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Diet PlanDiet, Food & Fitness

What is the Pritikin Diet ?

pritikin diet plan

pritikin diet plan

The Pritikin Diet Plan

The Pritikin Diet was invented by Nathan Pritikin in 1976 from his diet book “The Pritikin Program for Diet and Exercise” — where the dietary guidelines, also known as Very-Low-Fat-Diet and high fiber diet, are as follows:

  • less than 10% fat,
  • 10% to 15% protein and
  • the remainder 75% to 80% mainly from unrefined, complex carbohydrates.

In a small three-week study combining statins, diet, and vigorous exercise, those on the Pritikin diet resulted in a further 19% reduction in total cholesterol. There was also an incremental benefit in low-density lipoprotein (LDL) cholesterol and triglycerides for those on the diet, but also a slight reduction in HDL cholesterol 1.

In another very short-term therapy 2, 12-15 days, involving 67 subjects (52 men and 15 women; mean age, 60±10 years) diagnosed with Metabolic Syndrome. All subjects were obese (BMI ≥30 kg/m2). Forty (60%) of the subjects had diabetes, determined by either a prescription for medication to treat hyperglycemia or a fasting blood glucose of ≥126 mg/dL. Fifty-one (76%) subjects were taking medications to treat ≥1 clinical feature of the metabolic syndrome, which included antihypertensive, hypoglycemic, and lipid-lowering agents. At the start of treatment, subjects were taking an average of 2.4±2.0 medications. Subjects were excluded if they had severe uncontrolled hypertension (blood pressure ≥190/120 mm Hg), severe hypertriglyceridemia (serum triglycerides >600 mg/dL), untreated hypothyroidism, or were pregnant or lactating. Body weight; BMI; fasting blood glucose; blood pressure; and serum HDL-C, triglycerides, total cholesterol, and LDL-C concentrations were recorded at the beginning and end of 12–15 days of treatment.

All subjects 2 were treated with a comprehensive diet and exercise program. The diet consisted of 10%–15% of calories from fat, 15%–20% from protein (primarily from plants but also from seafood, fowl, or bison), and 65%–75% from carbohydrate (comprising whole grains, vegetables, and fruits), and contained about 40 g/1000 kcal of fiber. Salt was limited to <1500 mg/d and cholesterol to <100 mg/d. Alcohol, tobacco products, and caffeinated beverages were not allowed. Subjects were instructed on how to reduce total energy intake to achieve gradual weight loss, but meals and snacks were provided ad libitum, with the exception of seafood, fowl, or bison, which was limited to 3.5 oz/d. Subjects also received instruction for a personalized exercise program (outdoor walking plus daily exercise classes) for a total of 45–60 minutes of aerobic exercise performed to achieve a heart rate of 70%–85% of maximal heart rate.

At the end of treatment, 21 out of 67 (31%) subjects no longer met criteria for the metabolic syndrome 2. Moreover, with the exception of serum HDL-C concentration (serum “good” HDL cholesterol concentrations decreased in their subjects), all metabolic abnormalities of the metabolic syndrome improved with treatment. The number of medications used to treat the metabolic syndrome decreased in 16 (24%) subjects and increased in 6 (9%) subjects.

Comment: Due to the very small sample size, not a randomized clinical trial and the very short duration (12-15 days) of the study, we cannot determine whether Pritikin diet therapy is better (or worse) than other low-fat, high-fiber diets in treating obesity/overweight and Metabolic Syndrome X. Second, the participants in this study may not be representative of other patients who have the metabolic syndrome. Therefore, these results may not necessarily reflect the outcome that would be achieved in other subjects. Third, the duration of the intervention was approximately 2 weeks. Therefore, the results from this short-term intervention cannot determine long-term outcomes. For example, data from most lifestyle therapy interventions designed to achieve weight loss have shown that many obese persons who achieve short-term weight loss during therapy often regain much of their lost weight over time 3. Additional studies are needed to evaluate long-term effectiveness and compliance with this type of Pritikin diet and activity program.

There is currently no firm evidence 4 of the long-term (at least six months) effects of low-fat diets for otherwise healthy people with acquired, that is not familial hypercholesterolaemia (high cholesterol levels in the blood).

Since then his son Robert Pritikin has tweaked the Pritikin Diet concept to still a very low in fat diet (under 10% fat), but with a new focus on something he calls the calorie density solution.

There are 10 simple steps to The Pritikin Edge

  1. Start each meal with soup, salad, fruit, or whole grains. They fill you up, so you’re less likely to eat high-fat, high-calorie food.
  2. No more high-calorie drinks, especially soda. A daily glass of wine can be good for the heart, but skip most alcoholic beverages.
  3. Avoid high-calorie foods.
  4. Snack at set times and only on healthy foods.
  5. Choose whole, unprocessed foods as often as possible, and always avoid fast food.
  6. Exercise regularly, combining lots of walking with strength training.
  7. Go easy on meat, especially red meat. Instead, opt for fatty fish like salmon.
  8. Skip extra salt.
  9. Don’t smoke.
  10. Ease stress.

Foods on the Pritikin Diet include:

  • Fruits
  • Vegetables
  • Whole Grains like whole-wheat bread, brown rice, whole-wheat pasta, and oatmeal
  • Starchy Vegetables like potatoes, corn, and yams
  • Legumes such as beans (like black beans, pinto beans, and garbanzo beans); peas; and lentils
  • Lean Calcium-Rich Foods such as nonfat dairy milk, nonfat yogurt, and fortified soymilk
  • Fish (a rich source of omega-3-fatty acids)
  • Lean Sources of Protein (very low in saturated fat) such as skinless white poultry; lean red meat like bison and venison; and plant sources of protein, such as legumes and soy-based foods like tofu and edamame (soybeans)

Items to minimize include oils, refined sugars, salt, and refined grains. The plan recommends avoiding processed meats, foods high in saturated fat and those made with trans fat, organ meats, processed meats, and high-cholesterol foods like eggs.

1) Unrefined Complex Carbohydrates

5 or more servings daily of whole grains (such as whole wheat, oats, rye, brown rice, barley, quinoa, and millet); starchy vegetables (like potatoes, yams, and winter squashes); chestnuts; and legumes (beans, peas, and lentils). A serving is 1/2 cup cooked. For whole-grain bread products (like breads, bagels, and crackers), a serving is 1 ounce, which is generally half a common portion.

Limit refined grains (like white bread, white rice, and white pasta) as much as possible. But keep in mind that “white” does not necessarily mean “unhealthy.” There are many healthy foods that are white, such as cauliflower, white potatoes, jicama, and nonfat yogurt.

2) Vegetables

5 (preferably more) servings daily. A serving is 1 cup raw or 1/2 cup cooked. Enjoy a variety of colors, like dark green, yellow, red, and orange vegetables. The more vegetables and other low-calorie-dense foods you eat, the less need there is for counting calories. You’ll just naturally eat fewer calories, and shed excess weight.

3) Fruit

4 or more servings of whole fruits daily. For most fruits, a serving fits in your hand. Examples include all fresh and raw fruits, and frozen and canned fruits without added sugar. Enjoy whole fruit, not fruit juices. And don’t believe silly science that says fruit is fattening. To the contrary! People have shed 100 pounds and more with Pritikin’s fruit-rich diet.

4) Dairy and/or Dairy Substitutes

2 servings daily of dairy foods and/or dairy substitutes.

For dairy foods, choose from nonfat milk (1 cup), nonfat yogurt (3/4 cup), and nonfat varieties of ricotta and cottage cheese (1/2 cup). Choose plain nonfat milk, not flavored varieties like chocolate. Nonfat Lactaid is also acceptable.

For dairy milk substitutes, choose those that closely match the nutritional richness of nonfat cow’s milk for calcium, vitamins D and B-12, and protein. Optimal choices tend to be fortified soymilks (original or unsweetened). Almond and rice milks usually score well for calcium, D, and B-12, but poorly for protein. So if you drink a cup of almond or rice milk, add to your daily diet a lean, protein-rich food like 1/2 cup cooked legumes (beans) or 2 egg whites. Steer clear of coconut milk because it contains saturated fat.

For all dairy milk substitutes, make sure they contain very little or no added sugars, sodium, and saturated fat.

Note: Many plant foods are rich sources of calcium, such as leafy greens like collard greens, turnip greens and kale, as well as tofu and tempeh.

5) Protein-Rich Foods

  • Protein-Rich Animal Foods:
    Fish, White Poultry, Lean Meat

No more than 1 serving per day. A serving is about 3½ to 4 ounces cooked (the size of a deck of cards).

Below are fish/poultry/meat choices rated from “Best” to “Poor”:
Best: Omega-3-rich fish (such as salmon, sardines, herring, mackerel, and trout). Choose at least 2 times weekly. If you’re using canned fish, such as canned sardines, select very-low-sodium or no-salt-added varieties.
Good: Most other fish, plus shelled mollusks (clams, oysters, mussels, scallops).
Satisfactory: Crustaceans (shrimp, crab, lobster),
Poultry (white meat, skinless),
Game meat (bison, venison, elk), optimally free-range and grass-fed.
Poor: Red meat (beef, pork, veal, lamb, goat). For all red meat choices, select cuts that are under 30% fat.

For optimal heart-health results, limit “Satisfactory” choices to no more than 1 serving per week and “Poor” choices to no more than 1 serving per month.

Egg whites

Up to 2 daily. If you prefer egg whites instead of other land-based animal foods like white poultry and lean meat, you may eat more. About 7 egg whites is the protein equivalent of 1 serving of poultry or meat. Steer clear of egg yolks and their high dietary cholesterol.

  • Protein-Rich Plant Foods:
    Legumes like beans, peas, and lentils
    Soy products like tofu and edamame

For maximum cholesterol reduction and giving yourself the best chance at reversing atherosclerosis (heart disease), choose on most days protein-rich plant foods like beans instead of land-based animal foods like poultry and meat. And yes, you can get plenty of protein with a plant-based diet.

6) Miscellaneous Foods

  • Beverages

Water (plain, bottled, low-sodium, mineral); hot grain beverages (coffee substitutes); non-medicinal herbal teas (such as peppermint, rosehips, and chamomile); and cocoa – up to 2 tablespoons per day (use non-alkali processed cocoa). You do not have to drink large amounts of water daily. Simply drink when thirsty.

Caffeinated Beverages

If you choose to drink caffeinated beverages, Pritikin recommend green or black tea over coffee because of tea’s many health benefits. Pritikin also recommend moderation: no more than 400 mg of caffeine daily (the amount in about 4 eight-ounce cups of coffee or 8 eight-ounce cups of tea).

Coffee, both regular and decaf, does contain chemicals (diterpenes) that may modestly raise LDL cholesterol. However, by brewing with paper filters like paper cones or capsule filters like Keurig, the diterpenes are largely eliminated.

Alcoholic Beverages

Use in moderation or not at all. For women, up to 4 drinks per week, with no more than 1/2 to 1 drink per day. For men, up to 7 drinks per week, with no more than 1 to 2 drinks per day. A drink is approximately 5 oz of wine, 12 oz of beer, or 1½ oz of 80 proof liquor. Choose red wine over white wine, wine over beer, and either over liquor.

Herbs

Culinary herbs are rich sources of many beneficial phytonutrients, and are a good way to add flavor without extra calories, fat, or salt. Include at least 1 to 2 teaspoons of dried herbs or 1 to 2 tablespoons of fresh herbs each day.

Artificial Sweeteners

While artificial sweeteners have not been proven to aid weight loss, they may be of benefit to people with diabetes, elevated triglycerides, and those following the Pritikin Eating Plan to lose weight. Limit intake to no more than 10 to 12 packets per day. Sucralose (Splenda) and stevia (brand names include SweetLeaf and Truvia) appear to be the safest choices.

If You Want To Lose Weight

Go wild on vegetables. The more vegetables, including dark green, yellow, red, or orange vegetables, the better! They’re among the best foods for weight loss.

Limit calorie-dense foods such as dried grains (breads, crackers, cold cereals), dried fruits, nuts, and seeds. Avoid refined or concentrated sweeteners. They all pack a lot of calories into very small amounts of food. You’ll find it much easier to feel full and satisfied – and curb hunger – if you focus instead on high-water, high-fiber foods like cooked grains (such as oatmeal and brown rice), vegetables, and whole fruits. These foods are low in calorie density. You’ll eat more – and weigh less.

Steer clear of fruit and vegetable juices because they provide less satiety than whole fruits and vegetables.

Summary

The overall Pritikin diet is low in fat and high in fiber. The recommended foods are fruits, vegetables, low-fat dairy, legumes, lean protein, and fish. Items to minimize include oils, refined sugars, salt, and refined grains. The plan recommends avoiding processed meats, foods high in saturated fat and those made with trans fat, organ meats, processed meats, and high-cholesterol foods like eggs.

For weight loss, in recent randomized trial comparing 4 diet plans (Weight Watchers, Ornish, Pritikin and Atkins), found that all 4 diets resulted in modest statistically significant weight loss at 1 year, with no statistically significant differences between diets, but only for the minority of individuals who can sustain a high dietary adherence level.

Studies show the Pritikin diet can help reverse heart disease, lower cholesterol and blood pressure, and result in weight loss. Many people following the plan have been able to cut back on medications and use the diet and exercise program to help manage their condition.

It’s also heart-healthy. A Washington University School of Medicine study found that the Pritikin Program lowers many risk factors for heart disease, including weight (measured by body mass index, or BMI) and blood pressure.

References
  1. R.J. Barnard, S.C. DiLauro, S.B. Inkeles. Effects of intensive diet and exercise intervention in patients taking cholesterol-lowering drugsAm J Cardiol, 79 (1997), pp. 1112-1114
  2. Wiley Online Library. Effect of Short-Term Pritikin Diet Therapy on the Metabolic Syndrome. First published: September 2006. http://onlinelibrary.wiley.com/doi/10.1111/j.1559-4564.2006.05732.x/full
  3. Klein S, Wadden T, Sugerman HJ. AGA technical review on obesity. Gastroenterology. 2002;123:882–932. https://www.ncbi.nlm.nih.gov/pubmed/12198715
  4. Cochrane Review. 16 February 2011. Low-fat diets for acquired hypercholesterolaemia. http://www.cochrane.org/CD007957/ENDOC_low-fat-diets-for-acquired-hypercholesterolaemia
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Diet PlanDiet, Food & Fitness

Can a Ketogenic Diet help with my weight loss if I’m overweight or obese ?

ketogenic diet foods

What is a Ketogenic Diet ?

Developed in the 1920s by Hugh Conklin a faith healer in Battle Creek, Michigan, who treated children with epilepsy by depriving them of all foods by giving them nothing but water for up to 25 days, this diet induces a state that mimics carbohydrate starvation 1. As medications became available and effectively addressed seizures, the ketogenic diet fell out of favor. During the last few decades, researchers and clinicians have learned that ketogenic diet can be useful in children and adults with refractory epilepsy and a variety of other conditions. Once again, from the 1960s onwards keto diets — especially as the ‘Atkins Diet’ 2 have become widely known as one of the most common methods for obesity treatment. These very-low-carbohydrate high-fat ketogenic diets result in the substitution of ketone bodies as a source of energy (also known as nutritional ketosis). Ketosis is also produced during fasting periods, which is known as fasting ketosis. Recently, the combinations of nutritional ketosis and fasting ketosis, as well as nutritional ketosis alone, have been used as resources for weight loss management 3. Today’s ketogenic diet has been modified with scientifically proven adjustments to increase palatability and help with adherence. Recent work over the last decade or so has provided evidence of the therapeutic potential of ketogenic diets in many pathological conditions, such as diabetes, some forms of epilepsy, polycystic ovary syndrome, acne, Alzheimer’s disease, Parkinson’s disease, cancer, glaucoma, and the amelioration of respiratory and cardiovascular disease risk factors. And many Americans are using it to lose weight 4.

The keto diet (often termed ketogenic diet) is a very low-carb, high-fat diet that shares many similarities with the Atkins and low-carb diets. It lowers blood sugar and insulin levels, and shifts the body’s metabolism away from carbs and towards fat and ketones.

Ketogenic diet involves drastically reducing carbohydrate intake, and replacing it with fat. Ketogenic diets are characterized by a reduction in carbohydrates (usually to less than 50 g/day) and a relative increase in the proportions of protein and fat 5. The reduction in carbs puts your body into a metabolic state called ketosis. When this happens, your body becomes incredibly efficient at burning fat for energy. It also turns fat into ketones in the liver, which can supply energy for the brain.

This study showed that subjects with lower fat percentage, body mass index (BMI), as well as higher metabolic rate (resting energy expenditure or basal metabolic rate) have higher ketone buildups, and thus metabolize fat more efficiently 6. The researchers also found with no significant difference between ketogenic diets with 79% fat content and 90% fat content in terms of the significant buildup of ketone bodies.

The keto diet is so filling that you can lose weight without counting calories or tracking your food. One study found that people on a keto diet lost 2.2 times more weight than those on a calorie-restricted low-fat diet. Triglyceride and HDL cholesterol levels also improved. Another study found that participants on the keto diet lost 3 times more weight than those on the Diabetes USA recommended diet.

Keto diets can cause massive reductions in blood sugar and insulin levels. This, along with the increased ketones, has numerous health benefits.

When your body burns a lot of fat, the liver releases some of the partly burned fat molecules containing the last four carbon atoms into the blood; scientists call these ‘ketones’, which suppress hunger. It has been demonstrated that ketosis prevents the rise in ghrelin, a potent stimulator of appetite, which otherwise occurs as a result of diet-induced weight loss 7, that occurs after weight loss, and also increases the secretion of the hunger-suppressing hormone cholecystokinin 8. There are additional nutrient changes that contribute to hunger suppression 7. The heart and brain are the only two organs that can burn ketones, so the other possibility, not yet proven, is that ketones, like other nutrients such as glucose and fatty acids, suppress hunger directly by working on the brain. The point is that during the weight-loss phase, the patient can manufacture her own appetite suppressant. The downside to being mildly ketotic is that the ketones are volatile and, thus, can be breathed out, so the patient may develop ketotic breath. Chewing sugarless gum may help.

Although the mechanism of the efficacy of ketogenic diets has not been definitively established, it is commonly proposed that ketones suppress appetite 9 and it has been observed that study participants on ad libitum ketogenic diets spontaneously restrict their energy intake 10.

In the hypothalamus, signals from several circulating hormones and nutrients are integrated to regulate appetite and energy expenditure 11. The peripheral modulators of appetite include glucose 12, free-fatty acids 13 and hormones from the gastrointestinal tract, pancreas and adipose tissue, such as leptin, insulin, ghrelin, cholecystokinin (CCK), glucagon-like peptide 1, peptide YY and pancreatic polypeptide 14.

Following diet-induced weight loss, a number of compensatory changes occur, which encourage weight regain and restoration of energy balance. These include reductions in energy expenditure 15 and circulating leptin 16 and an increase in the orexigenic hormone ghrelin 17. It was recently reported that postprandial release of cholecystokinin (CCK), a hormone which increases satiety, was significantly reduced after diet-induced weight loss 18. However, when weight-reduced subjects were ketotic due to restriction of dietary carbohydrate, cholecystokinin (CCK) release was maintained at preweight loss concentrations, raising the possibility of an interaction between circulating ketones and hormonal mediators of appetite.

It should be noted that although the majority of randomized controlled trials comparing ad libitum ketogenic low-carbohydrate diets with low-fat diets have found greater weight loss over 6 months on the ketogenic diets, the difference is no longer observed at 12 months 19. In one of these studies, urinary ketones were significantly higher in the low-carbohydrate group compared with the low-fat group over the first 12 weeks, but no relationship was found between urinary ketones and weight loss 20. Only a minority of people have detectable urinary ketones after 3–6 months on low-carbohydrate diets 21.

Consumption of the ketogenic diet is characterized by elevated circulating levels of the ketone bodies acetoacetate, β-hydroxybutyrate and acetone, produced largely by the liver. During high rates of fatty acid oxidation, large amounts of acetyl-CoA are generated. These exceed the capacity of the tricarboxylic acid cycle and lead to the synthesis of the three ketone bodies within liver mitochondria. Plasma levels of ketone bodies rise, with acetoacetate and β-hydroxybutyrate increasing three-fold to four-fold from basal levels of 100 and 200 µmol/l, respectively 22. In the absence of glucose, the preferred source of energy (particularly of the brain), the ketone bodies are used as fuel in extrahepatic tissues. The ketone bodies are oxidized, releasing acetyl-CoA, which enters the tricarboxylic acid cycle.

In a double blind randomized crossover study on the safety and efficacy with respect to weight loss, cardiometabolic diseases of 21 days very low-calorie ketogenic diet (<800 kcal/day) 23.  The study showed ketogenic diet may be used safely for a limited period up to 3 weeks to stimulate fat loss, to ensure weight loss, ectopic and visceral fat reduction, improve metabolism, without running the risk of the possibility of cardiovascular, renal and hepatic diseases 23.

However, in a small New Zealand study involving 5 endurance athletes (4 females, 1 male), who underwent a 10-week ketogenic (low-carbohydrate, high-fat) dietary intervention 24. All five athletes reported experiencing reduced energy levels initially and an inability to easily undertake high intense bouts. On the other hand, each athlete reported experiencing enhanced well-being, included improved recovery, improvements in skin conditions, reduced body fat and reduced inflammation 24.

Figure 1. Metabolic pathway of ketosis and tissues ketolysis.

Metabolic pathway of ketosis and tissues ketolysis

Footnote: CHO = carbohydrate.

[Source 25 ]

What is Ketosis ?

Ketogenic diets have undoubtedly been shown to be effective, at least in the short to medium term, as a tool to fight obesity including people with diabetes who are obese 26, hyperlipidemia and some cardiovascular risk factors 27, 28, 29, but ketogenic diets also raise some concerns among physicians 30. Many of the concerns about the use of ketogenic diet as therapeutic tools could be attributed to a broad lack of knowledge about the physiological mechanisms involved. Ketogenic diets induce a metabolic condition named “physiological ketosis” by Hans Krebs, to distinguish it from the pathological diabetic ketosis 31.

Under normal diet with average amount of carbohydrates and fat, insulin activates key enzymes in the glucose metabolic pathways, which store energy derived from carbohydrates, and when there is an absence or scarcity of dietary carbohydrates the resulting reduced insulin level leads to a reduction in lipogenesis and fat accumulation. After a few days of fasting, or of drastically reduced carbohydrate consumption (below 20 g/day), glucose reserves become insufficient both for normal fat oxidation via the supply of oxaloacetate in the Krebs cycle (which gave origin to the phrase ‘fat burns in the flame of carbohydrate’) and for the supply of glucose to the central nervous system 32, 33, 34, 35.

Figure 2. Ketone bodies formation from acetyl-CoA (acetyl coenzyme A).

ketone bodies formation

Footnote: Ketone bodies are used by tissues as a source of energy through a pathway that involves firstly that β-hydroxybutyric acid is converted back to acetoacetate (AcAc) this is then transformed into acetoacetyl-CoA and, finally, two molecules of acetyl-CoA are formed from acetoacetyl-CoA which are used in the Krebs cycle.

[Source 25 ]

The central nervous system cannot use fat as an energy source; hence, it normally utilizes glucose. After 3–4 days without carbohydrate consumption the central nervous system is ‘forced’ to find alternative energy sources, and as demonstrated by the classic experiments of Cahill and colleagues 32 this alternative energy source is derived from the overproduction of acetyl coenzyme A (CoA). This condition seen in prolonged fasting, type 1 diabetes and high-fat/low-carbohydrate diets (aka ketogenic diets) leads to the production of higher-than-normal levels of so-called ketone bodies, that is, acetoacetate, β-hydroxybutyric acid and acetone—a process called ketogenesis and which occurs principally in the mitochondrial matrix in the liver (see Figures 1 and 2) 36. It is important to underline that the liver produces ketone bodies, but is unable to utilize them because the absence of the enzyme 3-ketoacyl CoA transferase required to convert acetoacetate into acetoacetyl-CoA 37. Even though the main ketone body produced in the liver is acetoacetate, the primary circulating ketone is β-hydroxybutyrate 38. Under normal conditions of adequate dietary carbohydrate, the production of free acetoacetic acid is negligible (<0.3 mmol/l) and this compound, transported via the blood stream, is rapidly metabolized by various tissues, especially the skeletal and heart muscles. In conditions of overproduction of acetoacetic acid, it accumulates above normal levels and part of it is converted to the other two ketone bodies leading to ketonemia and ketonuria (presence of ketone bodies in the blood and urine).

Acetone (produced by spontaneous decarboxylation of acetoacetate), being a very volatile compound, is eliminated mainly via respiration in the lungs, hence the characteristic sweet “fruity breath” breath odour of ketosis is caused by acetone, which, being a very volatile compound, is eliminated mainly via respiration in the lungs. Acetone even though it does not have metabolic functions, its presence can be useful from a clinical diagnostic point of view. Thus it is to be considered that a “fruity breath” indicates a condition of ketosis that could be physiological (fasting, low carbohydrate diet, post exercise) 38.

  • It should be stressed that, as shown in Table 1 (below), blood glucose level, even though reduced, remains within physiological levels 39. In fact glucose is formed from two sources: glucogenic amino acids and from glycerol liberated via lysis from triglycerides 40, 41. The importance of the second source increases progressively during the ketosis condition. In the first days of a ketogenic diet the main source of glucose is via neoglucogenesis from amino acids, as the days goes by, the contribution of amino acids decreases whilst the amount of glucose derived from glycerol increases. As a matter of fact glycerol (released from triglyceride hydrolysis) can produce more than 16% of glucose in the liver during a ketogenic diet and about 60% after a few days of complete fasting 40. According to Bortz (1972) of the new glucose formed from protein and glycerol 38% is derived from glycerol in the lean and 79% in the obese 42.

It is of interest to underline that ketosis is a metabolic state characteristic of humans. humans are more susceptible to ketosis-induced fasting due to the greater brain/body mass (this can explain why newborns are more susceptible to ketosis) 43. Under normal conditions the concentration of ketone bodies is very low (<0.3 mmol/L) compared to glucose (approx. 4 mmol) and since glucose and ketone bodies have a similar Km (or Michaelis-Menten constant) for glucose transport to the brain, the ketone bodies begin to be utilised as an energy source by the brain when they reach a concentration of about 4 mmol/L 44 which is close to the Km for the monocarboxylate transporter 45.

The ketone bodies begin to be utilized as an energy source by the central nervous system when they reach a concentration of about 4 mmol/l (normal level is <0.3 mmol/l), which is close to the Km for the monocarboxylate transporter 44, 36. The brain will use ketone bodies whenever provided with them (i.e., whenever blood ketone body levels rise). However, continued use of some glucose appears obligatory 46 and is supplied by way of hepatic gluconeogenesis 47.

Figure 3. Ketone bodies: Acetoacetate (AcAc) is the principal ketone body. It is produced and utilized during intermediary metabolism and other ketone bodies are derived from it. Acetone is produced by the spontaneous decarboxylation of acetoacetate and is important from the clinical point of view because it is responsible for the fruity sweet odour of infant ketoacidosis. β-Hydroxybutyric acid (3HB) is produced via the reduction of acetoacetate. From a strictly biochemical point of view it is not actually a ketone body since the ketonic moiety is reduced to a hydroxyl group; it is though grouped among the ketone bodies. 3HB is relatively stable biochemically and is transported to the tissues where it is reconverted to AcAc.

ketone bodies

[Source 25]

Ketosis or ketoacidosis is a physiological state of increased ketones (ketone bodies acetoacetate or acetoacetic acid, β-hydroxybutyrate or β -hydroxybutyric acid and acetone) level in the blood, blood and urine due to relatively high lipid oxidation rates. Detecting altered concentrations of ketones in the breath, blood, and urine is crucial for the diagnosis ketosis and for monitoring rapid and dramatic changes in ketones as valuable diagnoses for lipid oxidation and metabolism 48. Several studies have clearly demonstrated that metabolic imbalance in type I diabetes has led to ketoacidosis of blood, leading to elevated ketone levels with arterial pH < 7.3 and bicarbonate < 15 mEq/L, and causing arresting of major organ functions 49. In addition to acidosis, studies have also shown that elevated ketone levels are a natural metabolic response to negative energy balance, wherein caloric intake is smaller than total energy expenditure, and the body burns stored fat to produce the needed energy 50, leading to a state of ketosis known as fasting ketosis. Fasting ketosis has been used as an indicator of the effectiveness of weight loss 51, 52, 53. Ketosis also occurs in situations where caloric intake equals total energy expenditure, specifically in a diet that contains high percentage of fat (>60%) and/or low carbohydrate. This state of ketosis has been referred to as nutritional ketosis 54, 55. Nutritional ketosis has been investigated as a treatment for epilepsy because ketones are thought to provide energy to the brain, which reduces epileptic seizures 56, 57. In addition, ketosis buildup capability resulting from a combination of nutritional ketosis and fasting ketosis has been associated with weight loss efficiency and positive health outcomes 58, 59, 60.

Table 1. Blood levels during a normal diet, ketogenic diet and diabetic ketoacidosis 61
Blood levels
                  Normal diet               Ketogenic diet
            Diabetic ketoacidosis
Glucose (mg/dl)80–12065–80>300
Insulin (μU/l)6–236.6–9.4≅ 0
KB conc (mℳ/l)0.17/8>25
pH7.47.4<7.3

Note (Table 1): Nutritional and Functional Ketosis are completely physiological mechanism and it was the biochemist Hans Krebs who first referred to physiological ketosis to differentiate it from the pathological ketoacidosis seen in type 1 diabetes 62. In physiological ketosis (which occurs during very-low-calorie ketogenic diets and in fasting), ketonemia reaches maximum levels of 7/8 mmol/l (it does not go higher precisely because the central nervous system efficiently uses these molecules for energy in place of glucose) and with no change in pH, whereas in uncontrolled diabetic ketoacidosis it can exceed 20 mmol/l with a concomitant lowering of blood pH 63, 64. Diabetic patients know that the detection in their urine of the ketone bodies is a danger signal that their diabetes is poorly controlled. Indeed, in severely uncontrolled diabetes, if the ketone bodies are produced in massive supranormal quantities, they are associated with ketoacidosis. In this life-threatening complication of diabetes mellitus, the acids 3-hydroxybutyric acid and acetoacetic acid are produced rapidly, causing high concentrations of protons, which overwhelm the body’s acid-base buffering system 47.

It is very important to note the difference between physiological ketosis (nutritional and functional ketosis) and pathological ketoacidosis (diabetic ketoacidosis).

  • During Physiological ketosis, ketonemia (blood ketone bodies) reaches maximum levels of 7/8 mmol/L with no change in pH while in uncontrolled diabetic ketoacidosis it can exceed 20 mmol/L with a concomitant lowering of blood pH 65 (see Table 1). Blood levels of ketone bodies in healthy people do not exceed 8 mmol/L precisely because the central nervous system (brain) efficiently uses these molecules for energy in place of glucose.
  • Diabetic Ketoacidosis is an acute metabolic complication of type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. Diabetic ketoacidosis is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. It is characterized by hyperglycemia (high blood glucose), hyperketonemia (very high blood ketone bodies), and metabolic acidosis (low blood pH). Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. Diabetic ketoacidosis is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia 66.

Under physiological ketosis or ketoacidosis, the liver metabolizes fatty acids to produce two water-soluble types of ketones: acetoacetic acid and beta-hydroxybutyric acid. A third type of ketone, i.e., acetone, is also produced by the enzymatic decarboxylation of acetoacetic acid. Due to its high vapor pressure, acetone crosses the membrane barrier into the alveoli of the lung and the airway. As a result, acetone is normally present in breath. Since, the ketone level in breath is reflective of ketone level in blood, breath acetone has been considered a reliable indicator of ketosis in adults consuming ketogenic meals 22 and can be used to predict plasma ketone bodies in children with epilepsy who are on a ketogenic diet 67. Most recently, breath acetone has been used as a new ketone biomarker because it is non-invasive, convenient, and an accurate reflection of the body’s ketone level 68. Breath testing for ketones has a high sensitivity and specificity and appears to be a noninvasive, convenient, and repeatable method for the diagnosis and therapeutic monitoring of ketosis 69.

Furthermore, there are other conditions, such as exercise that can actually decrease ketone levels in the blood by using ketone as an energy source in the muscles 70, 71. For the reasons described above, ketone levels are affected by several factors, such as energy balance, diet composition, diabetes (type 1 and 2) and physical activities, all of which underscore the importance of determining the accuracy of ketone levels, blood glucose and pH levels.

Different Types of Keto Diets

There are several versions of the keto diet, the standard keto diet (SKD) is the most researched and most recommended.

  • Standard keto diet (SKD): This is a very low-carb, moderate-protein and high-fat diet. It typically contains 75% fat, 20% protein and only 5% carbs. A standard keto diet is an effective way to lose weight and lower risk factors for disease.
  • Cyclical keto diet (CKD): This diet involves periods of higher-carb refeeds, such as 5 keto days followed by 2 high-carb days.
  • Targeted keto diet (TKD): This diet allows you to add carbs around workouts.
  • High-protein keto diet: This is similar to a standard ketogenic diet, but includes more protein. The ratio is often 60% fat, 35% protein and 5% carbs.

However, only the standard and high-protein ketogenic diets have been studied extensively. Cyclical or targeted ketogenic diets are more advanced methods, and primarily used by bodybuilders or athletes. The information in this article mostly applies to the standard ketogenic diet, although many of the same principles also apply to the other versions.

**The keto diet can boost insulin sensitivity and cause fat loss, leading to drastic improvement for type 2 diabetes and prediabetes.

Studies have now shown that the diet can have benefits for a wide variety of different health conditions. However, keep in mind that research into many of these areas is far from conclusive:

  • Heart disease: The keto diet can improve risk factors like body fat, HDL levels, blood pressure and blood sugar.
  • Cancer: The diet is currently being used to treat several types of cancer and slow tumor growth.
  • Alzheimer’s disease: The diet may reduce symptoms of Alzheimer’s and slow down the disease’s progression.
  • Epilepsy: Research has shown that the ketogenic diet can cause massive reductions in seizures in epileptic children.
  • Parkinson’s disease: One study found that the diet helped improve symptoms of Parkinson’s disease.
  • Polycystic ovary syndrome: The ketogenic diet can help reduce insulin levels, which may play a key role in polycystic ovary syndrome.
  • Brain injuries: One animal study found that the diet can reduce concussions and aid recovery after brain injury.
  • Acne: Lower insulin levels and eating less sugar or processed foods may help improve acne.

ketogenic diet foods

The Ketogenic Diet Foods

Ketogenic diets allow you to eat real foods in the form of natural fats and protein (meat, fish, poultry) but  severely restrict the amount of carbohydrates (sugars and starches) you are allowed each day. The ketogenic diet is an extremely high-fat diet that requires you to eat four times as many fat calories as calories from protein or carbohydrates. A meal might include a small portion of chicken, a little bit of fruit, and a lot of fat, typically butter or cream. The diet was originally developed to treat epileptic children, but there are many variations, including the Atkins diet. You can achieve ketosis through fasting, diet, exogenous ketones, or a combination. Your brain and body begin to use ketones (derived from stored or ingested fat) for energy instead of blood sugar (glucose)—a state called ketosis.

On a standard American diet, carbohydrate intake is high (about 40-60% of calories) while fat intake, and especially saturated fat, is limited.  Diets high in carbohydrate have the effect of elevating blood sugar and a hormone called insulin over time. The chronically higher levels of blood sugar and insulin result in a condition called insulin resistance or metabolic syndrome which can result in constant hunger, weight gain and a long list of disease outcomes.

In contrast, carbohydrate intake on a keto diet is only about 2-4% of calories. By reducing the number of carbohydrates a person eats, the body is forced to burn fat for energy, a process called ketosis. This ketosis is the same process that kicks in when someone is fasting — on purpose or because of starvation. Fasting has been a traditional seizure treatment for centuries. When carb intake is low, meals are delicious and satiating.  Hunger goes away, and more importantly, this dietary change has some powerful and beneficial metabolic effects on the human body, in part because it lowers blood sugar and insulin levels. The bottom line here is that you can increase your energy and improve your health simply by changing the way you eat.

How Do Keto Diets Work ?

When carbohydrates (sugar and starch) are digested, they are broken down into blood sugar (glucose) in the body. More carbohydrate intake results in higher blood sugar.  If you reduce carb intake and instead eat more fat and protein, it results in a switch in metabolic pathways from using sugar as a primary fuel to burning stored and dietary fat as a primary fuel.

As more fat is burned, some of it is converted in ketone bodies.  As blood glucose and insulin levels drop and ketone levels rise, muscle tissue, including the heart, use the available fatty acids in the bloodstream as fuel and the brain begins using ketones as an energy source.  Being in this metabolic state of “nutritional ketosis” (blood sugar is low and ketone levels are moderate) has some powerful benefits. There is strong research evidence that low carb, high fat metabolic diets are effective for treating the following medical conditions:

  1. Diabetes:  Since carbohydrate is the prime driver of higher blood sugar, diet rich is carbohydrate is detrimental to diabetic health because it results in blood sugar spikes and crashes, which in turn causes a greater need for medication and insulin. Those high blood sugars also result in the complications of diabetes.  In contrast, a ketogenic diet reduces and in many cases, eliminates the need for diabetic medications and lowers the number of insulin units needed to manage blood sugar.  For people with Type 2 diabetes, ketogenic diets remove the trigger (carbohydrate intake) and reverse the underlying insulin resistance which causes the disease. As a result, long term complications are reversed or avoided.  Type 1 Diabetes: Lowering carb intake and increasing fat intake is also beneficial for people with Type 1 diabetes and can help lower the number and severity of hypoglycemic episodes, reduce HbA1c scores and minimize future complications.
  2. Weight Loss: There is no doubt that there is strong supportive evidence that the use of ketogenic diets – low carb, high fat keto diets have been proven in study after study as the best diet for weight loss because the diet works with your biochemistry instead of against it. However the mechanisms underlying the effects of ketogenic diets on weight loss is still a subject of debate. Atkins’ original hypothesis suggested that weight loss was induced by losing energy through excretion of ketone bodies, but more recently different hypotheses have been proposed: one hypothesis is that the use of energy from protein in ketogenic diet is an “expensive” process for the body and so can lead to a “waste of calories” and therefore increased weight loss compared to other “less expensive” diets. The hypothesized mechanisms of keto diet’s weight loss effects:
  3. (1)  Reduction in appetite due to higher satiety effect of proteins, effects on appetite control hormones and to a possible direct appetite suppressant action of the ketone bodies;
    (2) Reduction in lipogenesis and increased lipolysis;
    (3) Greater metabolic efficiency in consuming fats highlighted by the reduction in the resting respiratory quotient;
    (4) Increased metabolic costs of gluconeogenesis and the thermic effect of proteins.

The key to correctly implement a ketogenic diet plan is to remember that you are exchanging carbohydrate containing foods with a higher fat intake and a moderate protein consumption.

keto diet

Ketogenic Diet and Weight Loss

There is no doubt that there is strong supportive evidence that the use of ketogenic diets in weight-loss therapy is effective; however, there are contrasting theories regarding the mechanisms through which they work 38. Some researchers suggest that there are not in fact any metabolic advantages in low-carbohydrate diets and that weight loss results simply from reduced caloric intake, probably due to the increased satiety effect of protein 72. Others instead promote the hypothesis that there is indeed a distinct metabolic advantage, which has recently been explored in more detail, raising interest in the role of very-low-carbohydrate ketogenic diets 72 in weight loss and effects on metabolism in general 73. Adhering to these traditional concepts the US Department of Agriculture has concluded that diets, which reduce calories, will result in effective weight loss independent of the macronutrient composition, which is considered less important, even irrelevant 74, 75. In contrast with these views, the majority of studies demonstrate that subjects who follow a low-carbohydrate diet lose more weight during the first 3–6 months compared with those who follow balanced diets 76, 77, 78. One hypothesis is that the use of energy from proteins in very-low-carbohydrate ketogenic diets is an ‘expensive’ process for the body and so can lead to a ‘waste of calories’, and therefore increased weight loss compared with other ‘less-expensive’ diets 73, 79, 80. The average human body requires 60–65 g of glucose per day, and during the first phase of a diet very low in carbohydrates this is partially (16%) obtained from glycerol, with the major part derived via gluconeogenesis from proteins of either dietary or tissue origin 72. The energy cost of gluconeogenesis has been confirmed in several studies 81 and it has been calculated at ∼400–600 Kcal/day (due to both endogenous and food source proteins 79. Despite this, there is no direct experimental evidence to support this intriguing hypothesis; on the contrary, a recent study reported that there were no changes in resting energy expenditure after a very-low-carbohydrate ketogenic diets 82. A simpler, perhaps more likely, explanation for improved weight loss is a possible appetite-suppressant action of ketosis. The mechanism for this is not established but evidence supports direct action of ketone bodies together with modifications in levels of hormones, which influence appetite, such as ghrelin and leptin 83.

Here is the summary (listed in order of importance and available evidence) that the weight-loss effect of very-low-carbohydrate ketogenic diet seems to be caused by several factors:

  1. Reduction in appetite due to higher satiety effect of proteins 72, 84, effects on appetite control hormones 83 and to a possible direct appetite-suppressant action of the ketone bodies 85.
  2. Reduction in lipogenesis and increased lipolysis 86, 64.
  3. Reduction in the resting respiratory quotient and, therefore, greater metabolic efficiency in consuming fats 82, 87.
  4. Increased metabolic costs of gluconeogenesis and the thermic effect of proteins 73, 79.

Ketogenic Diet and Type 2 Diabetes

Recently, four studies have re-examined the effect of carbohydrate restriction on type 2 diabetes. One outpatient study enrolled 54 participants with type 2 diabetes (out of 132 total participants) and found that hemoglobin A1c improved to a greater degree over one year with a low-carbohydrate diet compared with a low-fat, calorie-restricted diet 88, 89. Another study enrolled 8 men with type 2 diabetes in a 5-week crossover outpatient feeding study that tested similar diets 90. The participants had greater improvement in glyco-hemoglobin (hemoglobin A1c or HbA1c) while on the low-carbohydrate diet than when on a eucaloric (normal calorie) low-fat diet. The third study was an inpatient feeding study in 10 participants with type 2 diabetes 91. After only 14 days, hemoglobin A1c improved from 7.3% to 6.8%. In the fourth study, 16 participants with type 2 diabetes who followed a 20% carbohydrate diet had improvement of hemoglobin A1c from 8.0% to 6.6% over 24 weeks 92. Only these latter three studies targeted glycemic control as a goal, and two of these were intensely-monitored efficacy studies in which all food was provided to participants for the duration of the study 90, 91. Three of the studies 91, 89, 92 mentioned that diabetic medications were adjusted but only one of them provided detailed information regarding these adjustments 92. This information is critical for patients on medication for diabetes who initiate a low-carbohydrate diet because of the potential for adverse effects resulting from hypoglycemia.

In studies that have evaluated well-formulated very-low-carbohydrate diets and documented high rates of compliance in individuals with type 2 diabetes, results have been nothing short of remarkable. Bistrian et al. 93 reported withdrawal of insulin and major weight loss in a matter of weeks in type 2 diabetes individuals who were fed a very-low-calorie and -carbohydrate diet. Gumbiner et al. 94 fed obese type 2 diabetes individuals two types of hypocaloric (650 kcal) diets for 3 weeks, they were matched for protein but one was much lower in carbohydrate content (24 vs 94 g/day). As expected, the lower-carbohydrate diet resulted in significantly greater levels of circulating ketones (∼3 mmol/l), which was strongly associated with a lower hepatic glucose output. Interestingly, there was a strong inverse correlation between circulating ketones and hepatic glucose output, suggesting that higher levels of ketones are associated with more favourable effects on glycaemic control in diabetics. More recently, Boden et al. 95 performed an in-patient study in obese type 2 diabetes individuals who were fed a low-carbohydrate (<20 g/day) diet for 2 weeks. Plasma glucose fell from 7.5 to 6.3 mmol/l, haemoglobin A1c decreased from 7.3 to 6.8% and there were dramatic improvements (75%) in insulin sensitivity.

In a longer study 96 obese type 2 diabetes individuals were prescribed a well-formulated ketogenic diet for 56 weeks, and significant improvements in both weight loss and metabolic parameters were seen at 12 weeks and continued throughout the 56 weeks as evidenced by improvements in fasting circulating levels of glucose (−51%), total cholesterol (−29%), high-density lipoprotein–cholesterol (63%), low-density lipoprotein–cholesterol (−33%) and triglycerides (−41%). It is of interest to note that in a recent study in overweight non-diabetic subjects, it was reported that during ketosis fasting glucose was not affected, but there was an elevation in post-prandial blood glucose concentration. This data suggests a different effect of ketosis on glucose homeostasis in diabetic and non-diabetic individuals 83. Other studies support the long-term efficacy of ketogenic diets in managing complications of type 2 diabetes 97, 98. Although significant reductions in fat mass often results when individuals restrict carbohydrate, the improvements in glycaemic control, haemoglobin A1c and lipid markers, as well as reduced use or withdrawal of insulin and other medications in many cases, occurs before significant weight loss occurs. Moreover, in normal caloric experiments individuals with insulin resistance showed dramatically improved markers of metabolic syndrome than diets lower in fat 99. It is interesting in this respect that a recent extremely large epidemiological study reported that diabetes risk is directly correlated, in an apparently causative manner, with sugar intake alone, independently of weight or sedentary lifestyle 100.

This very small study 101 with 28 subjects with type 2 diabetes (age 35–75 years; body mass index (BMI) >25 kg/m2; and fasting serum glucose >125 mg/dL or hemoglobin A1c >6.5% without medications, or treatment with oral hypoglycemic agents and/or insulin) to evaluate the effects of a low-carbohydrate, ketogenic diet (≤20 g carbohydrate per day and fats and oils were not restricted except that intake of trans fats was to be minimized) in overweight and obese patients with type 2 diabetes over 16 weeks. In summary, the low-carbohydrate ketogenic diet resulted in significant improvement of glycemia, as measured by fasting glucose and hemoglobin A1c, in patients with type 2 diabetes. More importantly, this improvement was observed while diabetes medications were reduced or discontinued in 17 of the 21 participants, and were not changed in the remaining 4 participants. Participants also experienced reductions in body weight, waist circumference, serum triglycerides and percent body fat but these improvements were moderate. While body weight decreased significantly (-8.5 kg) in these 21 diabetic participants, the mean weight loss was less compared with what we observed in the low-carbohydrate ketogenic diet participants of an another trial (-12.0 kg) 102. Most impressive is that improvement in hemoglobin A1c was observed 101.

In summary, individuals with metabolic syndrome, insulin resistance and type 2 diabetes (all diseases of carbohydrate intolerance) are likely to see symptomatic as well as objective improvements in biomarkers of disease risk if they follow a well-formulated very-low-carbohydrate diet. Glucose control improves not only because there is less glucose coming in, but also because systemic insulin sensitivity improves as well.

Ketogenic Diet and Cardiovascular disease

Several lines of evidence point to beneficial effects of low-carbohydrate ketogenic diet on cardiovascular risk factors. In the past, there have been doubts expressed about their long-term safety and increased effectiveness compared with ‘balanced’ diets 103, and clearly negative opinions regarding possible deleterious effects on triglycerides and cholesterol levels in the blood 104. However, the majority of recent studies seem instead to amply demonstrate that the reduction of carbohydrates to levels that induce physiological ketosis (see above ‘What is ketosis?’ section) can actually lead to significant benefits in blood lipid profiles 76, 78, 99. The low-carbohydrate ketogenic diet effect seems to be particularly marked on the level of blood triglycerides 87, 105, but there are also significant positive effects on total cholesterol reduction and increases in high-density (HDL) “good” cholesterol 87, 105, 106. Furthermore, low-carbohydrate ketogenic diet have been reported to increase the size and volume of low-density lipoprotein–cholesterol particles 106, which is considered to reduce cardiovascular disease risk, as smaller low-density lipoprotein particles have a higher atherogenicity. There are also direct diet-related effects on overall endogenous cholesterol synthesis. A key enzyme in cholesterol biosynthesis is 3-hydroxy-3-methylglutaryl–CoA reductase (the target for the drug statins), which is activated by insulin, which means that an increase in blood glucose and consequently of insulin levels will lead to increased endogenous cholesterol synthesis. A reduction in dietary carbohydrate will have the opposite effect and this, coupled with the additional inhibition by dietary cholesterol and fats on endogenous synthesis, is likely to be the mechanism via which physiological ketosis can improve lipid profiles. Hence, there are strong doubts about the negative effects of dietary fats when they are consumed as part of a low-carbohydrate ketogenic diet, on cholesterol and triglycerides blood levels, whereas there are strong pointers to the beneficial effects of low-carbohydrate ketogenic diet on these cardiovascular risk parameters 99, 105.

Ketogenic Diet and Polycystic Ovary Syndrome (PCOS)

Polycystic ovary syndrome (PCOS) is a common endocrine disorder in females, with a high prevalence (6–10%) 107; symptoms include hyperandrogenism, ovulatory dysfunction, obesity, insulin resistance and subfertility. Insulin resistance and related hyperinsulinaemia is actually a very common feature affecting about 65–70% of women with polycystic ovary syndrome 108; it is seen most frequently in obese patients, affecting 70–80%, compared with only 20–25% of lean polycystic ovary syndrome sufferers. Despite this observation, insulin resistance and hyperinsulinaemia appear to be linked to polycystic ovary syndrome independently of obesity, and modifications in the normal cellular mechanisms of insulin signalling have been demonstrated in both lean and obese patients. Furthermore, high blood levels of insulin can act by increasing androgenous hormonal stimulation of the ovarian theca cells as well as potentiating gonadotropin-stimulated ovarian androgen steroidogenesis—although recent data has suggested that the insulin-induced increase in ovarian hormone secretion is not accompanied by increased steroid metabolism 109. Hyperinsulinaemia may also affect the central actions of androgen by impairing progesterone inhibition of the gonadotropin-releasing hormone pulse generator 110. Insulin has also been shown to increase expression of adrenal steroidogenic enzyme mRNA47 as well as adrenal responsiveness to adrenocorticotropic hormone 111.

Women with PCOS frequently demonstrate many of the signs related to metabolic syndrome, such as insulin resistance, obesity, glucose intolerance, type 2 diabetes, dyslipidemia and also high levels of inflammation. Suggested treatments include those that reduce insulin resistance/hyperinsulinaemia, such as lifestyle modifications (exercise, diet and weight loss) and pharmacological treatments that include the administration of thiazolidinediones or metformin. It is evident that any interventions that improve insulinaemia and reduce body weight may also be effective in reducing hyperandrogenism, normalizing ovulation and reducing the various symptoms of polycystic ovary syndrome.

Finally, although we only have preliminary evidence of the positive effects of very-low-carbohydrate ketogenic diet in polycystic ovary syndrome 112, there are clear mechanisms that are consistent with the physiological plausibility of such dietary therapy.

Ketogenic Diet and Acne

In recent years there have been an increasing number of studies published, suggesting that at least for certain food types there is a nutritional influence on the development of acne. The negative effects seem to lie in the capacity of some foods/nutrients to stimulate proliferative pathways that in turn stimulate development of acne—suspect foods include those with a high glycaemic load and milk 61, 113, 114. Other evidence comes from several studies reporting that the prevalence of acne varies significantly between different populations and is substantially lower in non-Westernized populations that follow traditional diets 115, a common factor among these traditional diets being a low glycaemic load 116. Various studies have provided evidence that high-glycaemic-load diets are implicated in the cause of acne through their capacity to stimulate insulin, androgen bioavailability and insulin-like growth factor-1 (IGF-1) activity, whereas the beneficial effects of low-glycaemic-load diets, apart from weight and blood glucose levels, also include improved skin quality 114. The clinical and experimental evidence does in fact suggest ways in which insulin can increase androgen production and affect via induction of steroidogenic enzymes 117, the secretion by the pituitary gland of gonadotropin-releasing hormone and the production of sex hormone-binding globulin.48 Insulin is also able to reduce serum levels of IGF-binding protein-1 increasing the effect of IGF-1 118. These insulin-mediated actions can therefore influence diverse factors that underlie the development of acne such as:

  • The increased proliferation of basal keratinocytes within the pilosebaceous ducts.
  • An abnormal desquamation of the follicular epithelium.
  • Increased androgen-mediated sebum production.
  • Colonization of the stratum corneum by Propionibacterium acnes and consequent inflammation.46

In summary, there is persuasive, although not yet conclusive, clinical and physiological evidence that the ketogenic diet could be effective in reducing the severity and progression of acne and randomized clinical trials will be required to resolve the issue 61.

Ketogenic Diet and Epilepsy

At present, strong evidence exists that the ketogenic diet protects against seizures in children with difficult-to-treat epilepsy 119. Recent reports have raised the possibility that the diet may also improve the long-term outcome in such children 120, 121. In these studies, children with intractable epilepsy who remained on the ketogenic diet for more than 1 year and who experienced a good response to the diet, often had positive outcomes at long-term follow-up 3–6 years after the initiation of diet. Forty-nine percent of the children in this cohort experienced a nearly complete (≥ 90%) resolution in seizures. Surprisingly, even those children who remained on the diet for 6 months or less (most of these children terminated the diet because of an inadequate response) may have obtained a long-term benefit from exposure to the diet. Thirty-two percent of these children had a ≥ 90% decrease in their seizures and 22% became seizure free even without surgery. The diet also allowed a decrease or discontinuation of medications without a relapse in seizures. Of course, in the absence of a control group, it is not possible to be certain that the apparent good response in these children is simply the natural history of the epilepsy in the cohort studied, although these children had, by definition, intractable epilepsy before starting the diet. In any case, the results raise the possibility that the ketogenic diet, in addition to its ability to protect against seizures, may have disease-modifying activity leading to an improved long-term outcome. It is noteworthy that none of the currently marketed antiepileptic drugs has been demonstrated clinically to possess such a disease-modifying effect 122, 123. Determining whether the ketogenic diet truly alters long-term outcome will require prospective controlled trials.

Ketogenic Diet and Parkinson’s disease

One recently published clinical study tested the effects of the ketogenic diet on symptoms of Parkinson’s disease 124. In this uncontrolled study, Parkinson’s disease patients experienced a mean of 43% reduction in Unified Parkinson’s Disease Rating Scale scores after a 28-day exposure to the ketogenic diet. All participating patients reported moderate to very good improvement in symptoms. Further, as in Alzheimer’s disease, consumption of foods containing increased amounts of essential fatty acids has been associated with a lower risk of developing Parkinson’s disease 125.

Ketogenic Diet and Alzheimer’s disease

Recent studies have raised the possibility that the ketogenic diet could provide symptomatic benefit and might even be disease modifying in Alzheimer’s disease. Thus, Reger et al. 126 found that acute administration of medium-chain triglycerides improves memory performance in Alzheimer’s disease patients. Further, the degree of memory improvement was positively correlated with plasma levels of β-hydroxybutyrate produced by oxidation of the medium-chain triglycerides. If β-hydroxybutyrate is responsible for the memory improvement, then the ketogenic diet, which results in elevated β-hydroxybutyrate levels, would also be expected to improve memory function. When a patient is treated for epilepsy with the ketogenic diet, a high carbohydrate meal can rapidly reverse the antiseizure effect of the diet 127. It is therefore of interest that high carbohydrate intake worsens cognitive performance and behavior in patients with Alzheimer’s disease 128, 129.

It is also possible that the ketogenic diet could ameliorate Alzheimer’s disease by providing greater amounts of essential fatty acids than normal or high carbohydrate diets 130, 128. This is because consumption of foods or artificial supplements rich in essential fatty acids may decrease the risk of developing Alzheimer’s disease 131, 132, 133.

Keto Diet Plan

The ketogenic diet is a high-fat, adequate-protein, low-carbohydrate diet that actually originated as a tool for treating neurological diseases, such as difficult-to-control (refractory) epilepsy in children.

The ketogenic diet forces the body to burn fats rather than carbohydrates. Normally, the carbohydrates contained in food are converted into glucose, which is then transported around the body and is particularly important in fueling brain-function. However, if there is very little carbohydrate in the diet, the liver converts fat into fatty acids and ketone bodies. The ketone bodies pass into the brain and replace glucose as an energy source. An elevated level of ketone bodies in the blood, a state known as ketosis, leads to a reduction in the frequency of epileptic seizures. Over 20 studies show that this type of diet can also help you lose weight and improve health.

There are several reasons why a ketogenic diet is superior to a low-fat diet. One is the increased protein intake, which provides numerous benefits.

The increased ketones, lowered blood sugar levels and improved insulin sensitivity may also play a key role changes in metabolism, high blood sugar and impaired insulin function in pre-diabetes and type 2 diabetes. One study found that the ketogenic diet improved insulin sensitivity by a whopping 75%. The ketogenic diet can help you lose excess fat, which is closely linked to type 2 diabetes, prediabetes and metabolic syndrome.

Why high fat and moderate protein ?

Fats have little to no effect on blood sugar and insulin levels. Protein does affect both blood sugar and insulin. If you eat too much protein for your ideal body weight or lean muscle mass (usually more than 1.5-2.0 grams/kg lean body mass), it can spark gluconeogenesis and raise blood sugar and protein will also spike blood insulin levels temporarily.  Higher insulin levels will interfere with ketone body production. In addition, eating a diet that is heavy on lean protein (without enough fat) can make one sick with a condition know as “rabbit starvation”. Rabbit starvation is a form of malnutrition experienced by explorers and native Americans eating exclusively from the land during the Winter season, when food is scarce.  It’s caused by a diet restricted to the lean meat of animals such as rabbits, in the absence of carbohydrate and fat.

Other Beneficial Effects on Obesity

It could be argued that the ketogenic diet has beneficial effects other than simply fat and weight loss. For example, researchers recently suggested that ketones may protect from cognitive impairment caused by weight gain and obesity. Moreover there is some evidence that ketogenic diets may have positive effects on mood in overweight subjects. Even if during the very early phase of a ketogenic diet (the first 4 or 5 days) subjects may sometimes complain of lethargy this effect passes rapidly and subjects subsequently report an improved mood.

Although the prevalence of insulin resistance in obesity is not precisely known, it is quite common. Indeed the first demonstration of resistance to insulin stimulation of glucose uptake was obtained in obese subjects. A primary feature of insulin resistance is an impaired ability of muscle cells to take up circulating glucose and also the ability to slow down hepatic glucose output may be compromised. Thus, individuals with insulin resistance have a fundamental problem metabolizing dietary carbohydrate and will divert a greater proportion of dietary carbohydrate to the liver where much of it is converted to fat (i.e., de novo lipogenesis), as opposed to being oxidized for energy in skeletal muscle. Hence the beneficial effects of very low carbohydrate diets in obese subjects are not just a function of weight loss per se but also improved glycaemic control, haemoglobin A1c, and lipid markers, as well as reduced use or withdrawal of insulin and other medications in many cases, occurs before significant weight loss occurs. Moreover, in isocaloric experiments, individuals with insulin resistance showed dramatically improved markers of metabolic syndrome than diets lower in fat.

Is Keto Diet Safe for Obese People ?

In common opinion a low carbohydrate, high protein and fat diet is potentially unhealthy as it may cause a rise in LDL cholesterol and Triglycerides and this issue is of special importance in obese individuals. There are nevertheless several lines of evidence that point to beneficial effects of ketogenic diets on these cardiovascular risk factors. The majority of recent studies seem to amply demonstrate that the reduction of carbohydrates can actually lead to significant benefits in total cholesterol reduction, increases in HDL and reduction of blood triglycerides 25. Furthermore ketogenic diets have been reported to increase the size and volume of LDL-C particles which is considered to reduce cardiovascular disease risk since smaller LDL particles have a higher atherogenicity 134. There is a biochemical rational behind the effects of ketogenic diets on endogenous cholesterol synthesis. A key enyzme in cholesterol biosynthesis is HMGCoA reductase (the target for statins) which is activated by insulin, which means that an increase in blood glucose and consequently of insulin levels will lead to increased endogenous cholesterol synthesis. Thus a reduction in dietary carbohydrate together with a correct intake of cholesterol will lead to a inhibition of cholesterol biosynthesis.

Another point that must be addressed is the effect of ketogenic diet on bone metabolism. There is evidence showing that short-term ketogenic diets impair bone mass density and mechanical properties of bone in mouse. On the other side, it has been suggested recently that the metabolic complications of obesity, such as type 2 diabetes, metabolic syndrome, impaired glucose tolerance, insulin resistance, hyperglycemia, and inflammation may be associated with an increased risk of fracture and poor bone health. Moreover the amount of visceral fat (related to low-grade chronic inflammation) is associated with lower bone mineral density. Whilst there are many studies on the effects of dietary protein levels on bone metabolism in humans, the few investigations on ketogenic diet and bone metabolism were performed on epileptic children. But even in the recently published articles suggested that there is some negative effect on bone health. In any case in human subjects the effects of a very prolonged ketogenic diet are, as yet, not well investigated, for this reason, ketogenic diets may be used safely for a limited period (from 3 weeks to some months) to stimulate fat loss, improve metabolism and help the transition to a correct Mediterranean diet style.

Ketogenic Diet Risks

Regarding the overall safety of ketogenic diet on health there are differences in opinion about the research. Recently, in a recent systematic review based on limited observational studies, Noto and colleagues suggested a possible harmful effect of low carbohydrate/high protein diet (LC/HP) on health: i.e., an increase of all-cause mortality risk whilst there was no effect on cardiovascular disease mortality 135.

On the other hand, for example, a large European study demonstrated that an increase in protein content and a reduction in the glycaemic index led to better maintenance of weight loss without differences regarding adverse effects 136. The existing contradictory evidences on this matter lies in the complex interactions between low-carbohydrate diets and long-term outcomes. Moreover it is important to underline again that a ketogenic diet is not, strictly speaking, a low-carb/high-protein diet; ketogenic diet is mainly a very low carbohydrate diet with high fat and a normal amount of protein that produce a peculiar metabolic state that should not be assimilated to a low-carb/high-protein diet 25.

Some authors claims that a ketogenic diet could affect negatively glucose metabolism 137 but in the cited study the researchers performed the glucose load immediately after the cessation of the ketogenic diet. It is reasonable to suppose that after a period of very low carbohydrate diet there would be an increased glucose sensitively and for this reason is advisable to have a transition phase from ketogenic diet to a normal diet. Another very recently published study demonstrated that a long-term ketogenic diet (22 weeks) caused dyslipidemia, a pro-inflammatory state, signs of hepatic steatosis, glucose intolerance and a reduction in beta and alpha cell mass, without weight loss in mice 138. Two considerations need to be made: the first is that the induction of ketosis and the response to ketosis in man and mouse are quite different and this species metabolic differences could explain why insulin sensitivity is improved in man 139 whilst is decreased in mouse 140 after ketogenic diet. The second is that 22 weeks is a very long period for a mouse that could be compared to several years in human beings. In any case in human subjects the effects of a very prolonged ketogenic diet are, as yet, not well investigated, for this reason, ketogenic diet may be used safely for a limited period (from 3 weeks to some months) to stimulate fat loss, improve metabolism and help the transition to a correct Mediterranean diet style 141. Some authors report that a ketogenic diet induces a severe reduction of IGF-I concentration in rats 142 but, (even if we can compare rat with man) but as stated above a blunting of the IGF-1/AKT/mTOR pathway is not necessary a harmful effect.

Another point that must be addressed is the effect of ketogenic diet on bone metabolism. There is evidence showing that short-term ketogenic diets impair (suggested to be mediated by reductions in circulating IGF-1) bone mass density and mechanical properties of bone in mouse 143; whilst in humans very long term ketogenic diet in children with intractable epilepsy may lead to a progressive reduction of bone mineral content 144. The “caveat” about ketogenic diet and bone is indispensable but we have to take into account that the study of Bielohuby was performed on growing rats for 4 weeks (i.e., a very long time for humans) and thus we have to consider the above mentioned difference between ketosis in the two species, whilst the condition of a life-long ketogenic diet in intractable epilepsy is beyond the scope of this review.

On the other side, it has been suggested recently that the metabolic complications of obesity, such as type 2 diabetes, metabolic syndrome, impaired glucose tolerance, insulin resistance, hyperglycemia, and inflammation may be associated with an increased risk of fracture and poor bone health. Moreover the amount of visceral fat (related to low-grade chronic inflammation) is associated with lower bone mineral density 145. Whilst there are many studies on the effects of dietary protein levels on bone metabolism in humans the few investigations on ketogenic diet and bone metabolism were performed on epileptic children. But even if we assume a higher protein intake during a ketogenic diet (and it is not completely correct as stated above) recently published articles suggested that there is not a negative effect on bone health 146, 147, 148, 149.

Conclusions

A keto diet may provide many health benefits, especially with metabolic, neurological or insulin-related diseases. You should check with your physician if you have any concerns about starting a ketogenic diet plan with pre-existing health conditions, especially if those conditions involve kidney, bone or heart problems.  People with kidney disease should definitely consult with their physician about starting a ketogenic diet.

Talk to your doctor about implementing a ketogenic diet if you have any of these conditions:

  • History of pancreatitis
  • Active gall bladder disease
  • Impaired liver function
  • Impaired fat digestion
  • Poor nutritional status
  • Gastric bypass surgery
  • Abdominal tumors
  • Decreased gastrointestinal motility; this may be in conjunction with conventional cancer treatment and associated drugs
  • History of kidney failure
  • Pregnancy and lactation

A period of low carbohydrate ketogenic diet may help to control hunger and may improve fat oxidative metabolism and therefore reduce body weight. Furthermore new kinds of ketogenic diets using meals that mimic carbohydrate rich foods could improve the compliance to the diet. Attention should be paid to patient’s renal function and to the transition phase from ketogenic diet to a normal diet that should be gradual and well controlled. The duration of ketogenic diet may range from a minimum (to induce the physiological ketosis) of 2–3 weeks to a maximum (following a general precautionary principle) of many months (6–12 months). Correctly understood the ketogenic diet can be a useful tool to treat obesity in the hands of the physician.

References
  1. Conklin HW. Cause and treatment of epilepsy. J Am Osteopath Assoc. 1922;26;11-14
  2. Atkins RC. Dr Atkins’ Diet Revolution: The High Calorie Way to Stay Thin Forever. D. McKay Co: New York, NY, USA; 1972.
  3. Nutr J. 2015 Apr 22;14:41. doi: 10.1186/s12937-015-0028-x. Acetone as biomarker for ketosis buildup capability–a study in healthy individuals under combined high fat and starvation diets. https://www.ncbi.nlm.nih.gov/pubmed/25897953
  4. The Consultant Pharmacist®, Volume 32, Number 7, July 2017, pp. 388-396(9). https://doi.org/10.4140/TCP.n.2017.388. The Ketogenic Diet: Making a Comeback.https://www.ncbi.nlm.nih.gov/pubmed/28701250
  5. Prostaglandins Leukot Essent Fatty Acids. 2004 Mar;70(3):309-19. The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism. http://www.plefa.com/article/S0952-3278(03)00221-7/fulltext
  6. Prabhakar A, Quach A, Zhang H, et al. Acetone as biomarker for ketosis buildup capability – a study in healthy individuals under combined high fat and starvation diets. Nutrition Journal. 2015;14:41. doi:10.1186/s12937-015-0028-x. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4471925/
  7. Sumithran P, Prendergast LA, Delbridge E, et al. Ketosis and appetite-mediating nutrients and hormones after weight loss. Eur J Clin Nutr 2013;67:759–64. https://www.nature.com/articles/ejcn201390
  8. Chearskul S, Delbridge E, Shulkes A, Proietto J, Kriketos A. Effect of weight loss and ketosis on postprandial cholecystokinin and free fatty acid concentrations. Am J Clin Nutr 2008;87(5):1238–46.
  9. Astrup A, Meinert Larsen T, Harper A. Atkins and other low-carbohydrate diets: hoax or an effective tool for weight loss? Lancet 2004; 364: 897–899.
  10. Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP. Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med 2005; 142: 403–411.
  11. Schwartz MW, Woods SC, Porte D Jr., Seeley RJ, Baskin DG. Central nervous system control of food intake. Nature 2000; 404: 661–671.
  12. Campfield LA, Smith FJ, Rosenbaum M, Hirsch J. Human eating: evidence for a physiological basis using a modified paradigm. Neurosci Biobehav Rev 1996; 20: 133–137.
  13. Obici S, Feng Z, Morgan K, Stein D, Karkanias G, Rossetti L. Central administration of oleic acid inhibits glucose production and food intake. Diabetes 2002; 51: 271–275.
  14. Moran TH, Kinzig KP. Gastrointestinal satiety signals II. Cholecystokinin. Am J Physiol Gastrointest Liver Physiol 2004; 286: G183–G188.
  15. Leibel RL, Hirsch J. Diminished energy requirements in reduced-obese patients. Metabolism 1984; 33: 164–170.
  16. Geldszus R, Mayr B, Horn R, Geisthovel F, von zur Muhlen A, Brabant G. Serum leptin and weight reduction in female obesity. Eur J Endocrinol 1996; 135: 659–662.
  17. Cummings DE, Weigle DS, Frayo RS, Breen PA, Ma MK, Dellinger EP et al. Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. N Engl J Med 2002; 346: 1623–1630.
  18. Chearskul S, Delbridge E, Shulkes A, Proietto J, Kriketos A. Effect of weight loss and ketosis on postprandial cholecystokinin and free fatty acid concentrations. Am J Clin Nutr 2008; 87: 1238–1246.
  19. Nordmann AJ, Nordmann A, Briel M, Keller U, Yancy WS Jr., Brehm BJ et al. Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials. Arch Intern Med 2006; 166: 285–293
  20. Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003; 348: 2082–2090.
  21. Yancy WS Jr., Olsen MK, Guyton JR, Bakst RP, Westman EC. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med 2004; 140: 769–777.
  22. Breath acetone is a reliable indicator of ketosis in adults consuming ketogenic meals. Musa-Veloso K, Likhodii SS, Cunnane SC. Am J Clin Nutr. 2002 Jul; 76(1):65-70. https://www.ncbi.nlm.nih.gov/pubmed/12081817/
  23. C. Colica, G. Merra, A. Gasbarrini, A. De Lorenzo, G. Cioccoloni, P. Gualtieri, M.A. Perrone, S. Bernardini, V. Bernardo, L. Di Renzo, M. Marchetti. Eur Rev Med Pharmacol Sci 2017; 21 (9): 2274-2289. Efficacy and safety of very-low-calorie ketogenic diet: a double blind randomized crossover study. http://www.europeanreview.org/article/12711
  24. Caryn Zinn, Matthew Wood, Mikki Williden, Simon Chatterton, and Ed Maunder. J Int Soc Sports Nutr. 2017; 14: 22. Ketogenic diet benefits body composition and well-being but not performance in a pilot case study of New Zealand endurance athletes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5506682/
  25. Paoli A. Ketogenic Diet for Obesity: Friend or Foe? International Journal of Environmental Research and Public Health. 2014;11(2):2092-2107. doi:10.3390/ijerph110202092. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945587/
  26. Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials. Bueno NB, de Melo IS, de Oliveira SL, da Rocha Ataide T. Br J Nutr. 2013 Oct; 110(7):1178-87. https://www.ncbi.nlm.nih.gov/pubmed/23651522/
  27. Therapeutic role of low-carbohydrate ketogenic diet in diabetes. Al-Khalifa A, Mathew TC, Al-Zaid NS, Mathew E, Dashti HM. Nutrition. 2009 Nov-Dec; 25(11-12):1177-85. https://www.ncbi.nlm.nih.gov/pubmed/19818281/
  28. Beneficial effects of ketogenic diet in obese diabetic subjects. Dashti HM, Mathew TC, Khadada M, Al-Mousawi M, Talib H, Asfar SK, Behbahani AI, Al-Zaid NS. Mol Cell Biochem. 2007 Aug; 302(1-2):249-56. https://www.ncbi.nlm.nih.gov/pubmed/17447017/
  29. A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. Sharman MJ, Kraemer WJ, Love DM, Avery NG, Gómez AL, Scheett TP, Volek JS. J Nutr. 2002 Jul; 132(7):1879-85. https://www.ncbi.nlm.nih.gov/pubmed/12097663/
  30. Popular diets: a scientific review. Freedman MR, King J, Kennedy E. Obes Res. 2001 Mar; 9 Suppl 1():1S-40S. https://www.ncbi.nlm.nih.gov/pubmed/11374180/
  31. The regulation of the release of ketone bodies by the liver. Krebs HA. Adv Enzyme Regul. 1966; 4():339-54. https://www.ncbi.nlm.nih.gov/pubmed/4865971/
  32. Brain metabolism during fasting. Owen OE, Morgan AP, Kemp HG, Sullivan JM, Herrera MG, Cahill GF Jr. J Clin Invest. 1967 Oct; 46(10):1589-95. https://www.ncbi.nlm.nih.gov/pubmed/6061736/
  33. Amino acid metabolism during prolonged starvation. Felig P, Owen OE, Wahren J, Cahill GF Jr. J Clin Invest. 1969 Mar; 48(3):584-94. https://www.ncbi.nlm.nih.gov/pubmed/5773094/
  34. Owen O.E. Ketone bodies as a fuel for the brain during starvation. Biochem. Mol. Biol. Educ. 2005;33:246–251. doi: 10.1002/bmb.2005.49403304246.
  35. Liver and kidney metabolism during prolonged starvation. Owen OE, Felig P, Morgan AP, Wahren J, Cahill GF Jr. J Clin Invest. 1969 Mar; 48(3):574-83. https://www.ncbi.nlm.nih.gov/pubmed/5773093/
  36. Pathways and control of ketone body metabolism: on the fringe of lipid biochemistry. Fukao T, Lopaschuk GD, Mitchell GA. Prostaglandins Leukot Essent Fatty Acids. 2004 Mar; 70(3):243-51. https://www.ncbi.nlm.nih.gov/pubmed/14769483/
  37. Paoli A. Ketogenic Diet for Obesity: Friend or Foe? International Journal of Environmental Research and Public Health. 2014;11(2):2092-2107. doi:10.3390/ijerph110202092. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945587/
  38. Paoli A, Rubini A, Volek JS, Grimaldi KA. Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. European Journal of Clinical Nutrition. 2013;67(8):789-796. doi:10.1038/ejcn.2013.116. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826507/
  39. Targeting energy metabolism in brain cancer: review and hypothesis. Seyfried TN, Mukherjee P. Nutr Metab (Lond). 2005 Oct 21; 2:30. https://www.ncbi.nlm.nih.gov/pubmed/16242042/
  40. Lipolysis and gluconeogenesis from glycerol during weight reduction with very-low-calorie diets. Vazquez JA, Kazi U. Metabolism. 1994 Oct; 43(10):1293-9. https://www.ncbi.nlm.nih.gov/pubmed/7934983/
  41. Gluconeogenesis and energy expenditure after a high-protein, carbohydrate-free diet. Veldhorst MA, Westerterp-Plantenga MS, Westerterp KR. Am J Clin Nutr. 2009 Sep; 90(3):519-26. https://www.ncbi.nlm.nih.gov/pubmed/19640952/
  42. Glycerol turnover and oxidation in man. Bortz WM, Paul P, Haff AC, Holmes WL. J Clin Invest. 1972 Jun; 51(6):1537-46. https://www.ncbi.nlm.nih.gov/pubmed/5024045/
  43. Role of beta-hydroxybutyric acid in the central regulation of energy balance. Laeger T, Metges CC, Kuhla B. Appetite. 2010 Jun; 54(3):450-5. https://www.ncbi.nlm.nih.gov/pubmed/20416348/
  44. The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism. Veech RL. Prostaglandins Leukot Essent Fatty Acids. 2004 Mar; 70(3):309-19. https://www.ncbi.nlm.nih.gov/pubmed/14769489/
  45. Diet-induced ketosis increases monocarboxylate transporter (MCT1) levels in rat brain. Leino RL, Gerhart DZ, Duelli R, Enerson BE, Drewes LR. Neurochem Int. 2001 May; 38(6):519-27. https://www.ncbi.nlm.nih.gov/pubmed/11248400/
  46. Fernstrom JD, Fernstrom MH. Nutrition and the brain. In: Gibney MJ, Macdonald IA, Roche HM, editor. Nutrition & Metabolism. Oxford, UK: Blackwell Science; 2003. pp. 145–167.
  47. Manninen AH. Metabolic Effects of the Very-Low-Carbohydrate Diets: Misunderstood “Villains” of Human Metabolism. Journal of the International Society of Sports Nutrition. 2004;1(2):7-11. doi:10.1186/1550-2783-1-2-7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2129159/
  48. Ketone bodies, potential therapeutic uses. Veech RL, Chance B, Kashiwaya Y, Lardy HA, Cahill GF Jr. IUBMB Life. 2001 Apr; 51(4):241-7. https://www.ncbi.nlm.nih.gov/pubmed/11569918/
  49. Point-of-care blood ketone testing: screening for diabetic ketoacidosis at the emergency department. Charles RA, Bee YM, Eng PH, Goh SY. Singapore Med J. 2007 Nov; 48(11):986-9. https://www.ncbi.nlm.nih.gov/pubmed/17975686/
  50. Frayn K. Metabolic Regulation: A Human Perspective (3rd Edition) United Kingdom: Wiley-Blackwell; 2010.
  51. Brehm BJ, Seeley RJ, Daniels SR, D’Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metabol. 2003;88:1617–23. doi: 10.1210/jc.2002-021480. https://www.ncbi.nlm.nih.gov/pubmed/12679447
  52. Bueno NB, De Melo ISV, De Oliveira SL, Da Rocha Ataide T. Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: A meta-analysis of randomised controlled trials. Br J Nutr. 2013;110:1178–87. doi: 10.1017/S0007114513000548. https://www.ncbi.nlm.nih.gov/pubmed/23651522
  53. Paoli A, Rubini A, Volek J, Grimaldi K. Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. Eur J Clin Nutr. 2013;67:789–96. doi: 10.1038/ejcn.2013.116. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826507/
  54. Vining EP. The ketogenic diet. Adv Exp Med Biol. 2002;497:225–31. doi: 10.1007/978-1-4615-1335-3_20. https://www.ncbi.nlm.nih.gov/pubmed/11993735
  55. Garrow JS. Energy balance and obesity in man. Amsterdam/London: North-Holland Publishing Company; 1974.
  56. Keene DL. A systematic review of the use of the ketogenic diet in childhood epilepsy. Pediatr Neurol. 2006;35:1–5. doi: 10.1016/j.pediatrneurol.2006.01.005. https://www.ncbi.nlm.nih.gov/pubmed/16814077
  57. Mitchell G, Kassovska-Bratinova S, Boukaftane Y, Robert M, Wang S, Ashmarina L, et al. Medical aspects of ketone body metabolism. Clin Invest Med. 1995;18:193–216. https://www.ncbi.nlm.nih.gov/pubmed/7554586
  58. Mattson MP, Wan R. Beneficial effects of intermittent fasting and caloric restriction on the cardiovascular and cerebrovascular systems. J Nutr Biochem. 2005;16:129–37. doi: 10.1016/j.jnutbio.2004.12.007. https://www.ncbi.nlm.nih.gov/pubmed/15741046
  59. Johnson JB, Summer W, Cutler RG, Martin B, Hyun D-H, Dixit VD, et al. Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma. Free Radic Biol Med. 2007;42:665–74. doi: 10.1016/j.freeradbiomed.2006.12.005. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1859864/
  60. Yancy WS, Olsen MK, Guyton JR, Bakst RP, Westman EC. A Low-carbohydrate, ketogenic diet versus a Low-Fat diet to treat obesity and HyperlipidemiaA randomized. Controlled trial. Ann Intern Med. 2004;140:769–77. doi: 10.7326/0003-4819-140-10-200405180-00006. https://www.ncbi.nlm.nih.gov/pubmed/15148063
  61. Paoli A, Grimaldi K, Toniolo L, Canato M, Bianco A, Fratter A. Nutrition and acne: therapeutic potential of ketogenic diets. Skin Pharmacol Physiol. 2012;25:111–117. https://www.ncbi.nlm.nih.gov/pubmed/22327146
  62. Krebs HA. The regulation of the release of ketone bodies by the liver. Adv Enzyme Regul. 1966;4:339–354. https://www.ncbi.nlm.nih.gov/pubmed/4865971
  63. Paoli A, Canato M, Toniolo L, Bargossi AM, Neri M, Mediati M, et al. The ketogenic diet: an underappreciated therapeutic option. Clin Ter. 2011;162:e145–e153. https://www.ncbi.nlm.nih.gov/pubmed/22041813
  64. Cahill GF., Jr Fuel metabolism in starvation. Annu Rev Nutr. 2006;26:1–22. https://www.ncbi.nlm.nih.gov/pubmed/16848698
  65. Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. Paoli A, Rubini A, Volek JS, Grimaldi KA. Eur J Clin Nutr. 2013 Aug; 67(8):789-96. https://www.ncbi.nlm.nih.gov/pubmed/23801097/
  66. Merck Sharp & Dohme Corp., Merck Manual. Diabetic Ketoacidosis (DKA). https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/diabetes-mellitus-and-disorders-of-carbohydrate-metabolism/diabetic-ketoacidosis-dka
  67. Breath acetone predicts plasma ketone bodies in children with epilepsy on a ketogenic diet. Musa-Veloso K, Likhodii SS, Rarama E, Benoit S, Liu YM, Chartrand D, Curtis R, Carmant L, Lortie A, Comeau FJ, Cunnane SC. Nutrition. 2006 Jan; 22(1):1-8. https://www.ncbi.nlm.nih.gov/pubmed/16183255/
  68. Breath ketone testing: a new biomarker for diagnosis and therapeutic monitoring of diabetic ketosis. Qiao Y, Gao Z, Liu Y, Cheng Y, Yu M, Zhao L, Duan Y, Liu Y. Biomed Res Int. 2014;2014:869186. https://www.ncbi.nlm.nih.gov/pubmed/24900994/
  69. Biomed Res Int. 2014;2014:869186. doi: 10.1155/2014/869186. Epub 2014 May 11. Breath ketone testing: a new biomarker for diagnosis and therapeutic monitoring of diabetic ketosis. https://www.ncbi.nlm.nih.gov/pubmed/24900994/
  70. Post-exercise ketosis and the hormone response to exercise: a review. Koeslag JH. Med Sci Sports Exerc. 1982; 14(5):327-34. https://www.ncbi.nlm.nih.gov/pubmed/6759842/
  71. Sasaki H, Ishikawa S, Ueda H, KIMURA Y. Response of acetone in expired Air during graded and prolonged exercise. Adv Exerc Sports Physiol. 2011;16:97–100.
  72. Westerterp-Plantenga MS, Nieuwenhuizen A, Tome D, Soenen S, Westerterp KR. Dietary protein, weight loss, and weight maintenance. Annu Rev Nutr. 2009;29:21–41. https://www.ncbi.nlm.nih.gov/pubmed/19400750
  73. Feinman RD, Fine EJ. Nonequilibrium thermodynamics and energy efficiency in weight loss diets. Theor Biol Med Model. 2007;4:27. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1947950/
  74. Freedman MR, King J, Kennedy E. Popular diets: A scientific review. Obes Res. 2001;9 (Suppl 1:1S–40S. https://www.ncbi.nlm.nih.gov/pubmed/11374180
  75. Johnston BC, Kanters S, Bandayrel K, et al. Comparison of weight loss among named diet programs in overweight and obese adults: a network meta-analysis. JAMA. doi:10.1001/jama.2014.10397
  76. Brehm BJ, Seeley RJ, Daniels SR, D’Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab. 2003;88:1617–1623. https://www.ncbi.nlm.nih.gov/pubmed/12679447
  77. Gardner CD, Kiazand A, Alhassan S, Kim S, Stafford RS, Balise RR, et al. Comparison of the atkins, zone, ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: The A TO Z weight loss study: a randomized trial. JAMA. 2007;297:969–977. https://www.ncbi.nlm.nih.gov/pubmed/17341711
  78. Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, Witkow S, Greenberg I, et al. Weight loss with a low-carbohydrate, mediterranean, or low-fat diet. N Engl J Med. 2008;359:229–241. https://www.ncbi.nlm.nih.gov/pubmed/18635428
  79. Fine EJ, Feinman RD. Thermodynamics of weight loss diets. Nutr Metab (Lond) 2004;1:15. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC543577/
  80. Halton TL, Hu FB. The effects of high protein diets on thermogenesis, satiety and weight loss: a critical review. J Am Coll Nutr. 2004;23:373–385. https://www.ncbi.nlm.nih.gov/pubmed/15466943
  81. Veldhorst MA, Westerterp-Plantenga MS, Westerterp KR. Gluconeogenesis and energy expenditure after a high-protein, carbohydrate-free diet. Am J Clin Nutr. 2009;90:519–526.  https://www.ncbi.nlm.nih.gov/pubmed/19640952
  82. Paoli A, Grimaldi K, Bianco A, Lodi A, Cenci L, Parmagnani A. Medium term effects of a ketogenic diet and a mediterranean diet on resting energy expenditure and respiratory ratio BMC Proceedings 20126(Suppl 3): P37
  83. Sumithran P, Prendergast LA, Delbridge E, Purcell K, Shulkes A, Kriketos A, et al. Ketosis and appetite-mediating nutrients and hormones after weight loss Eur J Clin Nutr 2013;. e-pub ahead of print 1 May 2013; doi:10.1038/ejcn.2013.90. https://www.ncbi.nlm.nih.gov/pubmed/23632752
  84. Veldhorst M, Smeets A, Soenen S, Hochstenbach-Waelen A, Hursel R, Diepvens K, et al. Protein-induced satiety: effects and mechanisms of different proteins. Physiol Behav. 2008;94:300–307. https://www.ncbi.nlm.nih.gov/pubmed/18282589
  85. Johnstone AM, Horgan GW, Murison SD, Bremner DM, Lobley GE. Effects of a high-protein ketogenic diet on hunger, appetite, and weight loss in obese men feeding ad libitum. Am J Clin Nutr. 2008;87:44–55. https://www.ncbi.nlm.nih.gov/pubmed/18175736
  86. Veldhorst MA, Westerterp-Plantenga MS, Westerterp KR. Gluconeogenesis and energy expenditure after a high-protein, carbohydrate-free diet. Am J Clin Nutr. 2009;90:519–526. https://www.ncbi.nlm.nih.gov/pubmed/19640952
  87. Paoli A, Cenci L, Fancelli M, Parmagnani A, Fratter A, Cucchi A, et al. Ketogenic diet and phytoextracts comparison of the efficacy of mediterranean, zone and tisanoreica diet on some health risk factors. Agro Food Ind Hi-Tech. 2010;21:24.
  88. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Stern L, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams M, Gracely EJ, Samaha FF. Ann Intern Med. 2004 May 18; 140(10):778-85. https://www.ncbi.nlm.nih.gov/pubmed/15148064/
  89. A low-carbohydrate as compared with a low-fat diet in severe obesity. Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams T, Williams M, Gracely EJ, Stern L. N Engl J Med. 2003 May 22; 348(21):2074-81. https://www.ncbi.nlm.nih.gov/pubmed/12761364/
  90. Effect of a high-protein, low-carbohydrate diet on blood glucose control in people with type 2 diabetes. Gannon MC, Nuttall FQ. Diabetes. 2004 Sep; 53(9):2375-82. https://www.ncbi.nlm.nih.gov/pubmed/15331548/
  91. Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP. Ann Intern Med. 2005 Mar 15; 142(6):403-11. https://www.ncbi.nlm.nih.gov/pubmed/15767618/
  92. Lasting improvement of hyperglycaemia and bodyweight: low-carbohydrate diet in type 2 diabetes. A brief report. Nielsen JV, Jönsson E, Nilsson AK. Ups J Med Sci. 2005; 110(2):179-83. https://www.ncbi.nlm.nih.gov/pubmed/16075898/
  93. Nitrogen metabolism and insulin requirements in obese diabetic adults on a protein-sparing modified fast. Bistrian BR, Blackburn GL, Flatt JP, Sizer J, Scrimshaw NS, Sherman M. Diabetes. 1976 Jun; 25(6):494-504. https://www.ncbi.nlm.nih.gov/pubmed/1278601/
  94. Gumbiner B, Wendel JA, McDermott MP. Effects of diet composition and ketosis on glycemia during very-low-energy-diet therapy in obese patients with non-insulin-dependent diabetes mellitus. Am J Clin Nutr. 1996;63:110–115. https://www.ncbi.nlm.nih.gov/pubmed/8604657
  95. Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP. Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med. 2005;142:403–411. https://www.ncbi.nlm.nih.gov/pubmed/15767618
  96. Dashti HM, Al-Zaid NS, Mathew TC, Al-Mousawi M, Talib H, Asfar SK, et al. Long term effects of ketogenic diet in obese subjects with high cholesterol level. Mol Cell Biochem. 2006;286:1–9. https://www.ncbi.nlm.nih.gov/pubmed/16652223
  97. Yancy WS, Jr, Foy M, Chalecki AM, Vernon MC, Westman EC. A low-carbohydrate, ketogenic diet to treat type 2 diabetes. Nutr Metab (Lond) 2005;2:34. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1325029/
  98. Nielsen JV, Joensson EA. Low-carbohydrate diet in type 2 diabetes: Stable improvement of bodyweight and glycemic control during 44 months follow-up. Nutr Metab (Lond) 2008;5:14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2424054/
  99. Volek JS, Phinney SD, Forsythe CE, Quann EE, Wood RJ, Puglisi MJ, et al. Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Lipids. 2009;44:297–309. https://www.ncbi.nlm.nih.gov/pubmed/19082851
  100. Basu S, Yoffe P, Hills N, Lustig RH. The relationship of sugar to population-level diabetes prevalence: An econometric analysis of repeated cross-sectional data. PLoS One. 2013;8:e57873. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3584048/
  101. Yancy WS, Foy M, Chalecki AM, Vernon MC, Westman EC. A low-carbohydrate, ketogenic diet to treat type 2 diabetes. Nutrition & Metabolism. 2005;2:34. doi:10.1186/1743-7075-2-34.
  102. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Yancy WS Jr, Olsen MK, Guyton JR, Bakst RP, Westman EC. Ann Intern Med. 2004 May 18; 140(10):769-77. https://www.ncbi.nlm.nih.gov/pubmed/15148063/
  103. Nordmann AJ, Nordmann A, Briel M, Keller U, Yancy WS, Jr, Brehm BJ, et al. Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials. Arch Intern Med. 2006;166:285–293. https://www.ncbi.nlm.nih.gov/pubmed/16476868
  104. Blackburn GL, Phillips JC, Morreale S. Physician’s guide to popular low-carbohydrate weight-loss diets Cleve Clin J Med 200168761–766.768–9, 773–4. https://www.ncbi.nlm.nih.gov/pubmed/11563479
  105. Sharman MJ, Kraemer WJ, Love DM, Avery NG, Gomez AL, Scheett TP, et al. A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. J Nutr. 2002;132:1879–1885. https://www.ncbi.nlm.nih.gov/pubmed/12097663
  106. Volek JS, Sharman MJ, Forsythe CE. Modification of lipoproteins by very low-carbohydrate diets. J Nutr. 2005;135:1339–1342. https://www.ncbi.nlm.nih.gov/pubmed/15930434
  107. Fauser BC, Tarlatzis BC, Rebar RW, Legro RS, Balen AH, Lobo R, et al. Consensus on women’s health aspects of polycystic ovary syndrome (PCOS): the amsterdam ESHRE/ASRM-sponsored 3rd PCOS consensus workshop group Fertil Steril 20129728–38.e25. https://www.ncbi.nlm.nih.gov/pubmed/22153789
  108. DeUgarte CM, Bartolucci AA, Azziz R. Prevalence of insulin resistance in the polycystic ovary syndrome using the homeostasis model assessment. Fertil Steril. 2005;83:1454–1460. https://www.ncbi.nlm.nih.gov/pubmed/15866584
  109. Tosi F, Negri C, Perrone F, Dorizzi R, Castello R, Bonora E, et al. Hyperinsulinemia amplifies GnRH agonist stimulated ovarian steroid secretion in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2012;97:1712–1719. https://www.ncbi.nlm.nih.gov/pubmed/22419715
  110. Blank SK, McCartney CR, Chhabra S, Helm KD, Eagleson CA, Chang RJ, et al. Modulation of gonadotropin-releasing hormone pulse generator sensitivity to progesterone inhibition in hyperandrogenic adolescent girls–implications for regulation of pubertal maturation. J Clin Endocrinol Metab. 2009;94:2360–2366. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2708962/
  111. Moghetti P, Castello R, Negri C, Tosi F, Spiazzi GG, Brun E, et al. Insulin infusion amplifies 17 alpha-hydroxycorticosteroid intermediates response to adrenocorticotropin in hyperandrogenic women: apparent relative impairment of 17,20-lyase activity. J Clin Endocrinol Metab. 1996;81:881–886. https://www.ncbi.nlm.nih.gov/pubmed/8772544
  112. Mavropoulos JC, Yancy WS, Hepburn J, Westman EC. The effects of a low-carbohydrate, ketogenic diet on the polycystic ovary syndrome: a pilot study. Nutr Metab (Lond) 2005;2:35. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1334192/
  113. Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, et al. Origins and evolution of the western diet: health implications for the 21st century. Am J Clin Nutr. 2005;81:341–354. https://www.ncbi.nlm.nih.gov/pubmed/15699220
  114. Smith RN, Mann NJ, Braue A, Makelainen H, Varigos GA. The effect of a high-protein, low glycemic-load diet versus a conventional, high glycemic-load diet on biochemical parameters associated with acne vulgaris: A randomized, investigator-masked, controlled trial. J Am Acad Dermatol. 2007;57:247–256. https://www.ncbi.nlm.nih.gov/pubmed/17448569
  115. Smith R, Mann N. Acne in adolescence: a role for nutrition. Nutr Diet. 2007;64:S147–S149.
  116. Cordain L. Implications for the role of diet in acne. Semin Cutan Med Surg. 2005;24:84–91. https://www.ncbi.nlm.nih.gov/pubmed/16092796
  117. Kristiansen SB, Endoh A, Casson PR, Buster JE, Hornsby PJ. Induction of steroidogenic enzyme genes by insulin and IGF-I in cultured adult human adrenocortical cells. Steroids. 1997;62:258–265. https://www.ncbi.nlm.nih.gov/pubmed/9055386
  118. Powell DR, Suwanichkul A, Cubbage ML, DePaolis LA, Snuggs MB, Lee PD. Insulin inhibits transcription of the human gene for insulin-like growth factor-binding protein-1. J Biol Chem. 1991;266:18868–18876. https://www.ncbi.nlm.nih.gov/pubmed/1717456
  119. The efficacy of the ketogenic diet-1998: a prospective evaluation of intervention in 150 children. Freeman JM, Vining EP, Pillas DJ, Pyzik PL, Casey JC, Kelly LM. Pediatrics. 1998 Dec; 102(6):1358-63. https://www.ncbi.nlm.nih.gov/pubmed/9832569/
  120. The ketogenic diet: a 3- to 6-year follow-up of 150 children enrolled prospectively. Hemingway C, Freeman JM, Pillas DJ, Pyzik PL. Pediatrics. 2001 Oct; 108(4):898-905. https://www.ncbi.nlm.nih.gov/pubmed/11581442/
  121. The outcome of children with intractable seizures: a 3- to 6-year follow-up of 67 children who remained on the ketogenic diet less than one year. Marsh EB, Freeman JM, Kossoff EH, Vining EP, Rubenstein JE, Pyzik PL, Hemingway C. Epilepsia. 2006 Feb; 47(2):425-30. https://www.ncbi.nlm.nih.gov/pubmed/16499771/
  122. Current evidence indicates that antiepileptic drugs are anti-ictal, not antiepileptic. Schachter SC. Epilepsy Res. 2002 Jun; 50(1-2):67-70. https://www.ncbi.nlm.nih.gov/pubmed/12151118/
  123. Prevention of epilepsy after head trauma: do we need new drugs or a new approach? Benardo LS. Epilepsia. 2003; 44 Suppl 10():27-33. https://www.ncbi.nlm.nih.gov/pubmed/14511392/
  124. Treatment of Parkinson disease with diet-induced hyperketonemia: a feasibility study. Vanitallie TB, Nonas C, Di Rocco A, Boyar K, Hyams K, Heymsfield SB. Neurology. 2005 Feb 22; 64(4):728-30. https://www.ncbi.nlm.nih.gov/pubmed/15728303/
  125. Dietary fatty acids and the risk of Parkinson disease: the Rotterdam study. de Lau LM, Bornebroek M, Witteman JC, Hofman A, Koudstaal PJ, Breteler MM. Neurology. 2005 Jun 28; 64(12):2040-5. https://www.ncbi.nlm.nih.gov/pubmed/15985568/
  126. Effects of beta-hydroxybutyrate on cognition in memory-impaired adults. Reger MA, Henderson ST, Hale C, Cholerton B, Baker LD, Watson GS, Hyde K, Chapman D, Craft S. Neurobiol Aging. 2004 Mar; 25(3):311-4. https://www.ncbi.nlm.nih.gov/pubmed/15123336/
  127. Ketonemia and seizures: metabolic and anticonvulsant effects of two ketogenic diets in childhood epilepsy. Huttenlocher PR. Pediatr Res. 1976 May; 10(5):536-40. https://www.ncbi.nlm.nih.gov/pubmed/934725/
  128. High carbohydrate diets and Alzheimer’s disease. Henderson ST. Med Hypotheses. 2004; 62(5):689-700. https://www.ncbi.nlm.nih.gov/pubmed/15082091/
  129. A randomized, crossover trial of high-carbohydrate foods in nursing home residents with Alzheimer’s disease: associations among intervention response, body mass index, and behavioral and cognitive function. Young KW, Greenwood CE, van Reekum R, Binns MA. J Gerontol A Biol Sci Med Sci. 2005 Aug; 60(8):1039-45. https://www.ncbi.nlm.nih.gov/pubmed/16127110/
  130. Potential role of polyunsaturates in seizure protection achieved with the ketogenic diet. Cunnane SC, Musa K, Ryan MA, Whiting S, Fraser DD. Prostaglandins Leukot Essent Fatty Acids. 2002 Aug-Sep; 67(2-3):131-5. https://www.ncbi.nlm.nih.gov/pubmed/12324231/
  131. Prognosis of Alzheimer’s disease: the Rotterdam Study. Ruitenberg A, Kalmijn S, de Ridder MA, Redekop WK, van Harskamp F, Hofman A, Launer LJ, Breteler MM. Neuroepidemiology. 2001 Aug; 20(3):188-95. https://www.ncbi.nlm.nih.gov/pubmed/11490165/
  132. Fish, meat, and risk of dementia: cohort study. Barberger-Gateau P, Letenneur L, Deschamps V, Pérès K, Dartigues JF, Renaud S. BMJ. 2002 Oct 26; 325(7370):932-3. https://www.ncbi.nlm.nih.gov/pubmed/12399342/
  133. Dietary fats and the risk of incident Alzheimer disease. Morris MC, Evans DA, Bienias JL, Tangney CC, Bennett DA, Aggarwal N, Schneider J, Wilson RS. Arch Neurol. 2003 Feb; 60(2):194-200. https://www.ncbi.nlm.nih.gov/pubmed/12580703/
  134. Modification of lipoproteins by very low-carbohydrate diets. Volek JS, Sharman MJ, Forsythe CE. J Nutr. 2005 Jun; 135(6):1339-42. https://www.ncbi.nlm.nih.gov/pubmed/15930434/
  135. Low-carbohydrate diets and all-cause mortality: a systematic review and meta-analysis of observational studies. Noto H, Goto A, Tsujimoto T, Noda M. PLoS One. 2013; 8(1):e55030. https://www.ncbi.nlm.nih.gov/pubmed/23372809/
  136. Diets with high or low protein content and glycemic index for weight-loss maintenance. Larsen TM, Dalskov SM, van Baak M, Jebb SA, Papadaki A, Pfeiffer AF, Martinez JA, Handjieva-Darlenska T, Kunešová M, Pihlsgård M, Stender S, Holst C, Saris WH, Astrup A, Diet, Obesity, and Genes (Diogenes) Project. N Engl J Med. 2010 Nov 25; 363(22):2102-13. https://www.ncbi.nlm.nih.gov/pubmed/21105792/
  137. Impaired glucose tolerance in rats fed low-carbohydrate, high-fat diets. Bielohuby M, Sisley S, Sandoval D, Herbach N, Zengin A, Fischereder M, Menhofer D, Stoehr BJ, Stemmer K, Wanke R, Tschöp MH, Seeley RJ, Bidlingmaier M. Am J Physiol Endocrinol Metab. 2013 Nov 1; 305(9):E1059-70. https://www.ncbi.nlm.nih.gov/pubmed/23982154/
  138. Long-term ketogenic diet causes glucose intolerance and reduced β- and α-cell mass but no weight loss in mice. Ellenbroek JH, van Dijck L, Töns HA, Rabelink TJ, Carlotti F, Ballieux BE, de Koning EJ. Am J Physiol Endocrinol Metab. 2014 Mar 1; 306(5):E552-8. https://www.ncbi.nlm.nih.gov/pubmed/24398402/
  139. Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Volek JS, Phinney SD, Forsythe CE, Quann EE, Wood RJ, Puglisi MJ, Kraemer WJ, Bibus DM, Fernandez ML, Feinman RD. Lipids. 2009 Apr; 44(4):297-309. https://www.ncbi.nlm.nih.gov/pubmed/19082851/
  140. Induction of ketosis in rats fed low-carbohydrate, high-fat diets depends on the relative abundance of dietary fat and protein. Bielohuby M, Menhofer D, Kirchner H, Stoehr BJ, Müller TD, Stock P, Hempel M, Stemmer K, Pfluger PT, Kienzle E, Christ B, Tschöp MH, Bidlingmaier M. Am J Physiol Endocrinol Metab. 2011 Jan; 300(1):E65-76. https://www.ncbi.nlm.nih.gov/pubmed/20943751/
  141. Long term successful weight loss with a combination biphasic ketogenic Mediterranean diet and Mediterranean diet maintenance protocol. Paoli A, Bianco A, Grimaldi KA, Lodi A, Bosco G. Nutrients. 2013 Dec 18; 5(12):5205-17. https://www.ncbi.nlm.nih.gov/pubmed/24352095/
  142. Lack of dietary carbohydrates induces hepatic growth hormone (GH) resistance in rats. Bielohuby M, Sawitzky M, Stoehr BJ, Stock P, Menhofer D, Ebensing S, Bjerre M, Frystyk J, Binder G, Strasburger C, Wu Z, Christ B, Hoeflich A, Bidlingmaier M. Endocrinology. 2011 May; 152(5):1948-60. https://www.ncbi.nlm.nih.gov/pubmed/21427215/
  143. Short-term exposure to low-carbohydrate, high-fat diets induces low bone mineral density and reduces bone formation in rats. Bielohuby M, Matsuura M, Herbach N, Kienzle E, Slawik M, Hoeflich A, Bidlingmaier M. J Bone Miner Res. 2010 Feb; 25(2):275-84. https://www.ncbi.nlm.nih.gov/pubmed/19653818/
  144. Progressive bone mineral content loss in children with intractable epilepsy treated with the ketogenic diet. Bergqvist AG, Schall JI, Stallings VA, Zemel BS. Am J Clin Nutr. 2008 Dec; 88(6):1678-84. https://www.ncbi.nlm.nih.gov/pubmed/19064531/
  145. Divergent effects of obesity on bone health. Gower BA, Casazza K. J Clin Densitom. 2013 Oct-Dec; 16(4):450-4. https://www.ncbi.nlm.nih.gov/pubmed/24063845/
  146. Effects of a high protein diet on body weight and comorbidities associated with obesity. Clifton P. Br J Nutr. 2012 Aug; 108 Suppl 2():S122-9. https://www.ncbi.nlm.nih.gov/pubmed/23107523/
  147. Diet-induced weight loss: the effect of dietary protein on bone. Tang M, O’Connor LE, Campbell WW. J Acad Nutr Diet. 2014 Jan; 114(1):72-85. https://www.ncbi.nlm.nih.gov/pubmed/24183993/
  148. The effect of a low-carbohydrate diet on bone turnover. Carter JD, Vasey FB, Valeriano J. Osteoporos Int. 2006; 17(9):1398-403. https://www.ncbi.nlm.nih.gov/pubmed/16718399/
  149. Effect of protein intake on bone mineralization during weight loss: a 6-month trial. Skov AR, Haulrik N, Toubro S, Mølgaard C, Astrup A. Obes Res. 2002 Jun; 10(6):432-8. https://www.ncbi.nlm.nih.gov/pubmed/12055318/
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Diet PlanDiet, Food & Fitness

What is a Standard Serve Sizes ?

what is a serving size

What is a Serving Size

According to the 2015-2020 Dietary Guidelines for Americans, a serving size is defined as a standardized amount of a food, such as a cup or an ounce, used in providing information about a food within a food group, such as in dietary guidance. Serving size on the Nutrition Facts label is determined based on the Reference Amounts Customarily Consumed for foods that have similar dietary usage, product characteristics, and customarily consumed amounts for consumers to make “like product” comparisons 1.

The American Heart Association define serving size is the amount of food listed on a product’s Nutrition Facts label. So all of the nutritional values you see on the label are for the serving size the manufacturer suggests on the package 2.

The Australian Dietary Guidelines defines the ‘serve size’ as a set amount stated in the Australian Dietary Guidelines and this doesn’t change.

In Dietitians of Canada’s Food Guide, serving size refers to a recommended amount of food for “one Food Guide Serving.” A Food Guide Serving may not be the same as the amount of food you put on your plate. For example, one Food Guide Serving equals 1/2 cup (125 mL) of vegetables. On a Nutrition Facts table, the serving size refers to a specific amount of food that all of the label information is based on 3.

A Dietitians of Canada’s Food Guide Serving is simply a reference amount. It helps you understand how much food is recommended every day from each of the four food groups. In some cases, a Dietitians of Canada’s Food Guide Serving may be close to what you eat, such as an apple. In other cases, such as rice or pasta, you may serve yourself more than one Dietitians of Canada’s Food Guide Serving.

Look at the examples below to find out how much food is equal to one Food Guide Serving.

Examples of one Dietitians of Canada’s Food Guide Serving are:

Vegetables and Fruit

  • 125 mL (½ cup) fresh, frozen or canned
  • vegetable or fruit or 100% juice
  • 250 mL (1 cup) leafy raw vegetables or
  • salad
  • 1 piece of fruit

Grain Products

  • 1 slice (35 g) bread or ½ bagel (45 g)
  • ½ pita (35 g) or ½ tortilla (35 g)
  • 125 mL (½ cup) cooked rice, pasta, or couscous
  • 30 g cold cereal or 175 mL (¾ cup) hot cereal

Milk and Alternatives

  • 250 mL (1 cup) milk or fortified soy beverage
  • 175 g (¾ cup) yogurt
  • 50 g (1 ½ oz.) cheese

Meat and Alternatives

  • 75 g (2 ½ oz.)/125 mL (½ cup) cooked fish, shellfish, poultry or lean meat
  • 175 mL (¾ cup) cooked beans
  • 2 eggs
  • 30 mL (2 Tbsp) peanut butter

A recommended serving size is the amount of each food that you are supposed to eat during a meal or snack 4.

And a Portion Size—is defined as the amount of a food served or consumed in one eating occasion. A portion is not a standardized amount and the amount considered to be a portion is subjective and varies 1. Since the 1970s, portion sizes have increased both for food eaten at home and for food eaten away from home, in adults and children 5, 6. Short-term studies clearly demonstrate that when people are served larger portions, they eat more. One study, for example, gave moviegoers containers of stale popcorn in either large or medium-sized buckets; people reported that they did not like the taste of the popcorn-and even so, those who received large containers ate about 30 percent more popcorn than those who received medium-sized containers 7. Another study showed that people given larger beverages tended to drink significantly more, but did not decrease their subsequent food consumption 8. An additional study provided evidence that when provided with larger portion sizes, people tended to eat more, with no decrease in later food intake 9. Several well-controlled, laboratory-based studies have shown that providing older children and adults with larger food portions can lead to significant increases in energy intake. This effect has been demonstrated for snacks and a variety of single meals and shown to persist over a 2-day period. Despite increases in intake, individuals presented with large portions generally do not report or respond to increased levels of fullness, suggesting that hunger and satiety signals are ignored or overridden 10.

Once you understand the difference a serving size and portion size, it’s easier to determine how much to serve and easier to teach kids the difference between the two. Learn some suggested servings from each food groups you and your kids can eat at mealtime or between meals.

The following serving sizes are derived from the Australian Dietary Guidelines 11.

1) What is a serve of vegetables ?

A standard serve is about 75g (100–350kJ) or:

  • ½ cup cooked green or orange vegetables (for example, broccoli, spinach, carrots or pumpkin)
  • ½ cup cooked dried or canned beans, peas or lentils (preferably with no added salt)
  • 1 cup green leafy or raw salad vegetables
  • ½ cup sweet corn
  • ½ medium potato or other starchy vegetables (sweet potato, taro or cassava)
  • 1 medium tomato

vegetable serving size

2) What is a serve of fruit ?

A standard serve is about 150g (350kJ) or:

  • 1 medium apple, banana, orange or pear
  • 2 small apricots, kiwi fruits or plums
  • 1 cup diced or canned fruit (no added sugar)

Or only occasionally:

  • 125ml (½ cup) fruit juice (no added sugar)
  • 30g dried fruit (for example, 4 dried apricot halves, 1½ tablespoons of sultanas)

fruit serving size

3) What is a serve of rice, pasta and grain* (cereal) food ?

A standard serve is (500kJ) or:

  • 1 slice (40g) bread
  • ½ medium (40g) roll or flat bread
  • ½ cup (75-120g) cooked rice, pasta, noodles, barley, buckwheat, semolina, polenta, bulgur or quinoa
  • ½ cup (120g) cooked porridge
  • ²/³ cup (30g) wheat cereal flakes
  • ¼ cup (30g) muesli
  • 3 (35g) crispbreads
  • 1 (60g) crumpet
  • 1 small (35g) English muffin or scone

*Grain (cereal) foods, mostly wholegrain and/or high cereal fibre varieties

rice and grains serving size

4) How much is a serve of lean meat and chicken, fish, eggs, nuts and seeds, and legumes/beans ?

A standard serve is (500–600kJ):

  • 65g cooked lean red meats such as beef, lamb, veal, pork, goat or kangaroo (about 90-100g raw)
  • 80g cooked lean poultry such as chicken or turkey (100g raw)
  • 100g cooked fish fillet (about 115g raw) or one small can of fish
  • 2 large (120g) eggs
  • 1 cup (150g) cooked or canned legumes/beans such as lentils, chick peas or split peas (preferably with no added salt)
  • 170g tofu
  • 30g nuts, seeds, peanut or almond butter or tahini or other nut or seed paste (no added salt)*

*Only to be used occasionally as a substitute for other foods in the group (note: this amount for nuts and seeds gives approximately the same amount of energy as the other foods in this group but will provide less protein, iron or zinc).

serving size of chicken

5) How much is a serve of milk*, yoghurt*, cheese* and/or alternatives ?

A standard serve is (500–600kJ):

  • 1 cup (250ml) fresh, UHT long life, reconstituted powdered milk or buttermilk
  • ½ cup (120ml) evaporated milk
  • 2 slices (40g) or 4 x 3 x 2cm cube (40g) of hard cheese, such as cheddar
  • ½ cup (120g) ricotta cheese
  • ¾ cup (200g) yoghurt
  • 1 cup (250ml) soy, rice or other cereal drink with at least 100mg of added calcium per 100ml

*Choose mostly reduced fat

If you do not eat any foods from this group, try the following foods, which contain about the same amount of calcium as a serve of milk, yoghurt, cheese or alternatives (note: the kilojoule content of some of these serves (especially nuts) is higher so watch this if trying to lose weight).

  • 100g almonds with skin
  • 60g sardines, canned in water
  • ½ cup (100g) canned pink salmon with bones
  • 100g firm tofu (check the label as calcium levels vary)

serving size of dairy, yogurt and cheese

How many kilojoules are in a serve of each food group ?

  • Not all food groups provide the same number of kilojoules (kJ) per serve.

A serve of the grain (cereals) food group; milks/yoghurt/cheese and /or alternatives group; lean meats, poultry, fish, eggs and/or alternatives group; will provide about 500-600kJ.

About 2 serves of fruit, and from 2 serves (for starchy vegetables) to 5 serves (of green leafy vegetables) of different varieties in the vegetables group will provide about 500-600kJ. This is one reason that it makes good sense to fill up on leafy green and other lower kilojoule vegetables when you are trying to lose weight.

Also, while discretionary food serves can have similar kilojoules (about 600kJ) to a serve of the five food groups, they are usually much smaller and less filling, don’t provide you with the fibre and nutrients you need and contain too much saturated fat, added sugars and added salt for good health.

Recommended number of serves for adults

The dietary patterns in the table below provide the nutrients and energy needed by all men and women of average height with sedentary to moderate activity levels. Additional serves of the Five Food Groups or unsaturated spreads and oils or discretionary choices are needed only by adults who are taller, more active or in the higher end of a particular age band, to meet additional energy requirements.

Recommended average daily number of serves from each of the five food groups*Additional serves for taller or more active men and women
Vegetables & legumes/beansFruitGrain (cereal) foods, mostly wholegrainLean meat and poultry, fish, eggs, nuts and seeds, and legumes/beansMilk, yoghurt, cheese and/or alternatives (mostly reduced fat)Approx. number of additional serves from the five food groups or discretionary choices
Men
19-5062632 ½0-3
51-705 ½262 ½2 ½0-2 ½
70+524 ½2 ½3 ½0-2 ½
Women
19-505262 ½2 ½0-2 ½
51-70524240-2 ½
70+523240-2
Pregnant528 ½3 ½2 ½0-2 ½
Lactating7 ½292 ½2 ½0-2 ½

* Includes an allowance for unsaturated spreads or oils, nuts or seeds (4 serves [28-40g] per day for men less than 70 years of age; 2 serves [14-20g] per day for women and older men.)

(Source: National Health and Medical Research Council of Australia. Recommended number of serves for adults. 12).

Recommended number of serves for children, adolescents and toddlers

The dietary patterns in the table below provide the nutrients and energy needed for all children and adolescents of average height with sedentary to moderate activity levels.

Additional serves of the Five Food Groups or unsaturated spreads and oils or discretionary choices are needed only by children and adolescents who are taller, more active or in the higher end of a particular age band, to meet additional energy requirements.

Recommended average daily number of serves from each of the five food groups*Additional serves for more active, taller or older children and adolescents
Vegetables & legumes/beansFruitGrain (cereal) foods, mostly wholegrainLean meat and poultry, fish, eggs, nuts and seeds, and legumes/beansMilk, yoghurt, cheese and/or alternatives (mostly reduced fat)Approx. number of additional serves from the five food groups or discretionary choices
Toddlers **
1-22-3½411-1½
Boys
2-32 ½1411 ½0-1
4-84 ½1 ½41 ½20-2 ½
9-115252 ½2 ½0-3
12-135 ½262 ½3 ½0-3
14-185 ½272 ½3 ½0-5
Girls
2-32 ½1411 ½0-1
4-84 ½1 ½41 ½1 ½0-1
9-115242 ½30-3
12-135252 ½3 ½0-2 ½
14-185272 ½3 ½0-2 ½
Pregnant5283 ½3 ½0-3
Breastfeeding5 ½292 ½40-3

*Includes an allowance for unsaturated spreads or oils, nuts or seeds (½ serve [4.5g] per day for children 2-3 years of age, 1 serve [7-10g] per day for children 3-12 years of age; 1 ½ serves [11-15g] per day for children 12-13 years, and 2 serves [14-20g] per day for adolescents 14-18 years of age and for pregnant and breastfeeding girls).

** An allowance for unsaturated spreads or oils or nut/seed paste of 1 serve (7–10g) per day is included. Whole nuts and seeds are not recommended for children of this age because of the potential choking risk.

(Source: National Health and Medical Research Council of Australia. Recommended number of serves for children, adolescents and toddlers. 13).

References
  1. 2015–2020 Dietary Guidelines for Americans. https://health.gov/dietaryguidelines/2015/
  2. The American Heart Association. Portion Size Versus Serving Size. http://www.heart.org/HEARTORG/HealthyLiving/HealthyKids/HowtoMakeaHealthyHome/Portion-size-versus-serving-size—Whats-the-difference-for-kids_UCM_304051_Article.jsp
  3. Dietitians of Canada. Serving size. https://www.dietitians.ca/Your-Health/Nutrition-A-Z/Serving-size.aspx
  4. U.S. National Library of Medicine, Medline Plus. Portion size. https://medlineplus.gov/ency/patientinstructions/000337.htm
  5. Nielsen SJ, Popkin BM. Patterns and trends in food portion sizes, 1977-1998. JAMA. 2003;289:450-3. https://www.ncbi.nlm.nih.gov/pubmed/12533124
  6. Piernas C, Popkin BM. Food portion patterns and trends among U.S. children and the relationship to total eating occasion size, 1977-2006. J Nutr. 2011;141:1159-64. https://www.ncbi.nlm.nih.gov/pubmed/21525258
  7. Wansink B, Kim J. Bad popcorn in big buckets: portion size can influence intake as much as taste. J Nutr Educ Behav. 2005;37:242-5. https://www.ncbi.nlm.nih.gov/pubmed/16053812
  8. Rolls, B. J., L. S. Roe, et al. (2007). “The effect of large portion sizes on energy intake is sustained for 11 days.” Obesity (Silver Spring) 15(6): 1535-1543.
  9. Rosenheck R. Fast food consumption and increased caloric intake: a systematic review of a trajectory towards weight gain and obesity risk. Obes Rev. 2008;9:535-47. https://www.ncbi.nlm.nih.gov/pubmed/18346099
  10. Ello-Martin JA, Ledikwe JH, Rolls BJ. The influence of food portion size and energy density on energy intake: implications for weight management. Am J Clin Nutr. 2005;82(Suppl 1):236S–241S. https://www.ncbi.nlm.nih.gov/pubmed/16002828
  11. The Australian Dietary Guidelines. Serve sizes. https://www.eatforhealth.gov.au/food-essentials/how-much-do-we-need-each-day/serve-sizes
  12. National Health and Medical Research Council of Australia. Recommended number of serves for adults. https://www.eatforhealth.gov.au/food-essentials/how-much-do-we-need-each-day/recommended-number-serves-adults
  13. National Health and Medical Research Council of Australia. Recommended number of serves for children, adolescents and toddlers. https://www.eatforhealth.gov.au/food-essentials/how-much-do-we-need-each-day/recommended-number-serves-children-adolescents-and
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Diet PlanDiet, Food & Fitness

What is Mindful Eating and can it help with weight loss ?

mindful eating meditation

mindful eating meditation

What is Mindful Eating ?

Mindful eating includes awareness of physical hunger and satiety cues, environmental or emotional triggers to eat, and making healthier food choices 1. Many people eat mindlessly at meal time or when they snack. It’s common to eat while watching television, while on the computer, and while driving. Eating more slowly and relishing each bite could help people eat less or eat healthier, according to Dr. Lilian Cheung, lecturer in the Department of Nutrition at Harvard School of Public Health. Dr. Cheung, who also is the editorial director of the department’s nutrition website, The Nutrition Source, co-authored the 2010 book Savor: Mindful Eating, Mindful Life with Vietnamese Buddhist monk Thich Nhat Hanh 2. In Savor: Mindful Eating, Mindful Life, renowned spiritual leader Thich Nhat Hanh and Harvard nutritionist Dr. Lilian Cheung combine timeless Buddhist wisdom with nutrition science to deliver a new and insightful perspective on how people can end their struggles with weight for good.

In a recent literature review (published online 18 July 2017) involving sixty-eight publications: twenty-three interventions in obese/overweight populations; twenty-nine interventions in normal-weight populations; sixteen observational studies, three of which were carried out in overweight/obese populations. Mindfulness-based approaches appear most effective in addressing binge eating, emotional eating and eating in response to external cues 3. The authors found mindfulness-based approaches may prevent weight gain. Reduced food intake was seen in some of the studies in overweight and obese populations, but this was less apparent in the studies in normal-weight populations. Mindfulness appears to work by an increased awareness of internal, rather than external, cues to eat. Mindfulness and mindful eating have the potential to address problematic eating behaviours and the challenges many face with controlling their food intake. Encouraging a mindful eating approach would seem to be a positive message to be included in general weight management advice to the public 3.

This study 4 provides a description of mindfulness and mindful eating and addresses the application of mindful eating as a component of diabetes self-management education. Mindful eating helps individuals cultivate awareness of both internal and external triggers to eating, interrupt automatic eating, and eat in response to the natural physiological cues of hunger and satiety. Mindful eating interventions have been effective in facilitating improvement in dysregulated eating and dietary patterns. Through practice over time, eating mindfully can interrupt habitual eating behaviors and provide greater regulation of food choice.

Mindfulness is an ancient practice of “being completely aware of what’s happening in the present”—of all that’s going on inside and all that’s happening around you. It means not living your life on “autopilot.” Instead, you live your life “consciously in the present” in order to experience life as it unfolds moment to moment, good and bad, and without judgment or preconceived notions 5. “Many of us go through our lives without really being present in the moment,” being present in the now is the fundamental aspect of the spiritual practice to life and living.

As you start to learn how to be more mindful, it’s common and normal to realize how much your mind races and focuses on the past and future. You can just notice those thoughts and then return to the present moment. It is these little, regular steps that add up and start to create a more mindful, healthy life.

One National Institutes of Health-supported study found a link between mindfulness meditation and measurable changes in the brain regions involved in memory, learning and emotion. Another National Institutes of Health-funded researcher reported that mindfulness practices may reduce anxiety and hostility among urban youth and lead to reduced stress, fewer fights and better relationships 5.

The simple techniques involved in mindful eating—eating without watching the TV or computer, eating in silence, chewing slowly, taking breaths between bites—can help us focus more on what we are choosing to put into our bodies, and why, says Dr. Cheung 2.

More recently, self-help guru like Oprah Winfrey 6 has become cheerleaders for the practice of mindful eating. On Oprah’s site, she shared tips to eat mindfully from a Cornell University, Prof. Brian Wansink, the author of “Mindless Eating: Why We Eat More Than We Think.”

Here are seven essential tips from Prof. Brian Wansink from Oprah.com 6:

  1. People who stock up at discount stores eat up to 48 percent more. If you buy in bulk, put pretzels and other snacks in portion-size Baggies. Never, never, ever eat out of the box.
  2. The longer you sit at the table, the more you’ll eat. Dine with one friend, you’ll eat about 35 percent more. With a group of seven, you’ll eat 96 percent more. if you’re trying to lose weight, eat alone or with the smallest group possible, and pace yourself with the lightest eater.
  3. If you pre-plate your food in the kitchen, you’ll eat 14 percent less than if you serve yourself a smaller portion at the table and then take seconds.
  4. Brian’s rule of two: When eating at a buffet, put only two items at a time on your plate. Even if you make repeated trips, you’ll eat a lot less.
  5. Always eat in the same room of your house (but not in front of a TV or computer). You won’t snack as much.
  6. Don’t leave serving dishes on the table unless they’re filled with vegetables.
  7. Physical hunger builds gradually. Emotional hunger develops suddenly.

Simply put, mindful eating is learning to pay attention and eating with intention. Instead of eating mindlessly (and sometimes emotionally), putting food into your mouth almost unconsciously, not really tasting the food you’re eating, you notice your thoughts, feelings, and sensations. The look, smell, taste, feel of the food you’re eating.

Mindful eating is not a diet, or about giving up anything at all. It’s about experiencing food more intensely — especially the pleasure of it. You can eat a cheeseburger mindfully, if you wish. You might enjoy it a lot more. Or you might decide, halfway through, that your body has had enough. Or that it really needs some salad.

Eating is a natural, healthy, and pleasurable activity for satisfying hunger. However, in our food-abundant, diet-obsessed culture, eating is often mindless, consuming, and guilt-inducing instead. Mindful eating is an ancient mindfulness practice with profound modern implications and applications for resolving this troubled love-hate relationship with food.

Studies have shown that thinking about food and the way we eat it means we consume less. A small yet growing body of research suggests that a slower, more thoughtful way of eating could help with weight problems and maybe steer some people away from processed food and unhealthy choices.

This alternative approach has been dubbed “mindful eating.” It’s based on the Buddhist concept of mindfulness, which involves being fully aware of what is happening within and around you at the moment. Mindfulness techniques have also been offered as a way to relieve stress and alleviate problems like high blood pressure and chronic gastrointestinal difficulties.

Applied to eating, mindfulness includes noticing the colors, smells, flavors, and textures of your food; chewing slowly; getting rid of distractions like TV or reading; and learning to cope with guilt and anxiety about food. Some elements of mindful eating hark back to Horace Fletcher, an early 20th century food faddist who believed chewing food thoroughly would solve many different kinds of health problems.

The mind–gut connection

Digestion involves a complex series of hormonal signals between the gut and the nervous system, and it seems to take about 20 minutes for the brain to register satiety (fullness). If someone eats too quickly, satiety may occur after overeating instead of putting a stop to it. There’s also reason to believe that eating while we’re distracted by activities like driving or typing may slow down or stop digestion similar to how the “fight or flight” response does. And if we’re not digesting well, we may be missing out on the full nutritive value of some of the food we’re consuming.

When you eat mindfully, you slow down the process of eating, turn off autopilot, and focus on the present moment. Increasing your awareness of the present moment helps you become more conscious of your food choices, and requires you to use all five of your senses. This helps you truly taste and enjoy your food – without stuffing yourself. When you eat mindfully, it also makes you more aware of your body’s cues that tell you how hungry or full you are 7.

A starter kit for mindful eating

  • Awareness of your physical and emotional cues (your emotions during and after eating).
  • Recognition of your non-hunger triggers for eating (why you feel like eating, and what emotions or needs might be triggering the eating).
  • Learning to meet your other needs in more effective ways than eating
  • Choosing food for both enjoyment and nourishment (what you’re eating, and whether it is healthy or not).
  • Eating for optimal satisfaction and satiety (the look, smell, taste, feel of the food you’re eating).
  • Using the fuel you’ve consumed to live the vibrant life you crave (how full (or sated) you are before, during and after eating).
  • Where the food came from, who might have grown it, how much it might have suffered before it was killed, whether it was grown organically, how much it was processed, how much it was fried or overcooked, etc.

This broad application makes mindful eating a powerful tool for developing a healthier, happier relationship with food, which could result in healthy and long term weight loss.

Mindful Eating Tips

In your busy live, you often rush through meals sometimes not even pausing to sit while you eat. This hurried way of eating certainly deprives you of the pleasure of the meal, but could it also be impacting your health ? Could it be causing harm to our environment ? A new approach suggests that mindful eating may help you improve your health and the health of the planet through the practice of enjoying food with understanding and compassion. To understand this new philosophy, consider each of the four key principals:

  • how you eat mindfully,
  • what you eat,
  • why you eat, and
  • how much you eat.

How To Eat Mindfully

Eating more mindfully can start with something as simple as sitting down at a table for your meals. Eliminate distractions by removing your phone, television, computer or anything else that may compete for your attention. With typical distractions removed, you will be forced to focus on what is in front of you, your food. Enjoy how it looks, smells, feels and tastes. You can even listen to how it sounds when you chew it. You may notice something new about a food you have been eating for years.

Before you even put the food in your mouth, look at it closely. Notice the color, the texture, and the smell. Then, put the food in your mouth and let it sit on your tongue. Use your tongue to explore the shape and texture. You may even want to close your eyes at this point, so you can solely focus on the food in your mouth. Then, start to chew slowly and notice the flavors, textures, and smells that come in and out as the food breaks down. All this time, stay in the present moment. Think about the current taste of the food instead of anticipating the next bite or having more. Before reaching for another bite, notice whether you are doing so out of craving or because you are physically hungry.

A major benefit of mindfulness is that it encourages you to pay attention to your thoughts, your actions and your body. For example, studies have shown that mindfulness can help people achieve and maintain a healthy weight. It is so common for people to watch TV and eat snack food out of the box without really attending to how much they are eating. With mindful eating, you eat when you’re hungry, focus on each bite, enjoy your food more and stop when you’re full.

Once you’ve gotten a feel for it, try eating more mindfully at one meal or snack each day. Over time, you can gradually make it a habit that you practice at all meals of the day. You’ll find that you are actually tasting your food, enjoying meal time, and are more in control of what and how much you eat.

What You Eat

You know that the foods you choose will have an impact your personal health, in both the short and long term. Choosing more healthful foods like fruits, vegetables, beans, nuts, seeds and whole grains also has the added benefit of being more sustainable.

When You Eat

Sit down to eat. Avoid distractions like reading, the television, or the computer at meals and snacks. Don’t multi-task while you are eating.

Consciously tell yourself to slow down before eating. Take smaller bites and chew your food well. To slow down the process of eating, try putting your fork down between bites. You can also try eating with your opposite hand.

Eat from a smaller plate or bowl. Doing so actually makes us feel like we are eating more. When you eat from a larger plate or bowl, most people tend to fill it up and eat more.

Remember that you can’t eat what’s not there. If you have trouble with overeating or mindlessly eating certain foods, try not to buy them. Save them for a special occasion or just enjoy them when you are out to eat.

Why You Eat

Many factors influence why you eat. Nourishing your bodies and providing fuel for your daily activities should be the primary reason. Practicing mindfulness can help you filter out the other factors that may distract you (e.g. stress, anxiety, tiredness, boredom, fear, sadness, anger, depressed, lack of sleep, poor self-esteem, etc).

If you have recently eaten and find yourself craving food again, do a quick emotional check. Do you want food because you are hungry—or to fill an emotional need? Here are some tips to keep your eating in check:

  • Remember which emotions and situations trigger you to eat.
  • Write a list of other things to do to fulfill that emotional need, for example, call a friend, take a walk, drink some water or another zero-calorie beverage, send an email to a pal, or do a few yoga stretches.
  • Assess your physical hunger using the Hunger-Satiety Rating Scale.
  • Remember that food will not make your emotions go away (it won’t fix anything).
  • Track the food you eat, how hungry you are when you eat, and how you feel at the time. You may get a better idea of which emotions trigger eating when you are not physically hungry.
  • If you are having a hard time, reach out for help. Involve family members and friends to help support your weight loss efforts. Support groups, therapy, and members of your health care team can also help.

How Much Do You Eat

Rushing to fill your plates without consideration of how much you really need can lead to both overeating and increased food waste. Being more mindful during mealtime can help you pay attention to your hunger cues and understand when you are satisfied.

Studies suggest that mindfulness practices may help people manage stress, cope better with serious illness and reduce anxiety and depression. Many people who practice mindfulness report an increased ability to relax, a greater enthusiasm for life and improved self-esteem.

Finding time for mindfulness in our culture, however, can be a challenge. We tend to place great value on how much we can do at once and how fast. Still, being more mindful is within anyone’s reach.

You can practice mindfulness throughout the day, even while answering e-mails, sitting in traffic or waiting in line. All you have to do is become more aware—of your breath, of your feet on the ground, of your fingers typing, of the people and voices around you. So, before you roll your eyes again, take a moment and consider mindfulness.

Being Mindful

Research on mindfulness supports the idea that cultivating greater attention, awareness, and acceptance through meditation practice is associated with lower levels of psychological distress, including less anxiety, depression, anger, and worry 8, 9, 10, 11. Furthermore, studies have begun to elucidate how mindfulness training can reduce distress. One observational study found that more time spent on formal meditation practices (body scan, yoga, sitting meditation) at home during an 8-week intervention led to increased mindfulness, which, in turn, explained decreased psychological distress and increased psychological well-being 12. A recent randomized controlled trial in students showed that 4 weeks of mindfulness meditation training, relative to somatic relaxation training or a nonintervention control group, reduced distress by decreasing rumination, a cognitive process associated with depression and other mood disorders 13. Another clinical study found that 8 weeks of mindfulness meditation training significantly reduced ruminative thinking in persons with a history of depression 14. Together, these studies indicate that one beneficial mechanism of mindfulness appears to involve reshaping ways of thinking that engender improved emotional well-being.

Research further suggests that people with higher levels of mindfulness are better able to regulate their sense of well-being by virtue of greater emotional aware
ness, understanding, acceptance, and the ability to correct or repair unpleasant mood states 15, 9, 16. The
ability to skillfully regulate one’s internal emotional experience in the present moment may translate into good mental health long-term.

The concept of mindfulness is simple, but becoming a more mindful person requires commitment and practice. Here are some tips to help you get started:

  • Take some deep breaths. Breathe in through your nose to a count of 4, hold for 1 second and then exhale through the mouth to a count of 5. Repeat often.
  • Enjoy a stroll. As you walk, notice your breath and the sights and sounds around you. As thoughts and worries enter your mind, note them but then return to the present.
  • Practice mindful eating. Be aware of taste, textures and flavors in each bite, and listen to your body when you are hungry and full.
  • Find mindfulness resources in your local community, including yoga and meditation classes, mindfulness-based stress reduction programs and books. A great book to start with is the “The Power of Now: A Guide to Spiritual Enlightenment” by Eckhart Tolle.

 

mindful eating tips

Emotions and Eating

Emotions can influence what, when, and how much we eat. For example, you have probably heard that some people eat to cope with stress. Others eat to preoccupy themselves when they feel bored 17.

When you eat based on your emotions, it can hinder your weight loss efforts. Often, situations that trigger certain negative emotions prompt eating. Find out which emotions trigger your desire to eat using the chart below.

  1. Review the words below.
  2. Think about each of the emotions.
  3. Note any emotions that trigger your desire for food.
  4. Add any other emotions or situations that trigger you to eat.

Afraid, Alone, Angry, Anxious, Bad, Blue, Bored, Content, Depressed, Disappointed, Fat, Fearful, Frustrated, Good, Grief, Guilty, Happy, Hate, Hungry, Insecure, Jealous, Lonely,  Lust, Nervous, Peer Pressure, Regret, Sad, Scared, Self-pity, Shame, Sleepy, Stress, Time to eat, Tired, Unsure, Worried.

How does mindful eating help solve eating issues ?

Many people who struggle with food react mindlessly to their unrecognized or unexamined triggers, thoughts, and feelings. In other words, they re-act-repeating past actions again and again-feeling powerless to change. Mindfulness increases your awareness of these patterns without judgment and creates space between your triggers and your actions.

For example, whenever you notice that you feel like eating and pause to ask the question, “Am I hungry?”, you are able to observe your thoughts and choose how you will respond. Instead of reacting mindlessly, mindfulness gives you response-ability. That is how mindful eating empowers you to finally break old automatic or habitual chain reactions and discover options that work better for you.

  • You learn to eat when you’re hungry, and stop when you’re sated.
  • You learn to really taste food, and to enjoy the taste of healthy food.
  • You slowly start to realize that unhealthy food isn’t as tasty as you thought, nor does it make you feel very good.
  • As a result of the above three points, you will often lose weight if you’re overweight.
  • You begin to sort through the emotional issues you have around food and eating. This takes a bit longer, but it’s important.
  • Social overeating can become less of a problem — you can eat mindfully while socializing, with practice, and not overeat.
  • You begin to enjoy the eating experience more, and as a result enjoy life more, when you’re more present.
  • It can become a mindfulness ritual you look forward to.
  • You learn how food affects your mood and energy throughout the day.
  • You learn what food best fuels your exercise and work and play.

A treatment for bingers

Several studies have shown mindful eating strategies might help treat eating disorders and possibly help with weight loss. Psychologists at Indiana State University and colleagues at Duke University conducted an NIH-funded study of mindful eating techniques for the treatment of binge eating.

The randomized controlled study included 150 binge eaters and compared a mindfulness-based therapy to a standard psychoeducational treatment and a control group. Both active treatments produced declines in binging and depression, but the mindfulness-based therapy seemed to help people enjoy their food more and have less sense of struggle about controlling their eating. Those who meditated more (both at mealtimes and throughout the day) got more out of the program.

Experts suggest starting gradually with mindful eating, eating one meal a day or week in a slower, more attentive manner. Here are some tips (and tricks) that may help you get started:

  • Set your kitchen timer to 20 minutes, and take that time to eat a normal-sized meal.
  • Try eating with your non-dominant hand; if you’re a righty, hold your fork in your left hand when lifting food to your mouth.
  • Use chopsticks if you don’t normally use them.
  • Eat silently for five minutes, thinking about what it took to produce that meal, from the sun’s rays to the farmer to the grocer to the cook.
  • Take small bites and chew well.
  • Before opening the fridge or cabinet, take a breath and ask yourself, “Am I really hungry?” Do something else, like reading or going on a short walk.

As you can see, mindful eating is much more than “eating slowly, without distraction.” While that’s certainly an important part of it, at Am I Hungry? Mindful Eating Programs and Training, we believe that mindful eating encompasses the entire process of eating.

mindful eating exercise

Mindful Eating and Weight Loss

There is a growing evidence suggesting intervention techniques that enhance mindful self-awareness improve well-being, including anxiety and depression 18, eating disorders 19, 20, food cravings 21 and weight loss 22. Mindfulness-based interventions employ systematic procedures for developing greater awareness of moment-to-moment experience of physical sensations, affective states, and thoughts without judgment 23. Mindful eating, as taught in Mindfulness-Based Eating Awareness Training 24, includes making conscious food choices, developing awareness of physical vs. psychological hunger and satiety cues, and eating healthfully in response to those cues.

In a pilot study (a small scale preliminary study conducted in order to evaluate feasibility prior to performance of a full-scale study) on mindful eating and living (MEAL) involving 10 obese adults with a BMI of 36.9 kg/m² and average age of 44 yrs over 6 weeks 25. The mindful eating and living intervention involve six weekly two-hour group classes (with two monthly follow-up classes). Content included training in mindfulness meditation, mindful eating, and group discussion, with emphasis on awareness of body sensations, emotions, and triggers to overeat. At the end of the 12 week trial, participants had statistically significant weight loss, eating disinhibition, binge eating, depression, perceived stress, physical symptoms, negative affect, and C-reactive protein 25.

In a small randomised study involving 52 people with type 2 diabetes for more than 1 year with a body mass index (BMI) of ≥ 27.0 and glycosylated hemoglobin ≥ 7.0% (Hba1c), age 35 to 65 years not on insulin therapy 26. The participants were divided into 2 groups, group 1 to receive mindful eating intervention and group 2 were given the diabetes self-management education, which addresses knowledge, self-efficacy, and outcome expectations for improving food choices. Food was not provided to participants in the current study. Instead, participants purchased and prepared their own food and were encouraged to modify intake based on awareness of hunger and satiety cues in mindful eating or self-selected goals in the Diabetes Self-Management Intervention. Both mindful awareness of hunger and goal setting strategies were effective in helping participants reduce energy intake and lose weight. At the end of 3 months study period, there was significant reduction in energy intake for both groups following the interventions. There was no significant difference between groups with regard to the change in weight, body mass index (BMI), waist circumference, fasting glucose, A1c, or insulin at study end. In addition, significant improvement in intake of trans fats, fiber and glycemic load occurred. Physical activity and prescribed medications were similar between groups throughout the study and did not change significantly 26.

Mindful Eating and Type 2 Diabetes

In a small randomised study involving 52 people with type 2 diabetes for more than 1 year with a body mass index (BMI) of ≥ 27.0 and glycosylated hemoglobin ≥ 7.0% (Hba1c), age 35 to 65 years not on insulin therapy 1. The participants were divided into 2 groups, group 1 to receive mindful eating intervention and group 2 were given the diabetes self-management education, which addresses knowledge, self-efficacy, and outcome expectations for improving food choices. At the end of the 3 months study, there was no significant difference between groups with regard to the change in weight at study end, both groups lost weight. The weight loss findings have been discussed in more detail in the mindful eating and weight loss detailed above 26. Moreover, participants in both groups reported greater ability to minimize overeating in various situations. Correlational findings from the current study are consistent with these prior reports. Impulsivity or acting without thinking, was associated with higher scores on the disinhibition scale 27, suggesting a tendency to act impulsively is associated with a tendency to overeat. Training in mindful eating and the Diabetes Self-Management goal-based approach both raised conscious control of eating behaviors and reduced perceptions of uncontrolled eating in this study 1.

References
  1. Miller CK, Kristeller JL, Headings A, Nagaraja H. Comparison of a Mindful Eating Intervention to a Diabetes Self-Management Intervention Among Adults With Type 2 Diabetes: A Randomized Controlled Trial. Health education & behavior : the official publication of the Society for Public Health Education. 2014;41(2):145-154. doi:10.1177/1090198113493092. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4217158/
  2. Harvard School of Public Health. Lilian Cheung. https://www.hsph.harvard.edu/lilian-cheung/
  3. Warren JM, Smith N, Ashwell M. Nutr Res Rev. 2017 Jul 18:1-12. doi: 10.1017/S0954422417000154. [Published online: 18 July 2017]. A structured literature review on the role of mindfulness, mindful eating and intuitive eating in changing eating behaviours: effectiveness and associated potential mechanisms. https://www.cambridge.org/core/journals/nutrition-research-reviews/article/structured-literature-review-on-the-role-of-mindfulness-mindful-eating-and-intuitive-eating-in-changing-eating-behaviours-effectiveness-and-associated-potential-mechanisms/351A3D01E43F49CC9794756BC950EFFC
  4. Miller CK. Diabetes Spectr. 2017 May;30(2):89-94. doi: 10.2337/ds16-0039. Mindful Eating With Diabetes. https://www.ncbi.nlm.nih.gov/pubmed/28588374
  5. National Institutes of Health. Mindfulness Matters – Can Living in the Moment Improve Your Health ? https://newsinhealth.nih.gov/issue/Jan2012/feature2
  6. Oprah.com. 7 Ways to Eat Mindfully. http://www.oprah.com/health/Mindful-Eating
  7. American Diabetes Association. Eat More Mindfully. http://www.diabetes.org/mfa-recipes/tips/2014-10/mindful-eating-at-meals.html
  8. Baer, R. A. (2003). Mindfulness training as clinical intervention: A conceptual and empirical review. Clinical Psychology: Science and Practice, 10, 125-143.
  9. Brown, K. W., Ryan, R. M., & Creswell, J. D. (2007). Mindfulness: Theoretical foundations and evidence for salutary effects. Psychological Inquiry, 18, 211-237.
  10. Greeson, J., & Brantley, J. (2008). Mindfulness and anxiety disorders: Developing a wise relationship with the inner experience of fear. In F. Didonna (Ed.), Clinical handbook of mindfulness (pp. 171-188). New York, NY: Springer
  11. Grossman, P., Niemann, L., Schmidt, S., & Walach, H. (2004). Mindfulness-based stress reduction and health benefits. A meta-analysis. Journal of Psychosomatic Research, 57, 35-43.
  12. Carmody, J., & Baer, R. A. (2008). Relationships between mindfulness practice and levels of mindfulness, medical and psychological symptoms and well-being in a mindfulness-based stress reduction program. Journal of Behavioral Medicine, 31, 23-33.
  13. Jain, S., Shapiro, S. L., Swanick, S., Roesch, S. C., Mills, P. M., Bell, I., et al. (2007). A randomized controlled trial of mindfulness meditation versus relaxation training: Effects on distress, positive states of mind, rumination, and distraction. Annals of Behavioral Medicine, 33, 11-21.
  14. Ramel,W.,Goldin,P.R.,Carmona,P.E.,&McQuaid,J.R.(2004). The effects of mindfulness meditation training on cognitive processes and affect in patients with past depression. Cognitive Therapy and Research, 28, 433-455
  15. Baer, R. A., Smith, G. T., Lykins, E., Button, D., Krietemeyer, J., Sauer, S., et al. (2008). Construct validity of the five facet mindfulness questionnaire in meditating and nonmeditating samples. Assessment, 15, 329-342.
  16. Feldman, G., Hayes, A., Kumar, S., Greeson, J., & Laurenceau, J-P. (2007). Mindfulness and emotion regulation: The development and initial validation of the Cognitive and Affective Mindfulness Scale-Revised (CAMS-R). Journal of Psychopathology and Behavioral Assessment, 29, 177-190.
  17. American Diabetes Association. Emotions and Eating. http://www.diabetes.org/food-and-fitness/weight-loss/getting-started/emotions-and-eating.html
  18. The effect of mindfulness-based therapy on anxiety and depression: A meta-analytic review. Hofmann SG, Sawyer AT, Witt AA, Oh D. J Consult Clin Psychol. 2010 Apr; 78(2):169-83. https://www.ncbi.nlm.nih.gov/pubmed/20350028/
  19. The application of mindfulness to eating disorders treatment: a systematic review. Wanden-Berghe RG, Sanz-Valero J, Wanden-Berghe C. Eat Disord. 2011 Jan-Feb; 19(1):34-48. https://www.ncbi.nlm.nih.gov/pubmed/21181578/
  20. An Exploratory Study of a Meditation-based Intervention for Binge Eating Disorder. Kristeller JL, Hallett CB. J Health Psychol. 1999 May; 4(3):357-63. https://www.ncbi.nlm.nih.gov/pubmed/22021603/
  21. Coping with food cravings. Investigating the potential of a mindfulness-based intervention. Alberts HJ, Mulkens S, Smeets M, Thewissen R. Appetite. 2010 Aug; 55(1):160-3. https://www.ncbi.nlm.nih.gov/pubmed/20493913/
  22. Pilot study: Mindful Eating and Living (MEAL): weight, eating behavior, and psychological outcomes associated with a mindfulness-based intervention for people with obesity. Dalen J, Smith BW, Shelley BM, Sloan AL, Leahigh L, Begay D. Complement Ther Med. 2010 Dec; 18(6):260-4. https://www.ncbi.nlm.nih.gov/pubmed/21130363/
  23. Mindfulness-based stress reduction and health benefits. A meta-analysis. Grossman P, Niemann L, Schmidt S, Walach H. J Psychosom Res. 2004 Jul; 57(1):35-43. https://www.ncbi.nlm.nih.gov/pubmed/15256293/
  24. Mindfulness-based eating awareness training for treating binge eating disorder: the conceptual foundation. Kristeller JL, Wolever RQ. Eat Disord. 2011 Jan-Feb; 19(1):49-61. https://www.ncbi.nlm.nih.gov/pubmed/21181579/
  25. Dalen J, Smith BW, Shelley BM, Sloan AL, Leahigh L, Begay D. Complement Ther Med. 2010 Dec;18(6):260-4. doi: 10.1016/j.ctim.2010.09.008. Epub 2010 Nov 11. Pilot study: Mindful Eating and Living (MEAL): weight, eating behavior, and psychological outcomes associated with a mindfulness-based intervention for people with obesity.
  26. Miller CK, Kristeller JL, Headings A, Nagaraja H, Miser WF. Comparative Effectiveness of a Mindful Eating Intervention to a Diabetes Self-Management Intervention among Adults with Type 2 Diabetes: A Pilot Study. Journal of the Academy of Nutrition and Dietetics. 2012;112(11):1835-1842. doi:10.1016/j.jand.2012.07.036. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3485681/
  27. Impulsivity is associated with the disinhibition but not restraint factor from the Three Factor Eating Questionnaire. Yeomans MR, Leitch M, Mobini S. Appetite. 2008 Mar-May; 50(2-3):469-76. https://www.ncbi.nlm.nih.gov/pubmed/18069081/
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Diet PlanDiet, Food & Fitness

Why do many high-fiber foods still have a high GI value ?

foods high in fiber

What is Glycemic Index?

Carbohydrate is an essential part of our diets, but not all carbohydrate foods are equal. The glycemic index (GI) was first developed by Jenkins and colleagues 1 and the Glycemic Index (GI) is a relative ranking of carbohydrate in foods according to how they affect blood glucose levels 2. Carbohydrates with a low GI value (55 or less) are more slowly digested, absorbed and metabolised and cause a lower and slower rise in blood glucose and, therefore usually, insulin levels.

Research shows that both the amount and the type of carbohydrate in food affect blood glucose levels. Studies also show that the total amount of carbohydrate in food, in general, is a stronger predictor of blood glucose response than the GI.

The glycemic index or GI ranks carbohydrates according to their effect on blood glucose levels. The lower the GI, the slower the rise in blood glucose levels will be when the food is consumed. The effect may differ from person to person.

The GI index runs from 0–100 and usually uses glucose, which has a GI of 100, as the reference. Slowly absorbed carbohydrates have a low GI rating (55 or below), and include most fruits and vegetables, milk, some wholegrain cereals and bread, pulses and basmati rice. GI numbers are to be used as a guide only as individual foods do not have the same response in all people with diabetes.

  • Low GI foods are foods with a GI less than 55.
  • Intermediate GI foods are foods with a GI between 55 and 70.
  • High GI foods are foods with a GI greater than 70.

Below are examples of foods based on their GI.

Low GI Foods (55 or less)

  • 100% stone-ground whole wheat or pumpernickel bread
  • Oatmeal (rolled or steel-cut), oat bran, muesli
  • Pasta, converted rice, barley, bulgar
  • Sweet potato, corn, yam, lima/butter beans, peas, legumes and lentils
  • Most fruits, non-starchy vegetables and carrots

Not all low-GI foods are healthy choices – chocolate, for example, has a low-GI because of its fat content, which slows down the absorption of carbohydrate.

Medium GI (56-69)

  • Whole wheat, rye and pita bread
  • Quick oats
  • Brown, wild or basmati rice, couscous

High GI (70 or more)

  • White bread or bagel
  • Corn flakes, puffed rice, bran flakes, instant oatmeal
  • Shortgrain white rice, rice pasta, macaroni and cheese from mix
  • Russet potato, pumpkin
  • Pretzels, rice cakes, popcorn, saltine crackers
  • melons and pineapple

Table 1. The average glycemic index (GI) of 62 common foods derived from multiple studies by different laboratories

High-carbohydrate foodsGlycemic Index (GI)Breakfast cerealsGlycemic Index (GI)Fruit and fruit productsGlycemic Index (GI)VegetablesGlycemic Index (GI)
White wheat bread*75 ± 2Cornflakes81 ± 6Apple, raw36 ± 2Potato, boiled78 ± 4
Whole wheat/whole meal bread74 ± 2Wheat flake biscuits69 ± 2Orange, raw43 ± 3Potato, instant mash87 ± 3
Specialty grain bread53 ± 2Porridge, rolled oats55 ± 2Banana, raw51 ± 3Potato, french fries63 ± 5
Unleavened wheat bread70 ± 5Instant oat porridge79 ± 3Pineapple, raw59 ± 8Carrots, boiled39 ± 4
Wheat roti62 ± 3Rice porridge/congee78 ± 9Mango, raw51 ± 5Sweet potato, boiled63 ± 6
Chapatti52 ± 4Millet porridge67 ± 5Watermelon, raw76 ± 4Pumpkin, boiled64 ± 7
Corn tortilla46 ± 4Muesli57 ± 2Dates, raw42 ± 4Plantain/green banana55 ± 6
White rice, boiled*73 ± 4Peaches, canned43 ± 5Taro, boiled53 ± 2
Brown rice, boiled68 ± 4Strawberry jam/jelly49 ± 3Vegetable soup48 ± 5
Barley28 ± 2Apple juice41 ± 2
Sweet corn52 ± 5Orange juice50 ± 2
Spaghetti, white49 ± 2
Spaghetti, whole meal48 ± 5
Rice noodles53 ± 7
Udon noodles55 ± 7
Couscous65 ± 4

 

Dairy products and alternativesGlycemic Index (GI)LegumesGlycemic Index (GI)Snack productsGlycemic Index (GI)SugarsGlycemic Index (GI)
Milk, full fat39 ± 3Chickpeas28 ± 9Chocolate40 ± 3Fructose15 ± 4
Milk, skim37 ± 4Kidney beans24 ± 4Popcorn65 ± 5Sucrose65 ± 4
Ice cream51 ± 3Lentils32 ± 5Potato crisps56 ± 3Glucose103 ± 3
Yogurt, fruit41 ± 2Soya beans16 ± 1Soft drink/soda59 ± 3Honey61 ± 3
Soy milk34 ± 4Rice crackers/crisps87 ± 2
Rice milk86 ± 7

*Low-GI varieties were also identified.
Average of all available data.

Footnote: The GI should not be used in isolation; the energy density and macronutrient profile of foods should also be considered 3.

[Source 4 ]

The amount of carbohydrate you eat has a bigger effect on blood glucose levels than GI alone.

The GI value relates to the food eaten on its own and in practice we usually eat foods in combination as meals. Bread, for example is usually eaten with butter or margarine, and potatoes could be eaten with meat and vegetables. Therefore relying solely on the glycemic index of foods could result in eating unbalanced and un-healthy diets high in fat, salt and saturated fats.

An additional problem is that GI compares the glycaemic effect of an amount of food containing 50g of carbohydrate, but in real life we eat different amounts of food containing different amounts of carbohydrate.

The recommendation is to eat more low and intermediate GI foods, not to exclude high GI foods. By choosing the low glycaemic index foods and thus the minimally processed foods, people can lose more weight, feel fuller longer, and remain healthier.

The GI is only a small part of the healthy eating plan for people with diabetes. For people with diabetes, meal planning with the GI involves choosing foods that have a low or medium GI. If eating a food with a high GI, you can combine it with low GI foods to help balance the meal.

Carbohydrates are an essential nutrient. You need carbs as they break down into glucose in your body providing the:

  • main fuel for your brains and nervous systems,
  • preferred source of fuel for most organs and your muscles during exercise.

Consuming good quality carbohydrates aka Low GI ones help to facilitate the management of diabetes, weight loss and weight loss management and reducing the risk of developing type 2 diabetes, diabetes complications and other chronic lifestyle diseases.  In fact a low GI diet provides health benefits for everybody across all stages of life.

high in fiber foods

What can affect the Glycemic Index of Foods

Fat and fiber tend to lower the GI of a food. As a general rule, the more cooked or processed a food, the higher the GI; however, this is not always true.

Below are a few specific examples of other factors that can affect the GI of a food:

  • Ripeness and storage time — the more ripe a fruit or vegetable is, the higher the GI.
  • Processing — juice has a higher GI than whole fruit; mashed potato has a higher GI than a whole baked potato, stone ground whole wheat bread has a lower GI than whole wheat bread.
  • Cooking methods — how long a food is cooked (al dente pasta has a lower GI than soft-cooked pasta), frying, boiling and baking.
  • Fibre: wholegrains and high-fibre foods act as a physical barrier that slows down the absorption of carbohydrate. This is not the same as ‘wholemeal’, where, even though the whole of the grain is included, it has been ground up instead of left whole. For example, some mixed grain breads that include wholegrains have a lower GI than wholemeal or white bread.
  • Fat lowers the GI of a food. For example, chocolate has a medium GI because of it’s fat content, and crisps will actually have a lower GI than potatoes cooked without fat.
  • Protein lowers the GI of food. Milk and other diary products have a low GI because they are high in protein and contain fat.
  • Variety — converted long-grain white rice has a lower GI than brown rice but short-grain white rice has a higher GI than brown rice.

Starchy foods with a low GI are digested and absorbed more slowly than foods with a high GI. Some factors that influence glycemic properties of foods are listed in Table 2.

Table 2. Food factors influencing glycemic responses

Nature of the monosaccharide components
Glucose
Fructose
Galactose
Nature of the starch
Amylose
Amylopectin
Starch-nutrient interaction
Resistant starch
Cooking/food processing
Degree of starch gelatinization
Particle size
Food form
Cellular structure
Other food components
Fat and protein
Dietary fibre
Antinutrients
Organic acids
[Source 5 ]

What are High in Fiber Foods

Dietary fiber, also known as roughage or bulk, is the part of a plant that the body doesn’t absorb during digestion. Fibre is the part of food that is not digested in the small intestine. Dietary fibre moves largely unchanged into the large intestine or colon where it is fermented by friendly bacteria that live there. The scientific community define dietary fibre as intrinsic plant cell wall polysaccharides of vegetables, fruits and whole-grains, the health benefits of which have been clearly established, rather than synthetic, isolated or purified oligosaccharides and polysaccharides with diverse, and in some cases unique, physiological effects 6. The American Association of Cereal Chemists 7, define “dietary fiber is the edible parts of plants or analogous carbohydrates that are resistant to digestion and absorption in the human small intestine with complete or partial fermentation in the large intestine. Dietary fiber includes polysaccharides, oligosaccharides, lignin, and associated plants substances. Dietary fibers promote beneficial physiological effects including laxation, and/or blood cholesterol attenuation, and/or blood glucose attenuation” 7. The World Health Organization (WHO) and Food and Agriculture Organization (FAO) agree with the American Association of Cereal Chemists International (AACCI) definition but with a slight variation. They state “Dietary fibre means carbohydrate polymers1 with ten or more monomeric units, which are not hydrolysed by the endogenous enzymes in the small intestine of humans and belong to the following categories: that dietary fiber is a polysaccharide with ten or more monomeric units which is not hydrolyzed by endogenous hormones in the small intestine” 8.

Generally speaking, dietary fiber is the edible parts of plants or similar carbohydrates, that are resistant to digestion and absorption in the small intestine. Dietary fiber can be separated into many different fractions. Recent research has begun to isolate these components and determine if increasing their levels in a diet is beneficial to human health. These fractions include arabinoxylan, inulin, pectin, bran, cellulose, β-glucan and resistant starch. The study of these components may give us a better understanding of how and why dietary fiber may decrease the risk for certain diseases 9.

It was considered that the recommended intakes of fruit, vegetables, legumes and regular consumption of whole-grain cereals from Dietary Guidelines for Americans would provide adequate intakes of total dietary fibre 10. Low intakes of dietary fiber are due to low intakes of vegetables, fruits, and whole grains 10.

Dietary fiber and whole grains contain a unique blend of bioactive components including resistant starches, vitamins, minerals, phytochemicals and antioxidants. As a result, research regarding their potential health benefits has received considerable attention in the last several decades. Epidemiological and clinical studies demonstrate that consumption of dietary fiber and whole grain intake is inversely related to obesity 11, type two diabetes 12, cancer 13 and cardiovascular disease 14.

  • Eating fibre and wholegrain foods is linked to a lower risk of obesity, type 2 diabetes and heart disease, and may also reduce the risk of bowel cancer.
  • Eating high fibre foods can also help prevent constipation – this in turn can help to prevent hemorrhoids.
  • Because high fibre foods are filling they may also make it easier to stay at a healthy weight.
  • Foods high in fibre are generally good sources of vitamins and minerals, as well as other important nutrients.

The Food and Drug Administration (FDA) has approved two health claims for dietary fiber. The first claim states that, along with a decreased consumption of fats (<30% of calories), an increased consumption of dietary fiber from fruits, vegetables and whole grains may reduce some types of cancer 15. “Increased consumption” is defined as six or more one ounce equivalents, with three ounces derived from whole grains. A one ounce equivalent would be consistent with one slice of bread, ½ cup oatmeal or rice, or five to seven crackers. The second FDA claim supporting health benefits of dietary fiber states that diets low in saturated fat (<10% of calories) and cholesterol and high in fruits, vegetables and whole grain, have a decreased risk of leading to coronary heart disease 16. For most, an increased consumption of dietary fiber is considered to be approximately 25 to 35 g/d, of which 6 g are soluble fiber.

High intake of dietary fiber has been linked to a lower risk of heart disease in a number of large studies that followed people for many years 17. In a Harvard study of over 40,000 male health professionals, researchers found that a high total dietary fiber intake was linked to a 40 percent lower risk of coronary heart disease 18. A related Harvard study of female nurses produced quite similar findings 19.

Higher fiber intake has also been linked to a lower risk of metabolic syndrome, a combination of factors that increases the risk of developing heart disease and diabetes. These factors include high blood pressure, high insulin levels, excess weight (especially around the abdomen), high levels of triglycerides, and low levels of HDL (good) cholesterol. Several studies suggest that higher intake of fiber may offer protective benefits from this syndrome 20, 21.

Diets low in fiber and high in foods that cause sudden increases in blood sugar may increase the risk of developing Type 2 Diabetes. Both Harvard studies—of female nurses and of male health professionals—found that this type of diet more than doubled the risk of type 2 diabetes when compared to a diet high in cereal fiber and low in high-glycemic-index foods 22, 23, 24. A diet high in cereal fiber was linked to a lower risk of type 2 diabetes. Other studies, such as the Black Women’s Health Study 25 and the European Prospective Investigation Into Cancer and Nutrition–Potsdam, have shown similar results.

Recent studies support this inverse relationship between dietary fiber and the development of several types of cancers including colorectal, small intestine, oral, larynx and breast 13, 26, 27. Although most studies agree with these findings, the mechanisms responsible are still unclear. Several modes of actions however have been proposed. First, dietary fiber resists digestion in the small intestine, thereby allowing it to enter the large intestine where it is fermented to produce short chain fatty acids, which have anti-carcinogenic properties 28. Second, since dietary fiber increases fecal bulking and viscosity, there is less contact time between potential carcinogens and mucosal cells. Third, dietary fiber increases the binding between bile acids and carcinogens. Fourth, increased intake of dietary fiber yield increased levels of antioxidants. Fifth, dietary fiber may increase the amount of estrogen excreted in the feces due to an inhibition of estrogen absorption in the intestines 29. Obviously, many studies support the inverse relationship of dietary fiber and the risk for coronary heart disease. However, more recent studies found interesting data illustrating that for every 10 g of additional fiber added to a diet the mortality risk of coronary heart disease decreased by 17–35% 30, 14. Risk factors for CHD include hypercholesterolemia, hypertension, obesity and type two diabetes. It is speculated that the control and treatment of these risk factors underlie the mechanisms behind dietary fiber and coronary heart disease prevention. First, soluble fibers have been shown to increase the rate of bile excretion therefore reducing serum total and LDL “bad” cholesterol 31. Second, short chain fatty acid production, specifically propionate, has been shown to inhibit cholesterol synthesis 32. Third, dietary fiber demonstrates the ability to regulate energy intake thus enhancing weight loss or maintenance of a healthier body weight. Fourth, either through glycemic control or reduced energy intake, dietary fiber has been shown to lower the risk for type two diabetes. Fifth, dietary fiber has been shown to decrease pro-inflammatory cytokines such as interleukin-18 which may have an effect on plaque stability 33. Sixth, increasing dietary fiber intake has been show to decrease circulating levels of C-Reactive protein, a marker of inflammation and a predictor for coronary heart disease 34.

Fiber is found only in plant foods like whole-grain breads and cereals, beans and peas and other vegetables and fruits. Because there are different types of fiber in foods, choose a variety of foods daily. Eating a variety of fiber-containing plant foods is important for proper bowel function, can reduce symptoms of chronic constipation, diverticular disease, and hemorrhoids, and may lower the risk for heart disease and some cancers. However, some of the health benefits associated with a high-fiber diet may come from other components present in these foods, not just from fiber itself. For this reason, fiber is best obtained from foods rather than supplements.

Dietary fiber can be separated into many different fractions. Recent research has begun to isolate these components and determine if increasing their levels in a diet is beneficial to human health. These fractions include arabinoxylan, inulin, pectin, bran, cellulose, β-glucan and resistant starch. The study of these components may give us a better understanding of how and why dietary fiber may decrease the risk for certain diseases 35.

Types of Dietary Fiber

Many people think that if a food is rich in fibre it will automatically be low GI, but that’s not the case at all. To begin with, there’s not just one type of dietary fibre – there are many different kinds and is typically divided into three main categories: soluble fibre, insoluble fibre and resistant starch. In addition, processing makes a big difference to fibre’s digestibility. The American Association of Cereal Chemists 36, define “dietary fiber is the edible parts of plants or analogous carbohydrates that are resistant to digestion and absorption in the human small intestine with complete or partial fermentation in the large intestine. Dietary fiber includes polysaccharides, oligosaccharides, lignin, and associated plants substances. Dietary fibers promote beneficial physiological effects including laxation, and/or blood cholesterol attenuation, and/or blood glucose attenuation” 7. The World Health Organization (WHO) and Food and Agriculture Organization (FAO) agree with the American Association of Cereal Chemists International (AACCI) definition but with a slight variation. They state “Dietary fibre means carbohydrate polymers1 with ten or more monomeric units, which are not hydrolysed by the endogenous enzymes in the small intestine of humans and belong to the following categories: that dietary fiber is a polysaccharide with ten or more monomeric units which is not hydrolyzed by endogenous hormones in the small intestine” 8.

Table 3. Components of dietary fiber according to the American Association of Cereal Chemists

Non Starch Polysaccharides and Oligosaccharides
Cellulose
Hemicellulose
Arabinoxylans
Arabinogalactans
Polyfructoses
Inulin
Oligofructans
Galacto-oligosaccharides
Gums
Mucilages
Pectins
Analagous carbohydrates
Indigestible dextrins
Resistant maltodextrins
Resistant potato dextrins
Synthesized carbohydrates compounds
Polydextrose
Methyl cellulose
Hydroxypropylmethyl cellulose
Resistant starches
Lignin substances associated with the Non Starch Polysaccharides (NSP) and lignin complex
Waxes
Phytate
Cutin
Saponins
Suberin
Tannin
[Source: American Association of Cereal Chemists 36 ]

Recent research suggests that fiber should be categorized by its physical characteristics; how well it dissolves (solubility), how thick it is (viscosity) and how well it breaks down (fermentability). Some commonly known terms are described below:

  1. Soluble fiber including pectins and beta glucans is found in foods like oats, peas, beans, apples, citrus fruits, carrots, barley and psyllium. Soluble fiber dissolves in water to form a gel-like material. It can help lower blood cholesterol and glucose levels. Foods high in soluble fiber can help you feel full. They also help reduce constipation by speeding up the time it takes for feces (poop) to pass through your body. Soluble dietary fiber has been associated with lower postprandial glucose levels and increased insulin sensitivity in diabetic and healthy subjects; these effects were generally attributed to the viscous and/or gelling properties of soluble fiber 37. Soluble dietary fiber exerts physiological effects on the stomach and small intestine that modulate postprandial glycemic responses, including delaying gastric emptying 38, which accounts for ~35% of the variance in peak glucose concentrations following the ingestion of oral glucose 39, modulating gastrointestinal myoelectrical activity and delaying small bowel transit 40, 41, reducing glucose diffusion through the unstirred water layer 42, and reducing the accessibility of α-amylase to its substrates due to the increased viscosity of gut contents 43. Notably, the increased viscosity and gel-forming properties of soluble fiber are predominantly responsible for its glycemic effect, since the hypoglycemic effect can be reversed by the hydrolysis of guar gum or following ultra-high heating and homogenization 38. In addition, the intestinal absorption of carbohydrates was prolonged by soluble dietary fiber, which was partially due to altered incretin levels, including increased glucagon-like peptide 1 levels 43. In experimental clamp studies, soluble dietary fiber also influenced peripheral glucose uptake mechanisms 44, 45, including increasing skeletal muscle expression of the insulin-responsive glucose transporter type 4 (GLUT-4), which enhances skeletal muscle uptake, augments insulin sensitivity and normalizes blood glucose 45. In humans, various fatty acids stimulate the expression of peroxisome proliferator-activated receptor-γ, which increases adipocyte GLUT-4 levels 46. A more recent study to find out the health benefits of soluble fiber on type 2 diabetes 47. A total of 117 patients with type 2 diabetes between the ages of 40 and 70 were assessed. Patients were randomly assigned to one of two groups, and administered extra soluble dietary fiber (10 or 20 g/day), or to a control group (0 g/day) for one month. The 20 g/day soluble dietary fiber group exhibited significantly improved fasting blood glucose and low-density (LDL) lipoprotein “bad cholesterol” levels, as well as a significantly improved insulin resistance index. In addition, 10 and 20 g/day soluble dietary fiber significantly improved the waist and hip circumferences and levels of triglycerides and apolipoprotein A. The results of the present study suggested that increased and regular consumption of soluble dietary fiber led to significant improvements in blood glucose levels, insulin resistance and metabolic profiles 47.
  2. Insoluble fiber including cellulose is found in wheat bran and nuts. Insoluble fiber is a type of fibre that doesn’t dissolve in water. Because insoluble fiber absorbs water, it helps to soften the contents of your bowel, contributing to keep the bowels regular. Insoluble fiber promotes the movement of material through your digestive system and increases stool bulk, so it can be of benefit to those who struggle with constipation or irregular stools. Whole-wheat flour, wheat bran, nuts, beans and vegetables, such as cauliflower, green beans and potatoes, are good sources of insoluble fiber. Diverticulitis, an inflammation of the intestine, is one of the most common age-related disorders of the colon in Western society. Among male health professionals in a long-term follow-up study, eating dietary fiber, particularly insoluble fiber, was associated with about a 40 percent lower risk of diverticular disease 48.
  3. Resistant starch is a soluble fiber that is highly fermentable in the gut. While most starch is digested in the upper part of the gut, resistant starch resists digestion in the small intestine and so goes all the way to the large intestine 49. Once in the large intestine, good bacteria ferment resistant starch. This process produces short chain fatty acids (SCFAs) and gasses that help to keep the lining of the bowel healthy. Resistant starch is starch that is not easily absorbed. Different ways of cooking can create different amounts of resistant starch. For example, resistant starch is found in slightly undercooked (‘al dente’) pasta, cooked but cooled potatoes (including potato salad), cooked and cooled grains like rice, quinoa, barley and buckwheat, under-ripe bananas, beans, lentils and a product called Hi-maize used in some breads and breakfast cereals. Freekeh, a Middle Eastern grain available in some supermarkets, is another good source. In general, foods that are less highly processed contain more resistant starch. An important benefit of resistant starch is that it ferments, which produces substances that help to keep the lining of the bowel healthy. Resistant starch has been classified into five basic “types” 50.
    • Type 1 (resistant starch 1) is made up of starch granules surrounded by an indigestible plant matrix.
    • Type 2 (resistant starch 2) occurs in its natural form such as in an uncooked potato and high amylose maize.
    • Type 3 (resistant starch 3) are crystallized starches made by unique cooking and cooling processes.
    • Type 4 (resistant starch 4) is a starch chemically modified by esterification, crosslinking, or transglycosylation and is not found in nature.
    • Type 5 (resistant starch 5) is a starch consisting of amylose-lipid complex.
  4. Prebiotics are types of carbohydrate that only our gut bacteria can feed upon. Some examples are onions, garlic, asparagus and banana.

Table 4. Types of resistant starches

DesignationDescriptionExampleReference
Type 1 (resistant starch 1)Physically inaccessible starchCoarsely ground or whole-kernel grains51
Type 2 (resistant starch 2)Granular starch with the B- or C-polymorphHigh-amylose maize starch, raw potato, raw banana starch51
Type 3 (resistant starch 3)Retrograded starchCooked and cooled starchy foods52
Type 4 (resistant starch 4)Chemically modified starchesCross-linked starch and octenyl succinate starch53
Type 5 (resistant starch 5)Amylose-lipid complexStearic acid-complexed high-amylose starch54

Footnote: 1RSI, type I resistant starch; (RS); RSII, type II resistant starch; RSIII, type III resistant starch; RSIV, type IV resistant starch; RSV; type V resistant starch.

[Source 50 ]

Arabinoxylan

Arabinoxylan, a constituent of hemicelluloses, is comprised of a xylose backbone with arabinose side chains. Arabinoxylan is a major component of dietary fiber in whole grains having considerable inclusions in both the endosperm and bran. In wheat, Arabinoxylan account for around 64–69% of the structural carbohydrates (complex carbohydrates, non-starch polysaccharide are resistant to digestion in the small intestine and require bacterial fermentation located in the large intestine) in the bran and around 88% in the endosperm 55. During normal wheat flour processing, a majority of the arabinoxylan is removed as a by-product. In the GI tract, arabinoxylan acts much like a soluble fiber being rapidly fermented by the microflora of the colon.

Lu et al. 56, observed an inverse relationship between the intake level of an arabinoxylan rich bread and postprandial glucose response in healthy adult subjects. When compared to the control, postprandial glucose levels were significantly lower with only 6 g of arabinoxylan rich fiber supplementation while 12 g produced the greatest benefit. Breads high in arabinoxylan also appear to control blood glucose and insulin in adults with an already impaired glucose tolerance 57. Fasting blood glucose, postprandial blood glucose and insulin were all significantly lower when adults with type two diabetes were supplemented with 15 g/d of an arabinoxylan rich fiber. The mode of action behind arabinoxylan on improving glucose tolerance is unknown. However, it is thought to be due to the high viscosity of the fiber inside the lumen of the GI tract, thereby slowing the rate of glucose absorption.

The lower glycemic index of arabinoxylan may also play a role. Breads made with a flour rich in arabinoxylan have a relatively low glycemic index of around 59. Whole wheat flour, although high in fiber, has a glycemic index of around 99 56. Arabinoxylan rich bread has a similar glycemic index to that of whole grain bread but offers some distinct advantages such as improved mouth feel and tenderness. There was no significant difference in the sensory analysis between the control and a bread containing 14% arabinoxylan rich fiber 56.

Inulin

Inulin is a polymer of fructose monomers and is present in such foods as onions, garlic, wheat, artichokes and bananas and is used to improve taste and mouthfeel in certain applications. It is also used as a functional food ingredient due to its nutritional properties. Because of this, inulin products can be used as a replacement for fat or soluble carbohydrates without affecting the taste and texture and still contribute to a foods nutritional value.

Enzymatic hydrolyses in the small intestine is minimal (<10%) since inulin consists of beta bonds. Therefore, it enters the large intestine and is almost completely metabolized by the microflora. When fermented, they tend to favor propionate production which, in turn, decreases the acetate to propionate ratio leading to decreased total serum cholesterol and LDL 32, which are important risk factors for coronary heart disease.

Inulin has also demonstrated the ability to contribute to the health of the human large intestine as a prebiotic 58. They demonstrated that inulin stimulated the growth of bifidobacteria while restricting the growth of potential pathogenic bacteria such as E. coli, Salmonella, and Listeria. This could prove to be beneficial in such disorders as ulcerative colitis and C. difficile infections. Rafter et al. 59 agreed with these findings and suggested they were the underlying mechanisms behind the observation that inulin decreased biological compounds associated with colonic cancer, including reduced colorectal cell proliferation and water induced necrosis, decreased exposure to genotoxins, and decreased interleukin-2 release.

Increased mineral absorption may also contribute to the functionality of inulin. Increased calcium absorption, by approximately 20%, was reported in adolescent girls supplemented with inulin 60. Results from Abrams et al. 61, support these findings in a longer (one year) study of pubertal boys and girls consuming an inulin supplement. Subjects in the treatment group also experienced increased bone mineral density when compared to the control. The mechanisms behind these findings are still unclear but may be due to increased calcium absorption from the colon or possibly an increased solubility in the lumen of the GI tract due to short chain fatty acids. Finally, it may increase absorption through an enhancement of vitamin D.

Inulin may also provide a way to prevent and treat obesity. Cani et al. 62 demonstrated that oligofructose, a subgroup of inulin, increased satiety in adults which led to a decrease in total energy intake. This is thought to be due to short chain fatty acids and their ability to increase appetite suppressing hormones such as glucagon-like peptide 1 (GLP-1).

Beta-glucan

Beta-glucan (β-glucan) is a linear polysaccharide of glucose monomers with β(1→4) and β(1→3) linkages and found in the endosperm of cereal grains, primarily barley and oats. β-glucan concentrations in North American oat cultivars range from 3.9% to 6.8% 63. β-glucan is water soluble and highly viscous at low concentrations 63.

The physiological benefits due to β-glucan seem to stem from their effect on lipid metabolism and postprandial glucose metabolism. Many studies agree an inverse relationship exists between consumption levels of β-glucan and cholesterol levels. Several recent studies, in both hypercholesterolemic 64 and healthy 65 subjects, found that the daily consumption of 5 g of β–glucan significantly decreased serum total and LDL cholesterol. Davidson et al. 66 found that only a daily consumption of 3.6 g β-glucan was needed to produce the same significant effects. The same relationship also has been reported to occur between β-glucan and postprandial glucose and insulin responses in both diabetic and healthy subjects. Biorklund et al. 67 found that 5 g of β-glucan from oats significantly decreased postprandial glucose and insulin levels in healthy adults. Tappy et al. 68 reported the same results in adult subjects diagnosed with type two diabetes who consumed 4.0, 6.0 or 8.4 g of β-glucan.

Most authors agree that β-glucan’s viscosity in the GI tract is the most probable mechanism in which it decreases serum cholesterol levels as well as improves post prandial glucose metabolism. This gellation property may decrease bile acid absorption by increasing intestinal viscosity and increase bile acid excretion. This subsequently results in a higher hepatic cholesterol synthesis because of the higher need for bile acid synthesis 69. The same viscosity may also delay glucose absorption into the blood thus lowering post prandial glucose and insulin levels. Nazare et al. 70 observed that 5 g of oat β–glucan added to an oat concentrate cereal significantly delayed, but did not reduce, total glucose absorption.

The production of short chain fatty acids from β-glucan may also be a probable mechanism behind its observed metabolic effects. Fermentation of oat β-glucan has been shown to yield larger amounts of propionate 71, 72. Propionate has been shown to significantly inhibit cholesterol synthesis in humans 32 and is thought to be due to the inhibition of the rate limiting enzyme HMG CoA reductase 73.

Not all research however, agrees that β-glucan can affect lipid and glucose absorption/metabolism. Keogh et al. 74 observed that treatments of 8.1 to 11.9 g/d of barley β-glucan had no effect on total or LDL cholesterol in mildly hyperlipidemic adults. Cugent-Anceau et al. 75 not only observed that 3.5 g of oat β-glucan added to soup did not alter serum lipid profiles, but also produced no change in postprandial glucose levels.

Pectin

Pectin is a linear polymer of galacturonic acid connected with α (1→4) bonds. Regions of this backbone are substituted with α (1→2) rhamnopyranose units from which side chains of neutral sugars such as galactose, mannose, glucose and xylose occur. Pectin is a water soluble polysaccharide that bypasses enzymatic digestion of the small intestine but is easily degraded by the microflora of the colon. Citrus fruit contains anywhere from 0.5% to 3.5% pectin with a large concentration located in the peel. Commercially extracted pectins are also available and are typically used in food applications which require a gelling or a thickening agent.

Inside the GI tract, pectin maintains this ability to form a gel or thicken a solution. This is thought to be the likely mechanism behind its many beneficial effects on health including dumping syndrome, improved cholesterol and lipid metabolism and diabetes prevention and control. However, pectin also contains some unique abilities that may treat or prevent other diseases/disorders such as intestinal infections, atherosclerosis, cancer and obesity.

Several recent clinical studies, demonstrated that oral pectin supplementation to children and infants reduced acute intestinal infections and significantly slowed diarrhea. This is thought to be due to a reduction in pathogenic bacteria such as Shigella, Salmonella, Klebsiella, Enterobacter, Proteus and Citrobacter. This is supported by Olano–Martin et al. 76 who observed that pectin stimulated the growth of certain strains of Bifidobacteria and Lactobacillus in vitro. These bacteria are considered to be directly related to the health of the large intestine and their concentrations depict a healthy microflora population.

The quality of fibrin is thought to be an important risk factor for atherosclerosis, stroke and coronary heart disease. Pectin has been shown to increase fibrin permeability and decrease fibrin tensile strength in hyperlipidaemic men. Although the mechanism behind this is unknown, it is thought to be due in part to acetate production. Pectin yields predominantly acetate in the colon which is thought to enter peripheral circulation and alter fibrin architecture.

Pectin may also have a potential role in the complicated area of cancer prevention. Nangia–Makker et al. 77 found that pectin was able to bind to and decrease tumor growth and cancerous cell migration in rats fed modified citrus pectin. This is thought to be a result of pectin binding to galectin-3 and inhibiting some of its functions.

Bran

Bran is the outer most layer of a cereal grain and consists of the nucellar epidermis, seed coat, pericarp and aleurone. The aleurone consists of heavy walled, cube shaped cells which are composed primarily of cellulose. It is low in starch and high in minerals, protein, and fat. However, due to its thick cellulosic walls, these nutrients are virtually unavailable for digestion in monogastric species. The AACC defines oat bran as “the food which is produced by grinding clean oat groats or rolled oats and separating the resulting oat flour by sieving bolting, and/or other suitable means into fractions such that the oat bran fraction is not more than 50% of the original starting material and has a total betaglucan content of at least 5.5% (dry-weight basis) and a total dietary fiber content of at least 16.0% (dry-weight basis), and such that at least one-third of the total dietary fiber is soluble fiber.”

Bran from a wide array of cereal grains have been shown to have an effect on postprandial glucose levels, serum cholesterol, colon cancer, and body mass. Although the efficacy of bran may change due to its source, the purpose of this section will just evaluate bran’s general effect on the parameters listed above.

In a recent study of healthy adults, 31 g of rye bran decreased peak postprandial glucose levels by 35% when compared to the control 78. This effect may be due to the high arabinoxylan content in rye bran. Arabinoxylan, as discussed previously, may increase intestinal viscosity and slow nutrient absorption. In a more lengthy study, Qureshi et al. 79 found that subjects suffering type one and two diabetes decreased their fasting glucose levels due to the daily consumption of 10 g of stabilized rice bran over two months. The results may arise due to an increased intestinal viscosity, but is more likely a result of a decreased carbohydrate/caloric intake. Koh-Banerjee et al. 80, in a larger clinical study, supports this theory in their finding that for every 20 g/d increase in consumption of bran, body weight decreased by 0.80 lbs. It should be noted that this data remained significant even after adjustment for fat and protein intake, daily activity, caloric intake and baseline weight. In an earlier study, Zhang et al. 81 observed that adults with ileostomies, consuming bread rich in rye bran, significantly increased the ileal excretion of fat, nitrogen and energy. This study suggests bran did not delay nutrient absorption in the small intestine but hindered it.

In addition to a possible effect on carbohydrate absorption and metabolism, bran also seems to have the same effect on lipids. In a long term clinical study, Jensen et al. 82 reported that an increased daily consumption of bran significantly decreased the risk of coronary heart disease in healthy adult men. This is most likely due to the data reported by Qureshi et al. 79 who found that 10 g of rice bran consumed for eight weeks was able to decrease serum total cholesterol, LDL cholesterol and triglycerides. The mechanisms behind these effects may be two fold. The reduction in cholesterol levels is likely due to an increase in bile acid synthesis. Andersson et al. 83 found that oat bran doubled the serum concentration of 7α-hydroxy-4-cholesten-3-one (α-HC), which is a metabolite in the synthesis of bile acids that is oxidized from 7α-hydroxycholesterol. The reduction in serum triglyceride levels may be a result of a decreased absorption of fat from the small intestine.

Cellulose

Cellulose is a linear chain of β(1→4) linked glucose monomers and is the structural component of cell walls in green plants and vegetables. It is water insoluble and inert to digestive enzymes in the small intestine. However, it can go through microbial fermentation to a certain degree in the large intestine in turn producing short chain fatty acid.

Natural cellulose can be divided into two groups: Crystalline and amorphous. The crystalline component, which is made up of intra and intermolecular non covalent hydrogen bonds, make cellulose insoluble in water. However, many modified celluloses such as powdered cellulose, microcrystalline cellulose and hydroxypropylmethyl cellulose have been developed and are used as food ingredients. The difference between natural and modified celluloses is the extent of crystallization and hydrogen bonding. When these hydrogen bonds are disrupted and the crystallinity is lost, the cellulose derivative becomes water soluble 83.

Little research has been conducted evaluating the effects of cellulose in humans. Therefore, studies in other models such as the rat will be discussed. The translation to human relevance is poorly understood and debatable. Cellulose pills have been made available for human consumption with the theory that cellulose may decrease a person’s caloric intake. Although no human studies could be found to support this, several animal studies using cats, dogs and rats have shown that increasing dietary cellulose can reduce daily energy intake. This is most likely a dilution factor since cellulose is virtually undigested in the small intestine and only 51% metabolized by the microflora of the colon.

Many studies have evaluated the effect of cellulose on blood glucose and insulin levels in many different models. However, the data is extremely contradictory and may depend on the subject, type of cellulose and other unknown factors. Using the rat, dog and cat, natural cellulose was shown to decrease postprandial glucose and insulin levels. However, similar studies in pigs and humans 84 demonstrated that natural cellulose had no effect on these parameters. Studies using modified celluloses showed more consistent data. Microcrystalline cellulose has shown the ability to decrease blood glucose levels in the pig and rat. Complimenting this, methylcellulose had demonstrated the same effects in humans. Lightowler and Henry 85 found that adding only 1% high viscosity hydroxypropylmethylcellulose (HV-HPMC) to mashed potatoes decreased postprandial glucose levels by 37% in healthy adults. Also, Maki et al. 86 reported an acute 35% reduction in postprandial blood glucose due to 4 g of HV-HPMC in overweight subjects.

Modified cellulose has also been reported to effect lipid metabolism. Maki et al. 87, 88 both observed a significant reduction in total and LDL cholesterol in hypercholesterolemic adults consuming 5 g/d of HV-HPMC for four weeks. Interestingly, in subjects already receiving statin drugs, HV-HPMC was able to further reduce total and LDL cholesterol.

According to this, modified celluloses may be more beneficial than natural cellulose. These modified celluloses, as described above, act like soluble fiber thus adding to the viscosity of the GI tract. Therefore, it is assumed that increased intestinal viscosity delays nutrient absorption and increases bile acid excretion.

How much fiber do you need?

Depending on your age and sex, adults should get 25 to 31 grams of fiber a day 89. Older adults sometimes don’t get enough fiber because they may lose interest in food.

  • Men over the age of 50 should get at least 38 grams of fiber per day.
  • Women over the age of 50 should get 25 grams per day.
  • Children ages 1 to 3 should get 19 grams of fiber per day.
  • Children between 4 and 8 years old should get 25 grams per day.
  • Girls between 9 and 18 should get 26 grams of fiber each day. Boys of the same age range should get between 31 and 38 grams of fiber per day.

To get enough fiber every day, the U.S. Department of Health and Human Services 10 recommends that an individual eats:

  • at least 4 serves of wholegrain or wholemeal foods every day (or ensure about half of your daily serves of breads and cereals are wholegrain or wholemeal varieties)
  • at least 2 serves of fruit daily
  • 5 serves of vegetables daily including legumes (also known as ‘pulses’)
  • wholefoods rather than dietary fiber supplements as the benefits of fiber from food may be from the combination of nutrients in food working together.

Table 5. Below is an example of how an adult may meet their daily dietary fiber requirements:

FoodFiber Content
3/4 cup whole grain breakfast cereal4.5g
2 slices wholemeal bread4.5g
1 apple (with skin) and 1 orange5.5g
2 cups mixed raw vegetables10g
1/4 cup legumes eg. baked beans3g
Total27.5g

Footnote: Daily recommended fiber intake are highlighted in pink. (Source: U.S. Department of Health and Human Services and U.S. Department of Agriculture: Dietary Guidelines for Americans 2015-2020 10 ] [Source 90 ]

daily fiber requirement

Tips for including more fiber in your diet

  • Know which packaged foods are high in fibre by reading the nutrient panel on the pack. A food with at least 4g fibre per serve is a good source; food with at least 7g fibre per serve is an excellent source.
  • Enjoy wholegrain, wholemeal or mixed grain toast instead of white.
  • Use wholegrain pasta instead of white pasta.
  • Try brown rice or quinoa instead of white rice with casseroles or curries.
  • Use wholemeal flour to thicken sauces, gravies and stews.
  • Try wholegrain or wholemeal crisp breads with toppings such as creamed corn or salsa dip.
  • For breakfast choose a high-fiber breakfast cereal — 5 or more grams of fiber a serving. Opt for cereals with “whole grain,” “bran” or “fiber” in the name. Or add a few tablespoons of unprocessed wheat bran to your favorite cereal.
  • Switch to whole grains. Consume at least half of all grains as whole grains. Look for breads that list whole wheat, whole-wheat flour or another whole grain as the first ingredient on the label and have at least 2 grams of dietary fiber a serving. Experiment with brown rice, wild rice, barley, whole-wheat pasta and bulgur wheat.
  • Bulk up baked goods. Substitute whole-grain flour for half or all of the white flour when baking. Try adding crushed bran cereal, unprocessed wheat bran or uncooked oatmeal to muffins, cakes and cookies.
  • Lean on legumes. Beans, peas and lentils are excellent sources of fiber. Add kidney beans to canned soup or a green salad. Or make nachos with refried black beans, lots of fresh veggies, whole-wheat tortilla chips and salsa.
  • Eat more fruit and vegetables. Fruits and vegetables are rich in fiber, as well as vitamins and minerals. Try to eat five or more servings daily.
  • Make snacks count. Fresh fruits, raw vegetables, low-fat popcorn and whole-grain crackers are all good choices. A handful of nuts or dried fruits also is a healthy, high-fiber snack — although be aware that nuts and dried fruits are high in calories.

Foods High in Fiber

Good sources of dietary fiber include:

  • Pulses (like lentils and peas) and beans and legumes (think navy beans, small white beans, split peas, chickpeas, lentils, pinto beans)
  • Fruits and vegetables, vegetables such as carrots, broccoli, green peas, and collard greens; fruits especially those with edible skin (like pears and apples with the skin on) and those with edible seeds (like berries)
  • Nuts—try different kinds (pumpkin seeds, almonds, sunflower seeds, pistachios and peanuts are a good source of fiber and healthy fats, but be mindful of portion sizes, because they also contain a lot of calories in a small amount!)
  • Whole grains such as:
    • Quinoa, barley, bulgur, oats, brown rice and farro
    • Whole wheat pasta
    • Whole grain cereals, including those made from whole wheat, wheat bran and oats

Choose fiber rich foods from a variety of sources including wholegrains, fruit and vegetable, nuts and seeds, beans and pulses. When you read food labels check for the grams of fiber per serving or per 100g. Foods that are naturally high in fiber and contain at least 3 grams per 100 gram are often labeled as a “good source,” and foods labeled as “excellent source” contain more than 5 grams of fiber per serving.

Keep in mind that if you haven’t been eating a lot of foods high in fiber on a daily basis, it’s important to increase your intake slowly to allow your body to adjust. A sudden increase in eating foods high in fiber (especially foods with added fiber or when using supplements) can cause gas, bloating or constipation. Be sure you are drinking enough water too, because fiber needs water to move through your body, making your stool soft and bulky.

It is now known that diets rich in fiber are generally low in saturated fat and many national authorities including the U.S. Department of Health and Human Services and U.S. Department of Agriculture in their Dietary Guidelines for Americans 10 recommended you eat whole grains, vegetables, and fruits as parts of healthy diet and greater consumption of grain products to control weight 10. Whole grains may have beneficial effects on weight control through promoting satiety 91, 92, 93. Healthy eating patterns include whole grains and limit the intake of refined grains and products made with refined grains, especially those high in saturated fats, added sugars, and/or sodium, such as cookies, cakes, and some snack foods. The grains food group includes grains as single foods (e.g., rice, oatmeal, and popcorn), as well as products that include grains as an ingredient (e.g., breads, cereals,
crackers, and pasta). Grains are either whole or refined. Whole grains (e.g., brown rice, quinoa, and oats) contain the entire kernel, including the endosperm, bran, and germ. Refined grains differ from whole grains in that the grains have been processed to remove the bran and germ, which removes dietary fiber, iron, and other nutrients. The recommended amount of grains in the Healthy U.S.-Style Eating Pattern at the 2,000-calorie level is 6 ounce-equivalents per day. At least half of this amount should be whole grains 10. The intake of whole grains may also slow starch digestion or absorption, which leads to relatively lower insulin and glucose responses that favor the oxidation and lipolysis of fat rather than its storage 91, 92, 93. They are emphasized in the Dietary Guidelines for Americans because they provide vitamins, minerals, complex carbohydrates (starch and dietary fiber), and other substances that are important for good health. They are also generally low in fat, depending on how they are prepared and what is added to them at the table.  However, most grain products consumed in the United States are highly refined 93, 94. Refined-grain products have a higher starch content but a lower fiber content (ie, greater energy density) than do whole grains. Concentrations of vitamins, minerals, essential fatty acids, and phytochemicals that are important in carbohydrate metabolism are also lower in refined grains 95.

Indirect evidence from both epidemiologic and short-term experimental studies suggests a beneficial role of a high-fiber diet in weight control 95, 96, 97. Most Americans of all ages eat fewer than the recommended number of servings of grain products, vegetables, and fruits, even though consumption of these foods is associated with a substantially lower risk for many chronic diseases, including certain types of cancer 10.

Dietary fiber is widely prescribed 98, either alone or in combination with lipid-lowering therapies, to reduce cholesterol levels 99. The exact mechanism by which soluble fiber lowers serum levels of low-density lipoprotein (LDL) and cholesterol is not completely understood; however, it has been suggested that soluble fiber may interfere with lipid and/or bile acid metabolism 100. A reasonable increase in dietary fiber intake (20–35 g/day) is recommended by the American Diabetes Association based on the effects of soluble fiber on plasma levels of cholesterol 101. Recent epidemiological findings have suggested that there is an association between high dietary fiber intake and a reduced risk of developing diabetes and coronary heart disease 102, 103. In particular, soluble dietary fiber has been shown to reduce insulin resistance in female non-diabetic patients 104.

A more recent study to find out the health benefits of soluble fiber on type 2 diabetes 47. A total of 117 patients with type 2 diabetes between the ages of 40 and 70 were assessed. Patients were randomly assigned to one of two groups, and administered extra soluble dietary fiber (10 or 20 g/day), or to a control group (0 g/day) for one month. The 20 g/day soluble dietary fiber group exhibited significantly improved fasting blood glucose and low-density (LDL) lipoprotein “bad cholesterol” levels, as well as a significantly improved insulin resistance index. In addition, 10 and 20 g/day soluble dietary fiber significantly improved the waist and hip circumferences and levels of triglycerides and apolipoprotein A. The results of the present study suggested that increased and regular consumption of soluble dietary fiber led to significant improvements in blood glucose levels, insulin resistance and metabolic profiles 47.

Whole grains

Whole grains are an important source of dietary fiber and other nutrients 10. Whole grains are a source of nutrients, such as dietary fiber, iron, zinc, manganese, folate, magnesium, copper, thiamin, niacin, vitamin B6, phosphorus, selenium, riboflavin, and vitamin A 105 10. Healthful diets rich in dietary fiber have been shown to have a number of beneficial effects, including decreasing risk of coronary heart disease and promoting regularity. Some examples of whole-grain products could include whole wheat bread, whole wheat cereal, and brown rice.

Whole grains are just that whole. Nothing has been added or taken away by processing. When whole grains are processed, some of the dietary fiber and other important nutrients are removed. A processed grain is called a refined grain. Most refined grains are enriched, a process that adds back iron and four B vitamins (thiamin, riboflavin, niacin, and folic acid) 10. Because of this process, the term “enriched grains” is often used to describe these refined grains. These are called enriched grains. White rice and white bread are enriched grain products. If you read the packaging for these foods, you will see the word “enriched.” Some enriched grain foods have extra nutrients added. These are called fortified grains. Many ready-to-eat cereals are fortified. At least half of the grains you eat should be whole-grain; other grains should be fortified or enriched 10.

The following are some examples of how whole grains could be listed:

  • whole wheat
  • wild rice
  • quinoa
  • brown rice
  • whole oats/oatmeal
  • buckwheat
  • sorghum
  • whole rye
  • whole-grain corn
  • bulgur (cracked wheat)
  • popcorn
  • whole-grain barley
  • millet
  • triticale

foods that are high in fiberhigh fiber foods listhigh fiber foods list high fiber foods list high fiber foods listhigh fiber foods list

Note: Foods fiber content are highlighted in pink. (Source: U.S. Department of Health and Human Services and U.S. Department of Agriculture: Dietary Guidelines for Americans 2015-2020 10).

References
  1. Glycemic index of foods: a physiological basis for carbohydrate exchange. Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM, Bowling AC, Newman HC, Jenkins AL, Goff DV. Am J Clin Nutr. 1981 Mar; 34(3):362-6. https://www.ncbi.nlm.nih.gov/pubmed/6259925/
  2. American Diabetes Association. Glycemic Index and Diabetes. http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/understanding-carbohydrates/glycemic-index-and-diabetes.html
  3. FAO/WHO scientific update on carbohydrates in human nutrition: conclusions. Mann J, Cummings JH, Englyst HN, Key T, Liu S, Riccardi G, Summerbell C, Uauy R, van Dam RM, Venn B, Vorster HH, Wiseman M. Eur J Clin Nutr. 2007 Dec; 61 Suppl 1:S132-7. https://www.ncbi.nlm.nih.gov/pubmed/17992184/
  4. Atkinson FS, Foster-Powell K, Brand-Miller JC. International Tables of Glycemic Index and Glycemic Load Values: 2008 . Diabetes Care. 2008;31(12):2281-2283. doi:10.2337/dc08-1239. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2584181/
  5. Food and Agriculture Organization. Chapter 4 – The role of the glycemic index in food choice. http://www.fao.org/docrep/w8079e/w8079e0a.htm#factors%20influencing%20the%20blood%20glucose%20responses%20of%20foods
  6. European Journal of Clinical Nutrition (2007) 61 (Suppl 1), S132–S137; doi:10.1038/sj.ejcn.1602943. FAO/WHO Scientific Update on carbohydrates in human nutrition: conclusions. http://www.nature.com/ejcn/journal/v61/n1s/full/1602943a.html
  7. American Association of Cereal Chemists (AACC International). Dietary Fiber. http://www.aaccnet.org/initiatives/definitions/Pages/DietaryFiber.aspx
  8. Food and Agriculture Organization and World Health Organization. CODEX ALIMENTARIUS COMMISSION. Thirty second Session, Rome, Italy, 29 June – 4 July 2009. http://www.fao.org/input/download/report/710/al32_26e.pdf
  9. Lattimer JM, Haub MD. Effects of Dietary Fiber and Its Components on Metabolic Health. Nutrients. 2010;2(12):1266-1289. doi:10.3390/nu2121266. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257631/
  10. U.S. Department of Health and Human Services and U.S. Department of Agriculture: Dietary Guidelines for Americans 2015-2020. https://health.gov/dietaryguidelines/
  11. Increasing total fiber intake reduces risk of weight and fat gains in women. Tucker LA, Thomas KS. J Nutr. 2009 Mar; 139(3):576-81. https://www.ncbi.nlm.nih.gov/pubmed/19158230/
  12. Carbohydrates, dietary fiber, and incident type 2 diabetes in older women. Meyer KA, Kushi LH, Jacobs DR Jr, Slavin J, Sellers TA, Folsom AR. Am J Clin Nutr. 2000 Apr; 71(4):921-30. https://www.ncbi.nlm.nih.gov/pubmed/10731498/
  13. Dietary fiber intake and risk of breast cancer in postmenopausal women: the National Institutes of Health-AARP Diet and Health Study. Park Y, Brinton LA, Subar AF, Hollenbeck A, Schatzkin A. Am J Clin Nutr. 2009 Sep; 90(3):664-71. https://www.ncbi.nlm.nih.gov/pubmed/19625685/
  14. Dietary fiber intake in relation to coronary heart disease and all-cause mortality over 40 y: the Zutphen Study. Streppel MT, Ocké MC, Boshuizen HC, Kok FJ, Kromhout D. Am J Clin Nutr. 2008 Oct; 88(4):1119-25. https://www.ncbi.nlm.nih.gov/pubmed/18842802/
  15. FDA, authors. Code of Federal Regulations. Vol. 2 Food and Drug Administration; Silver Spring, MD, USA: 2008. Health claims: Fiber-contaning grain products, fruits and vegetables and cancer.
  16. FDA, authors. Code of Federal Regulations. Vol. 2 Food and Drug Administration; Silver Spring, MD, USA: 2008. Health claims: fruits, vegetables, and grain products that contain fiber, particularly soluble fiber, and risk of coronary heart disease.
  17. Pereira MA, O’Reilly E, Augustsson K, et al. Dietary fiber and risk of coronary heart disease: a pooled analysis of cohort studies. Arch Intern Med. 2004;164:370-6. https://www.ncbi.nlm.nih.gov/pubmed/14980987
  18. Rimm EB, Ascherio A, Giovannucci E, Spiegelman D, Stampfer MJ, Willett WC. Vegetable, fruit, and cereal fiber intake and risk of coronary heart disease among men. JAMA. 1996;275:447-51. https://www.ncbi.nlm.nih.gov/pubmed/8627965
  19. Brown L, Rosner B, Willett WW, Sacks FM. Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr. 1999;69:30-42. https://www.ncbi.nlm.nih.gov/pubmed/9925120
  20. McKeown NM, Meigs JB, Liu S, Wilson PW, Jacques PF. Whole-grain intake is favorably associated with metabolic risk factors for type 2 diabetes and cardiovascular disease in the Framingham Offspring Study. Am J Clin Nutr. 2002;76:390-8. https://www.ncbi.nlm.nih.gov/pubmed/12145012
  21. McKeown NM, Meigs JB, Liu S, Saltzman E, Wilson PW, Jacques PF. Carbohydrate nutrition, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort. Diabetes Care. 2004;27:538-46. https://www.ncbi.nlm.nih.gov/pubmed/14747241
  22. Fung TT, Hu FB, Pereira MA, et al. Whole-grain intake and the risk of type 2 diabetes: a prospective study in men. Am J Clin Nutr. 2002;76:535-40. https://www.ncbi.nlm.nih.gov/pubmed/12197996
  23. Liu S, Willett WC, Stampfer MJ, et al. A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in US women. Am J Clin Nutr. 2000;71:1455-61. https://www.ncbi.nlm.nih.gov/pubmed/10837285
  24. Schulze MB, Liu S, Rimm EB, Manson JE, Willett WC, Hu FB. Glycemic index, glycemic load, and dietary fiber intake and incidence of type 2 diabetes in younger and middle-aged women. Am J Clin Nutr. 2004;80:348-56. https://www.ncbi.nlm.nih.gov/pubmed/15277155
  25. Krishnan S, Rosenberg L, Singer M, et al. Glycemic index, glycemic load, and cereal fiber intake and risk of type 2 diabetes in US black women. Arch Intern Med. 2007;167:2304-9. https://www.ncbi.nlm.nih.gov/pubmed/18039988
  26. Dietary fiber and colorectal cancer risk: the multiethnic cohort study. Nomura AM, Hankin JH, Henderson BE, Wilkens LR, Murphy SP, Pike MC, Le Marchand L, Stram DO, Monroe KR, Kolonel LN. Cancer Causes Control. 2007 Sep; 18(7):753-64. https://www.ncbi.nlm.nih.gov/pubmed/17557210/
  27. Prospective study of dietary fiber, whole grain foods, and small intestinal cancer. Schatzkin A, Park Y, Leitzmann MF, Hollenbeck AR, Cross AJ. Gastroenterology. 2008 Oct; 135(4):1163-7. https://www.ncbi.nlm.nih.gov/pubmed/18727930/
  28. Dietary fibre and colorectal cancer: a model for environment–gene interactions. Young GP, Hu Y, Le Leu RK, Nyskohus L. Mol Nutr Food Res. 2005 Jun; 49(6):571-84. https://www.ncbi.nlm.nih.gov/pubmed/15864783/
  29. Adlercreutz H., Hamalainen E., Gorbach S.L., Goldin B.R., Woods M.N., Brunson L.S., Dwyer J.T. Association of Diet and Sex-Hormones in Relation to Breast-Cancer. Eur. J. Cancer Clin. Oncol. 1987;23:1725–1726.
  30. Dietary fiber and risk of coronary heart disease: a pooled analysis of cohort studies. Pereira MA, O’Reilly E, Augustsson K, Fraser GE, Goldbourt U, Heitmann BL, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman D, Stevens J, Virtamo J, Willett WC, Ascherio A. Arch Intern Med. 2004 Feb 23; 164(4):370-6. https://www.ncbi.nlm.nih.gov/pubmed/14980987/
  31. Dietary fiber and bile acid metabolism–an update. Story JA, Furumoto EJ, Buhman KK. Adv Exp Med Biol. 1997; 427():259-66. https://www.ncbi.nlm.nih.gov/pubmed/9361851/
  32. Amaral L., Morgan D., Stephen A.M., Whiting S. Effect of Propionate on Lipid-Metabolism in Healthy-Human Subjects. FASEB J. 1992;6:A1655.
  33. Meal modulation of circulating interleukin 18 and adiponectin concentrations in healthy subjects and in patients with type 2 diabetes mellitus. Esposito K, Nappo F, Giugliano F, Di Palo C, Ciotola M, Barbieri M, Paolisso G, Giugliano D. Am J Clin Nutr. 2003 Dec; 78(6):1135-40. https://www.ncbi.nlm.nih.gov/pubmed/14668275/
  34. Association between dietary fiber and serum C-reactive protein. Ma Y, Griffith JA, Chasan-Taber L, Olendzki BC, Jackson E, Stanek EJ 3rd, Li W, Pagoto SL, Hafner AR, Ockene IS. Am J Clin Nutr. 2006 Apr; 83(4):760-6. https://www.ncbi.nlm.nih.gov/pubmed/16600925/
  35. Nutrients. 2010 Dec; 2(12): 1266–1289. – Effects of Dietary Fiber and Its Components on Metabolic Health – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257631/
  36. American Association of Cereal Chemists (AACC International). Dietary Fiber. http://www.aaccnet.org/initiatives/definitions/Pages/DietaryFiber.aspx
  37. Therapeutic effects of psyllium in type 2 diabetic patients. Sierra M, García JJ, Fernández N, Diez MJ, Calle AP. Eur J Clin Nutr. 2002 Sep; 56(9):830-42. https://www.ncbi.nlm.nih.gov/pubmed/12209371/
  38. Dietary fibres, fibre analogues, and glucose tolerance: importance of viscosity. Jenkins DJ, Wolever TM, Leeds AR, Gassull MA, Haisman P, Dilawari J, Goff DV, Metz GL, Alberti KG. Br Med J. 1978 May 27; 1(6124):1392-4. https://www.ncbi.nlm.nih.gov/pubmed/647304/
  39. Gastric emptying in early noninsulin-dependent diabetes mellitus. Jones KL, Horowitz M, Carney BI, Wishart JM, Guha S, Green L. J Nucl Med. 1996 Oct; 37(10):1643-8. https://www.ncbi.nlm.nih.gov/pubmed/8862300/
  40. Action of guar gums on the viscosity of digestive contents and on the gastrointestinal motor function in pigs. Cherbut C, Albina E, Champ M, Doublier JL, Lecannu G. Digestion. 1990; 46(4):205-13. https://www.ncbi.nlm.nih.gov/pubmed/2178135/
  41. Effect of viscous fiber (guar) on postprandial motor activity in human small bowel. Schönfeld J, Evans DF, Wingate DL. Dig Dis Sci. 1997 Aug; 42(8):1613-7. https://www.ncbi.nlm.nih.gov/pubmed/9286225/
  42. Effect of gel-forming gums on the intestinal unstirred layer and sugar transport in vitro. Johnson IT, Gee JM. Gut. 1981 May; 22(5):398-403. https://www.ncbi.nlm.nih.gov/pubmed/7250752/
  43. Role of viscous guar gums in lowering the glycemic response after a solid meal. Leclère CJ, Champ M, Boillot J, Guille G, Lecannu G, Molis C, Bornet F, Krempf M, Delort-Laval J, Galmiche JP. Am J Clin Nutr. 1994 Apr; 59(4):914-21. https://www.ncbi.nlm.nih.gov/pubmed/7818627/
  44. Dietary guar gum improves insulin sensitivity in streptozotocin-induced diabetic rats. Cameron-Smith D, Habito R, Barnett M, Collier GR. J Nutr. 1997 Feb; 127(2):359-64. https://www.ncbi.nlm.nih.gov/pubmed/9039840/
  45. Soluble dietary fibre improves insulin sensitivity by increasing muscle GLUT-4 content in stroke-prone spontaneously hypertensive rats. Song YJ, Sawamura M, Ikeda K, Igawa S, Yamori Y. Clin Exp Pharmacol Physiol. 2000 Jan-Feb; 27(1-2):41-5. https://www.ncbi.nlm.nih.gov/pubmed/10696527/
  46. Troglitazone effects on gene expression in human skeletal muscle of type II diabetes involve up-regulation of peroxisome proliferator-activated receptor-gamma. Park KS, Ciaraldi TP, Lindgren K, Abrams-Carter L, Mudaliar S, Nikoulina SE, Tufari SR, Veerkamp JH, Vidal-Puig A, Henry RR. J Clin Endocrinol Metab. 1998 Aug; 83(8):2830-5. https://www.ncbi.nlm.nih.gov/pubmed/9709955/
  47. Chen C, Zeng Y, Xu J, et al. Therapeutic effects of soluble dietary fiber consumption on type 2 diabetes mellitus. Experimental and Therapeutic Medicine. 2016;12(2):1232-1242. doi:10.3892/etm.2016.3377. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950069/
  48. Aldoori WH, Giovannucci EL, Rockett HR, Sampson L, Rimm EB, Willett WC. A prospective study of dietary fiber types and symptomatic diverticular disease in men. J Nutr. 1998;128:714-9. https://www.ncbi.nlm.nih.gov/pubmed/9521633
  49. Resistant starch: metabolic effects and potential health benefits. Higgins JA. J AOAC Int. 2004 May-Jun; 87(3):761-8. https://www.ncbi.nlm.nih.gov/pubmed/15287677/
  50. Birt DF, Boylston T, Hendrich S, et al. Resistant Starch: Promise for Improving Human Health. Advances in Nutrition. 2013;4(6):587-601. doi:10.3945/an.113.004325. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3823506/
  51. Englyst HN, Kingman SM, Cummings JH. Classification and measurement of nutritionally important starch fractions. Eur J Clin Nutr. 1992;46(Supp 2):S33–50. https://www.ncbi.nlm.nih.gov/pubmed/1330528
  52. Woo KS, Seib PA. Cross-linked resistant starch: preparation and properties. Cereal Chem. 2002;79:819–25.
  53. Han J-A, BeMiller JN. Preparation and physical characteristics of slowly digesting modified food starches. Carbohydr Polym. 2007;67:366–74.
  54. Seneviratne HD, Biliaderis CG. Action of α-amylases on amylose-lipid complex superstructures. J Cereal Sci. 1991;13:129–43.
  55. Ring S.G., Selvendran R.R. Isolation and Analysis of Cell-Wall Material from Beeswing Wheat Bran (Triticum-Aestivum) Phytochemistry. 1980;19:1723–1730.
  56. Arabinoxylan fiber, a byproduct of wheat flour processing, reduces the postprandial glucose response in normoglycemic subjects. Lu ZX, Walker KZ, Muir JG, Mascara T, O’Dea K. Am J Clin Nutr. 2000 May; 71(5):1123-8. https://www.ncbi.nlm.nih.gov/pubmed/10799374/
  57. Arabinoxylan fibre improves metabolic control in people with Type II diabetes. Lu ZX, Walker KZ, Muir JG, O’Dea K. Eur J Clin Nutr. 2004 Apr; 58(4):621-8. https://www.ncbi.nlm.nih.gov/pubmed/15042130/
  58. Selective stimulation of bifidobacteria in the human colon by oligofructose and inulin. Gibson GR, Beatty ER, Wang X, Cummings JH. Gastroenterology. 1995 Apr; 108(4):975-82. https://www.ncbi.nlm.nih.gov/pubmed/7698613/
  59. Dietary synbiotics reduce cancer risk factors in polypectomized and colon cancer patients. Rafter J, Bennett M, Caderni G, Clune Y, Hughes R, Karlsson PC, Klinder A, O’Riordan M, O’Sullivan GC, Pool-Zobel B, Rechkemmer G, Roller M, Rowland I, Salvadori M, Thijs H, Van Loo J, Watzl B, Collins JK. Am J Clin Nutr. 2007 Feb; 85(2):488-96. https://www.ncbi.nlm.nih.gov/pubmed/17284748/
  60. Griffin I.J., Hicks P.M.D., Heaney R.P., Abrams S.A. Enriched chicory inulin increases calcium absorption mainly in girls with lower calcium absorption. Nutr. Res. 2003;23:901–909.
  61. A combination of prebiotic short- and long-chain inulin-type fructans enhances calcium absorption and bone mineralization in young adolescents. Abrams SA, Griffin IJ, Hawthorne KM, Liang L, Gunn SK, Darlington G, Ellis KJ. Am J Clin Nutr. 2005 Aug; 82(2):471-6. https://www.ncbi.nlm.nih.gov/pubmed/16087995/
  62. Oligofructose promotes satiety in healthy human: a pilot study. Cani PD, Joly E, Horsmans Y, Delzenne NM. Eur J Clin Nutr. 2006 May; 60(5):567-72. https://www.ncbi.nlm.nih.gov/pubmed/16340949/
  63. Wood P.J., Weisz J., Fedec P. Potential for Beta-Glucan Enrichment in Brans Derived from Oat (Avena sativa L.) Cultivars of Different (1→3),(1→4)-Beta-D-Glucan Concentrations. Cereal Chem. 1991;68:48–51.
  64. Simultaneous intake of beta-glucan and plant stanol esters affects lipid metabolism in slightly hypercholesterolemic subjects. Theuwissen E, Mensink RP. J Nutr. 2007 Mar; 137(3):583-8. https://www.ncbi.nlm.nih.gov/pubmed/17311944/
  65. Beta-glucan incorporated into a fruit drink effectively lowers serum LDL-cholesterol concentrations. Naumann E, van Rees AB, Onning G, Oste R, Wydra M, Mensink RP. Am J Clin Nutr. 2006 Mar; 83(3):601-5. https://www.ncbi.nlm.nih.gov/pubmed/16522906/
  66. Davidson M.H., McDonald A. Fiber: Forms and functions. Nutr. Res. 1998;18:617–624.
  67. Changes in serum lipids and postprandial glucose and insulin concentrations after consumption of beverages with beta-glucans from oats or barley: a randomised dose-controlled trial. Biörklund M, van Rees A, Mensink RP, Onning G. Eur J Clin Nutr. 2005 Nov; 59(11):1272-81. https://www.ncbi.nlm.nih.gov/pubmed/16015250/
  68. Regulation of hepatic glucose production in healthy subjects and patients with non-insulin-dependent diabetes mellitus. Tappy L. Diabete Metab. 1995 Oct; 21(4):233-40. https://www.ncbi.nlm.nih.gov/pubmed/8529757/
  69. Oat beta-glucan increases bile acid excretion and a fiber-rich barley fraction increases cholesterol excretion in ileostomy subjects. Lia A, Hallmans G, Sandberg AS, Sundberg B, Aman P, Andersson H. Am J Clin Nutr. 1995 Dec; 62(6):1245-51. https://www.ncbi.nlm.nih.gov/pubmed/7491888/
  70. Modulation of the postprandial phase by beta-glucan in overweight subjects: effects on glucose and insulin kinetics. Nazare JA, Normand S, Oste Triantafyllou A, Brac de la Perrière A, Desage M, Laville M. Mol Nutr Food Res. 2009 Mar; 53(3):361-9. https://www.ncbi.nlm.nih.gov/pubmed/18837470/
  71. In vitro bile-acid binding and fermentation of high, medium, and low molecular weight beta-glucan. Kim HJ, White PJ. J Agric Food Chem. 2010 Jan 13; 58(1):628-34. https://www.ncbi.nlm.nih.gov/pubmed/20020684/
  72. In vitro fermentation of oat flours from typical and high beta-glucan oat lines. Kim HJ, White PJ. J Agric Food Chem. 2009 Aug 26; 57(16):7529-36. https://www.ncbi.nlm.nih.gov/pubmed/19572543/
  73. Regulation by dietary fats of 3-hydroxy-3-methylglutaryl-Coenzyme A reductase in rat liver. Ide T, Okamatsu H, Sugano M. J Nutr. 1978 Apr; 108(4):601-12. https://www.ncbi.nlm.nih.gov/pubmed/632948/
  74. Randomized controlled crossover study of the effect of a highly beta-glucan-enriched barley on cardiovascular disease risk factors in mildly hypercholesterolemic men. Keogh GF, Cooper GJ, Mulvey TB, McArdle BH, Coles GD, Monro JA, Poppitt SD. Am J Clin Nutr. 2003 Oct; 78(4):711-8. https://www.ncbi.nlm.nih.gov/pubmed/14522728/
  75. A controlled study of consumption of beta-glucan-enriched soups for 2 months by type 2 diabetic free-living subjects. Cugnet-Anceau C, Nazare JA, Biorklund M, Le Coquil E, Sassolas A, Sothier M, Holm J, Landin-Olsson M, Onning G, Laville M, Moulin P. Br J Nutr. 2010 Feb; 103(3):422-8. https://www.ncbi.nlm.nih.gov/pubmed/19781120/
  76. Olano-Martin E., Gibson G.R., Rastell R.A. Comparison of the in vitro bifidogenic properties of pectins and pectic-oligosaccharides. J. Appl. Microbiol. 2002;93:505–511. doi: 10.1046/j.1365-2672.2002.01719.x. https://www.ncbi.nlm.nih.gov/pubmed/12174051
  77. Nangia-Makker P., Hogan V., Honjo Y., Baccarini S., Tait L., Bresalier R., Raz A. Inhibition of human cancer cell growth and metastasis in nude mice by oral intake of modified citrus pectin. J. Natl. Cancer Inst. 2002;94:1854–1862. https://www.ncbi.nlm.nih.gov/pubmed/12488479
  78. Ulmius M., Johansson A., Onning G. The influence of dietary fibre source and gender on the postprandial glucose and lipid response in healthy subjects. Eur. J. Nutr. 2009;48:395–402. https://www.ncbi.nlm.nih.gov/pubmed/19415409
  79. Qureshi A.A., Sami S.A., Khan F.A. Effects of stabilized rice bran, its soluble and fiber fractions on blood glucose levels and serum lipid parameters in humans with diabetes mellitus Types I and II. J. Nutr. Biochem. 2002;13:175–187. https://www.ncbi.nlm.nih.gov/pubmed/11893482
  80. Koh-Banerjee P., Franz M.V., Sampson L., Liu S.M., Jacobs D.R., Spiegelman D., Willett W., Rimm E. Changes in whole-grain, bran, and cereal fiber consumption in relation to 8-y weight gain among men. Am. J. Clin. Nutr. 2004;80:1237–1245. https://www.ncbi.nlm.nih.gov/pubmed/15531671
  81. Zhang J.X., Lundin E., Hallmans G., Adlercreutz H., Andersson H., Bosaeus I., Aman P., Stenling R., Dahlgren S. Effect of Rye Bran on Excretion of Bile-Acids, Cholesterol, Nitrogen, and Fat in Human-Subjects with Ileostomies. Am. J. Clin. Nutr. 1994;59:389–394. https://www.ncbi.nlm.nih.gov/pubmed/8310990
  82. Jensen M.K., Koh-Banerjee P., Hu F.B., Franz M., Sampson L., Gronbaek M., Rimm E.B. Intakes of whole grains, bran, and germ and the risk of coronary heart disease in men. Am. J. Clin. Nutr. 2004;80:1492–1499. https://www.ncbi.nlm.nih.gov/pubmed/15585760
  83. Andersson M., Ellegard L., Andersson H. Oat bran stimulates bile acid synthesis within 8 h as measured by 7 alpha-hydroxy-4-cholesten-3-one. Am. J. Clin. Nutr. 2002;76:1111–1116. https://www.ncbi.nlm.nih.gov/pubmed/12399287
  84. Schwartz S.E., Levine R.A., Singh A., Scheidecker J.R., Track N.S. Sustained pectin ingestion delays gastric emptying. Gastroenterology. 1982;83:812–817. https://www.ncbi.nlm.nih.gov/pubmed/6286402
  85. Lightowler H.J., Henry C.J. Glycemic response of mashed potato containing high-viscocity hydroxypropylmethylcellulose. Nutr. Res. 2009;29:551–557. https://www.ncbi.nlm.nih.gov/pubmed/19761889
  86. Maki K.C., Davidson M.H., Witchger M.S., Dicklin M.R., Subbaiah P.V. Effects of high‑fiber oat and wheat cereals on postprandial glucose and lipid responses in healthy men. Int. J. Vitam. Nutr. Res. 2007;77:347–356. https://www.ncbi.nlm.nih.gov/pubmed/18453320
  87. Maki K.C., Davidson M.H., Torri S., Ingram K.A., O’Mullane J., Daggy B.P., Albrecht H.H. High-molecular-weight hydroxypropylmethylcellulose taken with or between meals is hypocholesterolemic in adult men. J. Nutr. 2000;130:1705–1710. https://www.ncbi.nlm.nih.gov/pubmed/10867040
  88. Maki K.C., Carson M.L., Anderson W.H.K., Geohas J., Reeves M.S., Farmer M.V., Turowski M., Miller M., Kaden V.N., Dicklin M.R., Rains T.M. Lipid-altering effects of different formulations of hydroxypropylmethylcellulose. J. Clin. Lipidol. 2009;3:159–166. https://www.ncbi.nlm.nih.gov/pubmed/21291811
  89. U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2015-2020. https://health.gov/sites/default/files/2019-09/2015-2020_Dietary_Guidelines.pdf
  90. Dietitians Association of Australia. Dietary fibre: key for a happy, healthy gut. https://daa.asn.au/smart-eating-for-you/smart-eating-fast-facts/nourishing-nutrients/dietary-fibre-a-key-ingredient-in-gut-happiness/
  91. Jenkins DJ, Jenkins AL, Wolever TM, Collier GR, Rao AV, Thompson LU. Starchy foods and fiber: reduced rate of digestion and improved carbohydrate metabolism. Scand J Gastroenterol Suppl 1987;129:132-41. https://www.ncbi.nlm.nih.gov/pubmed/2820027?dopt=Abstract
  92. Jenkins DJ, Wesson V, Wolever TM, et al. Wholemeal versus wholegrain breads: proportion of whole or cracked grain and the glycaemic response. BMJ 1988;297:958-60.
  93. Slavin JL, Martini MC, Jacobs DR Jr, Marquart L. Plausible mechanisms for the protectiveness of whole grains. Am J Clin Nutr 1999;70(suppl):459S-63S. http://ajcn.nutrition.org/content/70/3/459s.full
  94. Putnam J, Allshouse J, Kantor LS. US per capita food supply trends: more calories, refined carbohydrates, and fats. Food Rev 2002;25:2-15.
  95. Liu S. Intake of refined carbohydrates and whole grain foods in relation to risk of type 2 diabetes mellitus and coronary heart disease.J Am Coll Nutr 2002;21:298-306. https://www.ncbi.nlm.nih.gov/pubmed/12166526?dopt=Abstract
  96. Roberts SB, Heyman MB. Dietary composition and obesity: do we need to look beyond dietary fat? J Nutr 2000;130:267S (editorial).
  97. Ludwig DS, Pereira MA, Kroenke CH, et al. Dietary fiber, weight gain, and cardiovascular disease risk factors in young adults. JAMA1999 ;282:1539-46. https://www.ncbi.nlm.nih.gov/pubmed/10546693?dopt=Abstract
  98. National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III): Third report of the national cholesterol education program (ncep) expert panel on detection, evaluation, and treatment of high blood cholesterol in Adults (Adult Treatment Panel III) final report. Circulation. 2002;106:3143–3421. https://www.ncbi.nlm.nih.gov/pubmed/12485966
  99. Ortega RM, Palencia A, López-Sobaler AM. Improvement of cholesterol levels and reduction of cardiovascular risk via the consumption of phytosterols. Br J Nutr. 2006;96(Suppl 1):S89–S93. doi: 10.1079/BJN20061708. https://www.ncbi.nlm.nih.gov/pubmed/16923260
  100. Theuwissen E, Mensink RP. Water-soluble dietary fibers and cardiovascular disease. Physiol Behav. 2008;94:285–292. doi: 10.1016/j.physbeh.2008.01.001. https://www.ncbi.nlm.nih.gov/pubmed/18302966
  101. American Diabetes Association: Nutrition recommendations and principles for people with diabetes mellitus. Diabetes Care. 2000;23(Suppl 1):S43–S46. https://www.ncbi.nlm.nih.gov/pubmed/12017676
  102. Bernaud FS, Rodrigues TC. Dietary fiber-adequate intake and effects on metabolism health. Arq Bras Endocrinol Metabol. 2013;57:397–405. doi: 10.1590/S0004-27302013000600001. https://www.ncbi.nlm.nih.gov/pubmed/24030179
  103. Frankenfeld CL. Cardiometabolic risk factors are associated with high urinary enterolactone concentration, independent of urinary enterodiol concentration and dietary fiber intake in adults. J Nutr. 2014;144:1445–1453. doi: 10.3945/jn.114.190512. https://www.ncbi.nlm.nih.gov/pubmed/24966407
  104. Breneman CB, Tucker L. Dietary fibre consumption and insulin resistance-the role of body fat and physical activity. Br J Nutr. 2013;110:375–383. doi: 10.1017/S0007114512004953. https://www.ncbi.nlm.nih.gov/pubmed/23218116
  105. in the form of provitamin A carotenoids
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Diet PlanDiet, Food & Fitness

What are Diabetes Superfoods ?

10 superfoods for diabetes

type 2 diabetes superfoods

A Healthy, Balanced Diet for Diabetes

Whether you are living with diabetes or not, eating a healthy balanced is important. Following a healthy, balanced diet will help to control blood glucose, blood fats and blood pressure, as well as helping to maintain a healthy weight. This can help to reduce your risk of diabetes complications, including heart disease and stroke.

The amount of carbohydrates you eat has the biggest effect on your blood glucose levels after eating. Therefore, reducing portions can help manage your glucose levels. It is also important to choose better sources of carbohydrates including wholegrains, pulses, fruits and vegetables and some dairy foods.

If you are overweight, reducing your overall portion sizes will also help you to lose weight. Losing excess weight has been shown to be beneficial in managing blood glucose, blood pressure and cholesterol levels. There are different approaches to losing weight.

Healthy eating helps keep your blood sugar in your target range. It is a critical part of managing your diabetes, because controlling your blood sugar can prevent the complications of diabetes.

  • The Centers for Disease Control and Prevention has a free recipes ebook for people and their families with diabetes, you download a free copy here 1.

A registered dietitian can also help you make an eating plan just for you. It should take into account your weight, medicines, lifestyle, and other health problems you have.

  • To find out about your body mass index (BMI), you can use a FREE online BMI calculators from the Centers for Disease Control and Prevention (CDC) – for Adults 2 and for Children 3
  • To find out What and How Much To Eat, you can use a FREE, award-winning, state-of-the-art, online diet and activity tracking tool called SuperTracker 4 from the United States Department of Agriculture Center for Nutrition Policy and Promotion 4. This free application empowers you to build a healthier diet, manage weight, and reduce your risk of chronic diet-related diseases. You can use SuperTracker 4 to determine what and how much to eat; track foods, physical activities, and weight; and personalize with goal setting, virtual coaching, and journaling.

SuperTracker website 4

  • To find out about how many calories you should eat to lose weight according to your weight, age, sex, height and physical activity, you can use a FREE online app Body Weight Planner 5
  • To find out about the 5 Food Groups you should have on your plate for a meal, you can use a FREE online app ChooseMyPlate 6

 

The foods you choose to eat in your daily diet make a difference not only to managing diabetes, but also to how well you feel and how much energy you have every day.

  • How much you need to eat and drink is based on your age, gender, how active you are and the goals you are looking to achieve.
  • Portion sizes have grown in recent years, as the plates and bowls we use have got bigger. Use smaller crockery to cut back on your portion sizes, while making the food on your plate look bigger.
  • No single food contains all the essential nutrients you need in the right proportion. That’s why you need to consume foods from each of the main food groups to eat well.

1) Fruit and vegetables

Naturally low in fat and calories and packed full of vitamins, minerals and fibre, fruit and vegetables add flavor and variety to every meal.

They may also help protect against stroke, heart disease, high blood pressure and some cancers.

  • Everyone should eat at least five portions a day. Fresh, frozen, dried and canned fruit in juice and canned vegetables in water all count. Go for a rainbow of colors to get as wide a range of vitamins and minerals as possible.

Try:

  • adding an apple, banana, pear, or orange to your lunchbox
  • sliced melon or grapefruit topped with low-fat yogurt, or a handful of berries, or fresh dates, apricots or prunes for breakfast
  • carrots, peas and green beans mixed up in a pasta bake
  • adding an extra handful of vegetables to your dishes when cooking – peas to rice, spinach to lamb or onions to chicken.

Vegetarian Diets Linked to Lower Mortality

Adults who eat a more plant-based diet may be boosting their chance of living longer, according to a large analysis.

Researchers studied more than 73,000 Seventh-day Adventist men and women ages 25 and older 7. The participants were categorized into dietary groups at the time of recruitment based on their reported food intake during the previous year. Nearly half of the participants were nonvegetarian, eating red meat, poultry, fish, milk and eggs more than once a week. Of the remaining, 8% were vegan (eating red meat, fish, poultry, dairy or eggs less than once a month); 29% were lacto-ovo vegetarians (eating eggs and/or dairy products, but red meat, fish or poultry less than once per month); 10% were pesco-vegetarians (eating fish, milk and eggs but rarely red meat or poultry); and 5% were semi-vegetarian (eating red meat, poultry and fish less than once per week).

Over about 6 years, there were 2,570 deaths among the participants. The researchers found that vegetarians (those with vegan, and lacto-ovo-, pesco-, and semi-vegetarian diets) were 12% less likely to die from all causes combined compared to nonvegetarians. The death rates for subgroups of vegans, lacto-ovo–vegetarians, and pesco-vegetarians were all significantly lower than those of nonvegetarians.

Those on a vegetarian diet tended to have a lower rate of death due to cardiovascular disease, diabetes, and renal disorders such as kidney failure. No association was detected in this study between diet and deaths due to cancer. The researchers also found that the beneficial associations between a vegetarian diet and mortality tended to be stronger in men than in women.

The researchers note several limitations to the study. Participants only reported their diet at the beginning of the study, and their eating patterns might have changed over time. In addition, they were only followed for an average of 6 years; it may take longer for dietary patterns to influence mortality 7.

2) Starchy foods

Potatoes, rice, pasta, bread, chapattis, naan and plantain all contain carbohydrate, which is broken down into glucose and used by your cells as fuel. Better options of starchy foods – such as wholegrain bread, wholewheat pasta and basmati, brown or wild rice – contain more fibre, which helps to keep your digestive system working well. They are generally more slowly absorbed (that is, they have a lower glycaemic index, or GI), keeping you feeling fuller for longer.

  • Try to include some starchy foods every day.

Try:

  • two slices of multigrain toast with a scraping of spread and peanut butter
  • rice, pasta or noodles in risottos, salads or stir-fries
  • potatoes any way you like – but don’t fry them – with the skin left on for valuable fibre. Choose low-fat toppings, such as cottage cheese or beans
  • baked sweet potato, with the skin left on for added fibre
  • boiled cassava, flavoured with chilli and lemon
  • chapatti made with brown or wholemeal atta.

3) Meat, fish eggs, pulses, beans and nuts

These foods are high in protein, which helps with building and replacing muscles. They contain minerals, such as iron, which are vital for producing red blood cells. Oily fish, such as mackerel, salmon and sardines, also provide omega-3, which can help protect the heart. Beans, pulses, soya and tofu are also good sources of protein.

  • Aim to have some food from this group every day, with at least 1–2 portions of oily fish a week.

Try:

  • serving meat, poultry or a vegetarian alternative grilled, roasted or stir-fried
  • a small handful of raw nuts and seeds as a snack or chopped with a green salad
  • using beans and pulses in a casserole to replace some – or all – of the meat
  • grilled fish with masala, fish pie, or make your own fish cakes
  • eggs scrambled, poached, dry fried or boiled – the choice is yours!

4) Dairy foods

Milk, cheese and yogurt contain calcium, which is vital for growing children as it keeps their bones and teeth strong. They’re good sources of protein, too.
Some dairy foods are high in fat, particularly saturated fat, so choose lower-fat alternatives (check for added sugar, though). Semi-skimmed milk actually contains more calcium than whole milk, but children under 2 should have whole milk because they may not get the calories or essential vitamins they need from lower-fat milks. Don’t give children skimmed milk until they’re at least 5.

  • Aim to have some dairy every day, but don’t overdo it.

Try:

  • milk straight in a glass, flavoured with a little cinnamon, or added to breakfast porridge
  • yogurt with fruit or on curry
  • cottage cheese scooped on carrot sticks
  • a bowl of breakfast cereal in the morning, with skimmed or semi-skimmed milk
  • a cheese sandwich at lunchtime, packed with salad
  • a refreshing lassi or some plain yogurt with your evening meal.

Changes you can make are:

  • Avoid foods labelled ‘diabetic’ or ‘suitable for diabetics’. These foods contain similar amounts of calories and fat, and they can affect your blood glucose levels. They are usually more expensive and can have a laxative effect. Stick to your usual foods. If you want to have an occasional treat, go for your normal treats and keep an eye on your portions.
  • Reduce Fried foods and other foods high in saturated fat and trans fat
  • Foods high in salt, also called sodium
  • Reduce intake of chips, cookies, cakes, full-fat ice cream, etc.
  • Cut back on high calorie snack foods and desserts.
  • Sweets, such as baked goods, candy, and ice cream
  • Beverages with added sugars, such as juice, regular soda, and regular sports or energy drinks
  • Eating too much of even healthful foods can lead to weight gain.
  • If you choose to drink alcohol, do so in moderation. (Two or less drinks per day for men and one or less drinks per day for women.)
  • Watch your portion sizes.
  • Reduce the fat (both saturated and trans fat), sugar or salt content of your food.
  • Drink water instead of sweetened beverages. Consider using a sugar substitute in your coffee or tea.

Making gradual and realistic changes over a longer period of time is more likely to lead to success. Be sure to get all of the tools you need to help you achieve these changes – structured education to make sure you have the right information, support from a healthcare professional such as a registered dietitian, and the backing of your family and friends. Although it may feel overwhelming now, it will get easier in the long run.

To successfully manage diabetes, you need to understand how foods and nutrition affect your body. Food portions and food choices are important. Carbohydrates, fat and protein need to be balanced to ensure blood sugar levels stay as stable as possible. (This is particularly important for people with Type 1 diabetes.)

The key to eating with diabetes is to eat a variety of healthy foods from all food groups, in the amounts your meal plan outlines. For that reason the American Diabetes Association has created:

  • The Diabetic Diet Meal Plans 8 and
  • A online tool called Create Your Plate 9. With Create Your Plate method, you fill your plate with more non-starchy veggies and smaller portions of starchy foods and protein—no special tools or counting required. You can practice with this interactive tool 9.

diet for better diabetes management

Summary

Healthy eating and an active lifestyle are important for everyone, including people with diabetes. To achieve and maintain a healthy weight, be physically active and choose amounts of nutritious foods and drinks to meet your energy needs. Having a healthy diet and being active is an important part of managing diabetes because it will help manage your blood glucose levels and your body weight.

  1. Meals that are recommended for people with diabetes are the same as for those without diabetes.
  2. There is no need to prepare separate meals or buy special foods.
  3. Everyone including family and friends can enjoy the same healthy and tasty meals together.
  4. As a guide, we recommend people with diabetes follow the American Dietary Guidelines Healthy Eating for Adults and Healthy Eating for Children.
  5. Everyone’s needs are different so we recommend everyone with diabetes visit a dietitian for personal advice.
  6. Enjoy a wide variety of nutritious from these five food groups every day:

a) Plenty of vegetables and different types and colors and legumes/beans.

b) Fruits

c) Grain (cereal) foods, mostly wholegrain and/or high cereal fiber varieties, such as breads, cereals, rice, pasta, noodles, polenta, couscous, quinoa, oats, and barley.

d) Lean meats and poultry, fish, eggs, tofu, nuts and seeds, and legumes/beans.

e) Milk, yogurt, cheese and/or their alternatives, mostly reduced fat.

And drink plenty of water. Limit intake of foods and drinks containing added salt, sugar and saturated and trans fats.

10 superfoods for diabetes

Vegetarian Diets and Diabetes

Reasons for switching to a vegetarian diet include:

  • the health benefits
  • ethical and moral reasons
  • religious or cultural reasons
  • concern for animal welfare
  • concern about the environment and sustainability
  • taste – some people just don’t like the taste of meat or fish.

A vegetarian diet, based on unprocessed foods, can provide many health benefits for us all, whether or not you have diabetes.

If you have diabetes, it’s important to be more aware of how what you eat affects your body and, in turn, you’ll hopefully become more health conscious.

So what is a vegetarian diet ? Are there any ways it could help manage diabetes ? Does it provide any health benefits for people with diabetes ?

According to the Vegetarian Society 10, a vegetarian is:

  • “Someone who lives on a diet of grains, pulses, legumes, nuts, seeds, vegetables, fruits, fungi, algae, yeast and/or some other non-animal-based foods (e.g. salt) with, or without, dairy products, honey and/or eggs. A vegetarian does not eat foods that consist of, or have been produced with the aid of products consisting of or created from, any part of the body of a living or dead animal. This includes meat, poultry, fish, shellfish*, insects, by-products of slaughter** or any food made with processing aids created from these.”
  • * Shellfish are typically ‘a sea animal covered with a shell’. We take shellfish to mean; Crustaceans (hard external shell) e.g. lobsters, crayfish, crabs, prawns, shrimps; Molluscs (most are protected by a shell) e.g. mussels, oysters, winkles, limpets, clams, etc. Also includes cephalopods such as cuttlefish, squid, octopus.
  • ** By-products of slaughter includes gelatine, isinglass and animal rennet.
  • Eggs: Many lacto-ovo vegetarians will only eat free-range eggs. This is because of welfare objections to the intensive farming of hens. Through its Vegetarian Society Approved trademark scheme, the Vegetarian Society will only license its trademark to products containing free-range eggs where eggs are used.

There are different types of vegetarians:

  • Lacto-ovo-vegetarians eat both dairy products and eggs (usually free range). This is the most common type of vegetarian diet 11.
  • Lacto-vegetarians eat dairy products, but avoid eggs.
  • Ovo-vegetarian. Eats eggs but not dairy products.
  • Vegans do not any products derived from animals – no meat, fish, dairy or eggs.

Why you may try a vegetarian diet ?

Plant-based foods, particularly fruit and vegetables, nuts, pulses and seeds have been shown to help in the treatment of many chronic diseases and are often associated with lower rates of Type 2 diabetes, less hypertension, lower cholesterol levels and reduced cancer rates 12.

These foods are also higher in fibre, antioxidants, folate and phytochemicals, which are all good for our general health.

Vegetarian diets have been shown to be beneficial for people with Type 2 diabetes where weight loss is often the most effective way to manage the condition. A wholefood vegetarian diet often contains fewer calories and can help you to maintain a healthy body weight.

In a review of scientific publications from 1946- December 2013, it was found that the consumption of vegetarian diets was associated with a significant reduction in HbA1c and a non-significant reduction in fasting blood glucose concentration 13.

In another randomised study with 74 patients with type 2 diabetes, who were given either calorie restricted (-500 kcal/day) vegetarian diet (37 subjects) or calorie restricted (-500 kcal/day) conventional diabetic diet (37 subjects) over 24 weeks 14. In the second 12 weeks of the study, the calorie restricted diets were combined with aerobic exercise. Participants were examined at baseline, 12 weeks and 24 weeks. Forty-three per cent of participants in the calorie restricted (-500 kcal/day) vegetarian diet group and 5% of participants in the calorie restricted (-500 kcal/day) conventional diabetic diet group reduce their diabetes medication. Body weight decreased more in the calorie restricted vegetarian diet group (-6.2 kg) than in the calorie restricted conventional diabetic diet group (-3.2 kg). An increase in insulin sensitivity was significantly greater in the calorie restricted vegetarian diet group than in the calorie restricted conventional diabetic diet group. A reduction in both visceral and subcutaneous fat was greater in the calorie restricted vegetarian diet group than in the calorie restricted conventional diabetic diet group. Plasma adiponectin increased (a protein hormone produced and secreted exclusively by adipocytes (fat cells) that regulates the metabolism of lipids and glucose. High blood levels of adiponectin are associated with a reduced risk of heart attack. Low levels of adiponectin are found in people who are obese (and who are at increased risk of a heart attack) and leptin decreased (a hormone produced mainly by adipocytes (fat cells) that is involved in the regulation of body fat. Leptin interacts with areas of the brain that control hunger and behavior and signals that the body has had enough to eat. Leptin tells your brain that you have enough energy stored in your fat cells to engage in normal) in the calorie restricted vegetarian diet group, with no change in the calorie restricted conventional diabetic diet group. Differences between groups were greater after the addition of exercise training. Changes in insulin sensitivity and enzymatic oxidative stress markers correlated with changes in visceral fat 14.

Diabetes Superfoods

Sources from the American Diabetes Association and the Diabetes UK 15.

All of the foods in the list have a low glycemic index or low GI and provide key nutrients that are lacking in the typical western diet such as:

  • calcium
  • potassium
  • fiber
  • magnesium
  • vitamins A (as carotenoids), vitamin C and vitamin E.

There isn’t research that clearly points to supplementation, so always think first about getting your nutrients from foods. Below is our list of superfoods to include in your diet.

Beans

Whether you prefer kidney, pinto, navy, or black beans, you can’t find better nutrition than that provided by beans. They are very high in fiber, a great source of protein, giving you about 1/3 of your daily requirement in just a ½ cup, and are also good sources of magnesium and potassium. Beans soluble fibre can lower your levels of “bad” cholesterol (low-density lipoprotein, or LDL) and lowers blood glucose levels.

They are considered starchy vegetables, beans are fairly high in carbohydrates, although it is a slower-acting carbohydrate but ½ cup provides as much protein as an ounce of meat without the saturated fat. To save time you can use canned beans, but be sure to drain and rinse them to get rid of as much sodium as possible.

Beans not only offer up a hefty variety of vitamins and minerals, but some studies 16 have shown that eating more beans can help to keep blood sugars lowered and keep HbA1c levels in line.

Incorporating beans into a low GI diet can improve both glycemic control and the risk the heart disease, especially in people with type 2 diabetes 17.

Healthy examples of beans include:

  • Black beans
  • White beans
  • Navy beans
  • Lima beans
  • Pinto beans
  • Garbanzo beans
  • Soy beans
  • Kidney beans

2) Dark Green Leafy Vegetables

Spinach, collards, kale – these powerhouse foods are so low in calories and carbohydrate. You can’t eat too much.

Non-starchy vegetables include dark, leafy greens, green beans and peppers (versus starchy veggies like corn and potatoes). Loading up at least a quarter of your plate with non-starchy veggies at each meal can help to fill you up on lots of fiber and fewer calories, which can aid in both blood glucose stabilization and weight reduction. Opting for more non-starchy veggies is also a great way to increase your intake of antioxidants and phytochemicals (a fancy name for healthy plant compounds) that help to ward off disease.

Examples of non-starchy vegetables include:

  • Cabbage
  • Lettuce
  • Spinach
  • Carrots
  • Courgette
  • Cucumber
  • Celery
  • Broccoli
  • Cauliflower
  • Mushrooms
  • Peppers
  • Tomato

3) Citrus Fruit

Citrus fruit is full of vitamin C. One large orange contains all the daily vitamin C you need. Citrus fruits also balance blood pressure.

On the other hand, citrus fruits contain a lot of carbohydrates. A medium grapefruit has 18.5g of carbohydrates, which is about the same amount as two bourbon biscuits.

People following a low-carb diet should eat citrus fruit in moderation. A single Satsuma per meal is about the limit.
Excessive amounts of the acid in citrus fruits can upset your stomach. Some people worry that citrus fruit damages the teeth, eroding the enamel, but this isn’t quite true.

Citrus fruit softens the enamel, which makes it more susceptible to damage from other sources, but doesn’t directly cause any damage. After about an hour, the enamel will harden again.

Citrus fruits offer a lot of benefits, but the carbohydrate content makes it advisable for people with diabetes only in moderation. That said, much of the carbohydrates in citrus fruit is fibre (about 4g of the 21g of carbohydrate in an orange), which lowers cholesterol and blood glucose levels. So it would be wise not to cut citrus fruit out of your diet altogether.

Good examples of citrus fruit include:

  • Oranges
  • Grapefruit
  • Lemon
  • Lime

4) Sweet Potatoes

A starchy vegetable packed full of vitamin A and fiber. Try in place of regular potatoes for a lower GI alternative.

Sweet potato comes in many different varieties and their GI values can range from low 45 (Ipomoea batatas) boiled to 94 (Ipomoea batatas) baked 18.

Table 1. Sweet Potato (Raw Unprepared) Nutrition Content

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. 19]

5) Berries

Which are your favorites: blueberries, strawberries or another variety ? Regardless, they are all packed with antioxidants, vitamins and fiber.

Several studies have linked berries to a number of health benefits for people with diabetes, particularly type 2 diabetes.

A study published in the Journal of Nutrition indicated that the benefits of berries are due to a group of compounds called anthocyanins 20, 21, 22.

The study showed that consumption of 160mg of anthocyanins twice a day led to:

  • 7.9 per cent reduction of low-density lipoprotein (LDL): LDL is also known, somewhat simplistically, as ‘bad cholesterol’. Generally, when people talk about “high cholesterol levels” they are referring to low-density lipoprotein
  • 19.4 per cent increase in levels of high-density lipoprotein (HDL). HDL is often known as “good cholesterol.” It clears LDL cholesterol out of the arteries
  • 8.5 per cent reduction in fasting plasma glucose levels
  • 13 per cent less insulin resistance
  • 23.4 per cent increase of adiponectin, a hormone that increases insulin sensitivity
  • The data suggest an inverse association between intake of anthocyanins and anthocyanin-rich foods (eg, blueberries and apples/pears) and type 2 diabetes in US men and women. It is possible that these findings reflect other dietary components that co-exist in anthocyanin-rich foods, and randomized trials will be needed to establish the effects that can be specifically attributed to anthocyanins. Further research on anthocyanin-rich foods may lead to more specific recommendations on consumption of fruit, which may contribute to the prevention of type 2 diabetes 21.

Berries are also a good source of vitamin C and fibre, and they don’t contain many carbohydrates. That said, although the research is promising, it isn’t yet conclusive 21. The signs are good, but the research is ongoing.

Berries are best incorporated into breakfast or dessert. They’re a great way of making often unhealthy or carb-heavy meals into something more nutritious.

Good examples of berries include:

  • Blueberries
  • Strawberries
  • Blackberries
  • Raspberries
  • Cherries

6) Tomatoes

An old standby where everyone can find a favorite. The good news is that no matter how you like your tomatoes, pureed, raw, or in a sauce, you’re eating vital nutrients like vitamin C, iron, vitamin E.

Table 2. Tomato (Red Raw) Nutrition Content

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. 19]

7) Fish High in Omega-3 Fatty Acids

Wild salmon is a favorite in this category. Stay away from the breaded and deep fat fried variety, they don’t count in your goal of 6-9 ounces of fish per week.

Few animal proteins offer up the amount of healthy omega-3 fatty acids quite like wild salmon or tuna. These cold-water fish have been shown to reduce inflammation in the body and have major heart-protecting properties that are particularly important for staving off coronary heart disease, a high risk factor for those living with diabetes.

  • Fish high in omega-3 fatty acids like Albacore tuna, herring, mackerel, rainbow trout, sardines, and salmon
  • Other fish including catfish, cod, flounder, haddock, halibut, orange roughy, and tilapia
  • Shellfish including clams, crab, imitation shellfish, lobster, scallops, shrimp, oysters.

The American Diabetes Association recommends eating fish at least two times per week to reap its omega-3 fatty acids benefits 23.

8) Whole Grains

It’s the germ and bran of the whole grain you’re after.  It contains all the nutrients a grain product has to offer. When you purchase processed grains like bread made from enriched wheat flour, you don’t get these. A few more of the nutrients these foods offer are magnesium, chromium, omega 3 fatty acids and folate.

Pearled barley and oatmeal are a source of fiber and potassium.

9) Nuts

An ounce of nuts can go a long way in providing key healthy fats along with hunger management. Other benefits are a dose of magnesium and fiber.

Some nuts and seeds, such as walnuts and flax seeds, also contain omega-3 fatty acids. Similar to fatty-fish, nuts have an excellent nutrition profile that research suggests can both reduce HbA1c levels and lower amounts of LDL or “bad” cholesterol in the body. It only takes about 2 ounces of nuts per day to see these great effects.

Try adding a tablespoon of chopped nuts to salads or oatmeal for an extra punch of protein and healthy fats. Or pair a handful of raw almonds or walnuts with a piece of fresh fruit for a great, mid-day snack that won’t send blood sugars surging.

10) Milk and Yogurt

Everyone knows dairy can help build strong bones and teeth. In addition to calcium, many fortified dairy products are a good source of vitamin D. More research is emerging on the connection between vitamin D and good health.

Greek yogurt is a very versatile ingredient that packs almost double the amount of protein of regular yogurt varieties and is typically lower in overall carbohydrates. Better yet, Greek yogurt is an excellent source of probiotics, also known as “friendly” gut bacteria that promote healthy digestion and may play a major role in the prevention and management of both Type 1 and Type 2 diabetes.

Seek out yogurts with few ingredients and no added sugars or thickeners. If you do like your yogurts sweetened, try adding fresh or frozen fruit to avoid spiking blood sugars. It can also be used in baking and as a substitute for sour cream in savory dishes.

References
  1. https://www.cdc.gov/diabetes/ndep/cdcinfo/ndep_pdf/tasty-recipes-508.pdf
  2. BMI Calculator Adults. https://www.cdc.gov/healthyweight/assessing/bmi/adult_BMI/english_bmi_calculator/bmi_calculator.html
  3. BMI Calculator Children. https://nccd.cdc.gov/dnpabmi/Calculator.aspx
  4. https://supertracker.usda.gov/
  5. Body Weight Planner. https://www.supertracker.usda.gov/bwp/index.html
  6. ChooseMyPlate. https://www.choosemyplate.gov/
  7. JAMA Intern Med. 2013;173(13):1230-1238. doi:10.1001/jamainternmed.2013.6473. Vegetarian Dietary Patterns and Mortality in Adventist Health Study 2. http://jamanetwork.com/journals/jamainternalmedicine/fullarticle/1710093
  8. American Diabetes Association. All of Our Meal Plans. http://www.diabetes.org/mfa-recipes/meal-plans/meal-plans.html
  9. American Diabetes Association. Create Your Plate. http://www.diabetes.org/food-and-fitness/food/planning-meals/create-your-plate/
  10. The Vegetarian Society. https://www.vegsoc.org/
  11. The Vegetarian Society. https://www.vegsoc.org/definition
  12. Diabetes UK. Vegetarian diets and diabetes. https://www.diabetes.org.uk/Guide-to-diabetes/Enjoy-food/Eating-with-diabetes/vegetarian-diets/
  13. Cardiovasc Diagn Ther. 2014 Oct; 4(5): 373–382. doi: 10.3978/j.issn.2223-3652.2014.10.04. Vegetarian diets and glycemic control in diabetes: a systematic review and meta-analysis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221319/
  14. Diabet Med. 2011 May;28(5):549-59. doi: 10.1111/j.1464-5491.2010.03209.x. Vegetarian diet improves insulin resistance and oxidative stress markers more than conventional diet in subjects with Type 2 diabetes. https://www.ncbi.nlm.nih.gov/pubmed/21480966
  15. Diabetes UK. Diabetes ‘Superfoods’. http://www.diabetes.co.uk/food/diabetes-superfoods.html
  16. Nutrition Journal 2012, 11:23. DOI: 10.1186/1475-2891-11-23. Bean and rice meals reduce postprandial glycemic response in adults with type 2 diabetes: a cross-over study. https://nutritionj.biomedcentral.com/articles/10.1186/1475-2891-11-23
  17. Arch Intern Med. 2012;172(21):1653-1660. doi:10.1001/2013.jamainternmed.70. Effect of Legumes as Part of a Low Glycemic Index Diet on Glycemic Control and Cardiovascular Risk Factors in Type 2 Diabetes Mellitus. A Randomized Controlled Trial. http://jamanetwork.com/journals/jamainternalmedicine/fullarticle/1384247
  18. http://glycemicindex.com
  19. United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. https://ndb.nal.usda.gov/ndb/
  20. J. Nutr. February 1, 2014. vol. 144 no. 2 202-208. Intakes of Anthocyanins and Flavones Are Associated with Biomarkers of Insulin Resistance and Inflammation in Women. http://jn.nutrition.org/content/144/2/202.full
  21. Am J Clin Nutr April 2012. vol. 95 no. 4 925-933. Dietary flavonoid intakes and risk of type 2 diabetes in US men and women. http://ajcn.nutrition.org/content/95/4/925.full.pdf+html
  22. Am J Clin Nutr. 2014 Feb;99(2):328-33. doi: 10.3945/ajcn.113.069641. Epub 2013 Nov 20. Intake of fruit, berries, and vegetables and risk of type 2 diabetes in Finnish men: the Kuopio Ischaemic Heart Disease Risk Factor Study. https://www.ncbi.nlm.nih.gov/pubmed/24257723
  23. American Diabetes Association. Protein Foods. http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/making-healthy-food-choices/meat-and-plant-based-protein.html
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Diet PlanDiet, Food & Fitness

What is Glycaemic (GI) Index ?

glycemic index food list

What is Glycemic Index?

Carbohydrate is an essential part of our diets, but not all carbohydrate foods are equal. The glycemic index (GI) was first developed by Jenkins and colleagues 1 and the Glycemic Index (GI) is a relative ranking of carbohydrate in foods according to how they affect blood glucose levels 2. Carbohydrates with a low GI value (55 or less) are more slowly digested, absorbed and metabolised and cause a lower and slower rise in blood glucose and, therefore usually, insulin levels.

Research shows that both the amount and the type of carbohydrate in food affect blood glucose levels. Studies also show that the total amount of carbohydrate in food, in general, is a stronger predictor of blood glucose response than the GI.

The glycemic index or GI ranks carbohydrates according to their effect on blood glucose levels. The lower the GI, the slower the rise in blood glucose levels will be when the food is consumed. The effect may differ from person to person.

Diabetes: There is no one diet or meal plan that works for everyone with diabetes. It is recommended that people with diabetes have moderate amounts of carbohydrate and include high fibre foods that also have a low GI (not all high fibre foods have a low GI). Because the type of carbohydrate can affect blood glucose, using the GI may be helpful in “fine-tuning” blood glucose management. In other words, combined with carbohydrate counting, it may provide an additional benefit for achieving blood glucose goals for individuals who can and want to put extra effort into monitoring their food choices. The amount of carbs you eat has a bigger effect on blood glucose levels than GI alone. For example, pasta has a lower GI than watermelon, but pasta has more carbs than watermelon, so if you eat similar amounts of either of these two foods, the pasta will have more of an impact on your blood glucose levels. The most important thing to do is get your portion size right – once you do this, you will get an added bonus for choosing low-GI alternatives.

Meats and fats don’t have a GI because they do not contain carbohydrate.

Some research has shown that by eating a diet with a lower GI, people with diabetes can reduce their average blood glucose levels. This is important in reducing the risk of developing diabetes-related complications.

The GI index runs from 0–100 and usually uses glucose, which has a GI of 100, as the reference. Slowly absorbed carbohydrates have a low GI rating (55 or below), and include most fruits and vegetables, milk, some wholegrain cereals and bread, pulses and basmati rice. GI numbers are to be used as a guide only as individual foods do not have the same response in all people with diabetes.

  • Low GI foods are foods with a GI less than 55.
  • Intermediate GI foods are foods with a GI between 55 and 70.
  • High GI foods are foods with a GI greater than 70.

Below are examples of foods based on their GI.

Low GI Foods (55 or less)

  • 100% stone-ground whole wheat or pumpernickel bread
  • Oatmeal (rolled or steel-cut), oat bran, muesli
  • Pasta, converted rice, barley, bulgar
  • Sweet potato, corn, yam, lima/butter beans, peas, legumes and lentils
  • Most fruits, non-starchy vegetables and carrots

Not all low-GI foods are healthy choices – chocolate, for example, has a low-GI because of its fat content, which slows down the absorption of carbohydrate.

Medium GI (56-69)

  • Whole wheat, rye and pita bread
  • Quick oats
  • Brown, wild or basmati rice, couscous

High GI (70 or more)

  • White bread or bagel
  • Corn flakes, puffed rice, bran flakes, instant oatmeal
  • Shortgrain white rice, rice pasta, macaroni and cheese from mix
  • Russet potato, pumpkin
  • Pretzels, rice cakes, popcorn, saltine crackers
  • melons and pineapple

Table 1. The average GI of 62 common foods derived from multiple studies by different laboratories

High-carbohydrate foodsGlycemic index (GI)Breakfast cerealsGlycemic index (GI)Fruit and fruit productsGlycemic index (GI)VegetablesGlycemic index (GI)
White wheat bread*75 ± 2Cornflakes81 ± 6Apple, raw†36 ± 2Potato, boiled78 ± 4
Whole wheat/whole meal bread74 ± 2Wheat flake biscuits69 ± 2Orange, raw†43 ± 3Potato, instant mash87 ± 3
Specialty grain bread53 ± 2Porridge, rolled oats55 ± 2Banana, raw†51 ± 3Potato, french fries63 ± 5
Unleavened wheat bread70 ± 5Instant oat porridge79 ± 3Pineapple, raw59 ± 8Carrots, boiled39 ± 4
Wheat roti62 ± 3Rice porridge/congee78 ± 9Mango, raw†51 ± 5Sweet potato, boiled63 ± 6
Chapatti52 ± 4Millet porridge67 ± 5Watermelon, raw76 ± 4Pumpkin, boiled64 ± 7
Corn tortilla46 ± 4Muesli57 ± 2Dates, raw42 ± 4Plantain/green banana55 ± 6
White rice, boiled*73 ± 4Peaches, canned†43 ± 5Taro, boiled53 ± 2
Brown rice, boiled68 ± 4Strawberry jam/jelly49 ± 3Vegetable soup48 ± 5
Barley28 ± 2Apple juice41 ± 2
Sweet corn52 ± 5Orange juice50 ± 2
Spaghetti, white49 ± 2
Spaghetti, whole meal48 ± 5
Rice noodles†53 ± 7
Udon noodles55 ± 7
Couscous†65 ± 4

 

Dairy products and alternativesGlycemic index (GI)LegumesGlycemic index (GI)Snack productsGlycemic index (GI)SugarsGlycemic index (GI)
Milk, full fat39 ± 3Chickpeas28 ± 9Chocolate40 ± 3Fructose15 ± 4
Milk, skim37 ± 4Kidney beans24 ± 4Popcorn65 ± 5Sucrose65 ± 4
Ice cream51 ± 3Lentils32 ± 5Potato crisps56 ± 3Glucose103 ± 3
Yogurt, fruit41 ± 2Soya beans16 ± 1Soft drink/soda59 ± 3Honey61 ± 3
Soy milk34 ± 4Rice crackers/crisps87 ± 2
Rice milk86 ± 7

Footnotes:

*Low-GI varieties were also identified.
†Average of all available data.

The GI should not be used in isolation; the energy density and macronutrient profile of foods should also be considered 3.

[Source 4 ]

Remember, GI is not a reflection of how healthy a food is.

  • Fat content – Foods high in fat often have a low GI (e.g. chocolate or corn chips) and should only be included occasionally.
  • The amount of food eaten– a small amount of a high GI food e.g. watermelon may only have a small effect on blood sugar levels.
  • The quality of food– always aim to eat a wide range of carbohydrate containing foods including wholegrain breads and cereals, fresh fruit and vegetables and dairy which provide important nutrients and fibre.

The GI value relates to the food eaten on its own and in practice we usually eat foods in combination as meals. Bread, for example is usually eaten with butter or margarine, and potatoes could be eaten with meat and vegetables. Therefore relying solely on the glycemic index of foods could result in eating unbalanced and un-healthy diets high in fat, salt and saturated fats.

An additional problem is that GI compares the glycaemic effect of an amount of food containing 50g of carbohydrate but in real life we eat different amounts of food containing different amounts of carbohydrate.

Note: The amount of carbohydrate you eat has a bigger effect on blood glucose levels than GI alone.

The recommendation is to eat more low and intermediate GI foods, not to exclude high GI foods. By choosing the low glycaemic index foods and thus the minimally processed foods, people can lose more weight, feel fuller longer, and remain healthier.

The GI is only a small part of the healthy eating plan for people with diabetes. For people with diabetes, meal planning with the GI involves choosing foods that have a low or medium GI. If eating a food with a high GI, you can combine it with low GI foods to help balance the meal.

Carbohydrates are an essential nutrient. You need carbs as they break down into glucose in your body providing the:

  • main fuel for your brains and nervous systems,
  • preferred source of fuel for most organs and your muscles during exercise.

Consuming good quality carbohydrates aka Low GI ones help to facilitate the management of diabetes, weight loss and weight loss management and reducing the risk of developing type 2 diabetes, diabetes complications and other chronic lifestyle diseases.  In fact a low GI diet provides health benefits for everybody across all stages of life.

A low GI diet is not a fad diet but a way of eating that is sustainable in the long term and backed by over 30 years of scientific evidence.

Recommendations for using GI in your diet

  • Aim to include at least 3 low GI foods throughout the day, ideally one with each meal or snack.
  • When eating high GI foods, try to combine these with a low GI food in order to decrease the overall GI of a meal.
  • Not all the carbohydrates you eat need to be low GI.

glycemic index chart

What Affects the GI of a Food?

Fat and fiber tend to lower the GI of a food. As a general rule, the more cooked or processed a food, the higher the GI; however, this is not always true 2.

Below are a few specific examples of other factors that can affect the GI of a food 5:

  • The type of starch present.
  • The type of sugar present – fructose (fruit sugar) and lactose (milk sugar) both have a lower GI than sucrose (table sugar).
  • Ripeness and storage time — the more ripe a fruit or vegetable is, the higher the GI.
  • Processing — juice has a higher GI than whole fruit; mashed potato has a higher GI than a whole baked potato, stone ground whole wheat bread has a lower GI than whole wheat bread.
  • Cooking methods — how long a food is cooked (al dente pasta has a lower GI than soft-cooked pasta), frying, boiling and baking. Cooking and processing food will usually increase the GI as there is less work required by the body to break the carbohydrates down.
  • Fibre: wholegrains and high-fibre foods act as a physical barrier that slows down the absorption of carbohydrate. This is not the same as ‘wholemeal’, where, even though the whole of the grain is included, it has been ground up instead of left whole. For example, some mixed grain breads that include wholegrains have a lower GI than wholemeal or white bread.
  • Fat lowers the GI of a food. For example, chocolate has a medium GI because of it’s fat content, and crisps will actually have a lower GI than potatoes cooked without fat.
  • Protein lowers the GI of food. Milk and other diary products have a low GI because they are high in protein and contain fat.
  • Adding acidity to the food will lower the GI (e.g. adding lemon juice).
  • Variety — converted long-grain white rice has a lower GI than brown rice but short-grain white rice has a higher GI than brown rice.

Low-GI foods in your healthy, balanced diet

It’s easy to include low-GI carbs in everyday meals:

  • Choose basmati or easy cook rice, pasta or noodles. Or, try plantain, quinoa or bulgur wheat for a change.
  • Eat wholemeal roti and include dhal in your meals.
  • Use new potatoes instead of old potatoes – try sweet potatoes for a change.
  • Instead of white and wholemeal bread, choose granary, pumpernickel or rye bread.
  • Swap frozen chips for pasta or noodles.
  • Try porridge, natural muesli or wholegrain breakfast cereals.

Fruits

Most fruits have a low glycemic index (GI) because of their fructose and fiber content. Melons and pineapple have medium GI values as do some dried fruits such as dates, raisins, and sweetened cranberries.

Fruit – all types such as apples, oranges, peaches, bananas, melons. Fruit is a good source of fibre; try to eat the whole fruit rather than drinking the juice. Include at least 2 serves of fruit a day (1 serve = 1 medium piece apple, orange or pear OR 2 small kiwifruit or plums).

The following is a list of common fruits:

  • Apples
  • Applesauce
  • Apricots
  • Avocado
  • Banana
  • Blackberries
  • Blueberries
  • Cantaloupe
  • Cherries
  • Dried fruit such as:
    • Cherries
    • Cranberries
    • Dates
    • Figs
    • Prunes
    • Raisins
  • Fruit cocktail
  • Grapefruit
  • Grapes
  • Honeydew melon
  • Kiwi
  • Mango
  • Nectarine
  • Orange
  • Papaya
  • Peaches
  • Pears
  • Pineapple
  • Plums
  • Raspberries
  • Strawberries
  • Tangerines
  • Watermelon

What is the difference between Glycemic Index (GI) and Glycemic Load (GL)?

Your blood glucose rises and falls when you eat a meal containing carbs. How high it rises and how long it remains high depends on the quality of the carbohydrates (the GI) and the quantity (the serve size). Glycemic load or GL combines both the quality and quantity of carbohydrate in one ‘number’. It’s the best way to predict blood glucose values of different types and amounts of food.

The formula is:
GL = (GI x available carbohydrate in a 100g serving) divided by 100.

Let’s take a single apple as an example.
It has a GI of 40 and it contains 15 grams of carbohydrate.
GL = 40 x 15/100 = 6 g

What about a small baked potato?
Its GI is 80 and it contains 15 g of carbohydrate.
GL = 80 x 15/100 = 12 g

You can think of GL as the amount of carbohydrate in a food “adjusted” for its glycemic potency.

  • Low GL = <10
  • Medium GL = 11-19
  • High GL = >20

Therefore the Glycemic Load takes into account the amount of carbohydrate consumed and is a more accurate measure of the impact of a food on blood sugars. As a general rule foods that have a low GL usually have a low GI and those with a medium to high GL value almost always have a very high GI value.

Here is an abbreviated chart of the glycemic index and glycemic load, per serving, for more than 100 common foods.

FOODGlycemic index (glucose = 100)Serving size (grams)Glycemic load per serving
BAKERY PRODUCTS AND BREADS
Banana cake, made with sugar476014
Banana cake, made without sugar556012
Sponge cake, plain466317
Vanilla cake made from packet mix with vanilla frosting (Betty Crocker)4211124
Apple muffin, made with rolled oats and sugar446013
Apple muffin, made with rolled oats and without sugar48609
Waffles, Aunt Jemima®763510
Bagel, white, frozen727025
Baguette, white, plain953014
Coarse barley bread, 80% kernels34307
Hamburger bun61309
Kaiser roll733012
Pumpernickel bread56307
50% cracked wheat kernel bread583012
White wheat flour bread, average753011
Wonder® bread, average733010
Whole wheat bread, average69309
100% Whole Grain® bread (Natural Ovens)51307
Pita bread, white683010
Corn tortilla525012
Wheat tortilla30508
BEVERAGES
Coca Cola® (US formula)63250 mL16
Fanta®, orange soft drink68250 mL23
Lucozade®, original (sparkling glucose drink)95250 mL40
Apple juice, unsweetened41250 mL12
Cranberry juice cocktail (Ocean Spray®)68250 mL24
Gatorade, orange flavor (US formula)89250 mL13
Orange juice, unsweetened, average50250 mL12
Tomato juice, canned, no sugar added38250 mL4
BREAKFAST CEREALS AND RELATED PRODUCTS
All-Bran®, average44309
Coco Pops®, average773020
Cornflakes®, average813020
Cream of Wheat®6625017
Cream of Wheat®, Instant7425022
Grape-Nuts®753016
Muesli, average563010
Oatmeal, average5525013
Instant oatmeal, average7925021
Puffed wheat cereal803017
Raisin Bran®613012
Special K® (US formula)693014
GRAINS
Pearled barley, average2515011
Sweet corn on the cob486014
Couscous651509
Quinoa5315013
White rice, boiled, type non-specified7215029
Quick cooking white basmati6315026
Brown rice, steamed5015016
Parboiled Converted white rice (Uncle Ben’s®)3815014
Whole wheat kernels, average455015
Bulgur, average4715012
COOKIES AND CRACKERS
Graham crackers742513
Vanilla wafers772514
Shortbread642510
Rice cakes, average822517
Rye crisps, average642511
Soda crackers742512
DAIRY PRODUCTS AND ALTERNATIVES
Ice cream, regular, average62508
Ice cream, premium (Sara Lee®)38503
Milk, full-fat, average31250 mL4
Milk, skim, average31250 mL4
Reduced-fat yogurt with fruit, average3320011
FRUITS
Apple, average361205
Banana, raw, average4812011
Dates, dried, average426018
Grapefruit251203
Grapes, black5912011
Oranges, raw, average451205
Peach, average421205
Peach, canned in light syrup521209
Pear, raw, average381204
Pear, canned in pear juice441205
Prunes, pitted296010
Raisins646028
Watermelon721204
BEANS AND NUTS
Baked beans401506
Black-eyed peas5015015
Black beans301507
Chickpeas101503
Chickpeas, canned in brine421509
Navy beans, average3915012
Kidney beans, average341509
Lentils281505
Soy beans, average151501
Cashews, salted22503
Peanuts13501
PASTA and NOODLES
Fettucini3218015
Macaroni, average5018024
Macaroni and Cheese (Kraft®)6418033
Spaghetti, white, boiled, average4618022
Spaghetti, white, boiled 20 min5818026
Spaghetti, whole-grain, boiled4218017
SNACK FOODS
Corn chips, plain, salted425011
Fruit Roll-Ups®993024
M & M’s®, peanut33306
Microwave popcorn, plain, average65207
Potato chips, average565012
Pretzels, oven-baked833016
Snickers Bar®, average516018
VEGETABLES
Green peas54804
Carrots, average39802
Parsnips52804
Baked russet potato11115033
Boiled white potato, average8215021
Instant mashed potato, average8715017
Sweet potato, average7015022
Yam, average5415020
MISCELLANEOUS
Hummus (chickpea salad dip)6300
Chicken nuggets, frozen, reheated in microwave oven 5 min461007
Pizza, plain baked dough, served with parmesan cheese and tomato sauce8010022
Pizza, Super Supreme (Pizza Hut®)361009
Honey, average612512

Footnotes: This kind of list does have its limitations. The GI value relates to the food eaten on its own and in practice you usually eat foods in combination as meals. Bread, for example is usually eaten with butter or vegetable-oil based spread, and potatoes could be eaten with meat and vegetables. An additional problem is that GI compares the glycemic effect of an amount of food containing 50g of carbohydrate but in real life you eat different amounts of food containing different amounts of carbohydrate. The amount of carbohydrate you eat has a bigger effect on blood glucose levels than GI alone.

The complete list of the glycemic index and glycemic load for more than 1,000 foods can be found in the article “International tables of glycemic index and glycemic load values: 2008” by Fiona S. Atkinson, Kaye Foster-Powell, and Jennie C. Brand-Miller in the December 2008 issue of Diabetes Care, Vol. 31, number 12, pages 2281-2283 6.

Low Glycaemic Index or Low Glycaemic Load Diets for Weight Loss in Overweight and Obesity

To assess the effects of low glycaemic index or low glycemic load diets for weight loss in overweight or obese people. Six eligible randomised controlled trials (total of 202 participants) comparing a low glycaemic index or low glycemic load diet (LGI) with a higher glycaemic index or load diet or other diet (Cdiet) in overweight or obese people, were reviewed  7. The dietary interventions ranged from five weeks to six months duration with up to six months follow-up after the intervention ceased. The decrease in body mass (-1.1 kg) and body mass index (BMI) -1.3 was significantly greater in participants receiving low glycaemic index or load diets compared to higher glycaemic index or load diets. The decrease in total cholesterol was significantly greater with low glycaemic index or load diets compared to higher glycaemic index or load diets (-0.22 mmol/L), as was the change in LDL-cholesterol (-0.24 mmol/L). No study reported adverse effects, mortality or quality of life data. The authors concluded, overweight or obese people on low glycaemic index or low glycemic load diets lost more weight and had more improvement in lipid profiles than those receiving higher glycaemic index or load diets. Body mass, total fat mass, body mass index, total cholesterol and LDL-cholesterol all decreased significantly more in the low glycaemic index or low glycemic load diets group. In studies comparing ad libitum low glycaemic index or low glycemic load diets to conventional restricted energy low-fat diets, participants fared as well or better on the low glycaemic index or low glycemic load diet, even though they could eat as much as desired. Lowering the glycaemic load of the diet appears to be an effective method of promoting weight loss and improving lipid profiles and can be simply incorporated into a person’s lifestyle. Further research with longer term follow-up will determine whether improvement continues long-term and improves quality of life 7.

In a large European study looked at the role of protein and glycemic index upon weight loss maintenance 8. Researchers first implemented a very low-calorie diet to produce weight loss, then examined whether protein and glycemic index impacted weight loss maintenance. The study involving 1209 overweight adults (average age 41 years) with a body mass index (BMI) of 34. The study population was made up of 938 overweight adults from European countries who were randomly entered into one of the 4 low-calorie-diet phase plus 1 control diet of the study groups over a 26-week period, a low-calorie diet consisting of:

  • a Low-Protein and Low-Glycemic-index diet;
  • a Low-Protein and High-Glycemic-index diet;
  • a High-protein and Low-Glycemic-index diet;
  • a High-protein and High-Glycemic-index diet;
  • or a Control diet.

The results 8, fewer participants in the high-protein and the low-glycemic-index groups than in the low-protein–high-glycemic-index group dropped out of the study (26.4% and 25.6%, respectively, vs. 37.4%). The mean initial weight loss with the low-calorie diet was 11.0 kg (at least 8% of their initial body weight). In the analysis of participants who completed the study, only the low-protein–high-glycemic-index diet was associated with subsequent significant weight regain (1.67 kg). The weight regain was 0.93 kg less in the groups assigned to a high-protein diet than in those assigned to a low-protein diet and 0.95 kg less in the groups assigned to a low-glycemic-index diet than in those assigned to a high-glycemic-index diet.

In conclusion, these results show that a modest increase in protein content (high-protein diet) and a modest reduction in the glycemic index (low-glycemic-index diet) led to an improvement in study completion and maintenance of weight loss 8.

Benefits of Low Glycaemic Index or Low Glycaemic Load Diets for Diabetes Mellitus

There is consensus that diets low in GI and GL were relevant to the prevention and management of diabetes and coronary heart disease, and probably obesity. Moderate to weak associations were observed for selected cancers 9.

To assess the effects of low glycaemic index or low glycaemic load, diets on glycaemic control in people with diabetes, eleven relevant randomised controlled trials, lasting 1 to 12 months, involving 402 participants were analysed 10.

There was a significant decrease in the glycated haemoglobin A1c (HbA1c) -0.5%. Episodes of hypoglycaemia were significantly fewer with low glycaemic index or low glycaemic load compared to high GI diet in one trial (difference of -0.8 episodes per patient per month), and proportion of participants reporting more than 15 hyperglycaemic episodes per month was lower for low-GI diet compared to measured carbohydrate exchange diet in another study (35% versus 66%). No study reported on mortality, morbidity or costs. The review authors concluded a low-GI diet can improve glycaemic control in diabetes without compromising hypoglycaemic events 10. This result is consistent with another smaller trial involving eight type 2 diabetes mellitus patients who were given carbohydrate foods with either a high or low glycemic index over a 2 weeks period 11.

Although a majority of studies show a positive correlation between high glycemic foods and type two diabetes, several studies disagree with these findings. Meyer et al. 12 found that glycemic index had no effect on the prevalence of type 2 diabetes in older aged women. However, there was a strong inverse relationship between dietary fiber intake and type 2 diabetes when adjusted for age and BMI. Women consuming an average of 26 g/day of dietary fiber had a 22% lower risk of developing diabetes when compared to women only consuming 13 g/d. Schulze et al. 13 agreed with these findings with men and women showing a decreased risk of diabetes with the consumption of an additional 12 g of dietary fiber per day. According to these findings, it may be more significant to focus on an increased consumption of dietary fiber to prevent diabetes than glycemic index/load. It is also important to note that the inverse relationship between dietary fiber and diabetes observed by Meyer et al. 14 and Schulze et al. 13 was independent of age and body weight. Hu et al. 15 supported these findings while correcting for age, fat intake, smoking, alcohol, family history, exercise, and body weight. Therefore, it seems that dietary fiber is associated with type two diabetes, independent of other compounding factors.

According to recent research, the soluble versus insoluble fraction of fiber may give some insight on the efficacy of dietary fiber on diabetes and its mechanisms. Although some studies have been contradictory, showing no differentiation between soluble and insoluble fiber on diabetes 13, a majority of the research demonstrates a strong inverse relationship between insoluble fiber and the risk of type two diabetes. Meyer et al. 12 using healthy middle aged women, observed a strong inverse relationship between insoluble fiber and the risk of type two diabetes while soluble fiber had no effect. Montonen et al. 16 also found the same results in healthy middle aged men and women consuming increased levels of whole rye bread. Interestingly, fiber from fruits and vegetables had no effect on the risk of developing type two diabetes. Earlier studies have agreed with these findings. A large epidemiological study of 42,000 men found that dietary fiber from fruits or vegetables had no effect on the risk of diabetes. However, dietary fiber from whole cereal grains showed a significant decrease in diabetes occurrence 17. Daily intakes of fiber among all groups were similar.

Insoluble fiber only has a small effect on macronutrient absorption 18. Therefore, another mode of action must be present and several hypotheses should be discussed. Some suggest that insoluble fiber increases the passage rate of foodstuff through the gastrointestinal tract thus resulting in a decreased absorption of nutrients, namely simple carbohydrates. However, Weicket et al. 19 found that an increased intake of cereal fiber significantly improved whole body glucose disposal resulting in an 8% improvement of insulin sensitivity. This suggests that the mechanisms behind insoluble fiber are more peripheral and not limited to nutrient absorption. First, an accelerated secretion of glucose-dependent insulintropic polypeptide was observed directly after the ingestion of an insoluble fiber in healthy women 20. Glucose-dependent insulintropic polypeptide is an incretin hormone which stimulates postprandial insulin release. Second, insoluble fiber can result in a reduced appetite and food intake 21. This may lead to a decreased caloric intake and BMI. Third, short chain fatty acids, via fermentation, have been shown to reduce postpandrial glucose response 22, 23. Early research demonstrated that lipid infusions impaired glucose utilization 24 and oral acetate could decrease free fatty acids in the blood 25. According to Kelley and Mandarino 26, increases in free fatty acid in the blood can inhibit glucose metabolism through the inhibition of GLUT 4 transporters. Therefore, short chain fatty acids, by way of decreasing serum free fatty acids, may reduce blood glucose levels through competition in insulin–sensitive tissues.

Low Glycaemic Index Diets for Coronary Heart Disease

Currently there is no evidence from randomised clinical trials to show an effect of low glycaemic index (low GI) diets on coronary heart disease 27. Weak evidence for minor effects on some coronary heart disease risk factors (weak evidence of slightly lower total cholesterol with low glycaemic index diets. However, when only studies on diabetics were included in the analysis, no evidence of an effect on total cholesterol was found) was found. Many of the trials identified were short-term, of poor quality and did not have sufficient power to detect clinically important differences. The combined evidence from the studies suggests that any beneficial effect of low glycaemic index diets on coronary heart disease and its risk factors is small. There is a need for well designed, adequately powered, randomised controlled studies, of greater than 12 weeks duration to assess the true effects of low glycaemic index diets for coronary heart disease.

In a systematic meta-analysis review 28 of available randomised controlled trials data on the effect of low glycemic index diets on blood lipids over at least 4 weeks. This meta-analysis 28 provides consistent evidence that low glycemic index diets reduce total and LDL-cholesterol and have no effect on HDL-cholesterol or triglycerides.

Glycaemic Index Diets and Cancer

In a study to find out if higher carbohydrate intake, glycaemic index (GI) and glycaemic load (GL) could increase your risk of developing cancer 29. Researchers reviewed the data from 3184 Caucasian American adults, what they found was that carbohydrate intake was not associated with risk of adiposity-related cancers combined or prostate and colorectal cancers 29. Furthermore, high-, medium- and low-GI foods were not associated with risk of adiposity-related cancers or prostate and colorectal cancers. Moreover, they also found that consuming healthier low-GI foods, were associated with 49 % lower breast cancer risk 29.

References
  1. Glycemic index of foods: a physiological basis for carbohydrate exchange. Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM, Bowling AC, Newman HC, Jenkins AL, Goff DV. Am J Clin Nutr. 1981 Mar; 34(3):362-6. https://www.ncbi.nlm.nih.gov/pubmed/6259925/
  2. American Diabetes Association. Glycemic Index and Diabetes. http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/understanding-carbohydrates/glycemic-index-and-diabetes.html
  3. FAO/WHO scientific update on carbohydrates in human nutrition: conclusions. Mann J, Cummings JH, Englyst HN, Key T, Liu S, Riccardi G, Summerbell C, Uauy R, van Dam RM, Venn B, Vorster HH, Wiseman M. Eur J Clin Nutr. 2007 Dec; 61 Suppl 1:S132-7. https://www.ncbi.nlm.nih.gov/pubmed/17992184/
  4. Atkinson FS, Foster-Powell K, Brand-Miller JC. International Tables of Glycemic Index and Glycemic Load Values: 2008 . Diabetes Care. 2008;31(12):2281-2283. doi:10.2337/dc08-1239. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2584181
  5. Glycemic Index International Database, University of Sydney. http://www.glycemicindex.com
  6. Diabetes Care 2008 Dec; 31(12): 2281-2283. https://doi.org/10.2337/dc08-1239. International Tables of Glycemic Index and Glycemic Load Values: 2008. http://care.diabetesjournals.org/content/31/12/2281.full
  7. Cochrane Review 18 July 2007. Low glycaemic index or low glycaemic load diets for overweight and obesity. http://www.cochrane.org/CD005105/ENDOC_low-glycaemic-index-or-low-glycaemic-load-diets-for-overweight-and-obesity
  8. N Engl J Med. 2010 Nov 25; 363(22): 2102–2113. doi: 10.1056/NEJMoa1007137. Diets with High or Low Protein Content and Glycemic Index for Weight-Loss Maintenance. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359496/
  9. Nutrition, Metabolism and Cardiovascular Diseases, 2015-09-01, Volume 25, Issue 9, Pages 795-815. https://www.clinicalkey.com.au/#!/content/playContent/1-s2.0-S0939475315001271
  10. Cochrane Review 21 January 2009. Low glycaemic index, or low glycaemic load, diets for diabetes mellitus. http://www.cochrane.org/CD006296/ENDOC_low-glycaemic-index-or-low-glycaemic-load-diets-for-diabetes-mellitus
  11. Am J Clin Nutr. 1988 Aug;48(2):248-54. Low-glycemic-index starchy foods in the diabetic diet. https://www.ncbi.nlm.nih.gov/pubmed/3407604
  12. Carbohydrates, dietary fiber, and incident type 2 diabetes in older women. Meyer KA, Kushi LH, Jacobs DR Jr, Slavin J, Sellers TA, Folsom AR. Am J Clin Nutr. 2000 Apr; 71(4):921-30. https://www.ncbi.nlm.nih.gov/pubmed/10731498/
  13. Glycemic index, glycemic load, and dietary fiber intake and incidence of type 2 diabetes in younger and middle-aged women. Schulze MB, Liu S, Rimm EB, Manson JE, Willett WC, Hu FB. Am J Clin Nutr. 2004 Aug; 80(2):348-56. https://www.ncbi.nlm.nih.gov/pubmed/15277155/
  14. Carbohydrates, dietary fiber, and incident type 2 diabetes mellitus in older women. Meyer KA, Kushi LH, Jacobs DR Jr, Slavin J, Sellers TA, Folsom AR. Am J Clin Nutr. 2000 Apr; 71(4):921-30. https://www.ncbi.nlm.nih.gov/pubmed/10731498/
  15. Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. Hu FB, Manson JE, Stampfer MJ, Colditz G, Liu S, Solomon CG, Willett WC. N Engl J Med. 2001 Sep 13; 345(11):790-7. https://www.ncbi.nlm.nih.gov/pubmed/11556298/
  16. Whole-grain and fiber intake and the incidence of type 2 diabetes. Montonen J, Knekt P, Järvinen R, Aromaa A, Reunanen A. Am J Clin Nutr. 2003 Mar; 77(3):622-9. https://www.ncbi.nlm.nih.gov/pubmed/12600852/
  17. Dietary fiber, glycemic load, and risk of NIDDM in men. Salmerón J, Ascherio A, Rimm EB, Colditz GA, Spiegelman D, Jenkins DJ, Stampfer MJ, Wing AL, Willett WC. Diabetes Care. 1997 Apr; 20(4):545-50. https://www.ncbi.nlm.nih.gov/pubmed/9096978/
  18. Dietary fibres, fibre analogues, and glucose tolerance: importance of viscosity. Jenkins DJ, Wolever TM, Leeds AR, Gassull MA, Haisman P, Dilawari J, Goff DV, Metz GL, Alberti KG. Br Med J. 1978 May 27; 1(6124):1392-4. https://www.ncbi.nlm.nih.gov/pubmed/647304/
  19. Metabolic effects of dietary fiber consumption and prevention of diabetes. Weickert MO, Pfeiffer AF. J Nutr. 2008 Mar; 138(3):439-42. https://www.ncbi.nlm.nih.gov/pubmed/18287346/
  20. Impact of cereal fibre on glucose-regulating factors. Weickert MO, Mohlig M, Koebnick C, Holst JJ, Namsolleck P, Ristow M, Osterhoff M, Rochlitz H, Rudovich N, Spranger J, Pfeiffer AF. Diabetologia. 2005 Nov; 48(11):2343-53. https://www.ncbi.nlm.nih.gov/pubmed/16172868/
  21. Insoluble cereal fiber reduces appetite and short-term food intake and glycemic response to food consumed 75 min later by healthy men. Samra RA, Anderson GH. Am J Clin Nutr. 2007 Oct; 86(4):972-9. https://www.ncbi.nlm.nih.gov/pubmed/17921373/
  22. Effect of neutralized and native vinegar on blood glucose and acetate responses to a mixed meal in healthy subjects. Brighenti F, Castellani G, Benini L, Casiraghi MC, Leopardi E, Crovetti R, Testolin G. Eur J Clin Nutr. 1995 Apr; 49(4):242-7. https://www.ncbi.nlm.nih.gov/pubmed/7796781/
  23. Barley bread containing lactic acid improves glucose tolerance at a subsequent meal in healthy men and women. Ostman EM, Liljeberg Elmståhl HG, Björck IM. J Nutr. 2002 Jun; 132(6):1173-5. https://www.ncbi.nlm.nih.gov/pubmed/12042429/
  24. Effect of fatty acids on glucose production and utilization in man. Ferrannini E, Barrett EJ, Bevilacqua S, DeFronzo RA. J Clin Invest. 1983 Nov; 72(5):1737-47. https://www.ncbi.nlm.nih.gov/pubmed/6138367/
  25. Role of acetate in the reduction of plasma free fatty acids produced by ethanol in man. Crouse JR, Gerson CD, DeCarli LM, Lieber CS. J Lipid Res. 1968 Jul; 9(4):509-12. https://www.ncbi.nlm.nih.gov/pubmed/5725882/
  26. Fuel selection in human skeletal muscle in insulin resistance: a reexamination. Kelley DE, Mandarino LJ. Diabetes. 2000 May; 49(5):677-83. https://www.ncbi.nlm.nih.gov/pubmed/10905472/
  27. Cochrane Review 18 October 2004. Low glycaemic index diets for coronary heart disease. http://www.cochrane.org/CD004467/VASC_low-glycaemic-index-diets-for-coronary-heart-disease
  28. Nutr Metab Cardiovasc Dis. 2013 Jan;23(1):1-10. doi: 10.1016/j.numecd.2012.06.002. Epub 2012 Jul 25. Low glycaemic index diets and blood lipids: a systematic review and meta-analysis of randomised controlled trials. https://www.ncbi.nlm.nih.gov/pubmed/22841185
  29. British Journal of Nutrition Volume 117, Issue 11, June 2017, pp. 1603-1614. Carbohydrate nutrition and risk of adiposity-related cancers: results from the Framingham Offspring cohort (1991–2013). https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/carbohydrate-nutrition-and-risk-of-adiposityrelated-cancers-results-from-the-framingham-offspring-cohort-19912013/FABC2997829AF7BE2ABF6EC0E21694AE
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Diet PlanDiet, Food & Fitness

What is the American Diabetes Association (ADA) diet ?

american diabetes association diet

diet for better diabetes management

The American Diabetes Association Diet

The diabetes diet is simply a healthy-eating plan that will help you control your blood sugar. Diabetic diet usually contains low-glycaemic index food, with similar amount of protein, complex carbohydrates, fibres, and unsaturated fatty acids as in food for general public 1. If you have diabetes, your body cannot make or properly use insulin. This leads to high blood glucose, or blood sugar, levels. What you eat is closely connected to the amount of sugar in your blood. The right food choices will help you control your blood sugar level and controlling your blood sugar can prevent the complications of diabetes 2.

General Dietary Goals for Diabetes

The nutrition therapy goals 3 for the individual with diabetes have evolved in the past few years and have become more flexible and user-friendly.

These goals include the following:

  • To promote and support healthful eating patterns, emphasizing a variety of nutrient dense foods in appropriate portion sizes in order to improve overall health and specifically to:
  • Attain individualized glycemic, blood pressure, and lipid goals. General recommended goals from the ADA for these markers are as follows:*
  • A1C <7%
  • Blood pressure,<140/80mmHg
  • LDL cholesterol ,<100 mg/dL
  • Triglycerides <150 mg/dL
  • HDL cholesterol >40 mg/dL for men
  • HDL cholesterol >50 mg/dL for women
  • Achieve and maintain body weight goals
  • Delay or prevent complications of diabetes
  • To address individual nutrition needs based on personal and cultural preferences, health literacy and numeracy, access to healthful food choices, willingness and ability to make behavioral changes, as well as barriers to change
  • To maintain the pleasure of eating by providing positive messages about food choices while limiting food choices only when indicated by scientific evidence
  • To provide the individual with diabetes with practical tools for day-to-day meal planning rather than focusing on individual macronutrients, micronutrients

*A1C, blood pressure, and cholesterol goals may need to be adjusted for the individual based on age, duration of diabetes, health history, and other present health conditions. Further recommendations for individualization of goals can be found in the ADA Standards of Medical Care in Diabetes 4.

If you go to the American Diabetes Association website, there is no such thing as the American Diabetes Association (ADA) diet per se. In other word, there is no one diet or meal plan that works for everyone with diabetes. Instead the American Diabetes Association promotes healthy diabetes meal plan. A diabetes meal plan is a guide that tells you how much and what kinds of food you can choose to eat at meals and snack times. A good meal plan should fit in with your schedule and eating habits. The important thing is to follow a meal plan that is tailored to personal preferences and lifestyle and helps achieve goals for blood glucose, cholesterol and triglycerides levels, blood pressure, and weight management.

Research shows that both the amount and the type of carbohydrate in food affect blood glucose levels. Studies also show that the total amount of carbohydrate in food, in general, is a stronger predictor of blood glucose response than the Glycemic Index (GI). Based on the research, for most people with diabetes, the first tool for managing blood glucose is some type of carbohydrate counting.

Because the type of carbohydrate can affect blood glucose, using the Glycemic Index may be helpful in “fine-tuning” blood glucose management. In other words, combined with carbohydrate counting, it may provide an additional benefit for achieving blood glucose goals for individuals who can and want to put extra effort into monitoring their food choices.

People with diabetes can eat the same foods the family enjoys and people with diabetes have to take extra care to make sure that their food is balanced with insulin and oral medications (if they take them), and exercise to help manage their blood glucose levels.

This might sound like a lot of work, but your doctor and/or dietitian can help you create a meal plan that is best for you. When you make healthy food choices, you will improve your overall health and you can even prevent complications such as heart disease and some cancers.

The right meal plan will help you improve your blood glucose, blood pressure, and cholesterol numbers and also help keep your weight on track. Whether you need to lose weight or stay where you are, your meal plan can help.

There is no one perfect food, so including a variety of different foods and watching portion sizes is key to a healthy diet. Also, make sure your choices from each food group provide the highest quality nutrients you can find. In other words, pick foods rich in vitamins, minerals and fiber over those that are processed.

Everyone benefits from healthy eating so the whole family can take part in healthy eating. It takes some planning but you can fit your favorite foods into your meal plan and still manage your blood glucose, blood pressure and cholesterol.

  • Avoid foods labelled ‘diabetic’ or ‘suitable for diabetics’. These foods contain similar amounts of calories and fat, and they can affect your blood glucose levels. They are usually more expensive and can have a laxative effect. Stick to your usual foods. If you want to have an occasional treat, go for your normal treats and keep an eye on your portions.

There isn’t one specific “diabetes diet.” Healthy eating helps keep your blood sugar in your target range. It is a critical part of managing your diabetes, because controlling your blood sugar can prevent the complications of diabetes.

  • The Centers for Disease Control and Prevention has a free recipes ebook for people and their families with diabetes, you download a free copy here 5.

A registered dietitian can also help you make an eating plan just for you. It should take into account your weight, medicines, lifestyle, and other health problems you have.

  • To find out about your body mass index (BMI), you can use a FREE online BMI calculators from the Centers for Disease Control and Prevention (CDC) – for Adults 6 and for Children 7
  • To find out What and How Much To Eat, you can use a FREE, award-winning, state-of-the-art, online diet and activity tracking tool called SuperTracker 8 from the United States Department of Agriculture Center for Nutrition Policy and Promotion 8. This free application empowers you to build a healthier diet, manage weight, and reduce your risk of chronic diet-related diseases. You can use SuperTracker 8 to determine what and how much to eat; track foods, physical activities, and weight; and personalize with goal setting, virtual coaching, and journaling.

SuperTracker website 8

  • To find out about how many calories you should eat to lose weight according to your weight, age, sex, height and physical activity, you can use a FREE online app Body Weight Planner 9
  • To find out about the 5 Food Groups you should have on your plate for a meal, you can use a FREE online app ChooseMyPlate 10

 

Energy balance

Matching the amount of food you eat with the amount of energy you burn through activity and exercise is important. Putting too much fuel in your body can lead to weight gain. Being overweight or obese can make it difficult to manage your diabetes and can increase the risk of heart disease, stroke and cancer.

Limit foods high in energy such as take away foods, sweet biscuits, cakes, sugar sweetened drinks and fruit juice, lollies, chocolate and savoury snacks. Some people have a healthy diet but eat too much. Reducing your portion size is one way to decrease the amount of energy you eat. Being active has many benefits. Along with healthy eating, regular physical activity can help you to manage your blood glucose levels, reduce your blood fats (cholesterol and triglycerides) and maintain a healthy weight.

Learn more about exercise and maintaining a healthy weight.

Carbohydrate

Carbohydrate foods play an important role in your diet. They are the best energy source for your body, especially your brain. When carbohydrates are digested they break down to form glucose in the bloodstream. Insulin takes the glucose out of the blood and puts it into the muscles, liver and other cells in the body where it is used to provide energy. Most carbohydrate containing foods are also very good sources of fibre, vitamins and minerals which keep our body and bowels healthy.

Of the three key nutrients in your food – fat, protein and carbohydrate, carbohydrate is the nutrient that will have the biggest impact on your blood glucose levels. The effect of carbohydrate will depend on i) the amount of carbohydrate you eat and ii) the type of carbohydrate you eat.

Everyone’s carbohydrate needs are different depending on your gender, how active you are, your age and your body weight. Anyone with diabetes should see an Accredited Practising Dietitian to work out the amount of carbohydrate to eat at each meal and snack.

All carbohydrate foods are digested to produce glucose but they do so at different rates – some slow, some fast. The glycemic index or GI is a way of describing how quickly a carbohydrate food is digested and enters the blood stream.

Low GI carbohydrate foods enter the blood stream slowly and have less of an impact on blood glucose levels. Examples of low GI foods include traditional rolled oats, dense wholegrain breads, lentils and legumes, sweet potato, milk, yoghurt, pasta and most types of fresh fruit. The type of carbohydrate you eat is very important as some can cause higher blood glucose after eating. The best combination is to eat moderate amounts of high fibre low GI carbohydrates.

For some people, a lower carbohydrate diet may help with diabetes management. If you are considering reducing the carbohydrate content of your diet, consult your healthcare team for individualised advice.

Sugar

A healthy eating plan for diabetes can include some sugar. It is ok to have a sprinkle of sugar on porridge or a scrape of jam on some low GI high fibre bread. However, foods that are high in added sugars and poor sources of other nutrients should be consumed sparingly. In particular, limit high energy foods such as sweets, lollies and standard soft drinks. Some sugar may also be used in cooking and many recipes can be modified to use less than the amount stated or substituted with an alternative sweetener. Select recipes that are low in fat (particularly saturated fat) and contain some fibre.

Alternative sweeteners

As mentioned above small amounts of sugar as part of a balanced meal plan shouldn’t have a large effect on blood glucose levels. However sweeteners such as Equal, Stevia, Sugarine and Splenda can be used in place of sugar especially if they are replacing large amounts of sugar. Foods and drinks that have been sweetened with an alternative sweetener, such as diet soft drinks and cordials, sugar-free lollies etc., are also best enjoyed occasionally, as they do not have any nutritional benefit and may often take the place of more nutritious foods and drinks, such as fruits, vegetables, dairy, nuts and water.

Protein

Protein foods are needed by the body for growth and repair. Protein does not break down into glucose, so it does not directly raise blood glucose levels.

The main protein foods are:

  • Meats, chicken, fish, & tofu
  • Eggs
  • Nuts & seeds
  • Cheese

There are some protein foods which also contain carbohydrate such as milk, yoghurt, lentils and legumes which will have an effect on blood glucose levels but these should still be included as part of a healthy diet.

Drink water

Water is needed for most of the body’s functions and the body needs to be kept hydrated every day. Water is the best drink to have because it contains no extra kilojoules and won’t have an effect on your blood glucose levels. Other good choices are:

  • Tea, coffee, herbal tea, water, soda water, plain mineral water
  • If you want a sweet drink occasionally products labelled ‘diet’ or ‘low joule’
  • If you choose to drink alcohol limit your intake to no more than 2 standard drinks per day with some alcohol free days each week.

To successfully manage diabetes, you need to understand how foods and nutrition affect your body. Food portions and food choices are important. Carbohydrates, fat and protein need to be balanced to ensure blood sugar levels stay as stable as possible. (This is particularly important for people with Type 1 diabetes.)

The key to eating with diabetes is to eat a variety of healthy foods from all food groups, in the amounts your meal plan outlines. For that reason the American Diabetes Association has created:

  • The Diabetic Diet Meal Plans 11 and
  • A online tool called Create Your Plate 12. With Create Your Plate method, you fill your plate with more non-starchy veggies and smaller portions of starchy foods and protein—no special tools or counting required. You can practice with this interactive tool 12.

 

The American Diabetes Association’s Create Your Plate online interactive meal planning tool

The American Diabetes Association’s Create Your Plate online interactive meal planning tool divides your daily food requirements according to the percentage daily requirement for each major food groups: 25 percent Protein, 25 percent Grains and Starchy Foods and 50 percent Non-starchy Vegetables 12. Creating your plate lets you still choose the foods you want, but changes the portion sizes so you are getting larger portions of non-starchy vegetables and a smaller portion of starchy foods. The healthy meal combinations are endless.

Using the 7 simple steps to Create Your Plate 12 you can simply and effectively manage your diabetes and lose weight at the same time. When you are ready, you can try new foods within each food category.

Try these seven steps to get started:

  1. Using your dinner plate, put a line down the middle of the plate. Then on one side, cut it again so you will have three sections on your plate.
  2. Fill the largest section with non-starchy vegetables.
  3. Now in one of the small sections, put grains and starchy foods.
  4. And then in the other small section, put your protein.
  5. Add a serving of fruit, a serving of dairy or both as your meal plan allows.
  6. Choose healthy fats in small amounts. For cooking, use oils. For salads, some healthy additions are nuts, seeds, avocado and vinaigrettes.
  7. To complete your meal, add a low-calorie drink like water, unsweetened tea or coffee.

The food groups are :

Vegetables

  • Non-starchy Vegetables 13

The following is a list of common non-starchy vegetables:

  • Amaranth or Chinese spinach
  • Artichoke
  • Artichoke hearts
  • Asparagus
  • Baby corn
  • Bamboo shoots
  • Beans (green, wax, Italian)
  • Bean sprouts
  • Beets
  • Brussels sprouts
  • Broccoli
  • Cabbage (green, bok choy, Chinese)
  • Carrots
  • Cauliflower
  • Celery
  • Chayote
  • Coleslaw (packaged, no dressing)
  • Cucumber
  • Daikon
  • Eggplant
  • Greens (collard, kale, mustard, turnip)
  • Hearts of palm
  • Jicama
  • Kohlrabi
  • Leeks
  • Mushrooms
  • Okra
  • Onions
  • Pea pods
  • Peppers
  • Radishes
  • Rutabaga
  • Salad greens (chicory, endive, escarole, lettuce, romaine, spinach, arugula, radicchio, watercress)
  • Sprouts
  • Squash (cushaw, summer, crookneck, spaghetti, zucchini)
  • Sugar snap peas
  • Swiss chard
  • Tomato
  • Turnips
  • Water chestnuts
  • Yard-long beans

Generally, non-starchy vegetables have about 5 grams of carbohydrate in ½ cup cooked or 1 cup raw. Most of the carbohydrate is fiber so unless you eat more than 1 cup of cooked or 2 cups of raw at a time, you may not need to count the carbohydrates from the non-starchy vegetables.

The best choices are fresh, frozen and canned vegetables and vegetable juices without added sodium, fat or sugar.

If using canned or frozen vegetables, look for ones that say low sodium or no salt added on the label.
As a general rule, frozen or canned vegetables in sauces are higher in both fat and sodium.
If using canned vegetables with sodium, drain the vegetables and rinse with water. Then cook the rinsed vegetables in fresh water. This will cut back on how much sodium is left on the vegetables.

For good health, try to eat at least 3-5 servings of vegetables a day. This is a minimum and more is better! A serving of vegetables is:

  • ½ cup of cooked vegetables or vegetable juice
  • 1 cup of raw vegetables

 

 

  • Starchy Starchy Vegetables and Grains 14

Grains

  • At least half of your grains for the day should be whole grains. A whole grain is the entire grain—which includes the bran, germ and endosperm (starchy part).

The most popular grain in the US is wheat so that will be our example. To make 100% whole wheat flour, the entire wheat grain is ground up. “Refined” flours like white and enriched wheat flour include only part of the grain – the starchy part, and are not whole grain. They are missing many of the nutrients found in whole wheat flour.

Examples of whole grain wheat products include 100% whole wheat bread, pasta, tortillas, and crackers. But don’t stop there! There are many whole grains to choose from.

Finding whole grain foods can be a challenge. Some foods only contain a small amount of whole grain but will say it contains whole grain on the front of the package. For all cereals and grains, read the ingredient list and look for the following sources of whole grains as the first ingredient:

Best Choices

  • Bulgur (cracked wheat)
  • Whole wheat flour/
  • Whole oats/oatmeal
  • Whole grain corn/corn meal
  • Popcorn
  • Brown rice
  • Whole rye
  • Whole grain barley
  • Whole farro
  • Wild rice
  • Buckwheat
  • Buckwheat flour
  • Triticale
  • Millet
  • Quinoa
  • Sorghum

If you suffer from Celiac disease or gluten intolerance :

  • Celiac disease is a digestive disorder. When someone with celiac disease eats food containing gluten, their body reacts by damaging the small intestine. Uncomfortable symptoms such as abdominal pain often occur. The damage to the small intestine also interferes with the body’s ability to make use of the nutrients in food. About 1% of the total population has celiac disease. It is more common in people with type 1 diabetes. An estimated 10% of people with type 1 also have celiac. The only way to manage celiac disease is to completely avoid all foods that have gluten. Following a gluten-free diet will prevent permanent damage to your body and will help you feel better.
  • Gluten Intolerance : There are also many people who are said to have a gluten intolerance. When these people eat foods that contain gluten, they also experience uncomfortable symptoms. However, they test negative for celiac disease and actual damage to their small intestine does not occur. More research about gluten intolerance is needed, but avoiding foods with gluten should help to relieve these symptoms.

Gluten is a protein found in wheat, rye, barley and all foods that are made with these grains.

Starchy Vegetables

Starchy vegetables are great sources of vitamins, minerals and fiber . The best choices do not have added fats, sugar or sodium.

Try a variety such as:

  • Parsnip
  • Plantain
  • Potato
  • Pumpkin
  • Acorn squash
  • Butternut squash
  • Green Peas
  • Corn

Best Choices of Dried Beans, Legumes, Peas and Lentils

Try to include dried beans into several meals per week. They are a great source of protein and are loaded with fiber, vitamins and minerals.

  • Dried beans such as black, lima, and pinto
  • Lentils
  • Dried peas such as black-eyed and split
  • Fat-free refried beans
  • Vegetarian baked beans

Fruits 15

Wondering if you can eat fruit ? Yes !

Fruits are loaded with vitamins, minerals and fiber just like vegetables.

Fruit contains carbohydrate so you need to count it as part of your meal plan. Having a piece of fresh fruit or fruit salad for dessert is a great way to satisfy your sweet tooth and get the extra nutrition you’re looking for.

The best choices of fruit are any that are fresh, frozen or canned without added sugars.

  • Choose canned fruits in juice or light syrup
  • Dried fruit and 100% fruit juice are also nutritious choices, but the portion sizes are small so they may not be as filling as other choices. Only 2 tablespoons of dried fruit like raisins or dried cherries contains 15 grams of carbohydrate so be cautious with your portion sizes!
  • Includes oranges, melon, berries, apples, bananas, and grapes

For Carbohydrate Counters

  • A small piece of whole fruit or about ½ cup of frozen or canned fruit has about 15 grams of carbohydrate. Servings for most fresh berries and melons are from ¾ – 1 cup.
  • Fruit juice can range from 1/3 -1/2 cup for 15 grams of carbohydrate.

Fruit can be eaten in exchange for other sources of carbohydrate in your meal plan such as starches, grains, or dairy.

 

Protein 16

The biggest difference among foods in this group is how much fat they contain, and for the vegetarian proteins, whether they have carbohydrate.

Meats do not contain carbohydrate so they do not raise blood glucose levels. A balanced meal plan usually has about 2-5 ounces of meat.

Most plant-based protein foods, like beans and soy products, and any breaded meats contain carbohydrate. It’s best to read food labels carefully for these foods.

In general there is about 15 grams of carbohydrate in ½ cup beans, and between 5 to 15 grams in soy-based products like veggie burgers and “chicken” nuggets.

The best choices are:

  • Plant-based proteins
  • Fish and seafood
  • Chicken and other poultry
  • Cheese and eggs

Fish and Seafood

Try to include fish at least 2 times per week.

  • Fish high in omega-3 fatty acids like Albacore tuna, herring, mackerel, rainbow trout, sardines, and salmon
  • Other fish including catfish, cod, flounder, haddock, halibut, orange roughy, and tilapia
  • Shellfish including clams, crab, imitation shellfish, lobster, scallops, shrimp, oysters.

Poultry

Choose poultry without the skin for less saturated fat and cholesterol.

  • Chicken, turkey, cornish hen

Game

  • Buffalo, ostrich, rabbit, venison
  • Dove, duck, goose, or pheasant (no skin)

Beef, Pork, Veal, Lamb

If you decide to have these, choose the leanest options, which are:

  • Select or Choice grades of beef trimmed of fat including: chuck, rib, rump roast, round, sirloin, cubed, flank, porterhouse, T-bone steak, tenderloin
  • Beef jerky
  • Lamb: chop, leg, or roast
  • Organ meats: heart, kidney, liver
  • Veal: loin chop or roast
  • Pork: Canadian bacon, center loin chop, ham, tenderloin

Cheese and Eggs

  • Reduced-fat cheese
  • Cottage cheese
  • Egg whites and egg substitutes

 

Dairy 17

Including sources of dairy in your diet is an easy way to get calcium and high-quality protein.

The best choices of dairy products are:

  • Fat-free or low-fat (1% milk)
  • Plain non-fat yogurt (regular or Greek yogurt)
  • non-fat light yogurt (regular or Greek yogurt)
  • unflavored fortified soy milk

If you are lactose intolerant or don’t like milk, you may want to try fortified soy milk, rice milk, or almond milk as a source of calcium and vitamin D.

Tips for Carb Counters

  • 1 cup of milk or yogurt is equal to 1 small piece of fruit or 1 slice of bread
  • Each 1 cup serving of milk or 6 ounce serving of yogurt has about 12 grams of carbohydrate and 8 grams of protein. Greek yogurt is higher in protein than regular yogurt, with about 12 grams per 6 ounce serving.
  • If you are trying to switch to lower fat dairy products, take the time to get used to the taste and texture difference. For example, first change from whole milk to 2%. Then to 1% or non-fat milk.
  • Switching from whole to 1% milk will save you 70 calories and 4 grams of saturated fat in every serving!

Eat more fiber by eating more whole-grain foods 18. Whole grains can be found in:

  • Breakfast cereals made with 100% whole grains.
  • Oatmeal.
  • Whole grain rice.
  • Whole-wheat bread, bagels, pita bread, and tortillas.

 

What Can you Drink ?

Food often takes center stage when it comes to diabetes. But don’t forget that the beverages you drink can also have an effect on your weight and blood glucose!

The American Diabetes Association recommends choosing zero-calorie or very low-calorie drinks 19. This includes:

  • Water
  • Unsweetened teas
  • Coffee no added sugar
  • Diet soda
  • Other low-calorie drinks and drink mixes

You can also try flavoring your water with a squeeze of lemon or lime juice for a light, refreshing drink with some flavor. All of these drinks provide minimal calories and carbohydrate. If you choose to drink juice, be sure the label says it is 100% juice with no sugar added. Juice provides a lot of carbohydrates in a small portion, so be sure to count it in your meal plan. Usually about 4 ounces or less of juice contains 15 grams of carbohydrate and 50 or more calories.

What to Avoid

Avoid sugary drinks like regular soda, fruit punch, fruit drinks, energy drinks, sweet tea, and other sugary drinks. These will raise blood glucose and can provide several hundred calories in just one serving! See for yourself:

  • One 12-ounce can of regular soda has about 150 calories and 40 grams of carbohydrate. This is the same amount of carbohydrate in 10 teaspoons of sugar!
  • One cup of fruit punch and other sugary fruit drinks have about 100 calories (or more) and 30 grams of carbohydrate.

Make your calories count with these nutritious foods:

  • Healthy carbohydrates. During digestion, sugars (simple carbohydrates) and starches (complex carbohydrates) break down into blood glucose. Focus on the healthiest carbohydrates, such as fruits, vegetables, whole grains, legumes (beans, peas and lentils) and low-fat dairy products.
  • Fiber-rich foods. Dietary fiber includes all parts of plant foods that your body can’t digest or absorb. Fiber moderates how your body digests and helps control blood sugar levels. Foods high in fiber include vegetables, fruits, nuts, legumes (beans, peas and lentils), whole-wheat flour and wheat bran.
  • Heart-healthy fish. Eat heart-healthy fish at least twice a week. Fish can be a good alternative to high-fat meats. For example, cod, tuna and halibut have less total fat, saturated fat and cholesterol than do meat and poultry. Fish such as salmon, mackerel, tuna, sardines and bluefish are rich in omega-3 fatty acids, which promote heart health by lowering blood fats called triglycerides. Avoid fried fish and fish with high levels of mercury, such as tilefish, swordfish and king mackerel.
  • “Good” fats. Foods containing monounsaturated and polyunsaturated fats can help lower your cholesterol levels. These include avocados, almonds, pecans, walnuts, olives, and canola, olive and peanut oils. But don’t overdo it, as all fats are high in calories.

The glycemic index, or GI, measures how a carbohydrate-containing food raises blood glucose. Foods are ranked based on how they compare to a reference food — either glucose or white bread.

A food with a high GI raises blood glucose more than a food with a medium or low GI.

Meal planning with the GI involves choosing foods that have a low or medium GI. If eating a food with a high GI, you can combine it with low GI foods to help balance the meal.

Examples of carbohydrate-containing foods with a low GI include dried beans and legumes (like kidney beans and lentils), all non-starchy vegetables, some starchy vegetables like sweet potatoes, most fruit, and many whole grain breads and cereals (like barley, whole wheat bread, rye bread, and all-bran cereal).

Meats and fats don’t have a GI because they do not contain carbohydrate.

Low GI Foods (55 or less)

  • 100% stone-ground whole wheat or pumpernickel bread
  • Oatmeal (rolled or steel-cut), oat bran, muesli
  • Pasta, converted rice, barley, bulgar
  • Sweet potato, corn, yam, lima/butter beans, peas, legumes and lentils
  • Most fruits, non-starchy vegetables and carrots

Medium GI (56-69)

  • Whole wheat, rye and pita bread
  • Quick oats
  • Brown, wild or basmati rice, couscous

High GI (70 or more)

  • White bread or bagel
  • Corn flakes, puffed rice, bran flakes, instant oatmeal
  • Shortgrain white rice, rice pasta, macaroni and cheese from mix
  • Russet potato, pumpkin
  • Pretzels, rice cakes, popcorn, saltine crackers
  • melons and pineapple

What Affects the GI of a Food ?

Fat and fiber tend to lower the GI of a food. As a general rule, the more cooked or processed a food, the higher the GI; however, this is not always true.

Below are a few specific examples of other factors that can affect the GI of a food:

  • Ripeness and storage time — the more ripe a fruit or vegetable is, the higher the GI.
  • Processing — juice has a higher GI than whole fruit; mashed potato has a higher GI than a whole baked potato, stone ground whole wheat bread has a lower GI than whole wheat bread.
  • Cooking methods — how long a food is cooked (al dente pasta has a lower GI than soft-cooked pasta), frying, boiling and baking.
  • Fibre: wholegrains and high-fibre foods act as a physical barrier that slows down the absorption of carbohydrate. This is not the same as ‘wholemeal’, where, even though the whole of the grain is included, it has been ground up instead of left whole. For example, some mixed grain breads that include wholegrains have a lower GI than wholemeal or white bread.
  • Fat lowers the GI of a food. For example, chocolate has a medium GI because of it’s fat content, and crisps will actually have a lower GI than potatoes cooked without fat.
  • Protein lowers the GI of food. Milk and other diary products have a low GI because they are high in protein and contain fat.
  • Variety — converted long-grain white rice has a lower GI than brown rice but short-grain white rice has a higher GI than brown rice.

Your food choices matter a lot when you’ve got diabetes. Some are better than others.

Nothing is completely off limits. Even items that you might think of as “the worst” could be occasional treats — in tiny amounts. But they won’t help you nutrition-wise, and it’s easiest to manage your diabetes if you mainly stick to the “best” options.

What is the difference between Glycemic Index (GI) and Glycemic Load (GL) ?

Your blood glucose rises and falls when you eat a meal containing carbs. How high it rises and how long it remains high depends on the quality of the carbohydrates (the GI) and the quantity (the serve size). Glycemic load or GL combines both the quality and quantity of carbohydrate in one ‘number’. It’s the best way to predict blood glucose values of different types and amounts of food.

The formula is:
GL = (GI x available carbohydrate in a 100g serving) divided by 100.

Let’s take a single apple as an example.
It has a GI of 40 and it contains 15 grams of carbohydrate.
GL = 40 x 15/100 = 6 g

What about a small baked potato?
Its GI is 80 and it contains 15 g of carbohydrate.
GL = 80 x 15/100 = 12 g

You can think of GL as the amount of carbohydrate in a food “adjusted” for its glycemic potency.

  • Low GL = <10
  • Medium GL = 11-19
  • High GL = >20

Therefore the Glycemic Load takes into account the amount of carbohydrate consumed and is a more accurate measure of the impact of a food on blood sugars. As a general rule foods that have a low GL usually have a low GI and those with a medium to high GL value almost always have a very high GI value.

Here is an abbreviated chart of the glycemic index and glycemic load, per serving, for more than 100 common foods.

FOODGlycemic index (glucose = 100)Serving size (grams)Glycemic load per serving
BAKERY PRODUCTS AND BREADS
Banana cake, made with sugar476014
Banana cake, made without sugar556012
Sponge cake, plain466317
Vanilla cake made from packet mix with vanilla frosting (Betty Crocker)4211124
Apple muffin, made with rolled oats and sugar446013
Apple muffin, made with rolled oats and without sugar48609
Waffles, Aunt Jemima®763510
Bagel, white, frozen727025
Baguette, white, plain953014
Coarse barley bread, 80% kernels34307
Hamburger bun61309
Kaiser roll733012
Pumpernickel bread56307
50% cracked wheat kernel bread583012
White wheat flour bread, average753011
Wonder® bread, average733010
Whole wheat bread, average69309
100% Whole Grain® bread (Natural Ovens)51307
Pita bread, white683010
Corn tortilla525012
Wheat tortilla30508
BEVERAGES
Coca Cola® (US formula)63250 mL16
Fanta®, orange soft drink68250 mL23
Lucozade®, original (sparkling glucose drink)95250 mL40
Apple juice, unsweetened41250 mL12
Cranberry juice cocktail (Ocean Spray®)68250 mL24
Gatorade, orange flavor (US formula)89250 mL13
Orange juice, unsweetened, average50250 mL12
Tomato juice, canned, no sugar added38250 mL4
BREAKFAST CEREALS AND RELATED PRODUCTS
All-Bran®, average44309
Coco Pops®, average773020
Cornflakes®, average813020
Cream of Wheat®6625017
Cream of Wheat®, Instant7425022
Grape-Nuts®753016
Muesli, average563010
Oatmeal, average5525013
Instant oatmeal, average7925021
Puffed wheat cereal803017
Raisin Bran®613012
Special K® (US formula)693014
GRAINS
Pearled barley, average2515011
Sweet corn on the cob486014
Couscous651509
Quinoa5315013
White rice, boiled, type non-specified7215029
Quick cooking white basmati6315026
Brown rice, steamed5015016
Parboiled Converted white rice (Uncle Ben’s®)3815014
Whole wheat kernels, average455015
Bulgur, average4715012
COOKIES AND CRACKERS
Graham crackers742513
Vanilla wafers772514
Shortbread642510
Rice cakes, average822517
Rye crisps, average642511
Soda crackers742512
DAIRY PRODUCTS AND ALTERNATIVES
Ice cream, regular, average62508
Ice cream, premium (Sara Lee®)38503
Milk, full-fat, average31250 mL4
Milk, skim, average31250 mL4
Reduced-fat yogurt with fruit, average3320011
FRUITS
Apple, average361205
Banana, raw, average4812011
Dates, dried, average426018
Grapefruit251203
Grapes, black5912011
Oranges, raw, average451205
Peach, average421205
Peach, canned in light syrup521209
Pear, raw, average381204
Pear, canned in pear juice441205
Prunes, pitted296010
Raisins646028
Watermelon721204
BEANS AND NUTS
Baked beans401506
Black-eyed peas5015015
Black beans301507
Chickpeas101503
Chickpeas, canned in brine421509
Navy beans, average3915012
Kidney beans, average341509
Lentils281505
Soy beans, average151501
Cashews, salted22503
Peanuts13501
PASTA and NOODLES
Fettucini3218015
Macaroni, average5018024
Macaroni and Cheese (Kraft®)6418033
Spaghetti, white, boiled, average4618022
Spaghetti, white, boiled 20 min5818026
Spaghetti, whole-grain, boiled4218017
SNACK FOODS
Corn chips, plain, salted425011
Fruit Roll-Ups®993024
M & M’s®, peanut33306
Microwave popcorn, plain, average65207
Potato chips, average565012
Pretzels, oven-baked833016
Snickers Bar®, average516018
VEGETABLES
Green peas54804
Carrots, average39802
Parsnips52804
Baked russet potato11115033
Boiled white potato, average8215021
Instant mashed potato, average8715017
Sweet potato, average7015022
Yam, average5415020
MISCELLANEOUS
Hummus (chickpea salad dip)6300
Chicken nuggets, frozen, reheated in microwave oven 5 min461007
Pizza, plain baked dough, served with parmesan cheese and tomato sauce8010022
Pizza, Super Supreme (Pizza Hut®)361009
Honey, average612512

The complete list of the glycemic index and glycemic load for more than 1,000 foods can be found in the article “International tables of glycemic index and glycemic load values: 2008” by Fiona S. Atkinson, Kaye Foster-Powell, and Jennie C. Brand-Miller in the December 2008 issue of Diabetes Care, Vol. 31, number 12, pages 2281-2283. (Source 20).

Benefits of Low Glycaemic Index or Low Glycaemic Load Diets for Diabetes Mellitus

To assess the effects of low glycaemic index or low glycaemic load, diets on glycaemic control in people with diabetes, eleven relevant randomised controlled trials, lasting 1 to 12 months, involving 402 participants were analysed 21.

There was a significant decrease in the glycated haemoglobin A1c (HbA1c) -0.5%. Episodes of hypoglycaemia were significantly fewer with low glycaemic index or low glycaemic load compared to high GI diet in one trial (difference of -0.8 episodes per patient per month), and proportion of participants reporting more than 15 hyperglycaemic episodes per month was lower for low-GI diet compared to measured carbohydrate exchange diet in another study (35% versus 66%). No study reported on mortality, morbidity or costs. The review authors concluded a low-GI diet can improve glycaemic control in diabetes without compromising hypoglycaemic events 21. This result is consistent with another smaller trial involving eight type 2 diabetes mellitus patients who were given carbohydrate foods with either a high or low glycemic index over a 2 weeks period 22.

 

I) Starches

Your body needs carbs. But you want to choose wisely. Use this list as a guide.

Best Choices

  • Whole grains, such as brown rice, oatmeal, quinoa, millet, or amaranth
  • Baked sweet potato
  • Items made with whole grains and no (or very little) added sugar

Worst Choices

  • Processed grains, such as white rice or white flour
  • Cereals with little whole grains and lots of sugar
  • White bread
  • French fries
  • Fried white-flour tortillas

II) Vegetables

Load up! You’ll get fiber and very little fat or salt (unless you add them).  Remember, potatoes and corn count as carbs.

Best Choices

  • Fresh veggies, eaten raw or lightly steamed, roasted, or grilled
  • Plain frozen vegetables, lightly steamed
  • Greens such as kale, spinach, and arugula. Iceberg lettuce is not as great, because it’s low in nutrients.
  • Low sodium or unsalted canned vegetables
  • Go for a variety of colors: dark greens, red or orange (think of carrots or red peppers), whites (onions) and even purple (eggplants). The 2015 U.S. guidelines recommend 2.5 cups of veggies per day.

Worst Choices

  • Canned vegetables with lots of added sodium
  • Veggies cooked with lots of added butter, cheese, or sauce
  • Pickles, if you need to limit sodium — otherwise, pickles are okay.
  • Sauerkraut, for the same reason as pickles — so, limit them if you have high blood pressure

 

III) Fruits

They give you carbohydrates, vitamins, minerals, and fiber. Most are naturally low in fat and sodium. But they tend to have more carbs than vegetables do.

Best Choices

  • Fresh fruit
  • Plain frozen fruit or fruit canned without added sugar
  • Sugar-free or low-sugar jam or preserves
  • No-sugar-added apple sauce

Worst Choices

  • Canned fruit with heavy sugar syrup
  • Chewy fruit rolls
  • Regular jam, jelly, and preserves (unless you have a very small portion)
  • Sweetened apple sauce
  • Fruit punch, fruit drinks, fruit juice drinks

IV) Protein

You have lots of choices, including beef, chicken, fish, pork, turkey, seafood, beans, cheese, eggs, nuts, and tofu.

Best Choices

The American Diabetes Association lists these as the top options:

  • Plant-based proteins, such as beans, nuts, seeds, or tofu
  • Fish and seafood
  • Chicken and other poultry (Choose the breast meat if possible.)
  • Eggs and low-fat dairy

If you eat meat, keep it low in fat. Trim the skin off poultry.

Try to include some plant-based protein from beans, nuts, or tofu, even if you’re not a vegetarian or vegan. You’ll get nutrients and fiber that aren’t in animal products.

Worst Choices

  • Fried meats
  • Higher-fat cuts of meat, such as ribs
  • Pork bacon
  • Regular cheeses
  • Poultry with skin
  • Deep-fried fish
  • Deep-fried tofu
  • Beans prepared with lard

V) Dairy

Keep it low in fat. If you want to splurge, keep your portion small.

Best Choices

  • 1% or skim milk
  • Low-fat yogurt
  • Low-fat cottage cheese
  • Low-fat or nonfat sour cream

Worst Choices

  • Regular yogurt
  • Regular cottage cheese
  • Regular sour cream
  • Regular ice cream
  • Regular half-and-half

VI) Fats, Oils, and Sweets

They’re tough to resist. But it’s easy to get too much and gain weight, which makes it harder to manage your diabetes.

Best Choices

  • Natural sources of vegetable fats, such as nuts, seeds, or avocados (high in calories, so keep portions small)
  • Foods that give you omega-3 fatty acids, such as salmon, tuna, or mackerel
  • Plant-based oils, such as canola, grapeseed, or olive oils

Worst Choices

  • Anything with artificial trans fat in it. It’s bad for your heart. Check the ingredient list for anything that’s “partially hydrogenated,” even if the label says it has 0 grams of trans fat.

VII) Drinks

When you down a favorite drink, you may get more calories, sugar, salt, or fat than you bargained for. Read the labels so you know what’s in a serving.

Best Choices

  • Water, unflavored or flavored sparkling water
  • Unsweetened tea (add a slice of lemon)
  • Coffee, black or with added low-fat milk and sugar substitute

Worst Choices

  • Light beer, small amounts of wine, or non-fruity mixed drinks
  • Regular sodas
  • Regular beer, fruity mixed drinks, dessert wines
  • Sweetened tea
  • Coffee with sugar and cream
  • Flavored coffees and chocolate drinks
  • Energy drinks

Summary

Healthy eating and an active lifestyle are important for everyone, including people with diabetes. To achieve and maintain a healthy weight, be physically active and choose amounts of nutritious foods and drinks to meet your energy needs. Having a healthy diet and being active is an important part of managing diabetes because it will help manage your blood glucose levels and your body weight.

  1. Meals that are recommended for people with diabetes are the same as for those without diabetes.
  2. There is no need to prepare separate meals or buy special foods.
  3. Everyone including family and friends can enjoy the same healthy and tasty meals together.
  4. As a guide, we recommend people with diabetes follow the American Dietary Guidelines Healthy Eating for Adults and Healthy Eating for Children.
  5. Everyone’s needs are different so we recommend everyone with diabetes visit a dietitian for personal advice.
  6. Enjoy a wide variety of nutritious from these five food groups every day:

a) Plenty of vegetables and different types and colors and legumes/beans.

b) Fruits

c) Grain (cereal) foods, mostly wholegrain and/or high cereal fiber varieties, such as breads, cereals, rice, pasta, noodles, polenta, couscous, quinoa, oats, and barley.

d) Lean meats and poultry, fish, eggs, tofu, nuts and seeds, and legumes/beans.

e) Milk, yogurt, cheese and/or their alternatives, mostly reduced fat.

And drink plenty of water. Limit intake of foods and drinks containing added salt, sugar and saturated and trans fats.

low calorie diet

Low Calorie Diet on Weight Loss and the Metabolic Profile of Obese Patients with Type 2 Diabetes Mellitus

A small study 23 with 60 patients (23 males and 37 postmenopausal females) who have type 2 diabetes and are obese, to compare the effects of low calorie diet (1800 kcal/day) plus intensive insulin therapy (4 insulin injections/day) versus low calorie diet (1800 kcal/day) plus conventional insulin therapy (2/3 insulin injections/day). At 6 months post-interventions, there were significant reductions were observed in the body weight, body mass index (BMI), HbA1c for all participants and cholesterol. At 1 year, median body weight reduction was 4.5 kg for patients on low calorie diet (1800 kcal/day) plus intensive insulin therapy and 4.8 kg for those on low calorie diet (1800 kcal/day) plus conventional insulin therapy. The conclusion was a 12-month 1800-kcal low calorie dietary intervention achieved significant body weight loss and HbA1c reductions irrespectively of insulin regimen. The  low calorie diet (1800 kcal/day) plus conventional insulin therapy was associated with body weight loss greater than 8.0%, whereas low calorie diet (1800 kcal/day) plus intensive insulin therapy was associated with higher rates of normoglycemia 23.

Very Low Calorie Diet in Obese Type 2 Diabetes

A small study was conducted with fifty-one obese subjects (24 with diabetes and 27 obese without diabetes) to compare weight loss and change in body composition in obese subjects with and without type 2 diabetes mellitus during a very-low-calorie diet (VLCD) program 24. After 24 weeks of intervention, there was no difference in weight loss between the 2 groups. Both groups completing the study per protocol had near-identical weight change during the program, with similar weight loss at 24 weeks (diabetes: 8.5 ± 1.3 kg vs control: 9.4 ± 1.2 kg). Change in fat mass index correlated with change in body mass index (BMI) in both groups, but change in fat mass index per unit change in BMI was less in the diabetic group compared with controls, which persisted after adjusting for age, sex, and baseline BMI. Insulin concentrations remained higher and peak β-hydroxybutyrate concentrations were lower in the diabetic compared with the control group. The conclusion was while following a 24-week very-low-calorie diet program, obese subjects with and without diabetes achieved comparable weight loss; but the decrease in body fat per unit weight loss was less in diabetic subjects. Hyperinsulinemia may have inhibited lipolysis in the diabetic group; however, further investigation into other factors is needed 24.

Low Carbohydrate Low Calorie Diet in type 2 Diabetes

In a very small study 25 comparing the effects of low carbohydrate low calorie diet (1800 kcal for men and 1600 kcal for women, distributed as 20 % carbohydrates, 30 % protein and 50 % fat) and high carbohydrate low calorie diet (1600-1800 kcal for men and 1400-1600 kcal for women, consisted of approximately 60 % carbohydrates, 15 % protein and 25 % fat) in two groups of obese patients with type 2 diabetes. The diets were tested with regard to glycaemic control and bodyweight. A group of 16 obese patients with type 2 diabetes was advised on a low-carbohydrate diet,  Fifteen obese diabetes patients on a high-carbohydrate diet were control group. Positive effects on the glucose levels were seen very soon. After 6 months a marked reduction in bodyweight of patients in the low-carbohydrate diet group was observed, and this remained one year later. After 6 months the mean changes in the low-carbohydrate group and the control (high carbohydrate low calorie diet) group respectively were fasting blood glucose: -3.4 and -0.6 mmol/l; HBA1c: -1.4 % and -0.6 %; Body Weight: -11.4 kg and -1.8 kg; BMI: -4.1 kg/m2 and -0.7 kg/m2. In conclusion, a low-carbohydrate diet is an effective tool in the treatment of obese patients with type 2 diabetes 25.

References
  1. J Health Popul Nutr. 2012 Dec; 30(4): 447–455. Factors Associated with Consumption of Diabetic Diet among Type 2 Diabetic Subjects from Ahmedabad, Western India. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3763616/
  2. U.S. National Library of Medicine, Medline Plus. Diabetic Diet. https://medlineplus.gov/diabeticdiet.html
  3. Evert, A.B. and Boucher, J.L. et al; Nutrition Therapy Recommendations For the Management of Adults with Diabetes,:Position Statement by the ADA, Diabetes Care 2013, 363821-42.
  4. Standards of Medical Care in Diabetes-2013 Diabetes Care 2013;36(Suppl. 1):S11–S66
  5. https://www.cdc.gov/diabetes/ndep/cdcinfo/ndep_pdf/tasty-recipes-508.pdf
  6. BMI Calculator Adults. https://www.cdc.gov/healthyweight/assessing/bmi/adult_BMI/english_bmi_calculator/bmi_calculator.html
  7. BMI Calculator Children. https://nccd.cdc.gov/dnpabmi/Calculator.aspx
  8. https://supertracker.usda.gov/
  9. Body Weight Planner. https://www.supertracker.usda.gov/bwp/index.html
  10. ChooseMyPlate. https://www.choosemyplate.gov/
  11. American Diabetes Association. All of Our Meal Plans. http://www.diabetes.org/mfa-recipes/meal-plans/meal-plans.html
  12. American Diabetes Association. Create Your Plate. http://www.diabetes.org/food-and-fitness/food/planning-meals/create-your-plate/
  13. American Diabetes Association. Non-starchy Vegetables. http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/making-healthy-food-choices/non-starchy-vegetables.html
  14. American Diabetes Association. Grains and Starchy Vegetables. http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/making-healthy-food-choices/grains-and-starchy-vegetables.html
  15. American Diabetes Association. Fruits. http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/making-healthy-food-choices/fruits.html
  16. American Diabetes Association. Protein Foods. http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/making-healthy-food-choices/meat-and-plant-based-protein.html
  17. American Diabetes Association. Dairy. http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/making-healthy-food-choices/dairy.html
  18. Centers for Disease Control and Prevention. Managing Diabetes: Eat Right ! https://www.cdc.gov/diabetes/managing/eatright.html
  19. American Diabetes Association. What Can I Drink ? http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/making-healthy-food-choices/what-can-i-drink.html
  20. Diabetes Care 2008 Dec; 31(12): 2281-2283. https://doi.org/10.2337/dc08-1239. International Tables of Glycemic Index and Glycemic Load Values: 2008. http://care.diabetesjournals.org/content/31/12/2281.full
  21. Cochrane Review 21 January 2009. Low glycaemic index, or low glycaemic load, diets for diabetes mellitus. http://www.cochrane.org/CD006296/ENDOC_low-glycaemic-index-or-low-glycaemic-load-diets-for-diabetes-mellitus
  22. Am J Clin Nutr. 1988 Aug;48(2):248-54. Low-glycemic-index starchy foods in the diabetic diet. https://www.ncbi.nlm.nih.gov/pubmed/3407604
  23. Adv Ther. 2016 Mar;33(3):447-59. doi: 10.1007/s12325-016-0300-2. Epub 2016 Feb 17. Obese Patients with Type 2 Diabetes on Conventional Versus Intensive Insulin Therapy: Efficacy of Low-Calorie Dietary Intervention. https://www.ncbi.nlm.nih.gov/pubmed/26886777
  24. Metabolism. 2012 Jun;61(6):873-82. doi: 10.1016/j.metabol.2011.10.017. Epub 2011 Dec 5. Less fat reduction per unit weight loss in type 2 diabetic compared with nondiabetic obese individuals completing a very-low-calorie diet program. https://www.ncbi.nlm.nih.gov/pubmed/22146094?dopt=Abstract
  25. Ups J Med Sci. 2005;110(1):69-73. Lasting improvement of hyperglycaemia and bodyweight: low-carbohydrate diet in type 2 diabetes–a brief report. https://www.ncbi.nlm.nih.gov/pubmed/15801687?dopt=Abstract
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Diet PlanDiet, Food & Fitness

What is low calorie diet ?

low calorie diet

What is a Calorie

Calories are units representing the ability of food to be converted by the body into energy. All food contains calories, and we need a certain amount of calories each day.

  • Large calorie (Cal) is the energy needed to increase 1 kg of water by 1°C at a pressure of 1 atmosphere.
  • Large calorie (Cal) is also called Food calorie and is used as a unit of food energy.
  • 1 Large Calorie (1 kilocalories) = 4.184 kilojoules (kJ)
  • 2000 Calories = 8368 kilojoules (kJ)

Because how much calories you eat and what food groups you need are highly dependent on your age, sex, and your level of physical activity. For the most accurate way calculate how much food and calories you need to eat per day from each food group, Go to >>>>>

  • To find out about your body mass index (BMI), you can use a FREE online BMI calculators from the Centers for Disease Control and Prevention (CDC) – for Adults 1 and for Children 2
  • To find out What and How Much To Eat, you can use a FREE, award-winning, state-of-the-art, online diet and activity tracking tool called SuperTracker 3 from the United States Department of Agriculture Center for Nutrition Policy and Promotion 3. This free application empowers you to build a healthier diet, manage weight, and reduce your risk of chronic diet-related diseases. You can use SuperTracker 3 to determine what and how much to eat; track foods, physical activities, and weight; and personalize with goal setting, virtual coaching, and journaling.

SuperTracker website 3

  • To find out about how many calories you should eat to lose weight according to your weight, age, sex, height and physical activity, you can use a FREE online app Body Weight Planner 4
  • To find out about the 5 Food Groups you should have on your plate for a meal, you can use a FREE online app ChooseMyPlate 5

Calories are the energy in food. Your body has a constant demand for energy and uses the calories from food to keep functioning. Energy from calories fuels your every action, from sleeping to marathon running.

It is true that all “calories” have the same amount of energy. One dietary Calorie contains 4184 Joules of energy. In that respect, a calorie is a calorie. But when it comes to your body, things are not that simple. Looking only at calories ignores the metabolic effects of each calorie; the source of the calorie changes how you digest it and how you retrieve energy from it. The human body is a highly complex biochemical system with elaborate processes that regulate energy balance. This is because some foods provide not only calories but also other ingredients that also are critically important, such as vitamins, minerals, antioxidants, and others. When a food provides primarily calories, and little else of value to our health, we say that food has “empty calories.”

Examples include beverages like sugary soda, and foods like buttery pastries. They provide little health value. You can get all the calories you need from foods other than these-foods that contain other healthful ingredients. Another problem with foods said to contain “empty calories” is that they usually contain lots of calories-more than we need to attain or sustain a healthy weight.

Counting calories alone doesn’t work because ultimately it matters where those calories come from; this matters more than the number of calories ingested.

Carbohydrates, fats and proteins are the types of nutrients that contain calories and are the main energy sources for your body. Regardless of where they come from, the calories you eat are either converted to physical energy or stored within your body as fat.

Your weight is a balancing act, but the equation is simple: If you eat more calories than you burn, you gain weight.

Because 3,500 calories equals about 1 pound (0.45 kilogram) of fat, you need to burn 3,500 calories more than you take in to lose 1 pound.

So, in general, if you cut 500 calories from your typical diet each day, you’d lose about 1 pound a week (500 calories x 7 days = 3,500 calories). A weight loss of 1 to 2 pounds a week is the typical recommendation. Although that may seem like a slow pace for weight loss, it’s more likely to help you maintain your weight loss for the long term. Remember that 1 pound (0.45 kilogram) of fat contains 3,500 calories. So to lose 1 pound a week, you need to burn 500 more calories than you eat each day (500 calories x 7 days = 3,500 calories).

However, it isn’t quite this simple,because you usually lose a combination of fat, lean tissue and water. Also, if you lose a lot of weight very quickly, you may not lose as much fat as you would with a more modest rate of weight loss. Instead, you might lose water weight or even lean tissue, since it’s hard to burn that many fat calories in a short period.

low calorie diet

What is Low Calorie Diet

A low calorie diet (LCD) limits calories, but not as much as a very low calorie diet (VLCD). A typical low calorie diet (LCD) may provide:

  • 1,000–1,200 calories/day for a woman
  • 1,200–1,600 calories/day for a man

A low calorie diet is a diet with a reduction in calorie intake without deprivation of essential nutrients.

Calorie restriction without malnutrition is the most powerful nutritional intervention that has consistently been shown to increase maximal and average lifespan in a variety of organisms, including yeasts, worms, flies, spiders, rotifers, fish and rodents 6, 7, 8, 9, 10. Far from merely stretching the life of an old, ill and weak animal, calorie restriction extends longevity by preventing chronic diseases, and by preserving metabolic and biological functions at more youthful-like state 11, 12, 13. In rodents, the calorie restriction-mediated preventive effects are widespread with major reductions in the occurrence and/or progression of cancer, nephropathy, cardiomyopathy, obesity, type 2 diabetes, neuro-degenerative disease, and several autoimmune diseases 14, 15, 16. Moreover, unlike ad-libitum fed rodents, ~30% of the calorie restriction rodents die in old age without any pathological sign of disease 17. Likewise, 25 to 50% of the longevous Ames/Snell dwarf mice and growth hormone receptor knock-out mice expire without pathological evidence of disease severe enough to be recorded as the cause of death 18, 19, suggesting that in mammals the occurrence of lethal chronic disease can be completely prevented by dietary and genetic manipulations that down-regulate the key cellular nutrient-sensing pathways 6. However, whether or not calorie restriction with adequate nutrition will significantly slow aging and extend lifespan in non-human primates, and most importantly in human beings, is not yet clear.

Whether or not calorie restriction without malnutrition will extend lifespan in humans is not known yet, but accumulating data indicate that moderate calorie restriction with adequate nutrition has a powerful protective effect against the development of obesity, type 2 diabetes, inflammation, hypertension and cardiovascular disease, which are major causes of morbidity, disability and mortality 20. Accordingly, Lloyd-Jones and colleagues found that in men and women from the Framingham Heart Study with normal cardiovascular risk profile at age 50 (i.e. total glycemia <125 mg/dl, blood pressure <120/80 mmHg, cholesterol <180 mg/dl, BMI <25 kg/m2 and no smoke) the lifetime probability of developing an atherosclerotic cardiovascular disease was very low (i.e., 6.7% versus 59.5% in participants with ≥2 cardiometabolic risk factors) and average lifespan markedly longer (i.e. >39 versus 29.5 years in participants with ≥2 cardiometabolic risk factors) 21. In humans calorie restriction without malnutrition also results in a consistent reduction in circulating levels of growth factors, anabolic hormones, adipokines and inflammatory cytokines, which are associated with an increased risk of some of the most common types of cancer 22.

In terms of calorie reduction, we know that one pound equals 3,500 calories.  By reducing daily calorie intake by 500 to 1,000 calories, it is reasonable to expect a weight loss of 1 to 2 pounds/week.

The number of calories may be adjusted based on your age, weight, and how active you are. A low calorie diet usually consists of regular foods, but could also include meal replacements. As a result, you may find this type of diet much easier to follow than a very low calorie diet. In the long term, low calorie diets have been found to lead to the same amount of weight loss as very low calorie diets.

In 2011, a Diabetes UK research trial at Newcastle University 23 tested a low-calorie diet in 11 people with Type 2 diabetes, which helped us to understand how Type 2 diabetes can be put into remission. After the 8-week diet, volunteers had reduced the amount of fat in their liver and pancreas. This helped to restore their insulin production and put their Type 2 diabetes into remission. Three months later, some had put weight back on, but most still had normal blood glucose control. This study was only a first step. It was designed to tell us about the underlying biology of Type 2 diabetes, and it followed the participants for only three months.

Another study, published in 2016, confirmed these findings and showed (in 30 people) that Type 2 diabetes could be kept in remission 6 months after the low-calorie diet was completed. It also suggested that the diet was effective in people that had had Type 2 diabetes for up to 10 years.

Both of these studies were very small, and were carried out in a research environment. We don’t yet understand the long-term effects of these diets, or how a low-calorie diet might be used to bring about and maintain Type 2 diabetes remission in a real-life setting, as part of routine general practice care.

Currently a new research is underway in Scotland and Tyneside (UK) called the Diabetes Remission Clinical Trial, where 20-65 year olds who are overweight and have been diagnosed with Type 2 diabetes in the last six years, will be randomised to receive either low calorie diet for between 8 and 20 weeks or the current best-available Type 2 diabetes care. This study will last until October 2018 and results will be released once all of the data has been analysed probably early 2019 23.

In the meantime there’s been a lot of buzz on the internet about using a low-calorie diet to live longer. A new study of overweight people who cut their calories by 25% for 6 months found some promising lab results that have been linked to longevity 24. The results aren’t enough for any major conclusions, but they point the way toward longer studies to see if low-calorie diets can really slow the aging process in people.

In that longevity study with low calorie diet, participants were randomly divided into 4 groups:

  • One group stayed on a diet to maintain their pre-study weight.
  • A calorie-restriction group ate 25% less calories.
  • A calorie-restriction with exercise group ate 12.5% less calories but exercised to burn 12.5% more.
  • A very low-calorie diet group ate 890 calories a day until they lost 15% of their weight. They then followed a weight-maintenance diet to hold the lower weight.

Fasting insulin levels were significantly lower in all three groups on the restricted-calorie diets. Core body temperature was reduced in both the calorie-restriction and calorie-restriction with exercise groups. The low-calorie diets may also affect some other measurements of metabolism that have been linked with living longer and aging. The calorie restriction significantly lowered several predictors of cardiovascular disease compared to the control group:

  • Decreasing average blood pressure by 4 percent
  • Decreasing total cholesterol by 6 percent.
  • Levels of HDL (“good”) cholesterol were increased.
  • Calorie restriction caused a 47-percent reduction in levels of C-reactive protein, an inflammatory factor linked to cardiovascular disease.
  • It also markedly decreased insulin resistance, which is an indicator of diabetes risk.
  • T3, a marker of thyroid hormone activity, decreased in the calorie restriction group by more than 20 percent, while remaining within the normal range. This is of interest since some studies suggest that lower thyroid activity may be associated with longer life span.

No increased risk of serious adverse clinical events was reported. However, a few participants developed transient anemia and greater-than-expected decreases in bone density given their degree of weight loss, reinforcing the importance of clinical monitoring during calorie restriction.

Calorie restriction without malnutrition has been consistently shown to increase longevity in a number of animal models, including yeast, C. elegans, and mice 6. However, the effect of calorie restriction on the lifespan of nonhuman primates remains controversial and may be heavily influenced by dietary composition 25, 26, 27, 28, 29, 30.

The lifespan extension associated with calorie restriction in model organisms is believed to operate through its effects on growth hormone (GH) and growth hormone receptor (GHR), leading to subsequent deficiencies in IGF-1 and insulin levels and signaling 6. The effect of the insulin/IGF-1 pathway on longevity was first described in C. elegans by showing that mutations in the insulin/IGF-1 receptor or in the downstream age-1 gene caused a several-fold increase in lifespan 31. Other studies revealed that mutations in genes functioning in insulin/IGF-1 signaling, but also activated independently of insulin/IGF-1, including TOR-S6K and RAS-cAMP-PKA, promoted aging in multiple model organisms, thus providing evidence for the conserved regulation of aging by pro-growth nutrient signaling pathways 32. Not surprisingly, in mice, growth hormone receptor deficiency (GHRD) or growth hormone deficiency (GHD), both of which display low levels of IGF-1 and insulin, cause the strongest lifespan extension but also reduction of age-related pathologies including cancer and insulin resistance/diabetes 33, 34, 35. Recently, this study 36 showed showed that humans with growth hormone receptor deficiency (GHRD), also exhibiting major deficiencies in serum IGF-1 and insulin levels, displayed no cancer mortality or diabetes. Despite having a higher prevalence of obesity, combined deaths from cardiac disease and stroke in this group were similar to those in their relatives 37. Similar protection from cancer was also reported in a study that surveyed 230 growth hormone receptor deficiency 38.

Protein restriction or restriction of particular amino acids, such as methionine and tryptophan, may explain part of the effects of calorie restriction and growth hormone receptor deficiency mutations on longevity and disease risk, since protein restriction is sufficient to reduce IGF-1 levels and can reduce cancer incidence or increase longevity in model organisms, independently of calorie intake 39, 40, 41.

Low Calorie Diet and Weight Loss

In a study published in The New England Journal of Medicine in 2009, followed 811 overweight adults over 2 years 42, who were prescribed Low Calorie Diets (a deficit of 750 kcal per day from baseline, as calculated from the person’s resting energy expenditure and activity level) and all the low calorie diets should include 8% or less of saturated fat, at least 20 g of dietary fiber per day, and 150 mg or less of cholesterol per 1000 kcal). Carbohydrate-rich foods with a low glycemic index were recommended in each diet. Each participant’s caloric prescription represented one of the four diets:

  • Fat 20%, Protein 15% and Carbohydrate 65% (Low-fat and Average-protein and High carb)
  • Fat 20%, Protein 25% and Carbohydrate 55% (Low-fat and High-protein and Average carb)
  • Fat 40%, Protein 15% and Carbohydrate 45% (High-fat and Average-protein and Average carb)
  • Fat 40%, Protein 25% and Carbohydrate 35% (High-fat and High-protein and Low carb)
  • All participants’ goal for physical activity was 90 minutes of moderate exercise per week. Participation in exercise was monitored by questionnaire and by the online self-monitoring tool.

Group sessions were held once a week, 3 of every 4 weeks during the first 6 months and 2 of every 4 weeks from 6 months to 2 years; individual sessions were held every 8 weeks for the entire 2 years. Daily meal plans in 2-week blocks were provided. Participants were instructed to record their food and beverage intake in a daily food diary and in a web-based self-monitoring tool that provided information on how closely their daily food intake met the goals for macronutrients and energy. Behavioral counseling was integrated into the group and individual sessions to promote adherence to the assigned diets. Contact among the groups was avoided.

At 6 months, participants assigned to each diet had lost an average of 6 kg, which represented 7% of their initial weight; they began to regain weight after 12 months.

  • By 2 years, weight loss remained similar in those who were assigned to a diet with 15% protein and those assigned to a diet with 25% protein (3.0 and 3.6 kg, respectively); in those assigned to a diet with 20% fat and those assigned to a diet with 40% fat (3.3 kg for both groups); and in those assigned to a diet with 65% carbohydrates and those assigned to a diet with 35% carbohydrates (2.9 and 3.4 kg, respectively).
  • Among the 80% of participants who completed the trial, the average weight loss was 4 kg; 14 to 15% of the participants had a reduction of at least 10% of their initial body weight. Satiety, hunger, satisfaction with the diet, and attendance at group sessions were similar for all diets; attendance was strongly associated with weight loss (0.2 kg per session attended). The diets improved lipid-related risk factors and fasting insulin levels.

Conclusions: Reduced-calorie diets result in clinically meaningful weight loss regardless of which macronutrients they emphasize. All of the diets resulted in meaningful weight loss, despite the differences in macronutrient composition 42.

The study also found that the more group counseling sessions participants attended, the more weight they lost, and the less weight they regained. This supports the idea that not only is what you eat important, but behavioral, psychological, and social factors are important for weight loss as well 42.

Low Calorie Diet Foods

  • Protein.

Protein should be no more than 15 percent of total calories and should be derived from plant sources and lean sources of animal protein.

Lean plant proteins include dry peas, beans, legumes, and soy protein (tofu). Lean animal protein includes lean cuts of meat, poultry, seafood, and low fat dairy (milk, yogurt, cheese,and cottage cheese).

  • Carbohydrate and Fiber.

Dietary carbohydrate should be approximately 55 percent or more of  total calories and should be rich in complex carbohydrates from different vegetables, fruits, and whole grains—all good sources of vitamins, minerals, and fiber.
• A diet high in all types of fiber may aid in weight management by promoting satiety at lower levels of calorie and fat intake.
• Some authorities recommend 20 to 30 grams of fiber daily, with an upper limit of 35 grams. A diet rich in soluble fiber, including oat bran, legumes, barley, and most fruits and vegetables, may be effective in reducing blood cholesterol levels.  A diet high in all types of fiber may also aid in weight management by promoting satiety at lower calorie and fat levels.

  • Calcium.

During weight loss, attention should be given to maintaining an adequate intake of vitamins and minerals, particularly calcium. Maintenance of the recommended calcium intake of 1,000 to 1,500 mg/day is especially important for women who may be at risk of osteoporosis.

  • Total Fat.

Fat-modified foods can be a great help to those who are trying to lose weight,  but only if the low-fat food is also low in calories and the lost calories are not compensated for by eating larger quantities of these low-fat foods or other foods.  Reducing fat can be an important way to save calories, but many low-fat products in the store have the same number of calories as the regular variety.  This is why it is important
to read the food label to compare fat as well as calories.




 

 

 

How Many Calories Do You Need ?

Estimated Calorie Needs per Day, by Age, Sex, and Physical Activity Level

MALES[d]
AGESedentary[a]Moderately
active[b]
Active[c]
21,0001,0001,000
31,0001,4001,400
41,2001,4001,600
51,2001,4001,600
61,4001,6001,800
71,4001,6001,800
81,4001,6002,000
91,6001,8002,000
101,6001,8002,200
111,8002,0002,200
121,8002,2002,400
132,0002,2002,600
142,0002,4002,800
152,2002,6003,000
162,4002,8003,200
172,4002,8003,200
182,4002,8003,200
19-202,6002,8003,000
21-252,4002,8003,000
26-302,4002,6003,000
31-352,4002,6003,000
36-402,4002,6002,800
41-452,2002,6002,800
46-502,2002,4002,800
51-552,2002,4002,800
56-602,2002,4002,600
61-652,0002,4002,600
66-702,0002,2002,600
71-752,0002,2002,600
76 and up2,0002,2002,400
FEMALES[d]
AGESedentary[a]Moderately
active[b]
Active[c]
21,0001,0001,000
31,0001,2001,400
41,2001,4001,400
51,2001,4001,600
61,2001,4001,600
71,2001,6001,800
81,4001,6001,800
91,4001,6001,800
101,4001,8002,000
111,6001,8002,000
121,6002,0002,200
131,6002,0002,200
141,8002,0002,400
151,8002,0002,400
161,8002,0002,400
171,8002,0002,400
181,8002,0002,400
19-202,0002,2002,400
21-252,0002,2002,400
26-301,8002,0002,400
31-351,8002,0002,200
36-401,8002,0002,200
41-451,8002,0002,200
46-501,8002,0002,200
51-551,6001,8002,200
56-601,6001,8002,200
61-651,6001,8002,000
66-701,6001,8002,000
71-751,6001,8002,000
76 and up1,6001,8002,000

Notes:

[a] Sedentary means a lifestyle that includes only the physical activity of independent living.
[b] Moderately Active means a lifestyle that includes physical activity equivalent to walking about 1.5 to 3 miles perd ay at 3 to 4 miles per hour, in addition to the
activities of independent living.
[c] Active means a lifestyle that includes physical activity equivalent to walking more than 3 miles per day at 3 to 4 miles per hour, in addition to the activities o f
independent living.
[d] Estimates for females do not include women who are pregnant or breastfeeding.

(SOURCE: 43)

Balancing Calories

Balancing the calories you eat and drink with the calories burned by being physically active helps to maintain a healthy weight.

Each person uses different amounts of calories doing the same type of activity. In general, heavier people use more calories. Those who weigh less use fewer. Women also probably use fewer.

How much physical activity ? Although any amount of regular physical activity is good for you, aim for at least 150 minutes of physical activity each week. Unless you are already that active, you won’t do that much all at once—10-minute sessions several times a day on most days are fine.

Balancing Calories
Balancing Calories

Different foods go through different biochemical pathways, some of which are inefficient and cause energy (calories) to be lost as heat.

You should choose nutrient-dense foods. These foods give you lots of nutrients without a lot of extra calories. Even more important is the fact that different foods and macronutrients have a major effect on the hormones and brain centers that control hunger and eating behavior.

On the other hand, foods that are high in calories for the amount of food are called calorie dense. They may or may not have nutrients. High-calorie foods with little nutritional value, like potato chips, sugar-sweetened drinks, candy, baked goods, and alcoholic beverages, are sometimes called “empty calories.”

Energy density means getting more for your calories.

Energy density is the number of calories (energy) in a given amount (volume) of food. By choosing foods that are low in calories, but high in volume, you can eat more and feel fuller on fewer calories.

Fruits and vegetables are good choices because they tend to be low in energy density and high in volume.

So what about raisins ? They’re actually high in energy density — they pack a lot of calories into a small package. For example, 1/4 cup of raisins has about 100 calories. For about the same number of calories you could have 1 cup of grapes — and get more bite for your calorie buck.

High versus low energy density

Foods high in energy density include fatty foods, such as many fast foods, and foods high in sugar, such as sodas and candies. For example, a small order of fast-food french fries has about 250 calories.

For about the same calorie count, you could have heaping helpings of fresh fruits and vegetables — such as this salad made with 10 cups of spinach, 1 1/2 cups of strawberries and a small apple.

And with fresh fruits and vegetables, you get a plethora of valuable nutrients — not just empty calories. These foods also take longer to eat and are filling, which helps curb your hunger.

Another way to think about the idea of nutrient-dense and calorie-dense foods is to look at a variety of foods that all provide the same calories. Which would make a better snack for you ?

Let’s say that you wanted to have a snack that contained about 100 calories. You might choose one of these:

  • 7- or 8-inch banana,
  • Two ounces baked chicken breast with no skin,
  • Three cups low-fat popcorn,
  • Two regular chocolate-sandwich cookies,
  • Half cup low-fat ice cream,
  • One scrambled large egg cooked with fat,
  • 20 peanuts,
  • Half of the average-size candy bar.

Although these examples all have about 100 calories, there are some big differences:

  • Banana, chicken, peanuts, or egg are more nutrient dense.
  • Popcorn or chicken are likely to help you feel more satisfied.
  • Chicken, peanuts, or egg have more protein.
  • Cookies, candy, and ice cream have more added sugars.

Can choosing a nutrient-dense food instead of a calorie-dense food really make a difference ? Here are some examples of nutrient-dense choices side by side with similar foods that are not nutrient-dense, have more calories, or both.

A) Hamburger patty, 4 oz. precooked, extra lean ground beef
167 calories

B) Hamburger patty, 4 oz. precooked, regular ground beef
235 calories

A) Large apple, 8 oz.
110 calories

B) Apple pie, eighth of a 2-crust 9″ pie
356 calories

A) Two slices of 100% whole wheat bread, 1 oz. each
138 calories

B) Medium croissant, 2 oz.
231 calories

A) Medium baked potato with peel, 2 tablespoons low-fat sour cream
203 calories

B) French fries, one medium fast-food order
457 calories

A) Roasted chicken breast, skinless (3 oz.)
141 calories

B) Fried chicken wings with skin and batter, (3 oz.)
479 calories

A) A candy bar
280 calories

B) A pita bread stuffed with low-fat chicken salad
280 calories

Healthy eating:

  • Emphasizes vegetables, fruits, whole grains, and fat-free or low-fat milk and milk products.
  • Includes lean meat, poultry, fish, cooked dry beans and peas, eggs, and nuts.
  • Is low in saturated fats, trans fats, salt, and added sugars.
  • Balances the calories from foods and beverages with calories burned through physical activity so that you can maintain a healthy weight.
References
  1. BMI Calculator Adults. https://www.cdc.gov/healthyweight/assessing/bmi/adult_BMI/english_bmi_calculator/bmi_calculator.html
  2. BMI Calculator Children. https://nccd.cdc.gov/dnpabmi/Calculator.aspx
  3. https://supertracker.usda.gov/
  4. Body Weight Planner. https://www.supertracker.usda.gov/bwp/index.html
  5. ChooseMyPlate. https://www.choosemyplate.gov/
  6. Fontana L, Partridge L, Longo VD. Dietary Restriction, Growth Factors and Aging: from yeast to humans. Science (New York, NY). 2010;328(5976):321-326. doi:10.1126/science.1172539. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3607354/
  7. Greer EL, Brunet A. Different dietary restriction regimens extend lifespan by both independent and overlapping genetic pathways in C. elegans. Aging Cell. 2009;8(2):113-127. doi:10.1111/j.1474-9726.2009.00459.x. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680339/
  8. Kennedy BK, Steffen KK, Kaeberlein M. Ruminations on dietary restriction and aging. Cell Mol Life Sci. 2007;64:1323–1328. https://www.ncbi.nlm.nih.gov/pubmed/17396225
  9. Mair W, Dillin A. Aging and survival: the genetics of life span extension by dietary restriction. Annu Rev Biochem. 2008;77:727–754. https://www.ncbi.nlm.nih.gov/pubmed/18373439
  10. Masoro EJ. Overview of caloric restriction and ageing. Mech Ageing Dev. 2005;126:913–922. https://www.ncbi.nlm.nih.gov/pubmed/15885745
  11. Martin B, Mattson MP, Maudsley S. Caloric restriction and intermittent fasting: Two potential diets for successful brain aging. Ageing research reviews. 2006;5(3):332-353. doi:10.1016/j.arr.2006.04.002. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2622429/
  12. Wang C, Maddick M, Miwa S, et al. Adult-onset, short-term dietary restriction reduces cell senescence in mice. Aging (Albany NY). 2010;2(9):555-566. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2984605/
  13. Ye J, Keller JN. Regulation of energy metabolism by inflammation: A feedback response in obesity and calorie restriction. Aging (Albany NY). 2010;2(6):361-368. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2919256/
  14. Weindruch R, Naylor PH, Goldstein AL, Walford RL. Influences of aging and dietary restriction on serum thymosin alpha 1 levels in mice. J Gerontol. 1988;43:B40–42. https://www.ncbi.nlm.nih.gov/pubmed/3346517
  15. Ahmet I, Tae H-J, de Cabo R, Lakatta EG, Talan MI. Effects of Calorie Restriction on Cardioprotection and Cardiovascular Health. Journal of molecular and cellular cardiology. 2011;51(2):263-271. doi:10.1016/j.yjmcc.2011.04.015. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3138119/
  16. Qin W, Zhao W, Ho L, et al. Regulation of forkhead transcription factor FoxO3a contributes to calorie restriction-induced prevention of Alzheimer’s disease-type amyloid neuropathology and spatial memory deterioration. Annals of the New York Academy of Sciences. 2008;1147:335-347. doi:10.1196/annals.1427.024. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605640/
  17. Shimokawa I, Higami Y, Hubbard GB, McMahan CA, Masoro EJ, Yu BP. Diet and the suitability of the male Fischer 344 rat as a model for aging research. J Gerontol. 1993;48:B27–32. https://www.ncbi.nlm.nih.gov/pubmed/8418135
  18. Ikeno Y, Bronson RT, Hubbard GB, Lee S, Bartke A. Delayed occurrence of fatal neoplastic diseases in ames dwarf mice: correlation to extended longevity. J Gerontol A Biol Sci Med Sci. 2003;58:291–296. https://www.ncbi.nlm.nih.gov/pubmed/12663691
  19. Vergara M, Smith-Wheelock M, Harper JM, Sigler R, Miller RA. Hormone-Treated Snell Dwarf Mice Regain Fertility But Remain Long Lived and Disease Resistant. The journals of gerontology Series A, Biological sciences and medical sciences. 2004;59(12):1244-1250. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2924623/
  20. Fontana L, Meyer TE, Klein S, Holloszy JO. Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Proceedings of the National Academy of Sciences of the United States of America. 2004;101(17):6659-6663. doi:10.1073/pnas.0308291101. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC404101/
  21. Yu BP, Masoro EJ, Lloyd-Jones DM, Leip EP, Larson MG, D’Agostino RB, Beiser A, Wilson PW, Wolf PA, Levy D. Prediction of lifetime risk for cardiovascular disease by risk factor burden at 50 years of age. Circulation. 2006;113:791–798. http://circ.ahajournals.org/content/113/6/791.long
  22. Longo VD, Fontana L. Calorie restriction and cancer prevention: metabolic and molecular mechanisms. Trends in pharmacological sciences. 2010;31(2):89-98. doi:10.1016/j.tips.2009.11.004. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2829867/
  23. Diabetes UK. Research spotlight – low-calorie diet for Type 2 diabetes. https://www.diabetes.org.uk/Research/Research-round-up/Research-spotlight/Research-spotlight-low-calorie-liquid-diet/
  24. J Gerontol A Biol Sci Med Sci (2015) 70 (9): 1097-1104. A 2-Year Randomized Controlled Trial of Human Caloric Restriction: Feasibility and Effects on Predictors of Health Span and Longevity. https://academic.oup.com/biomedgerontology/article/70/9/1097/2949096/A-2-Year-Randomized-Controlled-Trial-of-Human
  25. Mercken EM, Crosby SD, Lamming DW, et al. Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile. Aging cell. 2013;12(4):645-651. doi:10.1111/acel.12088. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714316/
  26. Stein PK, Soare A, Meyer TE, Cangemi R, Holloszy JO, Fontana L. Caloric restriction may reverse age-related autonomic decline in humans. Aging cell. 2012;11(4):644-650. doi:10.1111/j.1474-9726.2012.00825.x. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3598611/
  27. Mattison JA, Roth GS, Beasley TM, et al. Impact of caloric restriction on health and survival in rhesus monkeys: the NIA study. Nature. 2012;489(7415):10.1038/nature11432. doi:10.1038/nature11432. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3832985/
  28. Aging, adiposity, and calorie restriction. Fontana, L. and Klein, S. JAMA. 2007; 297: 986–994. https://www.ncbi.nlm.nih.gov/pubmed/17341713
  29. Colman RJ, Anderson RM, Johnson SC, et al. Caloric restriction delays disease onset and mortality in rhesus monkeys. Science (New York, NY). 2009;325(5937):201-204. doi:10.1126/science.1173635. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2812811/
  30. Cava E, Fontana L. Will calorie restriction work in humans? Aging (Albany NY). 2013;5(7):507-514. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765579/
  31. The genetics of ageing. Kenyon, C.J. Nature. 2010; 464: 504–512. https://www.ncbi.nlm.nih.gov/pubmed/20336132
  32. The plasticity of aging: insights from long-lived mutants. Kenyon, C. Cell. 2005; 120: 449–460. http://www.cell.com/cell/fulltext/S0092-8674(05)00110-8
  33. Brown-Borg HM, Bartke A. GH and IGF1: Roles in Energy Metabolism of Long-Living GH Mutant Mice. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences. 2012;67A(6):652-660. doi:10.1093/gerona/gls086. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3348496/
  34. Dwarf mice and the ageing process. Brown-Borg, H.M., Borg, K.E., Meliska, C.J., and Bartke, A. Nature. 1996; 384: 33. https://www.ncbi.nlm.nih.gov/pubmed/8900272
  35. Masternak MM, Bartke A. Growth hormone, inflammation and aging. Pathobiology of Aging & Age Related Diseases. 2012;2:10.3402/pba.v2i0.17293. doi:10.3402/pba.v2i0.17293. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3417471/
  36. Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population .Cell Metabolism Volume 19, Issue 3, p407–417, 4 March 2014. http://www.cell.com/cell-metabolism/fulltext/S1550-4131(14)00062-X
  37. Guevara-Aguirre J, Balasubramanian P, Guevara-Aguirre M, et al. Growth Hormone Receptor Deficiency is Associated With a Major Reduction in Pro-aging Signaling, Cancer and Diabetes in Humans. Science Translational Medicine. 2011;3(70):70ra13. doi:10.1126/scitranslmed.3001845. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3357623/
  38. Congenital IGF1 deficiency tends to confer protection against post-natal development of malignancies. Steuerman, R., Shevah, O., and Laron, Z. Eur. J. Endocrinol. 2011; 164: 485–489. http://www.eje-online.org/content/164/4/485.long
  39. Fontana L, Adelaiye RM, Rastelli AL, et al. Dietary protein restriction inhibits tumor growth in human xenograft models of prostate and breast cancer. Oncotarget. 2013;4(12):2451-2461. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3926840/
  40. Gallinetti J, Harputlugil E, Mitchell JR. Amino acid sensing in dietary-restriction-mediated longevity: roles of signal-transducing kinases GCN2 and TOR. The Biochemical journal. 2013;449(1):1-10. doi:10.1042/BJ20121098. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3695616/
  41. Surgical stress resistance induced by single amino acid deprivation requires Gcn2 in mice. Peng, W., Robertson, L., Gallinetti, J., Mejia, P., Vose, S., Charlip, A., Chu, T., and Mitchell, J.R. Sci. Transl. Med. 2012; 4: 18ra11.
  42. N Engl J Med. 2009 Feb 26;360(9):859-73. doi: 10.1056/NEJMoa0804748. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. https://www.ncbi.nlm.nih.gov/pubmed/19246357
  43. Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids.
    Washington (DC): The National Academies Press; 2002.
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Diet PlanDiet, Food & Fitness

What is very low calorie diet ?

very low calorie diet meal plan

 

very low calorie diet meal plan

What is Very Low Calorie Diet

Very low calorie diets (VLCDs) is a special diet that provides up to 800 calories per day (<3350 kJ/day) that have been used since the 1970s to induce rapid weight loss 1. Very low calorie diets use commercial formulas, usually liquid shakes, soups, or bars, which replace all your regular meals. These formulas are not the same as the meal replacements you can find at grocery stores or pharmacies, which are meant to replace one or two meals a day. This type of diet is used to promote quick weight loss, often as a way to jump-start an obesity treatment program. Very-Low-Calorie Diet formulas are designed to provide all of the nutrients you need while helping you lose weight quickly. However, this type of diet should only be used for a short time—usually about 12 weeks. Very low calorie diets (VLCDs) reached the height of their popularity in the United States in 1988 when Oprah Winfrey announced to her television audience that she had lost 67 pounds by consuming a liquid diet 1. Interest in this approach declined sharply in 1990 when Winfrey reported that she had regained her lost weight and would “never diet again.” In addition, three recent reviews concluded that VLCDs are associated with greater long-term weight losses than are conventional reducing diets 2, 3, 4.

An expert panel convened by the National Heart, Lung, and Blood Institute 5 defined very low calorie diets as diets providing fewer than 800 kcal/d 5, the same definition used by a recent European expert panel 6.

However, it’s very important to note that the definition of a very low calorie diet is arbitrary. A 700 kcal/day diet, for example, would induce a relatively modest energy deficit in a short, sedentary woman with an resting energy expenditure of 1100 kcal/d. In contrast, a 1200 kcal/day diet would induce a substantial energy deficit in a tall man with an resting energy expenditure of 2500 kcal/day. The man would seem to have a greater risk of adverse metabolic effects (described later), even though technically he was prescribed an Low Calorie Diet (LCD) and the woman a Very Low Calorie Diet (VLCD). Thus, an alternative definition of a Very Low Calorie Diet (VLCD) is a diet that provides <50% of an individual’s predicted resting energy expenditure 7.

The diets are designed to produce rapid weight loss while preserving lean body mass.

This is accomplished by providing large amounts of dietary protein, typically 70 to 100 g/day or 0.8 to 1.5 g protein/kg ideal body weight 8, 5.

Protein may be obtained from a milk, soy, or egg based powder, which is mixed with water and consumed as a liquid diet. Such diets may provide up to 80 g carbohydrate/d and 15 g fat/day, and they include 100% of the recommended daily allowance for essential vitamins and minerals. Alternatively, protein may be obtained from a protein-sparing modified fast, consisting of servings of lean meat, fish, and fowl 9, 10. The modified fast must be supplemented with a multivitamin and 2 to 3 g/d potassium. Both diets require patients to drink 2 L/d non-caloric fluids 8. The two approaches produce comparable short-term weight losses 11. Thus, the choice of diet may be left to patient preference. Some investigators severely restrict carbohydrate to induce ketosis, which is thought to reduce hunger 9, 10, 11. However, comparable hunger ratings have been reported with ketotic and non-ketotic VLCDs 12. In a comparison of psychological adjustment during the baseline and low-calorie diets, the initial 2 wk of dieting was associated with a decrease in appetite and elevation of psychological well-being, regardless of the composition of the diet. Thereafter, appetite and mood approached basal levels. Further changes in these psychological reactions to dieting did not vary with the type of diet. There was no support for the idea that a minimal-carbohydrate, protein-supplemented fast decreases appetite and elevates mood more in comparison with a similar diet containing enough carbohydrate to minimize ketosis 12.

Very Low Calorie Diet Results

A literature review of the very low calorie diets from 1966 through 1992 13 showed that weight loss on very low calorie diet averages 1.5 to 2.5 kg/wk; total loss after 12 to 16 weeks averages 20 kg. These results are superior to standard low-calorie diets of 5020 kJ/d (1200 kcal/d), which lead to weight losses of 0.4 to 0.5 kg/wk and an average total loss of only 6 to 8 kg. There is little evidence that intakes of less than 3350 kJ/d (800 kcal/d) result in better weight losses than 3350 kJ. Intake of at least 1 g/kg of ideal body weight per day of protein of high biologic value appears to be important in helping to preserve lean body mass. Serious complications of modern VLCDs are unusual, cholelithiasis (the formation of gallstones) being most common 13.

Another review of studies on long-term outcome for dietary treatment of obesity published between 1931 and 1999 14 included 17 publications and 21 study groups, comprising 3030 patients. Of these 2131 (70%) were followed-up for 3-14 years (median 5 years). Mean initial weight loss ranged from four to 28 kg (median 11 kg). The median success rate of 15% of followed-up patients fulfilled one of the criteria for success. Overall, success rates seemed stable for up to 14 years of observation. Diet combined with group therapy lead to better long-term success rates than did diet alone or diet combined with behaviour modification. Active follow-up was generally associated with better success rates than was passive follow-up (19% vs. 10%). Conventional diet seemed to be most efficacious in addition with group therapy, whereas Very Low-Calorie Diet apparently was most efficacious if combined with behaviour modification and active follow-up 14.

A meta-analysis of 29 reports on the long-term (more than 5 years post weight loss intervention program) weight-loss maintenance of individuals completing a structured weight-loss program 15. Five years after completing structured weight-loss programs, the average individual maintained a weight loss of >3 kg and a reduced weight of >3% of initial body weight. After very low calorie diets or in individuals who lost greater than 20 kg of body weight, individuals maintained significantly more weight loss than after hypoenergetic balanced diets (diets that were designed to provide 600 kcal/day (2,520 kilo joule (kJ)) less than the individually estimated energy requirement) or weight losses of <10 kg. Weight-loss maintenance did not differ significantly between women and men. Six studies reported that groups who exercised more had significantly greater weight-loss maintenance than did those who exercised less 15.

A multicenter evaluation of a proprietary weight reduction program for the treatment of marked obesity 16. A total of 517 obese patients (407 women and 110 men) participated in a proprietary program that included 12 weeks of treatment by very-low-calorie diet within a 26-week program of life-style modification. Patients were treated in two cohorts (6 months apart) according to a standardized protocol implemented at 18 hospital-based clinics across the nation. Fifty-six percent of women and 54% of men completed treatment, at which time their weight losses were 22.0 kg and 32.1 kg, respectively. Weight losses of women and men who discontinued treatment averaged 14.3 kg and 20.0 kg, respectively. Weight loss was associated with significant improvements in blood pressure and total serum cholesterol levels. A 1-year follow-up evaluation of 74% of patients in the second cohort who completed treatment revealed that they maintained 15.3 kg of their 24.8 kg end-of-treatment weight loss; 59% of patients maintained a loss of 10 kg or more 16.

In a small study 17 involving 40 type 2 diabetes subjects with body mass indexes (BMIs) of 30-40 kg/m2 were randomized to one of two 800-kcal diets for 12 weeks. Group A received liquid supplement only, and group B received supplement plus an evening meal. Both groups received an intensive behavioral education program. Results: weight loss and improvements in glycemic, blood lipid, and blood pressure parameters were similar for the two groups. Weight loss averaged 15.7 kg for the entire group. The need for insulin, anti-diabetes, and anti-hypertensive medication decreased significantly. No serious side effects were observed.
In conclusion, both food-containing and supplement diets providing 800 kcal a day effectively promote weight loss for obese individuals with type 2 diabetes 17.

The National Task Force on the Prevention and Treatment of Obesity, National Institutes of Health, concluded that the current very low-calorie diets are generally safe when used under proper medical supervision in moderately and severely obese patients (body mass index [weight in kilograms divided by height in meters squared] >30) and are usually effective in promoting significant short-term weight loss, with concomitant improvement in obesity-related conditions. Long-term maintenance of weight lost with very low-calorie diets is not very satisfactory and is no better than with other forms of obesity treatment. Incorporation of behavioral therapy and physical activity in very low-calorie diets treatment programs seems to improve maintenance 18.

Very Low Calorie Diet and Weight Loss Maintenance

An additional study, published in The New England Journal of Medicine in 2010 19, looked at the role of protein and glycemic index upon weight loss maintenance. Researchers first implemented a very low-calorie diet (800 kcal per day with the use of Modifast products (Nutrition et Santé). Participants could also eat up to 400 g of vegetables, providing a total, including the very low-calorie diet, of 800 to 1000 kcal per day) to produce the weight loss, then examined whether protein and glycemic index impacted weight loss maintenance.

The study population was made up of 773 overweight adults from European countries who had lost at least 8% of their initial body weight with a very low-calorie diet. Participants were then assigned one of five diets to prevent weight regain over a 26-week period:

  • Low-Protein and Low-Glycemic-Index diet,
  • Low-Protein and High-Glycemic-index diet,
  • High-Protein and Low-Glycemic-index diet,
  • High-Protein and High-glycemic-index diet,
  • or a control diet.

The low-protein-high-glycemic-index diet was associated with subsequent significant weight regain, and weight regain was less in the groups assigned to a high-protein diet than in those assigned to a low-protein diet, as well as less in the groups assigned to a low-glycemic-index diet than in those assigned to a high-glycemic-index diet.

These results show that a modest increase in protein content and a modest reduction in the glycemic index led to an improvement in maintenance of weight loss 19.

Very Low Calorie Diet in Obese Type 2 Diabetes

A small study was conducted with fifty-one obese subjects (24 with diabetes and 27 obese without diabetes) to compare weight loss and change in body composition in obese subjects with and without type 2 diabetes mellitus during a very-low-calorie diet (VLCD) program 20. After 24 weeks of intervention, there was no difference in weight loss between the 2 groups. Both groups completing the study per protocol had near-identical weight change during the program, with similar weight loss at 24 weeks (diabetes: 8.5 ± 1.3 kg vs control: 9.4 ± 1.2 kg). Change in fat mass index correlated with change in body mass index (BMI) in both groups, but change in fat mass index per unit change in BMI was less in the diabetic group compared with controls, which persisted after adjusting for age, sex, and baseline BMI. Insulin concentrations remained higher and peak β-hydroxybutyrate concentrations were lower in the diabetic compared with the control group. The conclusion was while following a 24-week very-low-calorie diet program, obese subjects with and without diabetes achieved comparable weight loss; but the decrease in body fat per unit weight loss was less in diabetic subjects. Hyperinsulinemia may have inhibited lipolysis in the diabetic group; however, further investigation into other factors is needed 20.

Very Low Calorie Diet for Weight Loss

Most evaluations of very low calorie diets have consisted of single-site case series conducted at academic medical centers or in individual physician practices. Most studies found that patients who completed a comprehensive very low calorie diet program (that included lifestyle modification) generally lost 15% to 25% of initial weight in 3 to 4 months 2, 3, 21, 22, 23, 24, 25. Attrition in these programs typically ranged from 25% to 50% during the first 3 to 6 months, and patients generally regained 40% to 50% of lost weight 1 to 2 years after treatment, in the absence of follow-up care 23, 24, 25.

The National Heart, Lung, and Blood Institute expert panel did not recommend the use of very low calorie diets over low calorie diets (LCDs) providing 1000 to 1500 kcal/d of conventional foods 5. The panel’s conclusion was based on data from randomized trials that showed no differences in long-term weight losses between very low calorie diets and low calorie diets, principally because of greater weight regain after very low calorie diets 5.

Despite this expert panel’s conclusion, the majority of individual randomized trials showed slightly larger long-term weight losses for persons prescribed very low calorie diets. Anderson and colleagues, in a meta-analysis of long-term studies, concluded that very low calorie diets were associated with greater long-term weight reductions than low calorie diets 2. The studies included in that review, however, were mostly case series, and the meta-analysis did not account for the possibility of differential attrition among patients consuming either a low calorie diet or a very low calorie diet. Astrup and Rossner 3, in a qualitative review of several studies, also concluded that the larger initial weight losses induced by very low calorie diets were associated with greater long-term weight losses. Their conclusion assumed that patients participated in a weight maintenance intervention that included lifestyle modification. In addition, the European SCOOP-VLCD report noted that long-term weight losses may be greater after larger initial reductions in weight 6. Given the conflicting conclusions of these reviews, a new meta-analysis of six randomized controlled trials that compared very low calorie diets (VLCD) and low calorie diets (LCD) that were published between 1989 and 1997 26, 27, 28, 29, 30, 31 were reviewed, to determine whether combining study results would reveal any incremental long-term benefit of very low calorie diets 1.

The majority of studies enrolled patients with a BMI of 35 to 40 kg/m2. Two studies enrolled only women and two other trials enrolled only patients with type 2 diabetes. Participants were prescribed very low calorie diets for 8 to 24 weeks, and the total length of treatment ranged from 6 to 26 months. Three studies used liquid meal replacements, one used a protein-sparing modified fast and two studies used a combination of the two approaches. In three studies, patients were provided with exercise goals, which consisted of daily walking. For the low calorie diet (LCD) group, all six studies prescribed hypocaloric diets comprised of conventional foods, with energy goals ranging from 1000 to 1800 kcal/d.

Short-Term Weight Loss: Participants in the very low calorie diet and low calorie diet (LCD) arms of the studies lost a mean of 16.1% and 9.7% of initial weight, respectively. The mean difference of 6.4% was highly significant, revealing the short-term superiority of the very low calorie diet regimen, which was prescribed for a mean of 12.7 ± 6.4 weeks.

Long-Term Weight Loss: At follow-up assessment, which ranged from 1 to 5 years after completing the very low calorie diet, mean weight losses in the very low calorie diet and low calorie diet groups were 6.3% and 5.0% of initial weight, respectively. The difference between groups was 1.3 %, which was not statistically significant. Very low calorie diet and low calorie diet patients regained 62% and 41% of lost weight, respectively.

Discussion: This meta-analysis 1 of six studies showed that very low calorie diets induced significantly greater short-term weight losses than low calorie diets but comparable long-term changes in weight. The equivalence of long-term losses was attributable to greater weight regain among the very low calorie diet-treated patients. The present findings support the conclusion of the National Heart Lung and Blood Institute expert panel 5 that very low calorie diets not be recommended in lieu of low calorie diets comprised of conventional foods 5. The strength of the present conclusion resides in the examination of studies that directly compared very low calorie diets and low calorie diets, in head-to-head trials, rather than extrapolating across investigations, in which only one or the other diet was used 2. Results of this analysis should resolve the conflicting conclusions of prior reviews. The relative absence of adverse events reported in very low calorie diet participants in these six trials (particularly that no patient developed symptomatic cholelithiasis (the formation of gallstones)) may have been attributable to lack of detailed assessment.

Conclusion: Except in highly selected cases, we do not recommend the use of expensive very low calorie diets to induce losses of 15% to 25% of initial weight. Although both weight-loss and dropout rates were more favorable for the VLCD group than for the 1200–1500-kcal/d Low Calorie Diet group and the 1500–1800-kcal/d restricted normal-food group, the present findings indicate that few patients will be able to maintain these losses, even under the best of circumstances. Furthermore, numerous studies have shown that obese individuals who lost 10% to 12% of initial weight, at follow up (for 1 year or more) were also associated with greater weight regain even when provided behavioral weight maintenance therapy 32, 33, 30, 34, 35, 36 or pharmacotherapy. Weight losses of this size clearly are associated with significant improvements in health and well being 5, including a reduction in the risk of developing type 2 diabetes 37, 38.

Further research is needed to determine the optimal macronutrient composition of meal replacements for treating obese persons with different weight-related conditions including type 2 diabetes, hypertension, and hyperlipidemia. Preliminary findings, for example, suggest that high-protein, low-carbohydrate diets may substantially improve glycemic control in obese patients with type 2 diabetes 39 and may be more effective, in this regard, than traditional, low-fat reducing diets 40. The first of two studies conducted by Wing et al. 41 similarly observed superior glycemic control among patients treated with a high-protein VLCD than with a more traditional, low-fat LCD, despite comparable weight losses. However, widespread adoption of the low-carbohydrate approach for diabetic patients should await further long-term safety data concerning lipids, cardiovascular and renal disease, and bone mineral density.

Very Low Calorie Diet Meal Plan

A very low-calorie diet is a special type of diet that replaces all of your meals with prepared formulas, often in the form of liquid shakes 42. VLCDs use commercial formulas, usually liquid shakes, soups, or bars, which replace all your regular meals. Others, such as the fad grapefruit diet (also called the Hollywood Diet), rely on eating a lot of the same low-calorie food or foods.

Very low-calorie diets formulas are not the same as the over-the-counter meal replacements you can find at grocery stores or pharmacies, which are meant to replace one or two meals a day.

Very low calorie diet formulas are designed to provide all of the nutrients you need while helping you lose weight quickly. However, this type of diet should only be used for a short time—usually about 12 weeks.

Depending on a number of factors, healthy adults need different amounts of calories to meet their daily energy needs. A standard amount is about 2,000 calories. A very low-calorie diets provide far fewer calories than most people need to maintain a healthy weight. This type of diet is used to promote quick weight loss, often as a way to jump-start an obesity treatment program.

  • Very low-calorie diet (VLCD) may be used for a short time to promote quick weight loss among some people who are considered to be obese.
  • The diet requires close care from your doctor and is usually combined with other ways to lose weight.
  • Do not go on a VLCD on your own. If you need to lose weight, talk to your health care provider about the approaches that may work best for you.

Clinical Use of Very Low Calorie Diets

In the United States, very low calorie diets are generally used as part of a comprehensive intervention that includes medical monitoring and a program of lifestyle modification. Care is provided by a physician, often in conjunction with a dietitian, psychologist, and/or exercise physiologist. Treatment, including the cost of the very low calorie diet, is typically $1800 to $2200 for the first 12 weeks, during the period of rapid weight loss 43. An additional 12 to 14 weeks of refeeding (in which conventional foods are reintroduced) and weight stabilization bring total costs for 6 months to $3000 to $3500 8.

In European Union nations, very low calorie diets are frequently used with less medical supervision than provided in the United States. In most countries, diet products can be purchased over-the-counter or from a pharmacist without a prescription (except in France). As recommended by the SCOOP-VLCD report, prepared by an expert European panel, consumers may use a very low calorie diet as a sole source of nutrition for 3 weeks before seeking medical supervision 6. The report, however, also states that persons with obesity-related conditions should consult their physician before starting a VLCD. Thus, although physicians may be involved in identifying appropriate persons for treatment with a VLCD and for providing medical monitoring after the first 3 weeks, they do not have the same gatekeeping role as their U.S. counterparts. Rossner and Torgerson 44 have reviewed the Swedish experience with VLCDs and concluded that such programs can be provided largely by dietitians and nurses, lessening the need for physician involvement. We note that some companies in the United States sell very low calorie diets directly to consumers 43, whom they tell to consult with their physician before dieting. However, medically unsupervised use of these diets falls outside the guidelines recommended by expert panels in the United States.

Very Low Calorie Diet Side Effects

VLCDs are considered safe and effective when used by appropriately selected individuals under careful medical supervision 8. The diets are designed for patients with a BMI ≥ 30 kg/m2, a group at increased risk of cardiovascular morbidity and mortality and that also may derive the most benefit from substantial weight loss. In the United States, all candidates for a VLCD are expected to undergo a history and physical examination to determine medical and behavioral contraindications to treatment, as described in previous reviews 8. As noted previously, a similar recommendation applies in Europe to individuals who have significant comorbidities 6.

Patients in medically supervised VLCD programs in the U.S. are monitored by a physician approximately every 2 weeks during the period of rapid weight loss (i.e., 1.5 to 2.5 kg/wk). During this time, they are at increased risk of gallstones, cold intolerance, hair loss, headache, fatigue, dizziness, volume depletion (with electrolyte abnormalities), muscle cramps, and constipation. These side effects are usually mild and easily managed.

Cholelithiasis has been studied in detail. In an early study, gallstones developed in 25% of patients during 8 weeks of VLCD, and 6% of patients eventually required cholecystectomy. In a second trial, asymptomatic gallstones occurred in ∼12% of patients within 6 months of starting a VLCD, and approximately one-half of these individuals eventually became symptomatic, requiring cholecystectomy. The risk of cholelithiasis can be decreased by administration of ursodeoxycholic acid, including a moderate amount of fat in the diet, and limiting the rate of weight loss to 1.5 kg/wk.

In Europe, VLCDs apparently have not been associated with a higher than expected rate of cholelithiasis. This has been attributed to the inclusion of at least 7 grams of fat in meal replacement regimens sold in Europe, as reported by Festi et al. 45.

Unsupervised use of VLCDs can result in serious complications, including sudden death 46, 47, 48, 49, 50, which have contributed to stricter rules in the United States (where VLCD programs must be managed by a physician) than in Europe 51. The great majority of fatalities related to VLCDs occurred in the 1970s when dieters consumed products that contained low-quality protein (i.e., hydrolyzed collagen) and were deficient in vitamins and minerals. Of 60 persons who died in the United States, most developed cardiac complications after a loss of ∼30% of initial weight, achieved in an average of 4 months. No deaths were reported in persons who dieted for 8 weeks or fewer.

The SCOOP-VLCD report 6 noted that there have been no documented deaths attributable to VLCDs since their inclusion in the early 1980s of high-quality proteins (i.e., milk, egg, or soy). Nonetheless, in the United States, there were six reports of death during this time in persons who consumed the Cambridge Diet (which provided 330 kcal/d at the time) 50. Observational data clearly can lead to different conclusions about the safety of a product because of differences in the way the product is used (e.g., duration of use) or in the populations that use it (e.g., lean vs. obese individuals). Thus, although VLCDs seem to be safe when consumed for brief periods without medical supervision, long-term unsupervised use of a VLCD could be associated with significant health complications (as could any hypocaloric, reducing diet).

Rapid weight loss, whether by VLCD or bariatric surgery, increases the risk of developing gallstones, and clinical recommendations advise physicians to inform patients about this risk 6, 46, 52. Gallstone formation has mainly been associated with VLCDs containing low amounts of fat (∼1 g/d) 53, 54, 55, 56, 57, and a higher fat content (12–30 g/d) seems to reduce gallstone formation 58, 59, 60, 61.

Should you use a very low calorie diet to lose weight ?

Most people who need to lose weight should not use a very low calorie diet. For many of them, a low-calorie diet (LCD) may work better (see The Low-calorie Diet (LCD)) 42, 48.

Very low calorie diets may be used to promote rapid weight loss among adults who have obesity. Health care providers must review risks and benefits on a case-by-case ​basis.

In general, VLCDs are not appropriate for children. In a few cases, they may be used with some adolescents who are being treated for obesity.

Not much is known about the use of VLCDs to promote weight loss among older adults. Some people over age 50 may have medical issues that may not make them good candidates for this type of diet.

How Effective Are Very Low-Calorie Diets ?

If you have a BMI over 30 (which your doctor will call “obese”), then a very low-calorie diet may let you lose about 3 to 5 pounds per week, for an average total weight loss of 44 pounds over 12 weeks.

Losing that amount of weight may improve weight-related medical conditions, including diabetes, high blood pressure, and high cholesterol. But in the long-run, very low-calorie diets aren’t more effective than more modest diets. Once you go off a diet, you need to change your lifestyle, committing to healthy eating and regular physical activity.

What are the health benefits of a Very Low-Calorie Diets ?

A VLCD may allow you to lose about 3 to 5 pounds per week. This may lead to an average total weight loss of 44 pounds over 12 weeks. Such a weight loss can rapidly improve medical conditions linked to obesity, including diabetes, high blood pressure, and high cholesterol.​

The rapid weight loss experienced by most people on a VLCD can be very motivating. Patients who participate in a VLCD program that also includes lifestyle changes may lose about 15 to 25 percent of their initial weight during the first 3 to 6 months. They may maintain a 5 percent weight loss after 4 years if they adopt a healthy eating plan and physical activity habits.

What are the health risks of a Very Low-Calorie Diets ?

Very low-calorie diets are NOT okay for everyone. Talk to your doctor to see if this kind of diet is appropriate for you.

If your BMI is greater than 30, then very low-calorie diets are generally safe when used under proper medical supervision. For people who are overweight but not obese (BMI of 27-30), very low-calorie diets should be reserved for those who have weight-related medical problems and are under medical supervision.

Very low-calorie-diets are NOT recommended for pregnant or breastfeeding women, and are not appropriate for children or teens except in specialized treatment programs. They also may not be OK for people over age 50, either, depending on the potential need for medications for pre-existing conditions, as well as the possibility of side effects.

Doctors must monitor all very low calorie diet patients regularly—ideally every 2 weeks in the initial period of rapid weight loss—to be sure patients are not experiencing serious side effects.

Many patients on a very low calorie diet for 4 to 16 weeks report minor side effects such as fatigue, constipation, nausea, or diarrhea. These conditions usually improve within a few weeks and rarely prevent patients from completing the program.

The most common serious side effect is gallstones. Gallstones, which often develop in people who are obese, especially women, may be even more commonly developed during rapid weight loss. Some medicines can prevent gallstones from forming during rapid weight loss. Your health care provider can determine if these medicines are appropriate for you.

What Are the Other Drawbacks of Very Low-Calorie Diets ?

To be healthy, you need a balance of foods from different food groups. It’s difficult to get good nutrition and feel satisfied on a very low-calorie diet. In addition, consuming as few as 800 calories daily may not give you the energy you need for daily living and regular physical activity, especially if you eat the same foods every day.

Will you regain the weight ?

Although the long-term results of very low calorie diets vary widely, weight regain is common. A randomized trial showed that VLCD-treated patients who lost 14.8 kg regained 50% to 80% of lost weight 18 months after the end of treatment and did not benefit from individualizing the rate of refeeding or using meal replacements during maintenance 62.

To prevent weight regain, the very low calorie diet should always be combined with other ways to lose weight and with an active follow-up program. Two studies of exercise to facilitate weight maintenance after a VLCD yielded mixed results 63, 64.

For most people who have obesity, the condition is long term and requires a lifetime of attention even after formal methods to treat the obesity end. You may need to commit to permanent changes of healthier eating, regular physical activity, and an improved outlook about food.

References
  1. Tsai, A. G. and Wadden, T. A. (2006), The Evolution of Very-Low-Calorie Diets: An Update and Meta-analysis. Obesity, 14: 1283–1293. doi:10.1038/oby.2006.146
  2. Anderson J. W., Konz E. C., Frederich R. C., Wood CL (2001) Long-term weight-loss maintenance: a meta-analysis of US studies. Am J Clin Nutr. 74: 579–584. https://www.ncbi.nlm.nih.gov/pubmed/11684524
  3. Astrup A., Rossner S. (2000) Lessons from obesity management programmes: greater initial weight loss improves long-term maintenance. Obes Rev. 1: 17–19. https://www.ncbi.nlm.nih.gov/pubmed/12119640
  4. Ayyad C., Andersen T. (2000) Long-term efficacy of dietary treatment of obesity: a systematic review of studies published between 1931 and 1999. Obes Rev. 1: 113–139. https://www.ncbi.nlm.nih.gov/pubmed/12119984
  5. National Heart Lung and Blood Institute. (1998) Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report: National Institutes of Health/National Heart Lung and Blood Institute. Obes Res. 6: 51–209S.
  6. SCOOP-VLCD Working Group. Scientific Co-operation on Questions Relating to Food: Directorate-General Health and Consumer Protection, European Union. http://www.foodedsoc.org/scoop.pdf
  7. Atkinson RL (1989) Low and very low calorie diets. Med Clin North Am. 73: 203–215. https://www.ncbi.nlm.nih.gov/pubmed/2643004
  8. National Task Force on the Prevention and Treatment of Obesity, National Institutes of Health (1993) Very low-calorie diets. JAMA. 270: 967–974. https://www.ncbi.nlm.nih.gov/pubmed/8345648
  9. Blackburn G. L., Bistrian B. R., Flatt JP (1975) Role of a protein-sparing modified fast in a comprehensive weight reduction program. Howard, AN eds. Recent Advances in Obesity Research 279–281. Newman Publishing London, UK.
  10. Blackburn G. L., Greenberg I. (1978) Multidisciplinary approach to adult obesity therapy. Int J Obes. 2: 133–142. https://www.ncbi.nlm.nih.gov/pubmed/711360
  11. Wadden T. A., Stunkard A. J., Brownell K. D., Day SC (1985) A comparison of two very-low-calorie diets: protein-sparing-modified fast versus protein-formula-liquid diet. Am J Clin Nutr. 4: 533–539.
  12. Rosen J. C., Gross J., Loew D., Sims EA (1985) Mood and appetite during minimal-carbohydrate and carbohydrate-supplemented hypocaloric diets. Am J Clin Nutr. 42: 371–379. https://www.ncbi.nlm.nih.gov/pubmed/4036844
  13. JAMA. 1993;270(8):967-974. doi:10.1001/jama.1993.03510080071034. Very Low-Calorie Diets. http://jamanetwork.com/journals/jama/article-abstract/408083
  14. Obes Rev. 2000 Oct;1(2):113-9. Long-term efficacy of dietary treatment of obesity: a systematic review of studies published between 1931 and 1999. https://www.ncbi.nlm.nih.gov/pubmed/12119984
  15. Am J Clin Nutr. 2001 Nov;74(5):579-84. Long-term weight-loss maintenance: a meta-analysis of US studies. http://ajcn.nutrition.org/content/74/5/579.long
  16. Arch Intern Med. 1992 May;152(5):961-6. A multicenter evaluation of a proprietary weight reduction program for the treatment of marked obesity. https://www.ncbi.nlm.nih.gov/pubmed/1580722
  17. Diabetes Care. 1994 Jun;17(6):602-4. Food-containing hypocaloric diets are as effective as liquid-supplement diets for obese individuals with NIDDM. https://www.ncbi.nlm.nih.gov/pubmed/8082533
  18. JAMA. 1993 Aug 25;270(8):967-74.Very low-calorie diets. National Task Force on the Prevention and Treatment of Obesity, National Institutes of Health. https://www.ncbi.nlm.nih.gov/pubmed/8345648
  19. N Engl J Med. 2010 Nov 25;363(22):2102-13. doi: 10.1056/NEJMoa1007137. Diets with high or low protein content and glycemic index for weight-loss maintenance. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359496/
  20. Metabolism. 2012 Jun;61(6):873-82. doi: 10.1016/j.metabol.2011.10.017. Epub 2011 Dec 5. Less fat reduction per unit weight loss in type 2 diabetic compared with nondiabetic obese individuals completing a very-low-calorie diet program. https://www.ncbi.nlm.nih.gov/pubmed/22146094?dopt=Abstract
  21. Mustajoki P., Pekkarinen T. (2001) Very low energy diets in the treatment of obesity. Obes Rev. 2: 61–72. https://www.ncbi.nlm.nih.gov/pubmed/12119638
  22. Saris WH (2001) Very-low-calorie diets and sustained weight loss. Obes Res. 9: 295–301S.
  23. Wadden T. A., Foster G. D., Letizia K. A., Stunkard AJ (1992) A multicenter evaluation of a proprietary weight reduction program for the treatment of marked obesity. Arch Intern Med. 152: 961–6. https://www.ncbi.nlm.nih.gov/pubmed/1580722
  24. Anderson J. W., Brinkman-Kaplan V., Hamilton C. C., Logan J. E., Collins R. W., Gustafson NJ (1994) Food-containing hypocaloric diets are as effective as liquid-supplement diets for obese individuals with NIDDM. Diabetes Care. 17: 602–4. https://www.ncbi.nlm.nih.gov/pubmed/8082533
  25. Anderson J., Brinkman-Kaplan V., Lee H., Wood C. (1994) Relationship of weight loss to cardiovascular risk factors in morbidly obese individuals. J Am Coll Nutr. 13: 256–261. https://www.ncbi.nlm.nih.gov/pubmed/8077574
  26. Wing R. R., Blair E., Marcus M., Epstein L. H., Harvey J. (1994) Year-long weight loss treatment for obese patients with type II diabetes: does including an intermittent very-low-calorie diet improve outcome? Am J Med. 97: 354–62. https://www.ncbi.nlm.nih.gov/pubmed/7942937
  27. Wadden T. A., Sternberg J. A., Letizia K. A., Stunkard A. J., Foster GD (1989) Treatment of obesity by very low calorie diet, behavior therapy, and their combination: a five-year perspective. Int J Obes. 13: 39–46. https://www.ncbi.nlm.nih.gov/pubmed/2613427
  28. Ryttig K. R., Flaten H., Rossner S. (1997) Long-term effects of a very low calorie diet (Nutrilett) in obesity treatment: a prospective, randomized, comparison between VLCD and a hypocaloric diet + behavior modification and their combination. Int J Obes. 21: 574–579. https://www.ncbi.nlm.nih.gov/pubmed/9226488
  29. Wing R. R., Marcus M. D., Salata R., Epstein L. H., Miaskiewicz S., Blair EH (1991) Effects of a very-low-calorie diet on long-term glycemic control in obese type 2 diabetic subjects. Arch Intern Med. 151: 1334–1340. https://www.ncbi.nlm.nih.gov/pubmed/2064484
  30. Wadden T. A., Foster G. D., Letizia KA (1994) One-year behavioral treatment of obesity: comparison of moderate and severe caloric restriction and the effects of weight maintenance therapy. J Consult Clin Psychol. 62: 165–171. https://www.ncbi.nlm.nih.gov/pubmed/8034818
  31. Torgerson J. S., Lissner L., Lindroos A. K., Kruijer H., Sjöström L. (1997) VLCD plus dietary and behavioural support versus support alone in the treatment of severe obesity: a randomised two-year clinical trial. Int J Obes. 21: 987–994. https://www.ncbi.nlm.nih.gov/pubmed/9368821
  32. Am J Clin Nutr. 2012 Nov; 96(5): 953–961. Published online 2012 Sep 18. doi: 10.3945/ajcn.112.038265. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471207/
  33. Obesity (Silver Spring). 2011 Oct; 19(10): 1987–1998. Published online 2011 Jul 21. doi: 10.1038/oby.2011.230. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183129/
  34. Perri M. G., McAdoo W. G., McAllister D. A., Lauer J. B., Yancey DZ (1986) Enhancing the efficacy of behavior therapy for obesity: effects of aerobic exercise and a multicomponent maintenance program. J Consult Clin Psychol. 54: 670–675. https://www.ncbi.nlm.nih.gov/pubmed/3771884
  35. Perri M. G., McAllister D. A., Gange J. J., Jordan R. C., McAdoo G., Nezu AM (1988) Effects of four maintenance programs on the long-term management of obesity. J Consult Clin Psychol. 56: 529–534. https://www.ncbi.nlm.nih.gov/pubmed/2848874
  36. Perri M. G., Nezu A. M., McKelvey W. F., Shermer R. L., Renjilian D. A., Viegener BJ (2001) Relapse prevention training and problem-solving therapy in the long-term management of obesity. J Consult Clin Psychol. 69: 722–726. https://www.ncbi.nlm.nih.gov/pubmed/11550740
  37. Knowler W. C., Barrett-Connor E., Fowler S. E., et al. (2002) Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 346: 393–403. https://www.ncbi.nlm.nih.gov/pubmed/11832527
  38. Tuomilehto J., Lindstrom J., Eriksson J., et al. (2001) G. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med. 344: 1343–1350. https://www.ncbi.nlm.nih.gov/pubmed/11333990
  39. Boden G., Sargrad K., Homko C., Mozzoli M., Stein TP (2005) Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med. 142: 403–411. https://www.ncbi.nlm.nih.gov/pubmed/15767618
  40. Stern L., Iqbal N., Seshadri P., et al. (2004) The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med. 140: 778–785. https://www.ncbi.nlm.nih.gov/pubmed/15148064
  41. Wing R. R., Marcus M. D., Salata R., Epstein L. H., Miaskiewicz S., Blair EH (1991) Effects of a very-low-calorie diet on long-term glycemic control in obese type 2 diabetic subjects. Arch Intern Med. 151: 1334–1340. http://www.ncbi.nlm.nih.gov/pubmed/2064484
  42. The National Institute of Diabetes and Digestive and Kidney Diseases Health Information Center. Very Low-calorie Diets. https://www.niddk.nih.gov/health-information/weight-management/very-low-calorie-diets
  43. Tsai A. G., Wadden TA (2005) Systematic review: an evaluation of major commercial weight loss programs in the United States. Ann Intern Med. 142: 56–66. https://www.ncbi.nlm.nih.gov/pubmed/15630109
  44. Rossner S., Torgerson JS (2000) VLCD a safe and simple treatment of obesity. Lakartidningen 97: 3876–3879. https://www.ncbi.nlm.nih.gov/pubmed/11036337
  45. Festi D., Colecchia A., Orsini M., et al. (1998) Gallbladder motility and gallstone formation in obese patients following very low calorie diets: use it (fat) to lose it (well). Int J Obes. 22: 592–600. https://www.ncbi.nlm.nih.gov/pubmed/9665682
  46. JAMA. 1993 Aug 25;270(8):967-74. Very low-calorie diets. National Task Force on the Prevention and Treatment of Obesity, National Institutes of Health. https://www.ncbi.nlm.nih.gov/pubmed/8345648
  47. Obes Res. 2001 Nov;9 Suppl 4:295S-301S. Very-low-calorie diets and sustained weight loss. https://www.ncbi.nlm.nih.gov/pubmed/11707557
  48. Obesity (Silver Spring). 2006 Aug;14(8):1283-93. The evolution of very-low-calorie diets: an update and meta-analysis. https://www.ncbi.nlm.nih.gov/pubmed/16988070
  49. Wadden T. A., Stunkard A. J., Brownell KD (1983) Very low calorie diets: their efficacy, safety, and future. Ann Intern Med. 99: 675–84. https://www.ncbi.nlm.nih.gov/pubmed/6357020
  50. Wadden T. A., Stunkard A. J., Brownell K. D., Van Itallie TB (1983) The Cambridge diet: more mayhem? JAMA 250: 2833–4. https://www.ncbi.nlm.nih.gov/pubmed/6644962
  51. Ann Intern Med. 2005 Jan 4;142(1):56-66. Systematic review: an evaluation of major commercial weight loss programs in the United States. https://www.ncbi.nlm.nih.gov/pubmed/15630109/
  52. Ann Intern Med. 1993 Nov 15;119(10):1029-35. Contributions of obesity and weight loss to gallstone disease. https://www.ncbi.nlm.nih.gov/pubmed/8214980
  53. N Engl J Med. 1988 Dec 15;319(24):1567-72. Effects of ursodeoxycholic acid and aspirin on the formation of lithogenic bile and gallstones during loss of weight. https://www.ncbi.nlm.nih.gov/pubmed/3200265
  54. Am J Clin Nutr. 1992 Jul;56(1 Suppl):255S-257S. Cholelithiasis in patients treated with a very-low-calorie diet. https://www.ncbi.nlm.nih.gov/pubmed/1615894
  55. Arch Intern Med. 1989 Aug;149(8):1750-3. Gallstone formation during weight-reduction dieting. https://www.ncbi.nlm.nih.gov/pubmed/2669662
  56. Ann Intern Med. 1995 Jun 15;122(12):899-905. Prophylaxis against gallstone formation with ursodeoxycholic acid in patients participating in a very-low-calorie diet program. https://www.ncbi.nlm.nih.gov/pubmed/7755224
  57. Dig Dis Sci. 1992 Jun;37(6):912-8. Risk factors for gallstone formation during rapid loss of weight. https://www.ncbi.nlm.nih.gov/pubmed/1587196
  58. Int J Obes Relat Metab Disord. 1998 Jun;22(6):592-600. Gallbladder motility and gallstone formation in obese patients following very low calorie diets. Use it (fat) to lose it (well). https://www.ncbi.nlm.nih.gov/pubmed/9665682
  59. Hepatology. 1996 Sep;24(3):544-8. The role of gallbladder emptying in gallstone formation during diet-induced rapid weight loss. https://www.ncbi.nlm.nih.gov/pubmed/8781321
  60. Am J Clin Nutr. 1994 Aug;60(2):249-54. Reduced risk of liver-function-test abnormalities and new gallstone formation with weight loss on 3350-kJ (800-kcal) formula diets. https://www.ncbi.nlm.nih.gov/pubmed/8030603
  61. Int J Obes Relat Metab Disord. 1995 Aug;19(8):593-5. Gallstone formation in obese women treated by a low-calorie diet. https://www.ncbi.nlm.nih.gov/pubmed/7489033
  62. Agras W. S., Berkowitz R. I., Arnow B. A., et al. (1996) Maintenance following a very-low-calorie diet. J Consult Clin Psychol. 64: 610–613. https://www.ncbi.nlm.nih.gov/pubmed/8698956
  63. Pavlou K. N., Krey S., Steffee WP (1989) Exercise as an adjunct to weight loss and maintenance in moderately obese subjects. Am J Clin Nutr. 49: 1115–1123. https://www.ncbi.nlm.nih.gov/pubmed/2655416
  64. Sikand G., Kondo A., Foreyt J. P., Jones P. H., Gotto A. M. Jr (1988) Two-year follow-up of patients treated with a very-lowcalorie diet and exercise training. J Am Diet Assoc. 88: 487–488. https://www.ncbi.nlm.nih.gov/pubmed/3351170
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