What is Ghee Butter ?

Ghee, also known as clarified butter or anhydrous milk fat, is prepared by heating butter or cream to just over 100°C to remove water content by boiling and evaporation, then filtering out the precipitated milk solids ¹. Ghee has been utilized for thousands of years in Ayurveda as a therapeutic agent. In ancient India, ghee was the preferred cooking oil. In the last several decades, however, ghee has been implicated in the increased prevalence of coronary artery disease  in Asian Indians due to its content of saturated fatty acids and cholesterol and, in heated ghee, cholesterol oxidation products ¹.

The American Heart Association recommends limiting the consumption of saturated fats to less than 7% of energy to reduce the risk of cardiovascular disease ².

Ghee is heavily utilized in Ayurveda for numerous medical applications, including the treatment of allergy, skin, and respiratory diseases. Many Ayurvedic preparations are made by cooking herbs into ghee. Ghee carries the therapeutic properties of herbs to all the body’s tissues. It is an excellent anupana (vehicle) for transporting herbs to the deeper tissue layers of the body ³. Proper digestion, absorption, and delivery to a target organ system are crucial in obtaining the maximum benefit from any therapeutic formulation; the lipophilic action of ghee facilitates transportation to a target organ and final delivery inside the cell since the cell membrane also contains lipid ⁴. A study that compared different forms of herbs and herb extracts found that the efficacy increased when they were used with ghee, compared to usage in powder or tablet form ⁵.

What is Saturated Fat ?

Saturated fat is a type of dietary fat. It is one of the unhealthy fats, along with trans fat. These fats are most often solid at room temperature. Foods like dairy butter, ghee butter, palm oil, palm kernel oil, beef tallow and coconut oil, cheese, pork lard and red meat have high amounts of saturated fat ⁶.

Too much saturated fat in your diet can lead to heart disease and other health problems.

In large randomized clinical trials that used polyunsaturated fat to replace saturated fat reduced the incidence of cardiovascular disease ⁷, ⁸. Cardiovascular disease is the leading global cause of death, accounting for 17.3 million deaths per year, comprising 31.5% of total global deaths in 2013. Nearly 808 000 people in the United States died of heart disease, stroke, and other cardiovascular diseases in 2014, translating to about 1 of every 3 deaths.

This large cohort study ⁹ found that higher intake of saturated fat (found in foods like butter, lard, tallow and red meat) and especially trans fat (predominantly from partially hydrogenated vegetable oil), was associated with greater risk of mortality (death) when compared with the same number of calories from carbohydrate. When compared with carbohydrates, every 5% increase of total calories from saturated fat was associated with an 8% higher risk of overall mortality, and every 2% higher intake of trans fat was associated with a 16% higher risk of overall mortality ⁹. The study investigated 83,349 women from the Nurses’ Health Study (July 1, 1980, to June 30, 2012) and 42,884 men from the Health Professionals Follow-up Study (February 1, 1986, to January 31, 2012) who were free of cardiovascular disease, cancer, and types 1 and 2 diabetes at baseline ⁹. Dietary fat intake was assessed at baseline and updated every 2 to 4 years. Information on mortality was obtained from systematic searches of the vital records of states and the National Death Index, supplemented by reports from family members or postal authorities. Of the 126,233 participants who were followed up for as long as 32 years, the study found that higher intakes of saturated fat and trans-fat were associated with increased mortality, whereas higher intakes of polyunsaturated (PUFA) and monounsaturated (MUFA) fatty acids were associated with lower mortality. Replacing 5% of energy from saturated fats with equivalent energy from PUFA and MUFA was associated with reductions in total mortality of 27% and 13%, respectively ⁹.

People who replaced saturated fats with carbohydrates had only slightly lower mortality risk. In addition, replacing total fat with carbohydrates was associated with modestly higher mortality. This was not surprising, the authors said, because carbohydrates in the American diet tend to be primarily refined starch and sugar, which have a similar influence on mortality risk as saturated fats.

“Our study shows the importance of eliminating trans fat and replacing saturated fat with unsaturated fats, including both omega-6 and omega-3 polyunsaturated fatty acids. In practice, this can be achieved by replacing animal fats with a variety of liquid vegetable oils,” said senior author Frank Hu, professor of nutrition and epidemiology at Harvard Chan School and professor of medicine at Harvard Medical School.

This study is the most detailed and powerful examination to date on how dietary fats impact health. It suggests that replacing saturated fats like butter, lard, and fat in red meat with unsaturated fats from plant-based foods—like olive oil, canola oil, and soybean oil—can confer substantial health benefits and should continue to be a key message in dietary recommendations.

Meaning: Different types of dietary fat had different associations with mortality, the researchers found. Trans fats—on their way to being largely phased out of food—had the most significant adverse impact on health. Every 2% higher intake of trans fat was associated with a 16% higher chance of premature death during the study period. Higher consumption of saturated fats was also linked with greater mortality risk. When compared with the same number of calories from carbohydrate, every 5% increase in saturated fat intake was associated with an 8% higher risk of overall mortality.

Conversely, intake of high amounts of unsaturated fats—both polyunsaturated and monounsaturated—was associated with between 11% and 19% lower overall mortality compared with the same number of calories from carbohydrates. Among the polyunsaturated fats, both omega-6, found in most plant oils, and omega-3 fatty acids, found in fish and soy and canola oils, were associated with lower risk of premature death.

Figure 1. Dietary Fats and Mortality Rates

[Source ¹⁰]

These findings support current dietary recommendations to replace saturated fat and trans-fat with unsaturated fat.

• Scientists concluded that saturated fat should be no more than 5 percent to 6 percent of daily calories. So, for a diet of 2,000 calories a day, that would mean no more than 120 of them should come from saturated fats. That’s about 13 grams of saturated fats a day ¹¹.

Saturated fats are found in all animal foods, and some plant sources.

The following foods are high in saturated fats. Many of them are also low in nutrients and have extra calories from sugar:

• Baked goods (cake, doughnuts, Danish)
• Fried foods (fried chicken, fried seafood, French fries)
• Fatty or processed meats (bacon, sausage, chicken with skin, cheeseburger, steak)
• Whole-fat dairy products (butter, ice cream, pudding, cheese, whole milk)
• Solid fats such as coconut oil, palm, and palm kernel oils (found in packaged foods)

Here are some examples of popular food items with the saturated fat content in a typical serving:

• 12 ounces (oz), or 340 g, steak — 20 g
• 12 oz (340 g) cream of mushroom soup — 22 g
• Cheeseburger — 10 g
• Vanilla shake — 8 g
• 1 tablespoon (15 mL) butter — 7 g

It is fine to treat yourself to these types of foods once in a while. But, it is best to limit how often you eat them and limit portion sizes when you do.

How Saturated Fats Affect Your Health

Saturated fats are bad for your health in several ways:

• Heart disease risk. Your body needs healthy fats for energy and other functions. But too much saturated fat can cause cholesterol to build up in your arteries (blood vessels). Saturated fats raise your LDL, or bad, cholesterol. High LDL cholesterol increases your risk for heart disease and stroke.

• Weight gain. Many high-fat foods such as pizza, baked goods, and fried foods have a lot of saturated fat. Eating too much fat can cause you to gain weight. All fats contain 9 calories per gram of fat. This is more than twice the amount found in carbohydrates and protein.

Cutting out high-fat foods can help keep your weight in check and keep your heart healthy. Staying at a healthy weight can reduce your risk of diabetes, heart disease, and other health problems.

The most recent American Heart Association and American College of Cardiology advisory ¹¹, reaffirms that longstanding advice. Here are some of the scientific highlights:

• Randomized controlled trials that lowered intake of dietary saturated fat and replaced it with polyunsaturated vegetable oil reduced cardiovascular disease by about 30 percent – similar to results achieved by some cholesterol-lowering drugs known as statins ¹².

• Prospective observational studies in many populations showed that a lower intake of saturated fat with a higher intake of polyunsaturated and monounsaturated fat is associated with lower rates of cardiovascular disease ¹³.

• Several studies found that coconut oil – which is predominantly saturated fat but has been widely touted recently as healthy – raised LDL cholesterol to the same degree as other saturated fats found in butter, beef fat, ghee and palm oil.

• Replacing saturated fat with mostly refined carbohydrate and sugars does not lower rates of heart disease, but replacing these fats with whole grains is associated with lower rates. This indicates that saturated fat and refined carbohydrate are equally bad relative to heart disease risk.

What is Cholesterol ?

Cholesterol is a waxy substance that your body needs it to build cells. But too much cholesterol can be a problem ¹⁴.

Cholesterol comes from two sources. Your body (specifically your liver) makes all the cholesterol you need. The rest you get from foods. For example, meat, poultry, ghee, butter, pork lard, beef tallow and full-fat dairy products contain cholesterol (called dietary cholesterol). More importantly, these foods are high in saturated and trans fat. That’s a problem because these fats cause your liver to make more cholesterol than it otherwise would. For some people, this added production means they go from a normal cholesterol level to one that’s unhealthy.

Some tropical oils, such as palm oil, palm kernel oil and coconut oil, also can trigger your liver to make more cholesterol. These oils are often found in baked goods.

There are actually two types of cholesterol: “bad” and “good.” LDL cholesterol is the “bad” kind. HDL is the “good” kind. Too much of the bad kind (LDL cholesterol) — or not enough of the good kind (HDL cholesterol) — increases the chances that cholesterol will start to slowly build up in the inner walls of arteries that feed the heart and brain. We talk more about these two kinds of cholesterol here: What is Cholesterol and Is there good and bad cholesterol ?

High LDL “bad” cholesterol is one of the major controllable risk factors for coronary heart disease, heart attack and stroke. High LDL “bad” cholesterol contributes to fatty buildups in arteries (atherosclerosis). Plaque buildups narrow arteries and raise the risk for heart attack, stroke and peripheral artery disease can narrowed arteries in the legs. If the blocked artery supplies the heart or brain, a heart attack or stroke occurs. If an artery supplying oxygen to the extremities (often the legs) is blocked, gangrene can result. Gangrene is tissue death. If you have other risk factors such as smoking, high blood pressure or diabetes, this risk increases even more. The more risk factors you have and the more severe they are, the more your overall risk rises.

Keeping your cholesterol levels healthy is a great way to keep your heart healthy – and lower your chances of getting heart disease or having a stroke.

Why cholesterol matters

Cholesterol circulates in the blood, and as blood cholesterol levels rise, so does the risk to your health. That’s why it’s important to have your cholesterol tested so you can know your levels.

Together with other substances, LDL “bad” cholesterol can form a thick, hard deposit that can narrow the arteries and make them less flexible. This condition is known as atherosclerosis. If a clot forms and blocks a narrowed artery, a heart attack or stroke can result.

A diet high in saturated (e.g. ghee, butter, beef tallow, pork lard) and trans fat is unhealthy because it tends to raise LDL “bad” cholesterol.

High LDL “bad” cholesterol is one of the major controllable risk factors for coronary heart disease, heart attack and stroke. If you have other risk factors such as smoking, high blood pressure or diabetes, this risk increases even more. The more risk factors you have and the more severe they are, the more your overall risk rises.

A low LDL cholesterol level is considered good for your heart health.

A Scientific Statement From the American Heart Association Nutrition Committee recommendations ² are:

• to balance caloric intake and physical activity to achieve and maintain a healthy body weight;
• consume a diet rich in vegetables and fruits;
• choose whole-grain, high-fiber foods;
• consume fish, especially oily fish, at least twice a week;
• limit intake of saturated fat to <7% of energy, trans fat to <1% of energy, and cholesterol to <300 mg/day by choosing lean meats and vegetable alternatives, fat-free (skim) or low-fat (1% fat) dairy products and minimize intake of partially hydrogenated fats;
• minimize intake of beverages and foods with added sugars; choose and prepare foods with little or no salt.

Ghee Nutrition Content

Table 1. Ghee Nutrition Content

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ¹⁵]

Is ghee healthy ?

Consuming high amounts of saturated fats linked to increased heart disease risk ! ¹⁶, ¹⁷, ¹⁸, ¹⁹.

In a new study appearing online in the Journal of the American College of Cardiology, Dr. Frank Hu and colleagues found that people who replace saturated fat (primarily found in meats and dairy foods) with refined carbohydrates do not lower their risk of heart disease, whereas those who replace saturated fats with unsaturated fats or whole grains lower their heart disease risk ²⁰.

Previous studies have shown that individual saturated fatty acids have different effects on blood lipids, but little is known about associations between individual saturated fatty acid intake and coronary heart disease risk. However, in a study that appeared online on 23rd November 2016, in The British Medical Journal ²¹, where the researchers analyzed data from 73,147 women involved in the Nurses’ Health Study between 1984 and 2012, and 42,635 men who were in the Health Professionals Follow-up Study between 1986 and 2010. Participants reported their diet and health status on questionnaires completed every four years. The study found that a higher intake of the most commonly consumed major saturated fatty acids—lauric acid, myristic acid, palmitic acid, and stearic acid—was associated with a 18% increased relative risk of coronary heart disease ²¹. This study dispels the notion that ‘butter is good’, said Dr. Hu the study co-author. Dr. Hu added, “individual saturated fatty acids share the same food sources, such as red meat, dairy, butter, lard, and palm oil. Therefore it is impractical to differentiate the types of saturated fatty acids in making dietary recommendations, an idea that some researchers have put forth. Instead, it is healthier to replace these fatty acids with unsaturated fats from vegetable oils, nuts, seeds, and seafood as well as high quality carbohydrates” ²¹. “Replacing sources of saturated fat in our diets with unsaturated fats is one of the easiest ways to reduce our risk of heart disease,” said Walter Willett, a co-author and professor of epidemiology and nutrition.

Replacing just 1% of daily consumption of these fatty acids with equivalent calories from polyunsaturated fats, whole grain carbohydrates, or plant proteins, was estimated to reduce relative coronary heart disease risk by 6%-8%. Replacing palmitic acid—found in palm oil, meat, and dairy fat—was associated with the strongest risk reduction.

Although fat is an important part of a healthy diet, it’s even more important to focus on eating beneficial “good” fats and avoiding harmful “bad” fats.  Choose foods with “good” unsaturated fats, limit foods high in saturated fat, and avoid “bad” trans fat.

• “Good” unsaturated fats — Monounsaturated and polyunsaturated fats — lower disease risk. Foods high in good fats include vegetable oils (such as olive oil, canola oil, sunflower oil, peanut oil, safflower, soybean oil, walnut oil and corn oil), nuts (peanuts,almonds, cashews, hazelnuts, pistachios and pecans), seeds, avocado and fish.

• “Bad” fats — trans fats — increase disease risk, even when eaten in small quantities. Foods containing trans fats are primarily in processed foods made with trans fat from partially hydrogenated oil. Fortunately, trans fats have been eliminated from many of these foods.

• “Bad” Saturated fats, while not as harmful as trans fats, by comparison with unsaturated fats negatively impact health and are best consumed in moderation. Foods containing large amounts of saturated fat include red meat, butter, ghee, coconut oil, palm oil, cheese and ice cream.

When you cut back on foods like red meat and butter, replace them with oily fish, beans, nuts, and healthy oils instead of refined carbohydrates.

Most foods have a combination of different fats. You are better off choosing foods higher in healthier fats, such as monounsaturated and polyunsaturated fats. These fats tend to be liquid at room temperature.

The latest Dietary Guidelines for Americans ²² Key Recommendations for healthy eating pattern limits:

• Saturated fats and trans fats, added sugars, and sodium.
• Consume less than 10 percent of calories per day from saturated fats.
• To further reduce your heart disease risk, limit saturated fats to less than 7% of your total daily calories.
• Consume less than 10 percent of calories per day from added sugars.
• Consume less than 2,300 milligrams (mg) per day of sodium (salt).
• If alcohol is consumed, it should be consumed in moderation—up to one drink per day for women and up to two drinks per day for men—and only by adults of legal drinking age.

You can cut how much saturated fat you eat by substituting healthier foods for less healthy options. Replace foods high in saturated fats with foods that have polyunsaturated and monounsaturated fats. Here is how to get started:

• Replace red meats with skinless chicken or fish a few days a week.
• Use canola or olive oil instead of butter, ghee and other solid fats.
• Replace whole-fat diary with low-fat or nonfat milk, yogurt, and cheese.
• Eat more fruits, vegetables, whole grains, and other foods with low or no saturated fat.

Ghee vs Butter

Ghee has slightly more vitamin A 560 IU vs butter with only 400 IU per tablespoon.

However, both are high in saturated fat and cholesterol.

Table 2. Butter (Unsalted) Nutrition Content

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ¹⁵]

Ghee vs Polyunsaturated Oils (Olive Oil & Peanut Oil)

Both olive and peanut oils are low in saturated fat and has O (zero) cholesterol. And from heart and cardiovascular point of view, they are much healthier for you than ghee or butter.

• An analysis of more than 100 published research studies dating as far back as the 1950s, pointed out there are great benefits to replacing saturated fats – such as coconut oil, butter, ghee, beef fat or palm oil – with healthier polyunsaturated fats.

• The American Heart Association, the American College of Cardiology and the U.S. Department of Agriculture’s Dietary Guidelines for Americans have been issuing dietary recommendations for decades. In 1961, the American Heart Association recommended for the first time that vegetable oils replace saturated fats. Governments, including in the United States and internationally, as well as other nonprofits have been cautioning about saturated fats, too.

• The basis for the American Heart Association’s advice about nutrition is a systematic review of the best available scientific information, conducted by volunteer committees of expert researchers and physicians. More information on the American Heart Association’s statements and guidelines development is available online here ²³. –> American Heart Association. About GUIDELINES & Statements. http://professional.heart.org/professional/GuidelinesStatements/UCM_316885_Guidelines-Statements.jsp

Table 3. Olive Oil Nutrition Content

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ¹⁵]

Table 4. Peanut Oil Nutrition Content

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ¹⁵] References

1. Sharma H, Zhang X, Dwivedi C. The effect of ghee (clarified butter) on serum lipid levels and microsomal lipid peroxidation. Ayu. 2010;31(2):134-140. doi:10.4103/0974-8520.72361. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3215354/
2. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. American Heart Association Nutrition Committee., Lichtenstein AH, Appel LJ, Brands M, Carnethon M, Daniels S, Franch HA, Franklin B, Kris-Etherton P, Harris WS, Howard B, Karanja N, Lefevre M, Rudel L, Sacks F, Van Horn L, Winston M, Wylie-Rosett J. Circulation. 2006 Jul 4; 114(1):82-96. http://circ.ahajournals.org/content/114/1/82.long
3. Lad V. New York: Harmony Books; 1998. The Complete Book of Ayurvedic Home Remedies.
4. Sharma HM. Butter oil (ghee) – Myths and facts. Indian J Clin Pract. 1990;1:31–2.
5. Illingworth D, Patil GR, Tamime AY. Anhydrous milk fat manufacture and fractionation. In: Tamime AY, editor. Dairy Fats and Related Products. Chichester, West Sussex: Wiley-Blackwell; 2009.
6. U.S. National Library of Medicine. Facts about saturated fats. https://medlineplus.gov/ency/patientinstructions/000838.htm
7. Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010;7:e1000252. doi: 10.1371/journal. pmed.1000252.
8. Hooper L, Martin N, Abdelhamid A, Davey Smith G. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev. 2015:CD011737. doi: 10.1002/14651858. CD011737.
9. Wang DD, Li Y, Chiuve SE, Stampfer MJ, Manson JE, Rimm EB, Willett WC, Hu FB. Association of Specific Dietary Fats With Total and Cause-Specific Mortality. JAMA Intern Med. 2016;176(8):1134–1145. doi:10.1001/jamainternmed.2016.2417. http://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2530902
10. Harvard University, Harvard School of Public Health. Different Dietary Fat, Different Risk of Mortality. https://www.hsph.harvard.edu/nutritionsource/2016/07/05/different-dietary-fat-different-risk-of-mortality/
11. American Heart Association. Cutting through the saturated fat – meats, butter and tropical oils still need limits. http://news.heart.org/cutting-saturated-fat-meats-butter-tropical-oils-still-need-limits/
12. American Heart Association. Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association. http://circ.ahajournals.org/content/early/2017/06/15/CIR.0000000000000510
13. American Heart Association. Advisory: Replacing saturated fat with healthier fat could lower cardiovascular risks. http://news.heart.org/advisory-replacing-saturated-fat-with-healthier-fat-could-lower-cardiovascular-risks/
14. American Heart Association. About Cholesterol. http://www.heart.org/HEARTORG/Conditions/Cholesterol/AboutCholesterol/About-Cholesterol_UCM_001220_Article.jsp
15. United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. https://ndb.nal.usda.gov/ndb/
16. Siri-Tarino, P.W., et al., Saturated fatty acids and risk of coronary heart disease: modulation by replacement nutrients. Curr Atheroscler Rep, 2010. 12(6): p. 384-90.
17. Hu, F.B., et al., Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med, 1997. 337(21): p. 1491-9.
18. Ascherio, A., et al., Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States. BMJ, 1996. 313(7049): p. 84-90.
19. Hu, F.B., J.E. Manson, and W.C. Willett, Types of dietary fat and risk of coronary heart disease: a critical review. J Am Coll Nutr, 2001. 20(1): p. 5-19.
20. Journal of the American College of Cardiology Volume 66, Issue 14, October 2015. DOI: 10.1016/j.jacc.2015.07.055. Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease. http://www.onlinejacc.org/content/66/14/1538
21. BMJ 2016;355:i5796. Intake of individual saturated fatty acids and risk of coronary heart disease in US men and women: two prospective longitudinal cohort studies. http://www.bmj.com/content/355/bmj.i5796
22. 2015–2020 Dietary Guidelines for Americans, https://health.gov/dietaryguidelines
23. American Heart Association. About GUIDELINES & Statements. http://professional.heart.org/professional/GuidelinesStatements/UCM_316885_Guidelines-Statements.jsp

What are Natural Sweeteners ?

First of all, we need to define what sweeteners are. Sweeteners are substances used to improve the palatability and shelf life of food products. Sweetness also balances bitterness, sourness, and saltiness. A preference for sweet taste is innate and sweeteners can increase the pleasure of eating.

Sweeteners can generally be divided into three types of sweeteners depending how there are made:

1. Natural Sweeteners come from plant origin e.g. sugar (sucrose), honey, molasses, maple syrup, coconut palm sugar, stevia, agave, brown sugar, fruit concentrates, Luo Han Guo (monk fruit) fruit extracts.
2. Artificial (synthetic) Sweeteners are man made high-intensity sweeteners e.g. Aspartame (NutraSweet® and Equal®); Acesulfame-K (Sweet One®); Neotame; Saccharin (Sweet’N Low®); Sucralose (Splenda®) and Advantame. Artificial sweeteners also known as sugar substitutes are called ‘high-intensity’ sweeteners, because small amounts pack a large punch when it comes to sweetness. Artificial sweeteners are regulated by the U.S. Food and Drug Administration (FDA) ¹. And because high-intensity sweeteners are many times sweeter than table sugar (sucrose), smaller amounts of high-intensity sweeteners are needed to achieve the same level of sweetness as sugar in food. People may choose to use high-intensity sweeteners in place of sugar for a number of reasons, including that they do not contribute calories or only contribute a few calories to the diet. High-intensity sweeteners also generally will not raise blood sugar levels ².
3. Sugar Alcohols (Polyols). Despite their name, sugar alcohols aren’t sugar, and they aren’t alcohol. They are carbohydrates that occur naturally in certain fruits and can also be manufactured. They get their name because they have a chemical structure similar to sugar and to alcohol. Examples of sugar alcohols, isomalt, maltitol, lactitol, trehalose, mannitol, erythritol, xylitol and D-tagatose.

To make it even more complicated, sweeteners can be further divided into two categories based on their calorie content:

• Nutritive sweeteners – those that contain more than 2 percent of the calories in an equivalent amount of sugar, therefore nutritive sweeteners add caloric value to the foods that contain them ³. For example, sugar (sucrose), honey, molasses, maple syrup, coconut palm sugar, agave, brown sugar, fruit concentrates, Xylitol, Sorbitol, isomalt, maltitol, lactitol, trehalose, mannitol, erythritol and D-tagatose.
• Non-nutritive sweeteners – since they offer no nutritional benefits such as vitamins and minerals and they are low or have no calories. Non-nutritive sweeteners are those that contain less than 2 percent of the calories in an equivalent amount of sugar or have no calories at all. Also known as artificial sweeteners, sugar substitutes, low-calorie sweeteners, noncaloric sweeteners, or high-intensity sweeteners ³. For example, Stevia, Luo Han Guo fruit extracts (Siraitia grosvenorii Swingle fruit extract), Aspartame (NutraSweet® and Equal®); Acesulfame-K (Sweet One®); Neotame; Saccharin (Sweet’N Low®); Sucralose (Splenda®) and Advantame. Food products are considered “no-calorie” if they have 5 calories or less per serving. Notice that even though the nutrition labels on sweetener packets claim to have zero calories and carbohydrate, there are a small amount calories and carbs from those added ingredients ³.

Table 1. Natural Sweetening Agents

[Source: ⁴]

Replacing sugary foods and drinks with sugar-free options containing non-nutritive sweeteners is one way to limit calories and achieve or maintain a healthy weight ⁵. Also, when used to replace food and drinks with added sugars, it can help people with diabetes manage blood glucose levels. For example, swapping a full-calorie soda with diet soda is one way of not increasing blood glucose levels while satisfying a sweet tooth.

We don’t know for sure if using non-nutritive sweeteners in food and drinks makes people actually eat or drink fewer calories every day. But reducing the amount of added sugar in your diet ? That we know for sure is a good thing.

According to the American Academy of Nutrition and Dietetics, consumers can safely enjoy a range of nutritive sweeteners and non-nutritive sweeteners when consumed within an eating plan that is guided by current federal nutrition recommendations, such as the Dietary Guidelines for Americans and the Dietary Reference Intakes, as well as individual health goals and personal preference ⁶. The Dietary Guidelines for Americans, recommends sugars are to be consumed in moderation, with calories from sugar making up no more than 10 percent of their total calorie intake. For example, 10 percent of 1800 calories per day is 180 calories from added sugars ⁷. The American Heart Association recommends that most women eat no more than 6 teaspoons or 100 calories a day of added sugar and men no more than 9 teaspoons or 150 calories a day of added sugar. Added sugars include any sugars or caloric sweeteners that are added to foods or beverages during processing or preparation (such as putting sugar in your coffee or adding sugar to your cereal). Added sugars (or added sweeteners) can include natural sugars such as white sugar, brown sugar and honey as well as other caloric sweeteners that are chemically manufactured (such as high fructose corn syrup). This recommendation is based on research that showed diets high in added sugars increase risk factors, such as obesity and triglycerides, for coronary heart disease. Additionally, foods and beverages high in added sugars tend to displace nutritious foods and are generally high in calories and low in nutritional value. Limiting intake of added sugars can help reduce calorie intake and can help people achieve or maintain a healthy body weight ⁸.

Nutritive sweeteners contain carbohydrate and provide energy. They occur naturally in foods or may be added in food processing or by consumers before consumption. Higher intake of added sugars is associated with higher energy intake and lower diet quality, which can increase the risk for obesity, pre-diabetes, type 2 diabetes and cardiovascular disease. On average, adults in the United States consume 14.6% of energy from added sugars. Polyols (also referred to as sugar alcohols) add sweetness with less energy and may reduce risk for dental caries. Foods containing polyols and/or no added sugars can, within food labeling guidelines, be labeled as sugar-free ⁶.

Non-nutritive sweeteners are those that sweeten with minimal or no carbohydrate or energy. They are regulated by the Food and Drug Administration as food additives or generally recognized as safe. The Food and Drug Administration approval process includes determination of probable intake, cumulative effect from all uses, and toxicology studies in animals. Seven non-nutritive sweeteners are approved for use in the United States: acesulfame K, aspartame, luo han guo fruit extract, neotame, saccharin, stevia, and sucralose. They have different functional properties that may affect perceived taste or use in different food applications. All non-nutritive sweeteners approved for use in the United States are determined to be safe ⁶.

Keep in mind that just because a product is “sugar free,” it doesn’t always mean that it’s healthy. Foods and beverages that contain non-nutritive sweeteners can be included in a healthy diet, as long as the calories they save you are not added back by adding more foods as a reward later in the day, adding back calories that take you over your daily limit. The current meta-analysis ⁹ provides a rigorous evaluation of the scientific evidence on low-calorie sweeteners and body weight and composition. Findings from observational studies showed no association between low-calorie sweeteners intake and body weight or fat mass and a small positive association with body mass index (BMI); however, data from randomised clinical trials, which provide the highest quality of evidence for examining the potentially causal effects of low-calorie sweeteners intake, indicate that substituting low-calorie sweeteners options for their regular-calorie versions results in a modest weight loss and may be a useful dietary tool to improve compliance with weight loss or weight maintenance plans ⁹.

However, in a recent (published 17 July 2017) systematic review and meta-analysis of randomized controlled trials and prospective cohort studies on the effects of non-nutritive sweeteners (artificial sweeteners) and cardio-metabolic health being conducted by Dr. Azad et al. ¹⁰ found that non-nutritive sweeteners (artificial sweeteners) had no significant effect on BMI (body mass index) on participants, in fact in the included cohort studies, consumption of non-nutritive sweeteners was associated with a modest increase in BMI. In the cohort studies, consumption of non-nutritive sweeteners was associated with increases in weight and waist circumference, and higher incidence of obesity, hypertension, metabolic syndrome, type 2 diabetes and cardiovascular events ¹⁰. Theories about why artificial sweeteners might not help weight loss tend to revolve around two schools of thought, Dr. Azad said. One school holds that the sweeteners might influence dieters’ behavior in unhealthy ways. For example, a person drinking a no-calorie soda might feel free to eat calorie-laden foods, Azad noted. Artificial sweeteners also might sharpen the person’s sweet tooth, making them more likely to indulge in sugary foods. The other school holds that artificial sweeteners might influence the body itself in some as-yet-unknown way, Azad said. The artificial sweeteners could alter the way that gut microbes function in the digestion of food, or possibly change the body’s metabolism over time by sending repeated false signals that something sweet has been ingested ¹¹. Another plausible explanation for why the study subjects gained weight and have higher incidence of obesity, hypertension, metabolic syndrome, type 2 diabetes and cardiovascular events, is that the study population involved people who are already overweight, obese, have metabolic syndrome, hypertension or suffer from type 2 diabetes ¹¹.

Natural Sweeteners List

When choosing the best natural sweetener one needs to consider calories, effect on blood sugar, effect on dental hygiene, beneficial effects, taste, price and usefulness in cooking.

The common natural sweeteners are:

• White sugar
• Brown sugar
• Raw sugar
• Powdered sugar
• Agave nectar
• Barley malt
• Brown rice syrup
• Corn syrup
• Corn syrup solids
• High-fructose corn syrup
• Invert sugar
• Dextrose
• Anhydrous dextrose
• Crystal dextrose
• Dextrin
• Evaporated cane juice
• Fructose sweetener
• Liquid fructose
• Glucose
• Lactose
• Honey
• Malt syrup
• Maltose
• Maple syrup
• Molasses
• Pancake syrup
• Stevia
• Monk Fruit (Nectresse and Luo Han Guo)
• Sucrose
• Syrup
• Trehalose
• Turbinado sugar

All of these contain calories with the exception of Stevia and Lou Han Gou (Monk Fruit) extracts.

Table 2. 100% Natural O Calorie Sweetener, Monk Fruit & Stevia Blend

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ¹²]

Stevia

Stevia (Truvia, Pure Via, Sun Crystals, Rebaudioside A, Reb A, rebiana) is a non-caloric plant-based sweetener; made from the plant Stevia rebaudiana, which is grown for its sweet leaves; common names include sweetleaf, sweet leaf, sugarleaf, or simply stevia ¹³. In addition to stevioside several other sweet principles such as steviosides A and B, Steviobioside, Rebaudioside A, B, C, D, E
and Dulcoside A were isolated from Stevia rebaudiana leaf ¹⁴. FDA approved as generally recognized as safe (GRAS) as a food additive and table top sweetener only certain high purity steviol glycosides purified from the leaves of Stevia rebaudiana (Bertoni). Stevia is 150 to 200 times sweeter than sucrose (table sugar) ¹⁵.

Stevia (Stevia rebaudiana) is a bushy shrub that is native to northeast Paraguay, Brazil and Argentina ¹⁶. It is now grown in other parts of the world, including Canada and part of Asia and Europe. It is probably best known as a source of natural sweeteners.

Extracts from the stevia leaves are available as sweeteners in Japan, South Korea, Malaysia, Taiwan, Russia, Israel, Mexico, Paraguay, Uruguay, Venezuela, Colombia, Brazil, and Argentina ¹⁷.

Some people take stevia by mouth for medical purposes such as lowering blood pressure, treating diabetes, heartburn, high uric acid levels in the blood, for weight loss, to stimulate the heart rate, and for water retention.

Studies on the glycemic effect of rebaudioside A is still not clear, but it seems that consumption of rebaudioside A did not worsen glycemic control in individuals with and without diabetes ¹⁸.

So how effective is Stevia when used for medical purposes ?

Natural Medicines Comprehensive Database rates effectiveness based on scientific evidence according to the following scale:

• Effective, Likely Effective, Possibly Effective, Possibly Ineffective, Likely Ineffective, Ineffective, and Insufficient Evidence to Rate.

The effectiveness ratings for STEVIA are as follows:

Insufficient evidence ¹⁹ to rate Stevia effectiveness for:

• Diabetes. Research on how stevia might affect blood sugar in people with diabetes is inconsistent. Some early research suggests that taking 1000 mg daily of stevia leaf extract containing 91% stevioside might reduce blood sugar levels after meals by 18% in people with type 2 diabetes. However, other research shows that taking 250 mg of stevioside three times daily does not decrease blood sugar levels or HbA1c (a measure over blood sugar levels over time) after three months of treatment.
• High blood pressure. How stevia might affect blood pressure is unclear. Some research suggests that taking 750-1500 mg of stevioside, a chemical compound in stevia, daily reduces systolic blood pressure (the upper number in a blood pressure reading) by 10-14 mmHg and diastolic blood pressure (the lower number) by 6-14 mmHg. However, other research suggests that taking stevioside does not reduce blood pressure.
• Heart problems.
• Heartburn.
• Weight loss.
• Water retention.
• Other conditions.

More evidence is needed to rate the effectiveness of stevia for these uses ¹⁹.

Is Stevia safe ?

The appropriate dose of stevia depends on several factors such as the user’s age, health, and several other conditions. At this time there is not enough scientific information to determine an appropriate range of doses for stevia. Keep in mind that natural products are not always necessarily safe and dosages can be important. Be sure to follow relevant directions on product labels and consult your pharmacist or physician or other healthcare professional before using.

Stevia and chemicals contained in stevia, including stevioside and rebaudioside A, are LIKELY SAFE when taken by mouth as a sweetener in foods ¹⁹. The U.S. Food and Drug Administration (FDA) has given the generally recognized as safe (GRAS) status for Rebaudioside A in the U.S. for use as a sweetener for foods ²⁰. Stevioside has been safely used in research in doses of up to 1500 mg daily for 2 years.

In March 2010, the European Food Safety Authority (EFSA) concluded that the stevia sweeteners are not carcinogenic, genotoxic or associated with any reproductive/developmental toxicity and established an Acceptable Daily Intake (ADI) of 4 mg/kg body weight/day. Conservative estimates of steviol glycosides exposure, both in adults and in children, suggest that it is likely that the ADI would be exceeded at the maximum proposed use levels. The use of Stevia is now authorised in the European Union at appropriate levels for 31 different food categories including soft drinks, desserts, confectionary and table top sweeteners ²¹.

Some people who take stevia or stevioside can experience bloating or nausea. Other people have reported feelings of dizziness, muscle pain, and numbness.

Special precautions & warnings:

• Pregnancy and breast-feeding: There is not enough reliable information about the safety of taking stevia if you are pregnant or breast feeding. Stay on the safe side and avoid use.

• Allergy to ragweed and related plants: Stevia is in the Asteraceae/Compositae plant family. This family includes ragweed, chrysanthemums, marigolds, daisies, and many other plants. In theory, people who are sensitive to ragweed and related plants may also be sensitive to stevia.

• Diabetes: Some developing research suggests that some of the chemicals contained in stevia might lower blood sugar levels and could interfere with blood sugar control. However, other research disagrees. If you have diabetes and take stevia or any of the sweeteners it contains, monitor your blood sugar closely and report your findings to your healthcare provider.

• Low blood pressure: There is some evidence, though not conclusive, that some of the chemicals in stevia can lower blood pressure. There is a concern that these chemicals might cause blood pressure to drop too low in people who have low blood pressure. Get your healthcare provider’s advice before taking stevia or the sweeteners it contains, if you have low blood pressure.

• Lithium: Stevia might have an effect like a water pill or “diuretic.” Taking stevia might decrease how well the body gets rid of lithium. In theory, this could increase how much lithium is in the body and result in serious side effects. Talk with your healthcare provider before using this product if you are taking lithium. Your lithium dose might need to be changed ¹⁹.

• Medications for diabetes (Antidiabetes drugs): Some research shows that stevia might decrease blood sugar in people with type 2 diabetes. In theory, stevia might cause an interaction with diabetes medications resulting in blood sugar levels going too low; however, not all research has found that stevia lowers blood sugar. Therefore, it is not clear if this potential interaction is a big concern. Until more is known, monitor your blood sugar closely if you take stevia. Some medications used for diabetes include glimepiride (Amaryl), glyburide (DiaBeta, Glynase PresTab, Micronase), insulin, pioglitazone (Actos), rosiglitazone (Avandia), chlorpropamide (Diabinese), glipizide (Glucotrol), tolbutamide (Orinase), and others. The dose of your diabetes medication might need to be changed ¹⁹.
• Medications for high blood pressure (Antihypertensive drugs): Some research shows that stevia might decrease blood pressure. In theory, taking stevia along with medications used for lowering high blood pressure might cause your blood pressure to go too low. However, some research shows that stevia does not affect blood pressure. Therefore, it’s not known if this potential interaction is a big concern. Some medications for high blood pressure include captopril (Capoten), enalapril (Vasotec), losartan (Cozaar), valsartan (Diovan), diltiazem (Cardizem), Amlodipine (Norvasc), hydrochlorothiazide (HydroDiuril), furosemide (Lasix), and many others ¹⁹.
• Herbs and supplements that might lower blood pressure: Stevia might lower blood pressure. Using it along with other herbs and supplements that have this same effect might increase the risk of blood pressure dropping too low in some people. Some of these products include andrographis, casein peptides, cat’s claw, coenzyme Q-10, fish oil, L-arginine, lycium, stinging nettle, theanine, and others ¹⁹.

• Herbs and supplements that might lower blood sugar: Stevia might lower blood sugar. Using it along with other herbs and supplements that have the same effect might cause blood sugar to drop too low in some people. Some of these products include alpha-lipoic acid, bitter melon, chromium, devil’s claw, fenugreek, garlic, guar gum, horse chestnut seed, Panax ginseng, psyllium, Siberian ginseng, and others ¹⁹.

Monk Fruit or Lou Han Guo Extracts

Monk Fruit (Nectresse and Luo Han Guo) also known as Siraitia grosvenori Swingle, has been used in China for centuries as a natural sweetening agent and has been reported to be beneficial for diabetic population ²², ²³. However, limited research has been conducted to elucidate the relationship between the sweetening action and biological parameters that may be related to potential health benefits of Luo Han Kuo fruit. The present study ²² examined the effect of LHK fruit and its chemical components on insulin secretion using an in vitro cell model system. Mogroside V is the most abundant and the sweetest chemical component among the mogrosides in Luo Han Kuo fruit. The experimental data demonstrated that the crude Luo Han Kuo fruit extract stimulated the secretion of insulin in pancreatic beta cells; furthermore, pure mogroside V isolated from Luo Han Kuo fruit also exhibited a significant activity in stimulating insulin secretion by the beta cells, which could partially be responsible for the insulin secretion activity of Luo Han Kuo fruit and fruit extract. The current study supports that Luo Han Kuo fruit/extract has the potential to be natural sweetener with a low glycemic index and that mogroside V, possible other related mogrosides, can provide a positive health impact on stimulating insulin secretion ²².

Luohanguo is collected as a round green fruit that turns brown upon drying. The sweet taste of the fruit comes mainly from mogrosides, a group of triterpene glycosides that make up about 1% of the flesh of the fresh fruit ²⁴. The mogrosides have been numbered 1-5 ²⁵ and the main component is called mogroside-5, previously known as esgoside. Other, similar compounds from luohanguo have been labeled siamenoside and neomogroside ²⁴. The mixed mogrosides are estimated to be about 300 times as sweet as sugar by weight, so that the 80% extracts are nearly 250 times sweeter than sugar; pure mogrosides 4 and 5 may be 400 times as sweet as sugar by weight ²⁴. Through solvent extraction, a powder containing 80% mogrosides can be obtained, the main one being mogroside-5 (esgoside). Other similar agents in the fruit are siamenoside and neomogroside ²⁴. The powdered extract of monk (Luo Han Kuo fruit) fruit, a round green melon that grows in central Asia; 150 to 200 times sweeter than sucrose (table sugar); heat stable and can be used in baking and cooking and is more concentrated than sugar (¼ teaspoon or 0.5 grams equals the sweetness of 1 teaspoon or 2.5 grams sugar). FDA approved as generally recognized as safe (GRAS) as a food additive and table top sweetener.

Natural Sweeteners for Diabetics

Non-nutritive or artificial sweeteners are not actually needed to help manage diabetes. People with diabetes can still use regular sugar to sweeten foods and beverages, as long as it is used in small amounts and generally eaten as part of a healthy meal. An example of this might be one teaspoon of sugar sprinkled over a hot bowl of plain rolled oats or a thin spread of regular jam on some grainy toast. This is the same advice that would be given to someone who does not have diabetes, as large amounts of added sugar is not good for anyone, regardless of whether or not they have diabetes.

• Stevia: This leafy herb also known as honey leaf has been used for centuries by native South Americans. The extract from stevia is approximately 100 to 300 times sweeter than white sugar. It can be used in cooking, baking and as a sugar substitute in most beverages. Stevia has been shown to have a positive effect on blood sugar levels by increasing insulin production, and decreasing insulin resistance.

Natural Sweeteners for Coffee

Choose any form of natural sweetener that you like or that suits your coffee or meal the best. Just use them in small amounts to reduce the impact on your blood glucose levels and weight. Apart from sugar, honey, coconut sugar, yacon syrup, maple syrup and blackstrap molasses, that contain calories, you may want to consider the low to zero calorie natural sweeteners:

• Erythritol: Erythritol is a naturally occurring sugar alcohol found in fruit and fermented foods. Erythritol has 0.2 calories per gram (0.8 calories per teaspoon) and 60% to 80% as sweet as sugar. Erythritol does not result in as much of a rise in blood sugar after meals or cause tooth decay. Unlike other sugar alcohols, it does not cause stomach upset. This sugar alcohol is a sweetener available in a powdered form. It is formed from the breaking down, fermenting, and filtering of sugar cane or corn starch. It has a cool taste that works well in coffee and tea.

• Xylitol: Xylitol has 2.4 calories per gram and the same sweetness as sugar Sugar alcohols like Xylitol (when consumed in large amounts) can cause abdominal pain, gas/bloating and diarrhea as common side effects. Other gastric symptoms may also occur in some people, especially in children.

Natural Sweeteners for Tea

Again choose any form of natural sweetener that you like or that suits your coffee or meal the best. Just use them in small amounts to reduce the impact on your blood glucose levels and weight. Apart from sugar, honey, coconut sugar, yacon syrup, maple syrup and blackstrap molasses, that contain calories, you may want to consider the low to zero calorie natural sweeteners:

• Erythritol: Erythritol is a naturally occurring sugar alcohol found in fruit and fermented foods. Erythritol has 0.2 calories per gram (0.8 calories per teaspoon) and 60% to 80% as sweet as sugar. Erythritol does not result in as much of a rise in blood sugar after meals or cause tooth decay. Unlike other sugar alcohols, it does not cause stomach upset. This sugar alcohol is a sweetener available in a powdered form. It is formed from the breaking down, fermenting, and filtering of sugar cane or corn starch. It has a cool taste that works well in coffee and tea.

References

1. U.S. Food and Drug Administration. Additional Information about High-Intensity Sweeteners Permitted for use in Food in the United States. https://www.fda.gov/food/ingredientspackaginglabeling/foodadditivesingredients/ucm397725.htm
2. U.S. Food and Drug Administration. High-Intensity Sweeteners. https://www.fda.gov/Food/IngredientsPackagingLabeling/FoodAdditivesIngredients/ucm397716.htm
3. American Diabetes Association. 5 Must-Know Facts About Sweeteners. http://www.diabetesforecast.org/2016/jan-feb/5-must-know-facts-about-sweeteners.html
4. ResearchGate. Natural sweeteners: A complete review. https://www.researchgate.net/publication/265163543_Natural_sweeteners_A_complete_review
5. American Heart Association. Non-Nutritive Sweeteners (Artificial Sweeteners). http://www.heart.org/HEARTORG/HealthyLiving/HealthyEating/Non-Nutritive-Sweeteners-Artificial-Sweeteners_UCM_305880_Article.jsp
6. Fitch C, Keim KS; Academy of Nutrition and Dietetics.J Acad Nutr Diet. 2012 May;112(5):739-58. doi: 10.1016/j.jand.2012.03.009. Epub 2012 Apr 25. Position of the Academy of Nutrition and Dietetics: use of nutritive and nonnutritive sweeteners. https://www.ncbi.nlm.nih.gov/pubmed/22709780/
7. 2015–2020 Dietary Guidelines for Americans. https://health.gov/dietaryguidelines
8. American Heart Association. Added Sugars Add to Your Risk of Dying from Heart Disease. http://www.heart.org/HEARTORG/HealthyLiving/HealthyEating/Nutrition/Added-Sugars-Add-to-Your-Risk-of-Dying-from-Heart-Disease_UCM_460319_Article.jsp
9. Miller PE, Perez V. Low-calorie sweeteners and body weight and composition: a meta-analysis of randomized controlled trials and prospective cohort studies. The American Journal of Clinical Nutrition. 2014;100(3):765-777. doi:10.3945/ajcn.113.082826. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4135487/
10. Azad MB, Abou-Setta AM, Chauhan BF, et al. Nonnutritive sweeteners and cardiometabolic health: a systematic review and meta-analysis of randomized controlled trials and prospective cohort studies. CMAJ : Canadian Medical Association Journal. 2017;189(28):E929-E939. doi:10.1503/cmaj.161390. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5515645/
11. U.S. National Library of Medicine. Medline Plus. Could Artificial Sweeteners Raise Your Odds for Obesity ?. https://medlineplus.gov/news/fullstory_167249.html
12. United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. https://ndb.nal.usda.gov/ndb/
13. Lemus-Mondaca R, Vega-Galvez A, Zura-Bravo L, Ah-Hen K. Stevia rebaudiana Bertoni, source of a high-potency natural sweetener: A comprehensive review on the biochemical, nutritional and functional aspects. Food Chem. 2012;132:1121-1132.
14. Jaroslav Pol, Batbora Hohnova, Tuulia Hyptylainen, Characterisation of Stevis rebaudiana by comphrehensive two-dimensional liquid chromatography time-of–flight mass spectroscopy, Journal of chromatography, 1150, 2007, 85-92.
15. Yadav, A. A review on the improvement of stevia [Stevia rebaudiana (Bertoni). Canadian Journal of Plant Science 2011;91:1-27.
16. Chaturvedula, V. S. and Prakash, I. Structures of the novel diterpene glycosides from Stevia rebaudiana. Carbohydr.Res 6-1-2011;346:1057-1060. https://www.ncbi.nlm.nih.gov/pubmed/21489412?dopt=Abstract
17. Li, J., Jiang, H., and Shi, R. A new acylated quercetin glycoside from the leaves of Stevia rebaudiana Bertoni. Nat.Prod Res 2009;23:1378-1383. https://www.ncbi.nlm.nih.gov/pubmed/19809909?dopt=Abstract
18. Shin DH, Lee JH, Kang MS, et al. Glycemic Effects of Rebaudioside A and Erythritol in People with Glucose Intolerance. Diabetes & Metabolism Journal. 2016;40(4):283-289. doi:10.4093/dmj.2016.40.4.283. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4995183/
19. U.S. National Library of Medicine. Medline Plus. Stevia. https://medlineplus.gov/druginfo/natural/682.html
20. U.S. Food and Drug Administration. Has Stevia been approved by FDA to be used as a sweetener ? https://www.fda.gov/aboutfda/transparency/basics/ucm194320.htm
21. European Union. Questions and Answers on Food Additives. http://europa.eu/rapid/press-release_MEMO-11-783_en.htm
22. Zhou Y, Zheng Y, Ebersole J, Huang CF. Yao Xue Xue Bao. 2009 Nov;44(11):1252-7. Insulin secretion stimulating effects of mogroside V and fruit extract of luo han kuo (Siraitia grosvenori Swingle) fruit extract. https://www.ncbi.nlm.nih.gov/pubmed/21351724
23. Suzuki YA, Tomoda M, Murata Y, Inui H, Sugiura M, Nakano Y. Br J Nutr. 2007 Apr;97(4):770-5. Antidiabetic effect of long-term supplementation with Siraitia grosvenori on the spontaneously diabetic Goto-Kakizaki rat. https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/antidiabetic-effect-of-longterm-supplementation-with-siraitia-grosvenori-on-the-spontaneously-diabetic-gotokakizaki-rat/FC59DC2955AA96A75154985DAE6809E6
24. Institute for Traditional Medicine. LUO HAN GUO. http://www.itmonline.org/arts/luohanguo.htm
25. Chaturvedula VSP, Prakash I. Kaempferol glycosides from Siraitia grosvenorii. J. Chem. Pharm. Resi. 2011;3:799–804.

What is Ezekiel Bread

Ezekiel bread is a type of organic bread made with these ingredients:

• Organic Sprouted Wheat
• Organic Sprouted Barley
• Organic Sprouted Millet
• Organic Malted Barley
• Organic Sprouted Lentils
• Organic Sprouted Soybeans
• Organic Sprouted Spelt
• Fresh Yeast
• Organic Wheat Gluten
• Sea Salt
• Filtered water

The standard Ezekiel bread are made with six organic grains (wheat, barley, spelt, millet) and legumes (lentils, soybeans) and according to the Ezekiel bread manufacturer, Food for Life Baking Company Inc., their don’t use any genetically modified organisms (GMOs) ¹. And instead of sugar, Ezekiel bread uses malted barley, a natural sweetener produced from sprouted barley, which is basically a carbohydrate comprised mostly of complex carbohydrates ¹.

The original Ezekiel bread was made by Max Torres in 1964 and now the Ezekiel bread company also makes English muffins, tortillas, cereals, tortillas, pocket breads, buns, waffles and pasta ².

What is Sprouting ?

Sprouting or germination is a common problem for grain when weather is moist during harvest or the environment is humid during storage ³. When kernels absorb moisture from their surroundings to a sufficient level, the embryo and endosperm are hydrated. Hydration switches on the metabolism of the embryo, which sends hormonal signals to the aleurone layer, triggering the synthesis of enzymes responsible for digesting components of the starchy endosperm. Sprouting promotes the development of cytolytic, proteolytic, and amylolytic enzymes that are not active in dry kernels ⁴, ⁵ and could cause significant changes in kernel composition and physical properties ⁴. Sprouting not only causes compositional changes in the grain but also initiates a series of biochemical and physiological changes. Intrinsic enzymes such as amylases, proteases, lipases, fiber-degrading enzymes, and phytases are activated; this disrupts protein bodies and degrades proteins, carbohydrates, and lipids to simpler molecules, which increases digestibility of proteins and carbohydrates in the kernel and makes nutrients available and accessible for enzymes ⁶, ⁷. Research on baby food showed that sprouting can activate enzymes, decrease the level of antinutritional factors (tannins, phytic acid), and increase digestibility of macronutrients, bioavailability of minerals, and content of essential amino acids ⁸, ⁶. In a 1989 meta-analysis of existing studies, JK Chavan and SS Kadam found evidence that sprouting of grains for a limited period causes increased activities of hydrolytic enzymes, improvement in the contents of certain essential amino acids, total sugars and B-group vitamins, and a decrease in dry matter, starch, and antinutrients. The digestibilities of storage proteins and starch are improved due to their partial hydrolysis during sprouting. The digestibilities of storage proteins and starch are improved due to their partial hydrolysis during sprouting. The magnitude of the nutritional improvement is, however, influenced by the type of cereal, seed quality, sprouting conditions, and it is not large enough to account for in feeding experiments with higher animals ⁹.

• Controlled Sprouting for Maximum Benefits

While a little sprouting appears to be good for us, there’s a sweet spot. Just the right amount of time, temperature, and moisture are necessary to start the germination process. Too much moisture, and the grain drowns, with the seed splitting open not from the force of an emerging, vibrant seedling but instead, simply from waterlogged swelling. Or, the sprout may begin to emerge but then, if the moisture source is not removed, it can begin to ferment or even to rot. Time is important too: if a healthy sprout continues to grow indefinitely, it becomes a new grass stalk, losing its digestibility, since humans can’t properly digest grasses.

• Dry or Wet Sprouting ?

Companies making sprouted grain products currently use two different approaches – dry and wet – once the grains are sprouted.

• The Dry Approach. Some companies sprout the grain then dry it , to lock in this ideal stage. At this point, the sprouted grain can be stored until it’s cooked as a side dish, or it can be milled into sprouted grain flour, which is in turn used to make a wide variety of products.

• The Wet Approach. Alternately, other companies mash the wet, sprouted grains into a thick purée which is used to make breads, tortillas, muffins and other products. These products are often described as “flourless” and are frequently sold frozen.

What are Sprouted Grains ?

Grains are the seeds of certain plants, largely cereal grasses. Like all seeds, grain kernels are a marvel of nature, containing the potential of a whole new plant, patiently waiting its turn in the sun.

All three edible parts of the whole grain – the germ, endosperm, and bran – are crucial to creating the new plant. The germ is the plant embryo, which, when it grows, will feed on the starchy endosperm. The bran layers provide some additional nutrients and — along with the inedible husk found on many grains – help protect the grain seed until it’s ready to start the growth cycle.

Until then, the seed counts on certain built-in growth inhibitors to keep it from germinating until temperature and moisture conditions are just right. Then, once sprouting starts, enzyme activity wipes out these growth inhibitors and transforms the long-term-storage starch of the endosperm to simpler molecules that are easily digested by the growing plant embryo.

Controlled sprouting of grains might lead to the development of specific enzymatic pattern (amylases, proteases, cellulases) that may improve cereals micronutrients bioavailability, color, taste and flavor. The inclusion of sprouted wheat has been shown to enhance flavor, increase digestibility and the nutrient content in bread formulations ¹⁰. Due to the phytochemical presence and bioavailability of vitamins and minerals, sprouted wheat can provide added nutritional value to baked goods. Dough processing challenges and quality issues exist with the addition of sprouted flour. Currently, little research exists showing how different concentrations of sprouted grains can affect the physical attributes and shelf-stability of pan bread. This study to evaluate the concentration effect of sprouted whole grain flour on the physical and textural qualities of a sponge-and-dough processed whole wheat pan bread. Texture analysis determined that the addition of 30% (110 g) and 50% (87 g) sprouted flour created a softer crumb than the control (120 g). In summary, moderate additions of whole grain sprouted flour to pan bread can lengthen shelf-life and increase loaf volume thereby improving consumer satisfaction ¹⁰.

The use of partially sprouted wheat as alternative to conventional flour improvers (e.g. xylanase, malt) has not been thoroughly investigated. In order to investigate the effects of sprouted wheat as flour improver, scientists at the ACCC (formerly known as American Association of Cereal Chemists) added Xylanase and malt to the control flour at 0.5% level, as conventionally used in bakeries, whereas sprouted wheat flour was used up to 2%. Adding xylanase, malt or sprouted wheat to control flour significantly decreased dough stiffness, though best performances were observed in the presence of 1.5% sprouted wheat ¹¹. Unlikely the mixtures containing xylanase or malt, the sprouted wheat blend showed gluten aggregation strength similar to that of the control, suggesting no worsening of the protein network characteristics. As for the leavening properties, dough development was increased from 52.8 mm to 70.4 mm, thanks to the enrichment with sprouted flour. In addition, presence of sprouted wheat improved the amount of gas production during leavening, resulting in dough with increased volume. As for the pasting properties, in the presence of sprouted wheat lower setback values were observed, thus indicating a lower starch retrogradation tendency, as demonstrated by analyzing the crumb texture after three days of storage. In conclusion, addition of 1.5% sprouted wheat may represent a valid alternative to xylanase or malt for improving the rheological properties and bread making performance of stiff flours ¹¹.

According to the Whole Grains Council – there is at this time no regulated definition of “sprouted grain”¹².

The AACC International and one of the world’s leading authorities on grains, defines sprouted grains as “malted or sprouted grains containing all of the original bran, germ, and endosperm shall be considered whole grains as long as sprout growth does not exceed kernel length and nutrient values have not diminished. These grains should be labeled as malted or sprouted whole grain” ¹³. And the AACC Internation definition has subsequently been endorsed by USDA.

Figure 1. Sprouted Grain

Is ezekiel bread gluten free ?

No. Ezekiel bread is made from wheat and wheat contains gluten.

Gluten is a protein naturally found in some grains including wheat, barley, rye, and spelt. It acts like a binder, holding food together and adding a “stretchy” quality—think of a pizza maker tossing and stretching out a ball of dough. Without gluten, the dough would rip easily ¹⁴.

Other grains that contain gluten are wheat berries, durum, emmer, semolina, farina, farro, graham, khorasan wheat, einkorn, and triticale (a blend of wheat and rye). Oats—though naturally gluten free—often contain gluten from cross-contamination, as they are processed in the same facilities as the grains listed above. Gluten is also sold as wheat gluten, or seitan, a popular vegan high-protein food. Less obvious sources of gluten include monosodium glutamate (MSG), soy sauce, lecithin, modified food starch, and occasionally medications and vitamins (from cross-contamination or the use of wheat starch as fillers or in the coatings).

Ezekiel Bread Nutrition and Ezekiel Bread Ingredients

The 2015-2020 Dietary Guidelines for Americans recommends eating 6 ounces of grain foods daily (based on a 2000-calorie diet) and getting at least half or 3 ounces of that grain intake from 100% whole grains ¹⁵.

An easy way to tell if a food product is high in 100% whole grains is to make sure it is listed first or second in the ingredient list. Or better yet, choose unprocessed whole grains:

Table 1. Whole Grains

Amaranth	Kamut	Spelt
Barley	Millet	Teff
Brown Rice	Quinoa	Triticale
Buckwheat	Rye	Wheat Berries
Bulgur	Oats	Wild Rice
Corn	Sorghum

Be careful when choosing foods labeled as whole grains: “Whole grain” doesn’t always mean healthy.

Figure 2. Ezekiel Bread – Sprouted Grain Ingredients and Nutritional Value (Carbs, Calories, Protein and Dietary Fiber)

[Source: Food for Life Baking Company Inc. Ezekiel Bread. ¹⁶]

Figure 3. Ezekiel Bread – Low Sodium Sprouted Grain Ingredients and Nutritional Value

[Source: Food for Life Baking Company Inc. Ezekiel Bread. ¹⁶]

Figure 4. Ezekiel Bread – Sesame Sprouted Grain Ingredients and Nutritional Value

[Source: Food for Life Baking Company Inc. Ezekiel Bread. ¹⁶]

Figure 5. Ezekiel Bread – Cinnamon Raisin Sprouted Grain Ingredients and Nutritional Value

[Source: Food for Life Baking Company Inc. Ezekiel Bread. ¹⁶]

Table 2. Ezekiel Bread – Sprouted Grain Bread Nutritional Value from the United States Department of Agriculture, USDA Food Composition Databases.

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ¹⁷]

Table 3. Basic Whole Grain Bread Nutritional Value from the United States Department of Agriculture, USDA Food Composition Databases.

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ¹⁷]

Health Benefits of Sprouted Whole Grains

Sprouting grains increases many of the grains’ key nutrients, including B vitamins, vitamin C, folate, fiber, and essential amino acids often lacking in grains, such as lysine. Sprouted grains may also be less allergenic to those with grain protein sensitivities ¹⁸.

In a 1989 meta-analysis of existing studies, JK Chavan and SS Kadam found evidence that sprouting of grains for a limited period causes increased activities of hydrolytic enzymes, improvement in the contents of certain essential amino acids, total sugars and B-group vitamins, and a decrease in dry matter, starch, and antinutrients. The digestibilities of storage proteins and starch are improved due to their partial hydrolysis during sprouting. The digestibilities of storage proteins and starch are improved due to their partial hydrolysis during sprouting. The magnitude of the nutritional improvement is, however, influenced by the type of cereal, seed quality, sprouting conditions, and it is not large enough to account for in feeding experiments with higher animals ⁹.

The pace of research is quickening, with studies documenting a wide range of health benefits for different sprouted grains. Here are just a few:

• Sprouted brown rice fights diabetes.
• Sprouted buckwheat protects against fatty liver disease.
• Cardiovascular risk reduced by sprouted brown rice.
• Sprouted brown rice decreases depression and fatigue in nursing mothers.
• Decreased blood pressure linked to sprouted barley.

• Sprouting Increases Antioxidant Activity in Millet

Research shows that millet, a nutritious staple crop in many developing countries, can be made even more nutritious when the grains are sprouted. In a study in India, scientists measured the phenolic composition, antioxidant activity, and inhibitory properties against alpha-glucosidase and alpha-amylase (a mechanism that helps prevent spikes in blood sugar) of raw millet, germinated (sprouted) millet, and microwaved and steamed millet. Compositional analysis of phenolics by HPLC revealed that vanillic and ferulic acids were the principal phenolic acids and kaempferol was the predominant flavonoid found in raw millets. Different processing treatments brought about relevant changes in the composition and content of certain phenolic acids and flavonoids in processed millets. The researchers found that germinated millets showed highest phenolic content as well as superior antioxidant and enzyme inhibitory activities. These results suggest that sprouted millet grains are potential source of phenolic antioxidants and also great sources of strong natural inhibitors for α-amylase and α-glucosidase ¹⁹.

• Sprouted Wheat Higher in Nutrients

We all know that whole grains are more nutritious than their refined counterparts (see our other post What is Whole Grain ?). But increasingly, research is showing that sprouted whole grains can offer even greater benefits. In a recent study, Vietnamese researchers sprouted wheat for 48 hours, and found it was higher in dietary fiber, free amino acids and antioxidant activity than unsprouted wheat. Germinated waxy wheat had a better nutritional composition, such as higher dietary fibre, free amino acid and total phenolic compound contents, than ungerminated waxy wheat. Therefore germinated waxy wheat should be used to improve the nutritional quality of cereal-based products ²⁰.

• Sprouting (Malting) Millet Makes Some Minerals More Bioavailable

In India and some other countries, sprouted (malted) grains are commonly used as weaning foods for infants and as easily-digested foods for the elderly and infirm. A study at the Central Food Technological Research Institute in Mysore, India, measured the changes caused by malting finger millet, wheat and barley ²¹. Malted grains are extensively used in weaning infants and geriatric foods. Malting generally improves the nutrient content and digestibility of foods. The present investigation examined the influence of malting of finger millet, wheat, and barley on the bioaccessibility of iron, zinc, calcium, copper, and manganese. Malting increased the bioaccessibility of iron by >3-fold from the two varieties of finger millet and by >2-fold from wheat, whereas such a beneficial influence was not seen in barley. The bioaccessibility of zinc from wheat and barley increased to an extent of 234 and 100%, respectively, as a result of malting. However, malting reduced the bioaccessibility of zinc from finger millet. Malting marginally increased the bioaccessibility of calcium from white finger millet and wheat. Whereas malting did not exert any influence on bioaccessibility of copper from finger millet and wheat, it significantly decreased (75%) the same from barley. Malting did increase the bioaccessibility of manganese from brown finger millet (17%) and wheat (42%). Thus, malting could be an appropriate food-based strategy to derive iron and other minerals maximally from food grains ²¹.

• Nutrient Changes Noted in Sprouted Wheat

German researchers sprouted wheat kernels for up to 168 hours (1 week) at 15, 20, 25, or 30 °C, analyzing them at different stages to learn the effects of sprouting on different nutrient levels. While different times and temperatures produced different effects, overall the sprouting process decreased gluten proteins substantially, while increasing folate. A maximum 3.6-fold concentration was obtained after 102 hours of sprouting at 20 °C and 25 °C including 5-methyltetrafolate as the major vitamer. The concentration of dietary fiber remained constant or decreased during the first 96 hours of germination. Prolonged sprouting times of up to 168 hours led to a substantial increase of total dietary fiber and to a strong increase of the soluble dietary fiber by a factor of 3, whereas the insoluble fiber decreased by 50% ²².

• Sprouted Millet is Higher in Key Nutrients

Researchers in India allowed proso millet (a minor millet) to germinate for 1-7 days, then analysed the changes in its composition of protein fractions, free amino acids, lysine, tryptophan, methionine, non-protein nitrogen, starch, and sugars ²³. They found that overnight soaking and germination up to 7 days significantly increased the free amino acids and total sugars while the content of dry weight and starch decreased. Increases in albumin and globulin and large decreases in prolamin accompanied sprouting. The percent protein in germinated grains was higher than in the initial grain as a result of dry matter loss during germination. Further, there was an increase in lysine, tryptophan and non-protein nitrogen contents during germination. No change was noticed in methionine ²³.

• Digestibility Changes in Sprouted Barley

In an experiment at the University of Alberta, barley and canola seeds were sprouted over a 5 day period, in laboratory conditions under room temperature (22 degrees C) and room lighting. Following initial hydration, seeds were kept moist by wetting the germination trays at 9 a.m., 1 p.m. and 6 p.m. daily. A parallel germination experiment using 200 g quantities of seeds in petri dishes was conducted. Starting from the second day of germination, and every day, dishes of germinating seeds were removed, oven-dried, weighed and milled for proximate and chemical analysis. Seeds from the main germination experiment were fed in a digestibility trial to Wistar rats. Results indicated that sprouting was associated with depletion of many nutrients in both barley and canola, the major losses being in respect of dry matter, gross energy and triglycerides ²⁴. In barley (but not in canola) sprouting was associated with significant increases in crude fiber and diglyceride content. In canola, there were significant losses in lipid content and increases in phytosterol and phospholipid content. Digestibility data showed an enhancement in digestibility of nutrients in barley but not in canola, implying that sprouting improved nutritional quality of barley but not canola ²⁴.

Is Ezekiel Bread Healthy

According to the AACC (formerly known as American Association of Cereal Chemists) International, sprouted grains can be considered as an improved version of whole grains with better taste and health-enhancing properties. However, nutritional and therapeutic properties of sprouted grains still remain unclear, particularly when assessing optimum seed-modification and consensus on method-development to make such assessment. Discussions on sprouted grains in terms of nutrient bioavailability, safety and regulatory, and their role in human health and disease prevention together with the associated transparency have never been needed more than in today’s competitive and health-driven food market and health-conscious consumers ²⁵.

Is Ezekiel bread good for you ?

Ezekiel bread is just a bread like any whole grain breads that are out there. There is no scientific evidence showing that eating Ezekiel bread is good for you and there is nothing good from eating Ezekiel bread than eating your basic wholegrain bread due to similar nutritional contents (calories, carbs, fiber) between the bread. Furthermore, most breads sold today (white plain bread, whole grain bread) have also been fortified with vitamins like Thiamin and Folate. Lastly if you have Celiac disease or suffer from wheat or gluten sensitivity, you must avoid eating anything that contain gluten including Ezekiel bread.

• The healthiest sources of carbohydrates—unprocessed or minimally processed whole grains, vegetables, fruits and beans—promote good health by delivering vitamins, minerals, fiber, and a host of important phytonutrients.
• Unhealthier sources of carbohydrates include white bread, pastries, sodas, and other highly processed or refined foods. These items contain easily digested carbohydrates that may contribute to weight gain, interfere with weight loss, and promote diabetes and heart disease.

A growing body of research shows that choosing whole grains and other less-processed, higher-quality sources of carbohydrates, and cutting back on refined grains, improves health in many ways. The 2015-2020 Dietary Guidelines for Americans recommends eating 6 ounces of grain foods daily (based on a 2000-calorie diet) and getting at least half or 3 ounces of that grain intake from 100% whole grains ¹⁵. Consumers should steer towards whole grain foods that are high in fiber and that have few ingredients in addition to whole grain. Moreover, eating whole grains in their whole forms—such as brown rice, barley, oats, corn, and rye—are healthy choices because they pack in the nutritional benefits of whole grains without any additional ingredients.

References

1. Food For Life. Ezekiel 4:9. http://www.foodforlife.com/about_us/ezekiel-49
2. Food For Life. Our Products. http://www.foodforlife.com/products
3. Journal of Cereal Science 51 (2010) 374-380. Properties of field-sprouted sorghum and its performance in ethanol production. https://www.ars.usda.gov/ARSUserFiles/30200510/2010%20-%20Properties%20of%20Field-Sprouted%20Sorghum.pdf
4. Bamforth, C.W., 2006. Scientific Principles of Malting and Brewing. American Society of Brewing Chemists, St. Paul, MN. pp. 21-58.
5. Klose, C., Schehl, B.D., Arendt, E.K., 2009. Fundamental study on protein changes taking place during malting of oats. Journal of Cereal Science 49, 83-91.
6. Dicko, M.H., Gruppen, H., Coucouho, O.C., Traoré, A.S., Van Berkel, W.J.H., Voragen, A.G.J., 2006. Effects of germination on the activities of amylases and phenolic enzymes in sorghum varieties grouped according to food end-use properties. Journal of the Science of Food and Agriculture 86, 953-963.
7. Yan, S., Wu, X., MacRitchie, F., Wang, D., 2009. Germination-improved ethanol fermentation performance of high-tannin sorghum in the laboratory dry grind process. Cereal Chemistry 86, 597-600.
8. Correia, I., Nunes, A., Barros, A.S., Delgadillo, I., 2008. Protein profile and malt activity during sorghum germination. Journal of the Science of Food and Agriculture 88, 2598-2605.
9. Chavan JK, Kadam SS. Crit Rev Food Sci Nutr. 1989;28(5):401-37. Nutritional improvement of cereals by sprouting. http://www.tandfonline.com/doi/abs/10.1080/10408398909527508
10. AACC International. Poster Presentation:Alternative Ingredients for Grain-Based Foods. http://www.aaccnet.org/meetings/Documents/2015Abstracts/aacci2015abs182.htm
11. AACC International. Technical: Researching Health Benefits of Grain and Components: Part 2. http://www.aaccnet.org/meetings/Documents/2016Abstracts/aacc2016abs262.htm
12. Whole Grains Council. Definitions of Sprouted Grains. https://wholegrainscouncil.org/whole-grains-101/whats-whole-grain/sprouted-whole-grains/definitions-sprouted-grains
13. AACC International. http://www.aaccnet.org
14. Harvard University, Harvard School of Public Health. Gluten: A Benefit or Harm to the Body ? https://www.hsph.harvard.edu/nutritionsource/gluten/
15. U.S. Department of Health and Human Services. 2015–2020 Dietary Guidelines for Americans. https://health.gov/dietaryguidelines
16. Food for Life Baking Company Inc. http://www.foodforlife.com/sites/default/files/sellsheet/ss-ezekiel-bread.pdf
17. United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. https://ndb.nal.usda.gov/ndb/
18. Whole Grains Council. Sprouted Whole Grains. https://wholegrainscouncil.org/whole-grains-101/whats-whole-grain-refined-grain/sprouted-whole-grains
19. Pradeep PM, Sreerama YN. Food Chem. 2015 Feb 15;169:455-63. doi: 10.1016/j.foodchem.2014.08.010. Epub 2014 Aug 13. Impact of processing on the phenolic profiles of small millets: evaluation of their antioxidant and enzyme inhibitory properties associated with hyperglycemia. http://www.sciencedirect.com/science/article/pii/S0308814614012254
20. Hung, P. V., Maeda, T., Yamamoto, S. and Morita, N. (2012), Effects of germination on nutritional composition of waxy wheat. J. Sci. Food Agric., 92: 667–672. doi:10.1002/jsfa.4628. http://onlinelibrary.wiley.com/doi/10.1002/jsfa.4628/abstract;jsessionid=B05A6D7B3BA60EDE606B674E232101D8.f03t04
21. Platel K, Eipeson SW, Srinivasan K. J Agric Food Chem. 2010 Jul 14;58(13):8100-3. doi: 10.1021/jf100846e. Bioaccessible mineral content of malted finger millet (Eleusine coracana), wheat (Triticum aestivum), and barley (Hordeum vulgare). https://www.ncbi.nlm.nih.gov/pubmed/20560601
22. Koehler P, Hartmann G, Wieser H, Rychlik M. J Agric Food Chem. 2007 Jun 13;55(12):4678-83. Epub 2007 May 12. Changes of folates, dietary fiber, and proteins in wheat as affected by germination. http://pubs.acs.org/doi/abs/10.1021/jf0633037
23. Parameswaran KP, Sadasivam S. Plant Foods Hum Nutr. 1994 Feb;45(2):97-102. Changes in the carbohydrates and nitrogenous components during germination of proso millet, Panicum miliaceum. https://www.ncbi.nlm.nih.gov/pubmed/8153070
24. Chung TY, Nwokolo EN, Sim JS. Plant Foods Hum Nutr. 1989 Sep;39(3):267-78. Compositional and digestibility changes in sprouted barley and canola seeds. https://www.ncbi.nlm.nih.gov/pubmed/2608636
25. AACC International. Symposium: Sprouted Grains: What is in it for Consumers ? http://www.aaccnet.org/meetings/Documents/2016Abstracts/aacc2016abs282.htm

What is Farro ?

Farro (Triticum turgidum L. group dicoccum) is also known as Emmer, an ancient strain of wheat, one of the first cereals ever domesticated in Western Asia and farro served as the standard daily ration of the Roman army in the Ancient Rome. It was widely cultivated in the ancient world, but over the centuries, farro (emmer) was gradually abandoned in favor of durum wheat, which is easier to hull ¹ and is now a relict crop in mountainous regions of Europe and Asia ².

Though farro has often been referred to as if it were one grain, it’s actually three. There’s farro piccolo (einkorn), farro medio (emmer), and farro grande (spelt). Emmer is what you’ll find sold most often in the U.S. It’s a harder grain than einkorn and is often confused with spelt, which is another type of grain altogether. Then there are farro’s Latin labels: einkorn, which is Triticum monococcum; emmer, which is Triticum dicoccum; and spelt, which is Triticum spelta. Emmer is by far the most common variety grown in Italy and it is also considered higher quality for cooking than the other two grains, and is sometimes called “true” farro. Farro is also sometimes defined as spelt (dinkel in German), specifically distinguished from both emmer and einkorn.

There’s also the question of whether you should choose whole farro, which retains all the grain’s nutrients; semipearled, in which the part of the bran has been removed but still contains some fiber; or pearled, which takes the least time to cook but has no bran at all.

In Italy and increasingly throughout the world – farro is known as emmer or grano farro or farro medio (“medium farro”) and is staging a comeback as a niche based gourmet specialty. Semolina flour made from farro is still used today for special soups and other dishes in Tuscany and Umbria, and farro is thought by some aficionados to make the best pasta.

Today, emmer bread is available in Switzerland and in Italy, emmer bread (pane di farro) can be found in bakeries in some areas. Higher in fiber than common wheat, emmer’s use is for making pasta. Emmer has also been used in beer production and an example is the Riedenburger eco-brewery in Bavaria, Germany which currently makes Emmerbier.

By the beginning of the 20th century, higher-yielding wheat strains had replaced emmer almost everywhere, except in Ethiopia, where emmer still constitutes about 7% of the wheat grown.

In terms of health benefits of farro (emmer), currently there is very little research on farro and human health. Farro is an excellent source for complex carbohydrates. Additionally, farro is high in fiber, antioxidants and protein than modern wheat. Different than some other whole grains, a carbohydrate in farro called cyanogenic glucosides has been found to stimulate the immune system, lower cholesterol and help maintain blood sugar levels.

In Ankara, Turkey, scientists at Hacettepe University’s Department of Food Engineering compared 18 ancients wheats (12 emmer, 6 einkorn) with 2 modern bread wheats, to assess their total phenolics and flavonoids, phenolic acids, lutein, total yellow pigment, and total radical scavenging capacities. Results showed “remarkably higher total antioxidant activity” in emmer varieties, and “quite high levels of lutein” in the einkorn samples. In conclusion, the findings were considered to be key to “breeding wheat varieties for higher concentration and better composition of health-beneficial phytochemicals” ³.

Is Farro Gluten Free ?

No. Farro is a type of wheat and as wheat, it contains the gluten protein, which is found in the grains wheat, barley and rye, and is most definitely not gluten-free. So if you have Celiac disease or gluten sensitivity, you need to choose other non-gluten whole grains like rice, sorghum, quinoa millet and corn. See our other post on “What is gluten free diet ?”

Table 1. Farro Nutrition Facts

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ⁴]

Table 2. Wheat Flour (Whole Grain) Nutrition Facts

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ⁴]

Nutrition credentials of whole grain wheat:

• Low in fat, most of which is unsaturated.
• High in carbohydrate (mainly starch) and high in insoluble dietary fibre.
• Relatively high in protein (11-13%) compared with other major grains and contains a protein complex which forms gluten.
• High in potassium and low in sodium.
• The endosperm contains glucofructan (similar in structure to inulin) which functions as a prebiotic agent and has similar properties to dietary fibre.
• Contains B-group vitamins such as thiamin, riboflavin, niacin, vitamin B6 (pyridoxine), folate and pantothenic acid.
• Contains vitamin E.
• Contains iron, zinc, magnesium, phosphorus and selenium (depending on the soil content of selenium).
• Contains small amounts of copper, manganese and calcium.
• Contains phytochemicals including lignans, phenolic acids, phytic acid, plant sterols and saponins.

Health Benefits of Wheat

Worldwide, wheat is the third most-produced grain, trailing only corn (maize) and rice. In the United States, wheat accounts for about two-thirds of all grains consumed. However, much of the wheat you eat is refined (missing its nutritious bran and germ) or enriched (refined grain with just five of the dozens of missing or reduced nutrients added back in) ⁵.

Since wheat is by far the most common grain used in breads, pastas and other grain foods eaten in the United States, most U.S. studies of “whole grains” in the aggregate can be considered to attest to the benefits of whole wheat in its common form. These benefits are well established, and include, among others:

• stroke risk reduced 30-36%
• type 2 diabetes risk reduced 21-30%
• heart disease risk reduced 25-28%
• better weight maintenance
• reduced risk of asthma
• healthier blood pressure levels
• reduction of inflammatory disease risk

How To Cook Farro / Wheat

Farro is prepared like brown rice and cooks in 50-60 minutes (or can be soaked overnight to reduce the cooking time). It makes a fabulous pilaf, grain salad, risotto, addition to soup, or sprouted for breads and salads. When cooked, its dark, plump berries add sweet, full-bodied flavor, chewy texture and high nutritional value (over 16% protein) to every meal. It is a lovely, versatile grain that is a staple in our household. When mixed with lentils or chickpeas it makes a complete protein.

Whole wheat is cook at home in four main ways: as flour in baked goods; as wheat berries for side dishes and in casseroles; as bulgur; and as pasta or couscous.

• Flour. Whole wheat flour behaves a bit differently in recipes than refined all-purpose flour. As a rule of thumb, you can generally substitute whole wheat flour for up to half the all-purpose flour in a recipe. To make foods using more whole wheat, we recommend you start with recipes specifically designed to be their most delicious with whole wheat.

In general, whole white wheat flour is milder in flavor and smoother in texture than “regular” whole wheat flour. There are also special flours available that combine whole white wheat flour and all-purpose flour in the same bag, to make it even easier to transition your taste buds over to whole grains.

• Wheat Berries. Whole wheat kernels are usually described as “wheat berries.” You cook them in water or broth (about 2 ½ cups liquid for each cup of wheat berries) for about 45-60 minutes. As always when cooking grains, taste a few as cooking progresses. When the grains are soft enough for you, they’re done. You can add more liquid and cook longer, or drain extra liquid off if the grains are done to your taste before all the liquid is absorbed.

• Bulgur. Bulgur is wheat that’s been pre-cooked and broken into pieces, so you can quickly “finish it off” in your kitchen. Generally, you can simply add boiling water or broth to bulgur (about 1 ¾ to 2 cups liquid per cup of bulgur) and let it soak for about 20-25 minutes in a covered pot.

• Pasta and couscous: Couscous is not a grain (there is no couscous plant) – it’s more like a small grain-shaped pasta. Whole wheat couscous is so small it can usually be “cooked” simply by soaking in boiling water, while pasta takes about 8 minutes to cook.

Main culinary uses of wheat:

Wheat is typically milled into flour which is then used to make a wide range of foods including bread, crumpets, muffins, noodles, pasta, biscuits, cakes, pastries, cereal bars, sweet and savoury snack foods, crackers, crisp-breads, sauces and confectionery (e.g. liquorice).

Other culinary applications of wheat include:

• Flaked, puffed and extruded wheat – All three forms are commonly used to manufacture breakfast cereals and cereal snack bars.
• Wheat bran – Added to biscuits, cakes, muffins and breads to increase the dietary fibre content. Wheat bran is also used in the manufacture of some breakfast cereals.
• Wheat germ – Can be added to breads, pastries, cakes and biscuits or sprinkled onto yoghurt, breakfast cereal or fruit dishes.
• Semolina – Mainly used for making pasta. The preferred variety of wheat for pasta is Triticum durum. It can also be cooked in milk to make semolina pudding or fried golden brown and then mixed with plenty of sugar to make Halva, as eaten in the Middle East. In Greece, semolina is used in baked cakes.
• Couscous – Used widely in North Africa, couscous is made from semolina grains which are sprinkled with slightly salted water and rubbed to make tiny pellets which are steamed and then dried. Instant couscous is available in Australia which needs only 5 minutes soaking in hot water.
• Burghul (also known as bulgur or cracked wheat) – Is made by parboiling wheat, drying it and then coarsely grinding it. It can be steamed or boiled and used in a wide range of dishes, such as tabouleh, kofta or kibbeh.
• Kibbled wheat – Grains are cracked or broken into smaller particles and then moistened or steamed and dried. Kibbled wheat is used as an ingredient in mixed grain bread or cooked as a side dish.
• Boiled wheat – Puddings are made from boiled wheat in Lebanon and the Balkans.
• Wheat starch – Used as ‘cornflour’ or converted to glucose, dextrose and other sugars for use in confectionery and other manufactured foods.

References

1. Whole Grains Council. Whole Grains A to Z. https://wholegrainscouncil.org/whole-grains-101/whole-grains-z
2. Cooper R. Re-discovering ancient wheat varieties as functional foods. Journal of Traditional and Complementary Medicine. 2015;5(3):138-143. doi:10.1016/j.jtcme.2015.02.004. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4488568/
3. Serpen A, Gökmen V, Karagöz A, Köksel H. J Agric Food Chem. 2008 Aug 27;56(16):7285-92. doi: 10.1021/jf8010855. Epub 2008 Jul 2. Phytochemical quantification and total antioxidant capacities of emmer (Triticum dicoccon Schrank) and einkorn (Triticum monococcum L.) wheat landraces. http://pubs.acs.org/doi/abs/10.1021/jf8010855
4. United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. https://ndb.nal.usda.gov/ndb/
5. Whole Grains Council. Wheat July Grain of the Month. https://wholegrainscouncil.org/whole-grains-101/easy-ways-enjoy-whole-grains/grain-month-calendar/wheat-july-grain-month

What is Buckwheat ?

Common buckwheat (Fagopyrum esculentum) is a pseudo-cereal crop that produces short, wide-spreading plants bearing bright green, heart-shaped leaves and small white flowers ¹.

Buckwheat technically speaking is not classified as a ‘true’ grain, but rather a ‘pseudo-cereal’. However due to its nutritional profile, nutty flavour, appearance and culinary applications have led it to be commonly referred to as a grain ². It is neither a grain or a relative of wheat, but rather, its seeds so closely resemble the much larger seeds of the beech tree that the plant has been called “beech wheat,” or buckwheat, ever since ². Buckwheat has played an important role in diets around the world, mainly in Asia and Eastern Europe for around 8,000 years.

As a grain, buckwheat more than makes up for its less-than-striking appearance as a plant. Buckwheat groats are shaped almost like a pyramid, or a triangle with a rounded bottom and gently tapered sides. This unusual seed shape is actually how buckwheat got its common name ¹.

Buckwheat has a gene that lets it make red or green immature fruit, but the hull of common buckwheat becomes dark brown or almost black as the seeds reach maturity and are ready to harvest ¹.

As a short-season crop that performs well in acidic and under-fertilized soil, buckwheat can perform as a “smother” crop, used to keep weeds at bay, and to keep soil erosion to a minimum while fields “rest” during crop rotation ¹. It performs best when sown in June, and because it blooms for quite a while (even into September), its nectar provides for late-season honey that can be dark amber in color and rich in flavor. Once the flowers have yielded buckwheat groats and it’s time to harvest, the plant stalks can be dried further and used as straw for livestock, or the entire plants can be tilled under to help next year’s soil retain more moisture ¹.

Tartary Buckwheat

Another type of buckwheat is Tartary buckwheat (Fagopyrum tataricum) also known as duckwheat, India buckwheat, India wheat, green buckwheat, ku qiao or bitter buckwheat. Tartary buckwheat was domesticated in east Asia, and is also cultivated in Europe and North America. While it is an unfamiliar food in the West, it is common in the Himalayan region today, as well as other regions in Southwest China such as Guizhou province.

Tartary buckwheat (Fagopyrum tataricum) contains approximately 100-fold higher amounts of rutin in its seeds compared to common buckwheat ³, ⁴. Tartary buckwheat contains a range of nutrients including bioactive carbohydrates and proteins, polyphenols, phytosterols, vitamins, carotenoids, and minerals. Compared with the more widely cultivated and utilised cousin the common buckwheat (F. esculentum), tartary buckwheat tends to contain higher amounts of certain bioactive components such as rutin, which contributes to tartary buckwheat’s various health benefits such as anti-oxidative, anti-cancer, anti-hypertension, anti-diabetic, cholesterol-lowering, and cognition-improving ⁵.

Rutin is a flavonoid of the flavonol type, which is commonly found in plants ⁶. Rutin shows antioxidant effects via scavenging of radiation-induced free radicals ⁷. In addition, it has several pharmacological functions such as anti-inflammatory, anti-diabetic, and blood capillary strengthening properties ⁸. Kamalakkannan and Prince ⁹ reported that oral administration of rutin decreased blood glucose levels and increased insulin secretion in streptozotocin-induced diabetic rats. Other reports suggested that oral administration of rutin significantly decreased the levels of lipids in plasma and tissues in streptozotocin-induced diabetic rats ¹⁰. In addition, rutin has cardioprotective effects ¹¹, which are related to its ability to inhibit platelet aggregation ¹². Although it has been reported that rutin has several pharmacological effects, its exact mechanism and metabolism were not fully elucidated.

Is Buckwheat Gluten Free ?

Yes. Buckwheat is a naturally gluten-free whole grain ¹, ¹³.

Buckwheat Nutrition Value

Buckwheat provides a very high level of protein, second highest only to oats. Not only is buckwheat protein well-balanced and rich in lysine, its amino acid score is 100, which is one of the highest amino acid scores among plant sources as well ¹. It’s important to note there is some evidence that buckwheat protein digestibility in humans can be somewhat low ¹. While this makes it a less than ideal source of protein for growing children or anyone with digestive tract issues, it’s perfectly fine for the grown-ups of the world. Besides, humans are meant to have a varied, omnivorous diet, so it’s good to obtain protein from a variety of sources.

Nutrition values of buckwheat:

• Gluten free.
• Buckwheat contains higher levels of zinc, copper, potassium, manganese and magnesium than other cereal grains, and the bioavailability of zinc, copper, and potassium from buckwheat is also quite high.
• High in protein (13-15%), second highest only to oats, and rich in the amino acid lysine.
• Rich in carbohydrates (mainly starch).
• Rich in polyunsaturated essential fatty acids, such as linoleic acid.
• Contains vitamins B1, C and E.
• High in soluble fibre.
• Provides a potential source of resistant starch, as certain treatments of buckwheat starch or foods containing buckwheat increase the amount of retrograded, non-digestible starch.
• A rich source of polyphenol compounds.
• Contains rutin, a bioflavonoid thought to help control blood pressure and possess anti-inflammatory and anti-carcinogenic properties.

Table 1. Buckwheat Nutrition Content

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ¹⁴]

Table 2. Buckwheat Groats (Roasted Dry) Nutrition Content

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ¹⁴]

Table 3. Buckwheat Flour Nutrition Content

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ¹⁴]

Buckwheat Health Benefits

Buckwheat play two important roles for most adults:

• It’s high in soluble fiber, helping to slow down the rate of glucose absorption. This can be especially important in people with diabetes and anyone else trying to maintain balanced blood sugar levels. One Slovenian study in 2001 showed boiled buckwheat groats or bread made with at least 50% buckwheat flour induce much lower postprandial (after-meal) blood glucose and insulin responses than white wheat bread.

• It’s a potential source of resistant starch, a type of starch that escapes digestion in the small intestine. Resistant starch is often considered the third type of dietary fiber because it possesses some of the benefits of insoluble fiber and some of the benefits of soluble fiber. While most of the starch in buckwheat is readily digestible, the small portion that is resistant (about 4-7%) can be highly advantageous to overall colon health.

Buckwheat potassium helps your body to maintain the water and acid balance in blood and tissue cells, whilst its zinc helps to bolster your immune system. The copper in buckwheat may help prevent copper deficiency that can lead to a number of neurodegenerative diseases and disorders. Having buckwheat in your diet can help you stay fit, nimble, and healthy.

Buckwheat is also a good source of antioxidants, biologically high-valued amino acids ¹⁵, ¹⁶, dietary fiber ¹⁷, and minerals such as zinc, copper and manganese ¹⁸.

 

In Shanxi province, China, both common (Fagopyrum esculentum) and tartary (Fagopyrum tataricum) buckwheats are used to improve the health of patients with diabetes and cardiovascular diseases ¹⁹. A previous experimental buckwheat study concluded that intake of common buckwheat leaf tea could prevent further development of leg edema ²⁰, and a study by He et al. ²¹ showed a cholesterol-lowering effect of buckwheat. However, there are very few studies on the health effects of buckwheat, especially buckwheat products in humans.

• Eating Tartary Buckwheat may reduce body weight (cause weight loss)
  

In this study involving 149 subjects (42 males and 107 females aged 30–69 years) who had their body weight, body mass index (BMI), and body fat percentage  measured, at weeks 0 (baseline), 4, 8, and 12 after the start of rutin ingestion, and 3 weeks after the end of rutin ingestion ²². The active test foods were: rutin-rich tartary buckwheat food contains ‘Manten-Kirari’ buckwheat flour 50%, wheat flour 47%, wheat albumin 3% and the placebo food (wheat flour 97% and wheat albumin 3%). The results of that study showed subjects who were eating rutin-rich tartary buckwheat have significantly lower body weight and BMI than those in the placebo group at week 8. The body fat percentage in the subjects who were eating rutin-rich tartary buckwheat group at week 4 was lower than that in the placebo group. The researchers concluded that consuming rutin-rich Tartary buckwheat may be effective for body weight due to its antioxidant properties ²².

• Eating Buckwheat Products Produces Lower GI Response

In a joint effort to determine the characteristics of buckwheat starch and its potential for a reduced metabolic response after meals, researchers from Slovenia and Sweden scored human test subject’s responses to an assortment of buckwheat products, including boiled buckwheat groats, breads baked with 30-70% buckwheat flour, and bread baked from buckwheat groats. The highest level of resistant starch was found in the boiled buckwheat groats, while the resistant starch levels in the buckwheat breads were significantly lower, depending on whether flour or grouts had been used. The conclusion: All buckwheat products scored significantly lower on the after-meal blood glucose tests, while also scoring higher in satiety, than the control group’s white wheat bread ²³.

• Buckwheat Enhanced Gluten-free Bread a Healthier Gluten-free Alternative

Researches from the Polish Academy of Sciences recently published a study suggesting substituting some or all of the corn starch in many traditional gluten-free bread recipes with buckwheat flour. In addition to providing higher levels of antioxidants, B vitamins, magnesium, phosphorus and potassium, the study indicated that swapping 40% of the corn starch for buckwheat flour also increased its “overall sensory quality” when compared to the gluten-free bread used in the control. Although recipes were tested with anywhere from 10-40% buckwheat flour, the conclusion clearly points to the 40% buckwheat flour results as having the most nutritional benefits for Celiac sufferers ²⁴.

• Buckwheat Starch is A Good Energy Source

In a study found via the China National Knowledge Infrastructure, researchers at the Graduate University of the Chinese Academy of Sciences explored the digestibility of starch derived from oats, wheat, buckwheat, and sweet potatoes. The goal of this study was to determine which of the four starch sources might prove useful in high-energy diets. Pigs were fed diets containing vitamins, minerals, and starch from one of the four sources, and after 15 days, it was determined that buckwheat, along with oats and wheat, provided a better source of dietary energy than sweet potatoes ²⁵.

• Buckwheat Protein Shows Promise For Lowering Blood Glucose

A study from the Jilin Agricultural University in China investigated the blood glucose lowering potential of buckwheat protein, pitting it against a toxic glucose analogue called alloxan. This insidious chemical selectively destroys insulin-producing cells in the pancreas, causing characteristics similar to type 1 diabetes when found in rodents and many other animal species. Different doses of buckwheat protein were administered, and researchers discovered that the blood glucose levels of test subjects were indeed lowered when compared to the control group ²⁶.

• Germinated Buckwheat Extract Decreases Blood Pressure

A team of Korean researchers extracted the bioflavonoid rutin, thought to have blood-pressure lowering properties, from both raw buckwheat and germinated buckwheat. The team then studied the effects of both extracts on body weight and systolic blood pressure in rats. They also searched for any indication of the formation of peroxynitrite, an oxidant and nitrating agent that can damage a wide array of molecules in cells, including DNA and proteins. After five weeks, the systolic blood pressure of the rats treated with germinated buckwheat was lower than the group treated with raw buckwheat, but both groups showed significantly reduced oxidative damage in aortic cells when compared to the control group ²⁷.

• Buckwheat Provides Prebiotic-like Benefits And Can Be Considered a Healthy Food

In 2003, a study out of Madrid, Spain examined the high nutrient levels in buckwheat to determine whether it could behave as a prebiotic and be considered a healthy food. Prebiotics, of course, are indigestible food ingredients that stimulate the helpful bacteria in our digestive systems. Not only did the buckwheat-fed group emerge with a lower bodyweight when compared to the control, some of the best types of helpful bacteria were found, along with a decrease in some types of pathogenic bacteria ²⁸.

• Buckwheat Protein may have Cholesterol lowering activity
  

In a small animal experiment, 45 male hamsters were divided into five groups fed either the control diet or one of the four experimental diets containing 24% Tartary buckwheat protein, 24% rice protein, 24% wheat protein, or 5 g/kg of cholestyramine (cholestrol lowering medicine), respectively. Tartary buckwheat protein reduced plasma total cholesterol more effectively than cholestyramine (45% versus 37%), while rice and wheat proteins only reduced plasma total cholesterol by 10–13% ²⁹. In another experiment involving lab rats and mice, the consumption of tartary buckwheat protein product and common buckwheat protein product, both of which contain a compound quercetin, showed a mice and rats had reduction in total cholesterol which was associated with enhanced excretion of fecal fats ³⁰. In experiment number 2, the consumption of tartary buckwheat protein product and common buckwheat protein product for 27 day caused 62% and 43% reductions in the lithogenic index (gallstone forming) in mice fed cholesterol, respectively. The reduction in lithogenic index was associated with enhanced excretion of fecal bile acids ³¹. Taken together, these results suggest a potential source of tartary buckwheat protein as a functional food ingredient as well as common buckwheat protein.

In a small human study to find out if eating buckwheat could lower cholesterol, 62 female day-care centre staffs in Japan were fed either common buckwheat cookies or tartary buckwheat cookies for a total of weeks ³². At the end of two weeks, the type of buckwheat cookies were switched, so the group receiving common buckwheat are now eating tartary buckwheat and vice versa. When grouping the two types of buckwheat cookies together, there was a reduction of total serum cholesterol and HDL cholesterol, suggesting intake of buckwheat cookies may lower cholesterol levels ³².

How To Cook Buckwheat

Main culinary uses of buckwheat:

• Buckwheat flour – may be used to make gluten free crepes and pancakes. Up to half the rice, bean, sorghum or soy flour in gluten-free recipes may be used to make muffins, rolls, bread and cookies. Buckwheat flour also works well as a thickener for sauces, soups and casseroles.

• Buckwheat groats – are dehulled buckwheat kernels. The groats are used in many dishes throughout the world. In Asia they are consumed as noodles, dumplings and as unleavened chapattis, whereas in Europe, Kasha (toasted buckwheat groats) is used in dishes ranging from pilafs to mixtures with meat. In the US and Australia, the main use has been in pancakes, although, buckwheat is increasingly being eaten in the form of noodles, various ethnic dishes and gluten free foods.

• Soba noodles – buckwheat flour is mixed with wheat flour to produce Japanese noodles called ‘soba noodles’. The buckwheat flour content ranges from 50% to 80% depending on the type of noodle produced.

For more information on buckwheat recipes you may want to try out the Whole Grains Council recipes section here:

• Kasha and Beet Salad with Celery and Feta ³³,
• Kasha Varnishkes ³⁴,
• Buckwheat Pumpkin Muffins with Molasses-Cinnamon Glaze ³⁵,
• Buckwheat Mushroom Kreplach in Dill Tomato Sauce ³⁶.

Buckwheat Safety

Although eating buckwheat containing products is considered safe, there have been a very small and rarely reported cases of an allergic reaction to buckwheat. In this first reported case, there was an allergic rhinitis and asthma caused by sleeping on pillow filed with buckwheat ³⁷. Another buckwheat allergy cases were reported in the UK, one involving a 57-year-old man presented with anaphylaxis after eating home-baked bread prepared using buckwheat flour bought in France. In the second case, a 63-year-old lady presented with bronchospasm (narrowing of the airways) and urticaria (a round itchy skin rash) after consuming health-food muesli. Sensitisation was confirmed in both cases by positive skin prick testing and specific IgE to buckwheat ³⁸.

References

1. Whole Grains Council. Buckwheat – December Grain of the Month. https://wholegrainscouncil.org/whole-grains-101/easy-ways-enjoy-whole-grains/grain-month-calendar/buckwheat-december-grain-month
2. Grains & Legumes Nutrition Council. Buckwheat. http://www.glnc.org.au/grains-2/types-of-grains/buckwheat/
3. N. Fabjan, J. Rode, I.J. Kosir, Wang Z., Zhang Z., I. Kreft. Tartary buckwheat (Fagopyrum tataricum Gaertn.) as a source of dietary rutin and quercitrin. Journal of Agricultural and Food Chemistry, 51 (22) (2003), pp. 6452-6455. http://pubs.acs.org/doi/abs/10.1021/jf034543e
4. T. Morishita, H. Yamaguchi, K. Degi. The contribution of polyphenols to antioxidative activity in common buckwheat and Tartary buckwheat grain. Plant Production Science, 10 (1) (2007), pp. 99-104.
5. Zhu F. Food Chem. 2016 Jul 15;203:231-45. doi: 10.1016/j.foodchem.2016.02.050. Epub 2016 Feb 9. Chemical composition and health effects of Tartary buckwheat. https://www.ncbi.nlm.nih.gov/pubmed/26948610
6. N.A. Al-Dhabi, M.V. Arasu, C.H. Park, S.U. Park. An up-to-date review of rutin and its biological and pharmacological activities. EXCLI Journal, 14 (2015), pp. 59-63, 10.17179/excli2014-663. http://www.excli.de/vol14/Park_09012015_proof.pdf
7. C. Carrasco-Pozo, M.L. Mizgier, H. Speisky, M. Gotteland. Differential protective effects of quercetin, resveratrol, rutin and epigallocatechin gallate against mitochondrial dysfunction induced by indomethacin in Caco-2 cells. Chemico-Biological Interactions, 195 (3) (2012), pp. 199-205. http://www.sciencedirect.com/science/article/pii/S0009279711003450
8. L.S. Chua. A review on plant-based rutin extraction methods and its pharmacological activities. Journal of Ethnopharmacology, 150 (3) (2013), pp. 805-817. http://www.sciencedirect.com/science/article/pii/S0378874113007435
9. N. Kamalakkannan, P.S. Prince. Antihyperglycaemic and antioxidant effect of rutin, a polyphenolic flavonoid, in streptozotocin-induced diabetic Wistar rats. Basic and Clinical Pharmacology and Toxicology, 98 (1) (2006), pp. 97-103. http://onlinelibrary.wiley.com/doi/10.1111/j.1742-7843.2006.pto_241.x/abstract
10. P. Stanely Mainzen Prince, N.K. Kannan. Protective effect of rutin on lipids, lipoproteins, lipid metabolizing enzymes and glycoproteins in streptozotocin-induced diabetic rats. The Journal of Pharmacy and Pharmacology, 58 (10) (2006), pp. 1373-1383. http://onlinelibrary.wiley.com/doi/10.1211/jpp.58.10.0011/abstract
11. A. Annapurna, C.S. Reddy, R.B. Akondi, Rao S.R. Cardioprotective actions of two bioflavonoids, quercetin and rutin, in experimental myocardial infarction in both normal and streptozotocin-induced type I diabetic rats. The Journal of Pharmacy and Pharmacology, 61 (10) (2009), pp. 1365-1374. http://onlinelibrary.wiley.com/doi/10.1211/jpp.61.10.0014/abstract
12. C.R. Pace-Asciak, S. Hahn, E.P. Diamandis, G. Soleas, D.M. Goldberg. The red wine phenolics trans-resveratrol and quercetin block human platelet aggregation and eicosanoid synthesis: Implications for protection against coronary heart disease. Clinica Chimica Acta, 235 (2) (1995), pp. 207-219. http://www.sciencedirect.com/science/article/pii/0009898195060451
13. Grains & Legumes Nutrition Council. Hot Topics: Gluten Free Doesn’t Mean Grain Free. http://www.glnc.org.au/grains/hot-topics-whats-the-deal-with-gluten/
14. United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. https://ndb.nal.usda.gov/ndb/
15. Krkoškova, B. & Mrazova, Z. (2005) Prophylactic components of buckwheat. Food Res. Intern., 38, 561-568.
16. Jiang, P., Burczynski, F., Campbell, C., Pierce, G., Austria, J.A. & Briggs, C.J. (2007) Rutin and flavonoid contents in three buckwheat species Fagopyrum esculentum, F. tataricum, and F. homotropicum and their protective effects against lipid peroxidation. Food Res. Inter., 40, 356-364.
17. Bonafaccia, G., Marocchini, M. & Kreft, I. (2003) Composition and technological properties of the flour and bran from common and tartary buckwheat. Food Chem., 80, 9-15.
18. Ikeda, S. & Yamashita, Y. (1994) Buckwheat as a dietary source of zinc, copper and manganese. Fagopyrum, 14, 29-34.
19. Wieslander, G., Norbäck, D., Wang, Z.H., Zhang, Z., Yahong, M. & Lin, R.F. (2000) Buckwheat allergy and reports on asthma and atopic disorders in Taiyuan City, Northern China. Asian Pac. J. Allergy Immunol., 18, 147-152.
20. Ihme, N., Kiesewetter, H., Jung, F., Hoffmann, K.H., Birk, A., Muller, A. & Grutzner, K. (1996) Leg oedema protection from buckwheat herb tea in patients with chronic venous insufficiency: a single-centre, randomised, double blind, placebo-controlled clinical trial. Eur. J. Clin. Pharmacol., 40, 443-447.
21. He, J., Klag, M.J., Whelton, P.K., Mo, J.P., Chen, J.Y., Qian, M.C., Mo, P.S. & He, G.Q. (1995) Oats an buckwheat intakes and cardiovascular disease risk factors in an ethnic minority of China. Am. J. Clin. Nutr., 61, 366-372.
22. Journal of Functional Foods Volume 26, October 2016, Pages 460-469. Effectiveness of rutin-rich Tartary buckwheat (Fagopyrum tataricum Gaertn.) ‘Manten-Kirari’ in body weight reduction related to its antioxidant properties: A randomised, double-blind, placebo-controlled study. http://www.sciencedirect.com/science/article/pii/S1756464616302122
23. J. Agric. Food Chem., 2001, 49 (1), pp 490–496. DOI: 10.1021/jf000779w. Nutritional Properties of Starch in Buckwheat Products:  Studies in Vitro and in Vivo. http://pubs.acs.org/doi/full/10.1021/jf000779w
24. International Journal of Food Science and Technology, October 2010; 45(10):1993–2000. Epub August 25, 2010.
25. China’s Research of Agricultural Modernization Journal, April 2009
26. Journal of Jilin Agricultural University, 2009; 31(1):102-4
27. Phytotherapy Research, July 2009; 23(7):993–998. Epub January 12, 2009.
28. Nutrition Research, June 2003; 23(6):803-14
29. J Agric Food Chem. 2017 Mar 8;65(9):1900-1906. doi: 10.1021/acs.jafc.7b00066. Epub 2017 Feb 24. Cholesterol-Lowering Activity of Tartary Buckwheat Protein. http://pubs.acs.org/doi/abs/10.1021/acs.jafc.7b00066
30. Tomotake H, Yamamoto N, Kitabayashi H, Kawakami A, Kayashita J, Ohinata H, Karasawa H, Kato N. J Food Sci. 2007 Sep;72(7):S528-33. Preparation of tartary buckwheat protein product and its improving effect on cholesterol metabolism in rats and mice fed cholesterol-enriched diet. https://www.ncbi.nlm.nih.gov/pubmed/17995668
31. steroid carboxylic acids derived from cholesterol produced by the liver and excreted in the bile
32. Wieslander G, Fabjan N, Vogrincic M, Kreft I, Janson C, Spetz-Nyström U, Vombergar B, Tagesson C, Leanderson P, Norbäck D. Tohoku J Exp Med. 2011 Oct;225(2):123-30. Eating buckwheat cookies is associated with the reduction in serum levels of myeloperoxidase and cholesterol: a double blind crossover study in day-care centre staffs. https://www.ncbi.nlm.nih.gov/pubmed/21931228
33. Kasha and Beet Salad with Celery and Feta. https://wholegrainscouncil.org/recipes/kasha-and-beet-salad-celery-and-feta
34. Kasha Varnishkes. https://wholegrainscouncil.org/recipes/kasha-varnishkes
35. Buckwheat Pumpkin Muffins with Molasses-Cinnamon Glaze. https://wholegrainscouncil.org/recipes/buckwheat-pumpkin-muffins-molasses-cinnamon-glaze
36. Buckwheat Mushroom Kreplach in Dill Tomato Sauce. https://wholegrainscouncil.org/recipes/buckwheat-mushroom-kreplach-dill-tomato-sauce
37. Fritz SB, Gold BL. Ann Allergy Asthma Immunol. 2003 Mar;90(3):355-8. Buckwheat pillow-induced asthma and allergic rhinitis. https://www.ncbi.nlm.nih.gov/pubmed/12669902
38. Sammut D, Dennison P, Venter C, Kurukulaaratchy RJ. Buckwheat allergy: a potential problem in 21st century Britain. BMJ Case Reports. 2011;2011:bcr0920114882. doi:10.1136/bcr.09.2011.4882. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214221/

What is Xylitol ?

Xylitol is a sugar alcohol, a class of compounds that have been used for decades to sweeten chewing gum, sugar-free candy (such as mints and chocolate bars), fruit spreads, baked goods, breath mints, mouthwash, toothpaste, cough syrup, household sugar alternatives, children’s and adult chewable vitamins and other products. Sugar alcohols are also called “polyols” ¹. Pure xylitol is a white crystalline substance that looks and tastes like sugar. And unlike sugar, sugar alcohols like Xylitol does not react with plaque bacteria in your mouth and does not cause tooth cavities.

Sugar alcohols are carbohydrates that occur naturally in certain fruits and can also be manufactured.

Despite their name, sugar alcohols aren’t sugar and they aren’t alcohol. They are carbohydrates that occur naturally in certain fruits and can also be manufactured. They get their name because they have a chemical structure similar to sugar and to alcohol. Sugar alcohols are now found in many processed foods, including hard candies, ice cream, puddings, baked goods, and chocolate. They may be used in combination with another sugar substitute.

Polyols are hydrogenated monosaccharides and include such sugars as sorbitol, mannitol, erythritol, xylitol and D-tagatose as well as the hydrogenated disaccharides isomalt, maltitol, lactitol and trehalose. The polysaccharide derived hydrogenated starch hydrolysates are also included in this category. Polyols are used as sweeteners and bulking agents, and designated generally recognized as safe (GRAS) by the FDA ².

Newer, cheaper ways to make sugar alcohols from corncobs, wood, and other plant materials, along with their sugar-like taste, are fueling their use in a growing array of foods.

What is Sugar Alcohol

Sugar alcohols are also called “polyols” ¹. Polyols are hydrogenated monosaccharides and include such sugars as sorbitol, mannitol, erythritol, xylitol and D-tagatose as well as the hydrogenated disaccharides isomalt, maltitol, lactitol and trehalose. The polysaccharide derived hydrogenated starch hydrolysates are also included in this category. Polyols are used as sweeteners and bulking agents, and designated generally recognized as safe (GRAS) by the FDA ².

Despite their name, sugar alcohols aren’t sugar and they aren’t alcohol.

Sugar alcohols are carbohydrates that chemically have characteristics of both sugars and alcohols. They get their name because they have a chemical structure similar to sugar and to alcohol. However, sugar alcohols do not contain the type of alcohol found in alcoholic beverages ³.

Newer, cheaper ways to make sugar alcohols from corncobs, wood, and other plant materials, along with their sugar-like taste, are fueling their use in a growing array of foods.

The most common sugar alcohols found in foods include:

• Erythritol – 0.2 calories per gram and 60% to 80% as sweet as sugar. Erythritol is a naturally occurring sugar alcohol found in fruit and fermented foods. Erythritol does not result in as much of a rise in blood sugar after meals or cause tooth decay. Unlike other sugar alcohols, it does not cause stomach upset.
• Isomalt– 2 calories per gram and 45% to 65% as sweet as sugar
• Lactitol – 2 calories per gram and 30% to 40% as sweet at sugar
• Maltitol – 2.1 calories per gram and 90% as sweet as sugar
• Mannitol – 1.6 calories per gram and 50% to 70% as sweet as sugar
• Sorbitol – 2.6 calories per gram and 50% to 70% as sweet as sugar
• Xylitol – 2.4 calories per gram and the same sweetness as sugar (but only has a Glycemic Index of 7)
  

By comparison, there are 4 calories per gram of sugar.

Keep in mind that just because a product is “sugar free,” it doesn’t always mean that it’s healthy. Foods and beverages that contain non-nutritive sweeteners can be included in a healthy diet, as long as the calories they save you are not added back by adding more foods as a reward later in the day, adding back calories that take you over your daily limit. The current meta-analysis ⁴ provides a rigorous evaluation of the scientific evidence on low-calorie sweeteners and body weight and composition. Findings from observational studies showed no association between low-calorie sweeteners intake and body weight or fat mass and a small positive association with body mass index (BMI); however, data from randomised clinical trials, which provide the highest quality of evidence for examining the potentially causal effects of low-calorie sweeteners intake, indicate that substituting low-calorie sweeteners options for their regular-calorie versions results in a modest weight loss and may be a useful dietary tool to improve compliance with weight loss or weight maintenance plans ⁴.

Where Sugar Alcohols Are Found

Sugar alcohols are found naturally in small amounts in a variety of fruits and vegetables and are also commercially produced from sugars and starch.
Commercially produced sugar alcohols are added to foods as reduced-calorie sweeteners and are found in many sugar-free and reduced-sugar products, including:

• Chewing gum
• Dairy desserts (such as ice cream, other frozen desserts, and puddings)
• Frostings
• Grain-based desserts (such as cakes and cookies)
• Sweets (such as hard and soft candies, flavored jam, and jelly spreads)

Sugar alcohols are one type of reduced-calorie sweetener. You can find them in ice creams, cookies, puddings, candies and chewing gum that is labeled as “sugar-free”, “diabetic”, “low carb”or “no sugar added.” Sugar alcohols provide fewer calories than sugar and have less of an effect on blood glucose (blood sugar) than other carbohydrates.

Figure 1. Nutrition Facts Label

[Source ³]

Note: Look for sugar alcohols on the ingredient list on a food package. Some examples of sugar alcohols are: erythritol, hydrogenated starch hydrolysates, isomalt, lactitol, maltitol, mannitol, sorbitol, and xylitol. When choosing “sugar-free” foods containing sugar alcohols, remember to use the Nutrition
Facts Label to compare the calories and nutrients in the sugar-free version to the regular version of a particular food. These products may still have a significant amount of calories, carbohydrate, and fat.

Tip: Ingredients are listed in descending order by weight — the closer they are to the beginning of the list, the more of that ingredient is in the food.

How To Monitor Sugar Alcohols in Your Diet

Use the Nutrition Facts Label as your tool for monitoring consumption of sugar alcohols. The Nutrition Facts Label on food and beverage packages shows the amount in grams (g) of total carbohydrate and sugars and the Percent Daily Value (%DV) of total carbohydrate in one serving of the food.

Foods with low- or reduced-calorie sweeteners like Xylitol can have fewer calories than foods made with sugar and other caloric sweeteners. That can be helpful if you’re trying to lose weight or even to prevent weight gain. These products often times also have less carbohydrate which can be helpful in managing blood glucose levels. However, you need to read the food labels carefully because many of the food products containing these types of sweeteners still have a significant amount of carbohydrate, calories and fat, so never consider them a “free food” without checking the label. By comparing the calories in the sugar-free version to the regular version, you’ll see whether you’re really getting fewer calories.

Low-calorie sweeteners are useful for adding extra flavor or sweetness to your food, with few if any extra calories. In addition, these sweeteners are useful for reducing calories and carbohydrates when used instead of sugar in coffee, tea, cereal and on fruit. You can experiment with your own recipes to include low-calorie sweeteners.

What Sugar Alcohols Do

• Sugar alcohols provide a sweet taste with fewer calories per gram than table sugar (sucrose), and are commonly used in place of sugar and often in combination with artificial sweeteners.
• Sugar alcohols in food add bulk and texture, help retain moisture, and prevent browning that occurs during heating.
• Sugar alcohols produce a “cooling” sensation in the mouth when added to foods in high concentrations — for example, in sugar-free hard candy or
  chewing gum.
• Unlike sugar, sugar alcohols do not react with plaque bacteria in the mouth. So, they do not cause cavities (also known as “dental caries”).

Sugar Alcohols Health Facts

Sugar alcohols are slowly and incompletely absorbed from the small intestine into the blood. As a result, they provide fewer calories per gram than sugar and produce a smaller change in blood glucose (often referred to as blood sugar) than other carbohydrates.

Polyols (sugar alcohols like Xylitol) are only partially absorbed from the small intestine, allowing for the claim of reduced energy per gram. Polyols contain, on average, 2 kcals/gm, or 1/2 the calories of other nutritive sweeteners. Studies of subjects with and without diabetes have shown that sugar alcohols cause less of a postprandial glucose response than sucrose or glucose ⁵. However, polyols can cause diarrhea at ≥20 gms especially in children. Although a diet high in polyols could reduce overall energy intake or provide long-term improvement in glucose control in diabetes, such studies have yet to be done ⁶.

Sugar Alcohols Side Effects

Sugar alcohols can also produce abdominal gas, bloating, and diarrhea in some individuals because they are not completely absorbed by the body and are fermented by bacteria in the large intestine. For this reason, foods that contain the sugar alcohols sorbitol or mannitol must include a warning on their label that states “excess consumption may have a laxative effect.”

Xylitol Side Effects

Sugar alcohols like Xylitol (when consumed in large amounts) can cause abdominal pain, gas/bloating and diarrhea as common side effects. Other gastric symptoms may also occur in some people, especially in children.

Xylitol when consumed in water, 35 grams and 50 grams xylitol was associated with significant gastrointestinal symptoms when compared with 45 grams sucrose (table sugar). Consumption of a single oral, bolus dose of 50 g xylitol in water significantly increased the number of subjects reporting nausea, bloating, borborygmi (a rumbling or gurgling noise made by the movement of fluid and gas in the intestines), colic (severe pain in the abdomen), watery faeces (diarrhea) and total bowel movement frequency. Also 35 grams of xylitol increased significantly bowel movement frequency to pass watery faeces (diarrhea), compared to the sucrose control ⁷.

Is Xylitol Safe ?

Xylitol like all the Polyols (sugar alcohols) are used as sweeteners and bulking agents, and designated generally recognized as safe (GRAS) by the FDA ².

On a study of Xylitol toxicity 13 healthy children, aged seven to 16 years was investigated. Xylitol was administered as a supplement in addition to the children’s regular diet. The daily dose was increased during successive 10-day periods from 10 to 25, 45, 65 and 80 grams. Gastrointestinal symptoms (flatulence, occasional abdominal pain and diarrhea) were recorded daily throughout the study. Prior to xylitol supplementation and after 20-50 days of dietary supplement serum uric acid and total cholesterol were measured. Flatulence was the most common side effect occurring relatively infrequently in almost every other subject during the 45 g/day intake, and in most subjects with greater frequency at the 80 g/day intake. Transient diarrhea occurred in four children on 65 g xylitol/day and in one child at 80 g/day. After 50 days of xylitol consumption, there was an increase in serum uric acid and cholesterol. However, the values were within the normal ranges for children ⁸.

A study on the tolerance of xylitol involving 18 male and one female non-diabetic students aged 21-27 years, where the students were given xylitol for 21 days in increasing dose levels from five up to a maximum of 75 g/day. After one month of interruption the same group received xylitol in increasing dose levels from 40 g up to 220 g again during 21 days (19 students received during the first week 40-100 g/day, 18 during the second week 100-150 g, and six during the third week 150-220 g). The subjects themselves recorded quantity, daily division of xylitol intake, number and consistency of bowel movements as well as general condition and obvious side effects. Body weights were estimated weekly. At the third day of each experimental period and seven days after termination, fasting blood sugar analyses and urinalyses on presence of reducing sugar were carried out. From a 130 g/day dose level diarrhea was observed when the single doses were poorly distributed over the day. No other significant effects were noticed. In a similar study 23 men and three women were given xylitol or sorbitol. The initial dose was 5 g which was increased to 75 g/day after 14 days. In addition to the parameters investigated in the first experiment, xylitol and glucose analyses in 24 hour urine were carried out. Identically to the first experiment diarrhea was the only effect observed ⁹.

In a two year tolerance study, three groups of 125 volunteers remained on strict diet containing respectively, fructose, sucrose and xylitol. The highest daily doses of fructose and xylitol were 200-400 g. Serum samples were analyzed for sodium, potassium, calcium, magnesium, inorganic phosphates, ascorbate, bilirubin, amylase, alkaline phosphatase, amino-acids, immunoglobulin A, immunoglobulin G and immunoglobulin M. In addition saliva analyses of immunoglobulin A, immunoglobulin G and immunoglobulin M and amylase were carried out. The number of occurrences of diarrhea and flatulence-like conditions were also scored. Body weights of the volunteers were recorded weekly. The numbers of pregnancies in the groups were as follows; eight in the sucrose, six in the fructose and eight in the xylitol group. No significant changes of clinico-chemical parameters in serum and saliva were observed in the xylitol group. A significant rise in the occurrence of diarrhea and flatulence-like conditions was noted in the xylitol group. All pregnancies, deliveries and infants were normal ¹⁰.

Xylitol is Poisonous to Your Dog

In both people and dogs, the level of blood sugar is controlled by the release of insulin from the pancreas. In people, xylitol does not stimulate the release of insulin from the pancreas. However, it’s different in canines: When dogs eat something containing xylitol, the xylitol is more quickly absorbed into the bloodstream, and may result in a potent release of insulin from the pancreas ¹¹.

This rapid release of insulin may result in a rapid and profound decrease in the level of blood sugar (hypoglycemia), an effect that can occur within 10 to 60 minutes of eating the xylitol. Untreated, this hypoglycemia can quickly be life-threatening ¹¹.

Over the past several years, the Center for Veterinary Medicine at the U.S. Food and Drug Administration (FDA) has received several reports—many of which pertained to chewing gum—of dogs being poisoned by xylitol ¹¹.

Symptoms of xylitol poisoning in dogs include vomiting, followed by symptoms associated with the sudden lowering of your dog’s blood sugar, such as decreased activity, weakness, staggering, incoordination, collapse and seizures.

If you think your dog has eaten xylitol, take him to your vet or an emergency animal hospital immediately.

(A note to cat owners: The toxicity of xylitol for cats has not been documented. They appear to be spared, at least in part, by their disdain for sweets.)

[Source: U.S. Food and Drug Administration. Xylitol and Your Dog: Danger, Paws Off. ¹¹]

Xylitol and Prevention of Dental Caries (tooth decay or cavities)

Tooth cavities (dental caries) are decayed areas in the teeth, the result of a process that gradually dissolves a tooth’s hard outer surface (enamel) and progresses toward the interior.

Dental caries is a diet-associated disease which continues to be a serious health problem in most industrialized and developing countries. Although all carbohydrates can cause tooth decay to some degree, the biggest culprits are sugars. All simple sugars, including table sugar (sucrose) and the sugars in honey (levulose and dextrose), fruit (fructose), and milk (lactose), have the same effect on the teeth. Whenever sugar comes in contact with plaque, Streptococcus mutans bacteria in the plaque produce acid. The amount of sugar eaten is of little consequence. The amount of time the sugar stays in contact with the teeth is what matters. Thus, sipping a sugary soft drink over an hour is more damaging than eating a candy bar in 5 minutes, even though the candy bar may contain more sugar. Infants who go to bed with a bottle, even if it contains only milk or formula, are also at risk of cavities. Bedtime bottles should contain only water.

For tooth decay to develop, a tooth must be susceptible, acid-producing bacteria must be present, and nutrients (such as sugar) must be available for the bacteria to thrive and produce acid. A susceptible tooth has relatively little protective fluoride incorporated into the enamel or has pronounced pits, grooves, or cracks (fissures) that retain plaque. Poor oral hygiene that allows plaque and tartar to accumulate can accelerate this process. Although the mouth contains large numbers of bacteria, only certain types generate acid, which causes decay. The most common decay-causing bacteria are Streptococcus mutans ¹².

• Bacteria and debris build up on tooth surfaces, and the bacteria produce acids that cause decay.
• Tooth pain occurs after decay reaches the inside of the tooth.
• Dentists can detect cavities by examining the teeth and taking x-rays periodically.
• Good oral hygiene and regular dental care plus a healthy diet can help prevent cavities.

Fluoride treatments can help cavities in the enamel heal, but for deeper cavities, dentists must drill out the decay and fill the resulting space.

Risk factors for tooth cavities

There are many risk factors for cavities:

• Plaque: Plaque is a filmlike substance composed of bacteria, saliva, food debris, and dead cells that is continually being deposited on teeth.
• Tartar: Tartar, also scientifically known as calculus, is hardened plaque. It may be white but is more often yellow and forms at the base of teeth.
• Defects in the tooth surface
• Sugary or acidic foods
• Too little fluoride in the teeth
• Reduced saliva flow

The nutrients that decay-causing bacteria need come from the person’s diet. Large amounts of sugar in the diet also provide food for the bacteria. Acid in the diet (for example, in cola beverages, which contain phosphoric acid) accelerates tooth decay.

Types of Tooth Cavities

• Smooth surface decay, the most preventable and reversible type, grows the slowest. In smooth surface decay, a cavity begins as a white spot where bacteria dissolve the calcium of the enamel. Smooth surface decay between the permanent teeth usually begins between the ages of 20 and 30.
• Pit and fissure decay, which usually starts during the teen years in the permanent teeth, forms in the narrow grooves on the chewing surface and on the cheek side of the back teeth. Decay at these locations progresses rapidly. Many people cannot adequately clean these cavity-prone areas because the grooves are narrower than the bristles of a toothbrush.
• Root decay begins on the root surface covering (cementum) that has been exposed by receding gums, usually in people past middle age. This type of decay often results from difficulty cleaning the root areas, a lack of adequate saliva flow, a diet high in sugar, or a combination of these factors. Root decay can be the most difficult type of tooth decay to prevent and treat.

Prevention of Cavities

Several general strategies are key to preventing cavities:

• Good oral hygiene and regular dental care
• Healthy diet
• Fluoride (in water, toothpaste, or both)
• Sometimes fluoride sealants and antibacterial therapy

Strategies to maximize caries prevention should automatically consider the use of sugar substitutes. Clinical studies have shown that xylitol, a natural, physiologic sugar alcohol of the pentitol type, can be used as a safe and effective caries-limiting sweetener ¹³. Habitual use of xylitol-containing food and oral hygiene adjuvants has been shown to reduce the growth of dental plaque, to interfere with the growth of caries-associated bacteria, to decrease the incidence of dental caries, and to be associated with remineralization of caries lesions ¹³. And studies have also shown the effect of Xylitol or Sorbitol or the combination of the two as  sugar substitutes consistently decrease dental caries (tooth decay or cavities), ranging from 30 to 60 percent, among children compared to children not using Xylitol or Sorbitol in a control group ¹⁴. These dental caries rate reductions were observed in subjects using xylitol or sorbitol as the sugar substitute in chewing gum or toothpaste. The highest tooth decay or cavities reductions were observed in subjects using xylitol. These findings suggest that the replacement of sugar with sorbitol and xylitol may significantly decrease the incidence of dental caries ¹⁴.

Other Uses of Xylitol

In this pilot study, Xylitol in water has been used as sinonasal irrigation in the short term treatment of chronic rhinosinusitis (inflammation of the paranasal sinuses and nasal cavity) and this pilot study showed xylitol irrigations result in greater improvement of symptoms of chronic rhinosinusitis as compared to saline irrigation ¹⁵.

Recent Cochrane Review showed a “fair evidence that the prophylactic administration of xylitol among healthy children  up to 12 years of age attending day care centres reduces the occurrence of acute otitis media (middle ear infection) by 25% ¹⁶. However, the review authors also added that the data arise from a small number of studies, mainly from the same research group, which may not be applicable in a wider community and in a larger group.

References

1. American Academy of Family Physicians. Sugar Substitutes. https://familydoctor.org/sugar-substitutes
2. U.S. Food and Drug Administration. Sugar Alcohols. https://www.accessdata.fda.gov/scripts/interactivenutritionfactslabel/sugar-alcohol.html
3. U.S. Food and Drug Administration. Sugar Alcohols Fact Sheet. https://www.accessdata.fda.gov/scripts/interactivenutritionfactslabel/factsheets/Sugar_Alcohols.pdf
4. Miller PE, Perez V. Low-calorie sweeteners and body weight and composition: a meta-analysis of randomized controlled trials and prospective cohort studies. The American Journal of Clinical Nutrition. 2014;100(3):765-777. doi:10.3945/ajcn.113.082826. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4135487/
5. Position of the Academy of Nutrition and Dietetics:Use of Nutritive and Nonnutritive SweetenersJ Acad Nutr Diet. 2012;112:739-758
6. MDText.com, Inc.; 2000-.2015 May 31. Nutritional Recommendations for Individuals with Diabetes. https://www.ncbi.nlm.nih.gov/pubmed/25905243
7. European Journal of Clinical Nutrition (2007) 61, 349–354. doi:10.1038/sj.ejcn.1602532; published online 20 September 2006. Gastrointestinal tolerance of erythritol and xylitol ingested in a liquid. http://www.nature.com/ejcn/journal/v61/n3/full/1602532a.html
8. National Institutes of Health, Health & Human Services. Xylitol. https://toxnet.nlm.nih.gov/cgi-bin/sis/search2/r?dbs+hsdb:@term+@rn+87-99-0
9. WHO/FAO: Expert Committee on Food Additives. Summary of Toxicological Data of Certain Food Additives Series 12: Xylitol (87-99-0) (1977).
10. Mäkinen KK.Int Z Vitam Ernahrungsforsch Beih. 1976;15:92-104. Long-term tolerance of healthy human subjects to high amounts of xylitol and fructose: general and biochemical findings. https://www.ncbi.nlm.nih.gov/pubmed/783060
11. U.S. Food and Drug Administration. Xylitol and Your Dog: Danger, Paws Off. https://www.fda.gov/ForConsumers/ConsumerUpdates/ucm499988.htm
12. Merck Sharp & Dohme Corp., Merck Manual. Caries. www.merckmanuals.com/professional/dental-disorders/common-dental-disorders/caries
13. Mäkinen KK. Sugar alcohol sweeteners as alternatives to sugar with special consideration of xylitol. Med Princ Pract. 2011;20(4):303-20. doi: 10.1159/000324534. Epub 2011 May 11. https://www.karger.com/Article/Abstract/324534
14. Hayes C. J Dent Educ. 2001 Oct;65(10):1106-9. The effect of non-cariogenic sweeteners on the prevention of dental caries: a review of the evidence. http://www.jdentaled.org/content/65/10/1106.long
15. Weissman JD, Fernandez F, Hwang PH. Laryngoscope. 2011 Nov;121(11):2468-72. doi: 10.1002/lary.22176. Epub 2011 Oct 12. Xylitol nasal irrigation in the management of chronic rhinosinusitis: a pilot study. https://www.ncbi.nlm.nih.gov/pubmed/21994147
16. Azarpazhooh A, Limeback H, Lawrence HP, Shah PS. Cochrane Database Syst Rev. 2011 Nov 9;(11):CD007095. doi: 10.1002/14651858.CD007095.pub2. Xylitol for preventing acute otitis media in children up to 12 years of age. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD007095.pub2/abstract

What is Sucralose

Sucralose is a synthetic organochlorine sweetener (also known as Splenda®) is an artificial sweetener, also called sugar substitute or non-nutritive sweetener, is a substance that is used instead of sucrose (table sugar) to sweeten foods and beverages. Because artificial sweeteners are many times sweeter than table sugar, smaller amounts are needed to create the same level of sweetness.

Sucralose has the chemical name 1,6-dichloro-1,6-dideoxy-[beta]-D-fructofuranosyl-4-chloro-4-deoxy-[alpha]-D-galactopyranoside ¹.

Sugar substitutes are chemical or plant-based substances used to sweeten or enhance the flavor of foods and drinks. You may have heard them called “artificial sweeteners” or “non-caloric sweeteners.” They can be used as a tabletop sweetener (for example, to sweeten a glass of iced tea) and/or as an ingredient in processed foods and drinks.

Sucralose is about 600 times sweeter than sugar ².

Sugar substitutes are regulated as food additives by the U.S. Food and Drug Administration (FDA). This means that the FDA reviews scientific evidence to be sure that a sugar substitute is safe before it can be used in foods and drinks ².

Sucralose has been used as a general purpose sweetener that can be found in thousands of processed foods including baked goods, beverages, chewing gum, gelatins and frozen dairy desserts. Some examples include soft drinks, juices, sauces, syrups, candy, desserts, baked goods, and canned fruits. It is used in medicines, nutritional supplements, and vitamins. It is also used as a tabletop sweetener.

It is heat stable, meaning that it stays sweet even when used at high temperatures during baking, making it suitable as a sugar substitute in baked goods. Sucralose can be used in baking because it does not lose its sweet taste at high temperatures. For best results, follow the package instructions for using it in your recipes.

The range of product utilization is more extensive for sucralose than for other artificial sweeteners due to its physicochemical properties. For example, sucralose is readily soluble in ethanol, methanol, and water ³, ⁴, ⁵ and this solubility profile contributes to its versatility in both fat- and water-based food and beverage applications including alcoholic drinks. Other common artificial sweeteners such as aspartame, sodium saccharin, and acesulfame-potassium (ace-K) are only slightly or sparingly soluble in ethanol and/or methanol ⁶ and have more limited product applications. The Acceptable Daily Intake (ADI) level for sucralose was set at 5 mg/kg body weight per day (mg/kg/d) in the United States ⁷ and 15 mg/kg/d in the EU as recommended by Scientific Committee on Food of the European Commission ⁸, and there are no exclusions or restrictions for vulnerable population groups, including pregnant women, nursing mothers, infants, children, elderly, persons with medical conditions, and patients taking multiple medications.

What is the difference between nutritive and non-nutritive high-intensity artificial sweeteners ?

Nutritive sweeteners add caloric value to the foods that contain them, while non-nutritive sweeteners are very low in calories or contain no calories at all ².

Nutritive sweeteners: those that contain more than 2 percent of the calories in an equivalent amount of sugar ⁹.

Nonnutritive sweeteners: those that contain less than 2 percent of the calories in an equivalent amount of sugar or have no calories at all. Also known as artificial sweeteners, sugar substitutes, low-calorie sweeteners, noncaloric sweeteners, or high-intensity sweeteners ⁹.

Food products are considered “no-calorie” if they have 5 calories or less per serving. Notice that even though the nutrition labels on sweetener packets claim to have zero calories and carbohydrate, there are a small amount calories and carbs from those added ingredients ⁹.

Specifically, aspartame, the only approved nutritive high-intensity sweetener, contains more than two percent of the calories in an equivalent amount of sugar, as opposed to non-nutritive sweeteners that contain less than two percent of the calories in an equivalent amount of sugar.

Keep in mind that just because a product is “sugar free,” it doesn’t always mean that it’s healthy. Foods and beverages that contain non-nutritive sweeteners can be included in a healthy diet, as long as the calories they save you are not added back by adding more foods as a reward later in the day, adding back calories that take you over your daily limit. The current meta-analysis ¹⁰ provides a rigorous evaluation of the scientific evidence on low-calorie sweeteners and body weight and composition. Findings from observational studies showed no association between low-calorie sweeteners intake and body weight or fat mass and a small positive association with body mass index (BMI); however, data from randomised clinical trials, which provide the highest quality of evidence for examining the potentially causal effects of low-calorie sweeteners intake, indicate that substituting low-calorie sweeteners options for their regular-calorie versions results in a modest weight loss and may be a useful dietary tool to improve compliance with weight loss or weight maintenance plans ¹⁰.

Comparison of some different sweeteners to regular sugar below:

1 packet Sugar = 11 calories + 3 grams of carbohydrate

or

1 packet Splenda (Sucralose) = 4 calories + < 1 gram of carbohydrate

or

1 packet of Sugar Twin (Aspartame) = 3 calories + < 1 gram of carbohydrate

or

1 packet of Equal (Aspartame) = 4 calories + < 1 gram of carbohydrate

or

1 teaspoon of Agave = 21 calories + 5.3 to 5.7 grams carbohydrate

or

1 teaspoon of Sugar (brown, powdered, raw, and white) and Maple syrup have 2.5 to 4.6 grams of carbohydrate per teaspoon and 10 to 18 calories.

or

1 teaspoon of Powdered Sugar = 10 calories + 2.5 grams carbohydrate

or

1 teaspoon of Maple syrup = 10 to 18 calories + 2.5 to 4.6 grams of carbohydrate

or

1 teaspoon of Honey = 21 calories + 5.3 to 5.7 grams carbohydrate

When you use a large amount of these products, it can start to add up. As with all foods, it is important not to go overboard.

[Source: American Diabetes Association. ¹¹]

Other Sugar Substitutes/Artificial Sweeteners are Approved by the FDA

The following sugar substitutes are FDA approved as food additives in the United States:

• Acesulfame K (brand names: Sunett and Sweet One)
• Advantame
• Aspartame (two brand names: Equal and Nutrasweet)
• Neotame (brand name: Newtame)
• Saccharin (two brand names: Sweet ‘N Low and Sweet Twin)
• Sucralose (brand name: Splenda)

According to the FDA, some sugar substitutes are “generally recognized as safe” (GRAS) ². This means they do not require FDA approval because qualified experts agree the scientific evidence shows these products are safe for use in foods and drinks.

These artificial sweeteners are used by food companies to make diet drinks, baked goods, frozen desserts, candy, light yogurt and chewing gum. You can buy them to use as table top sweeteners. Add them to coffee, tea, or sprinkle them on top of fruit. Some are also available in “granular” versions which can be used in cooking and baking.

Sugar substitutes in this category include highly purified stevia extracts called “steviol glycosides” (two brand names: Pure Via and Truvia) and monk fruit extracts (two brand names: Monk Fruit in the Raw and PureLo).

Sugar alcohols are another class of sweeteners that can be used as sugar substitutes. Examples include mannitol, sorbitol, and xylitol. The FDA has determined that sugar alcohols are generally recognized as safe for use in foods and drinks.

Table 1. FDA Approved Artificial Sweeteners

[Source: U.S. Food and Drug Administration. Additional Information about High-Intensity Sweeteners Permitted for use in Food in the United States.  ²]

Note: Table 1. FDA Approved Artificial Sweeteners

ADI indicates Acceptable Daily Intake; Joint Expert Commission on Food Additives of the World Health Organization and the Food and Agriculture Organization JECFA ¹². ADI is a measure of the amount of a specific substance in food or drinking water that can be ingested over a lifetime without an appreciable health risk. Measurement is usually expressed in milligrams of sweetener per kilogram of body weight (mg/kg bw). The amount is usually set at 1/100 of the maximum level at which no adverse effect was observed in animal experiments.

* Number of Tabletop Sweetener Packets a 60 kg (132 pound) person would need to consume to reach the ADI. Calculations assume a packet of high-intensity sweetener is as sweet as two teaspoons of sugar.
**ADI established by the Joint FAO/WHO Expert Committee on Food Additives (JECFA)
*** NS means not specified. A numerical ADI may not be deemed necessary for several reasons, including evidence of the ingredient’s safety at levels well above the amounts needed to achieve the desired effect (e.g., as a sweetener) in food.

Additional Note:

Saccharin and sucralose are heat stable and are easiest to use baking and cooking. However, to keep the desirable taste, volume, color, and/or texture of a baked product, you usually will not substitute all of the sugar in a recipe for artificial sweetener. Read the package carefully for specific instructions on the best way to substitute the low-calorie sweetener for sugar in your recipes. The company’s website can also be a helpful resource for baking tips.

Some brands offer pre-made blends of sugar and low-calorie sweeteners. These blends are meant to be used in baking. They are half sugar and half low-calorie sweetener, so they have half the calories and carbohydrate as sugar. As with all low-calorie sweeteners, you will want to read the instructions for substituting these blends for sugar. For example, when replacing regular sugar with Splenda’s Sugar Blend (half-granular Splenda, half-sugar), they suggest using half as much:

1/2 cup Splenda (sucralose) Sugar Blend = 387 calories + 97 grams of carbohydrate

[Source: American Diabetes Association. Using Sugar Substitutes in the Kitchen. ¹³]

Is sucralose safe ?

Although early studies asserted that sucralose passes through the gastrointestinal tract unchanged, subsequent analysis suggested that some of the ingested sweetener is metabolized in the gastrointestinal tract, as indicated by multiple peaks found in thin-layer chromatograms profiles of methanolic fecal extracts after oral sucralose administration. The identity and safety profile of these putative sucralose metabolites are not known at this time ¹⁴. The identity and safety profile of these putative sucralose metabolites are not known at this time ¹⁵, ¹⁶, ¹⁷. Sucralose and one of its hydrolysis products were found to be mutagenic at elevated concentrations in several testing methods. Cooking with sucralose at high temperatures was reported to generate chloropropanols, a potentially toxic class of compounds ¹⁴. Taken together, these findings indicate that sucralose is not a biologically inert compound. The thin-layer chromatograms data of Sims et al. ¹⁷ and Roberts et al. ¹⁸ appear inconsistent with the claim that sucralose is not metabolized in the gastrointestinal tract as asserted by Grice and Goldsmith ¹⁹, Molinary and Quinlan ²⁰, and Grotz and Munro ²¹.

Potential toxicity from habitual sucralose ingestion. Historical in vitro genotoxicity tests found that sucralose was weakly mutagenic in a mouse lymphoma mutation assay, and that one of its hydrolysis products was weakly mutagenic in both the Ames test and mouse lymphoma mutation assay ²², ⁷. A subsequent comet test by Sasaki et al. ²³ found that sucralose induced DNA damage in mouse gastrointestinal tract. Three independent labs showed that sucralose undergoes thermal decomposition at temperatures used in baking ²⁴, ²⁵, ²⁶, ²⁷ and heating sucralose with glycerol, the backbone of triglycerides, generated chloropropanols, a potentially toxic class of compounds ²⁷.

The FDA approved sucralose for use in 15 food categories in 1998 and for use as a general purpose sweetener for foods in 1999 , under certain conditions of use ². In 2004, sucralose (termed food additive E 955) was approved in the European Union (EU) in a variety of products including water- and fat-based desserts, certain alcoholic beverages, fat-based sandwich spreads, breakfast cereals, marinades, and chewing gum ²⁸.

Sucralose safety has been extensively studied and more than 110 safety studies were reviewed by FDA in approving the use of sucralose as a general purpose sweetener for food. Before approving these sweeteners, the FDA reviewed more than 100 safety studies that were conducted on each sweetener, including studies to assess cancer risk. The results of these studies showed no evidence that these sweeteners cause cancer or pose any other threat to human health ²⁹.

According to the National Cancer Institute (an agency of the Department of Health and Human Services), there is no evidence that sucralose and other sugar substitutes approved for use in the United States cause cancer or other serious health problems ²⁹.

This study suggested sucralose may trigger a migraine headache ³⁰.

Effect of sucralose on the number and relative proportions of different intestinal bacterial types

Early studies of sucralose with bacteria in culture indicated that sucralose was not utilized as a carbon source by oral bacteria ³¹ or by bacteria from environmental samples ³². Abou-Donia et al. ³³ extended these studies to bacteria cultured from the GIT of rats that had been administered sucralose daily. An overall reduction of the existing microflora was found (≥50%) at sucralose doses that were lower than the human ADI. Beneficial bacteria including lactobacilli and bifidobacteria were disproportionately affected compared to pathogenic bacteria including enterobacteria. Further, the reduction in fecal microflora was not fully reversible even 3 mo after cessation of sucralose. Sucralose was also reported to exhibit antimicrobial activity against two oral bacterial species involved in periodontal disease ³⁴.

Is Sucralose Bad ?

In the last several years, numerous studies in rodents reported that sucralose modulates physiological processes involved in nutrient absorption and body weight regulation via its interaction with sweet taste receptors (called T1R2/T1R3) located in enteroendocrine cells of the gastrointestinal tract ³⁵, ³⁶, pancreatic ß cells ³⁷, and the hypothalamus ³⁸.

Ren et al. ³⁸ found that sucralose modulated the expression of the gene for the sweet taste receptor T1R2 in cells from the hypothalamus, a nutrient-sensing region of the brain, in rodents. Data showed that T1R2 expression was elevated when the hypothalamic cells were exposed to low (compared to high) extracellular glucose concentrations, and this was reversed with addition of sucralose to the low-glucose medium. That is, addition of sucralose resulted in expression levels of T1R2 that would be expected if higher extracellular glucose levels were actually present. Thus, activation of the sweet taste receptor in the brain by nonnutritive sucralose might potentially affect appetite regulation by providing an inaccurate signal regarding the actual levels of extracellular glucose in the brain ¹⁵. However, it is not yet known if the portion of sucralose that is absorbed into the systemic circulation can traverse the blood–brain barrier to reach the hypothalamus ¹⁴.

Recently, there have been significant advances in our understanding of how hormonal signals released from the gastrointestinal (GI) tract interact with circuits within the central nervous system to control appetite and energy intake ³⁹. The gut hormones peptide YY (PYY) and glucagon-like peptide (GLP)-1 are co-secreted from intestinal enteroendocrine L-cells and released post-prandially in proportion to the amount of energy ingested ⁴⁰, ⁴¹, ⁴². Glucagon-like peptide (GLP)-1 is an incretin hormone secreted in the gut that (1) induces glucose-dependent stimulation of insulin by the pancreas, (2) reduces glucagon secretion by the liver, (3) delays gastric emptying, and (4) increases satiety ⁴³. Incretins are a group of metabolic hormones that stimulate a decrease in blood glucose levels. Incretins are released after eating and augment the secretion of insulin released from pancreatic beta cells of the islets of Langerhans by a blood glucose-dependent mechanism. The incretin effect of GLP-1, augmentation of insulin secretion in response to an oral glucose load, has been well characterised.

The gut hormones peptide YY (PYY) and glucagon-like peptide (GLP)-1 have both been shown to be satiety factors, reducing food intake when administered to rodents ⁴⁴, ⁴⁵, ⁴⁶, ⁴⁷, ⁴⁸ and to humans ⁴⁹, ⁵⁰, ⁴⁴, ⁵¹, ⁴².

In a research to study the effects of oral ingestion of sucralose on gut hormone response (PYY and GLP-1) and appetite in healthy normal-weight subjects ⁵². Ford et al. gave subjects to consume 50 ml of either water, sucralose, a non-sweet, glucose-polymer matched for sweetness with sucralose addition (50% w/v maltodextrin+0.083% sucralose) or a modified sham-feeding protocol of sucralose (0.083% w/v). Appetite ratings and plasma GLP-1, PYY, insulin and glucose were measured at regular time points for 120 min. At 120 min, energy intake at a buffet meal was measured. The results of the study showed sucralose ingestion did not increase plasma GLP-1 or PYY. Sucralose did not elicit a cephalic phase response for insulin or GLP-1. Maltodextrin ingestion significantly increased insulin and glucose compared with water. Appetite ratings and energy intake were similar for all groups. Ford et al. concluded oral ingestion of sucralose does not increase plasma GLP-1 or PYY concentrations and hence, does not reduce appetite in healthy subjects. Oral stimulation with sucralose had no effect on GLP-1, insulin or appetite ⁵². Both human and rodent studies demonstrated that sucralose may alter glucose, insulin, and glucagon-like peptide 1 (GLP-1) levels. Furthermore, sucralose was shown to elevate glucose and insulin levels in a small study of obese women ⁵³, who are at increased risk for further weight gain and development of diabetes.

According to the American Heart Association news report 7th October 2014 ⁵⁴, a recent scientific study published in the science journal Nature ⁵⁵, a study on the effects of artificial sweeteners on blood glucose homeostasis and gut microbiota. The study was conducted largely on mice and included an experiment on seven people who did not normally consume artificial sweeteners. The researchers primarily used saccharin in the experiments, however some of the experiments also included aspartame and sucralose. They found that some mice and people had a two- to four-times increase in blood sugars and changes in the types of microbes in their intestines. In summary, their results suggest that artificial sweeteners consumption in both mice and humans enhances the risk of glucose intolerance and that these adverse metabolic effects are mediated by modulation of the composition and function of the gut microbiota. Notably, several of the bacterial taxa that changed following artificial sweeteners consumption were previously associated with type 2 diabetes in humans ⁵⁵. The findings counter the perception that artificial sweeteners, which are not meant to be absorbed by the digestive tract, don’t affect blood sugar or glucose tolerance – which can be a harbinger of diabetes ⁵⁴. Moreover, the study’s authors, Eran Elinav and Eran Segal of the Weizmann Institute of Science in Israel, said more information and confirmation of their results are needed ⁵⁵.

The American Heart Association and the American Diabetes Association reviewed the safety of artificial sweeteners in a 2012 statement and concluded they should be used “judiciously” as a way to reduce sugar intake. The findings of the American Heart Association research “at this time, there are insufficient data to determine conclusively whether the use of non-nutritive sweeteners (artificial sweeteners) to displace caloric sweeteners in beverages and foods reduces added sugars or carbohydrate intakes, or benefits appetite, energy balance, body weight, or cardiometabolic risk factors. There are some data to suggest that non-nutritive sweeteners (artificial sweeteners) may be used in a structured diet to replace sources of added sugars and that this substitution may result in modest energy intake reductions and weight loss. The impact of incorporating non-nutritive sweeteners (artificial sweeteners) and non-nutritive sweeteners-containing beverages and foods on overall diet quality should be included in assessing the overall balance of benefits and risks. Apparent from the available literature is the paucity of data from well-designed human trials exploring the potential role of non-nutritive sweeteners in achieving and maintaining a healthy body weight and minimizing cardiometabolic risk factors. The evidence reviewed suggests that when used judiciously, non-nutritive sweeteners could facilitate reductions in added sugars intake, thereby resulting in decreased total energy and weight loss/weight control, and promoting beneficial effects on related metabolic parameters. However, these potential benefits will not be fully realized if there is a compensatory increase in energy intake from other sources ⁵⁶.

Sucralose and Body Weight

In a recent (published 17 July 2017) systematic review and meta-analysis of randomized controlled trials and prospective cohort studies on the effects of non-nutritive sweeteners (artificial sweeteners) and cardio-metabolic health being conducted by Dr. Azad et al. ⁵⁷ found that non-nutritive sweeteners (artificial sweeteners) had no significant effect on BMI (body mass index) on participants, in fact in the included cohort studies, consumption of non-nutritive sweeteners was associated with a modest increase in BMI. In the cohort studies, consumption of non-nutritive sweeteners was associated with increases in weight and waist circumference, and higher incidence of obesity, hypertension, metabolic syndrome, type 2 diabetes and cardiovascular events ⁵⁷. Theories about why artificial sweeteners might not help weight loss tend to revolve around two schools of thought, Dr. Azad said. One school holds that the sweeteners might influence dieters’ behavior in unhealthy ways. For example, a person drinking a no-calorie soda might feel free to eat calorie-laden foods, Azad noted. Artificial sweeteners also might sharpen the person’s sweet tooth, making them more likely to indulge in sugary foods. The other school holds that artificial sweeteners might influence the body itself in some as-yet-unknown way, Azad said. The artificial sweeteners could alter the way that gut microbes function in the digestion of food, or possibly change the body’s metabolism over time by sending repeated false signals that something sweet has been ingested ⁵⁸. Another plausible explanation for why the study subjects gained weight and have higher incidence of obesity, hypertension, metabolic syndrome, type 2 diabetes and cardiovascular events, is that the study population involved people who are already overweight, obese, have metabolic syndrome, hypertension or suffer from type 2 diabetes ⁵⁸.

Epidemiological studies in humans ⁵⁹, ⁶⁰, ⁶¹, ⁶², ⁶³ and lab studies in animals ⁶⁴, ⁶⁵, ⁶⁶ both suggest an association between use of artificial sweeteners and body weight gain. Epidemiological studies also demonstrated that artificial sweetener use increased the risk for metabolic syndrome, type 2 diabetes, hypertension, and cardiovascular disease ⁶⁷. Most human epidemiological studies have not distinguished among the different types of artificial sweeteners (e.g., sucralose, saccharin, acesulfame-K, aspartame, neotame, stevioside, and rebaudioside) but rather treated them as a group. One exception is the Nurses’ Health Study cohort ⁶⁸, which did specifically associate saccharin use with weight gain. This finding is consistent with recent animal experiments ⁶⁴, ⁶⁵ in which saccharin intake was related to weight gain in rats. Because synthetic organochlorine compounds and artificial sweeteners have both been associated with weight gain, and because sucralose is a member of both categories, it is important to determine its effect on mechanisms that regulate body weight.

To date, the effect of chronic oral consumption of sucralose on body weight at levels approved by the FDA and EU has not been studied prospectively in adults. In a lab setting, ingestion of sucralose tends to increase intake after a 60-min interval ⁶⁹; however, it is not yet known whether this finding transfers into chronic body weight gain in free-living adult populations. In an 18-mo trial with children, participants were randomly assigned to receive an 8-oz can per day of either a noncalorically sweetened or a sugar-sweetened beverage that provided 104 kcal ⁷⁰. Each can of sugar-free beverage contained 34 mg sucralose and 12 mg acesulfame-K, and the mean sucralose dosage for the sugar-free group was 1.1 mg/kg/d. The mean duration of the study was 541 d (77.3 wk), during which 477 of 641 children completed the intervention by consuming an average of 5.8 beverages per week. Measurement of urinary sucralose levels was one of several markers used to monitor compliance with the protocol. The calorie consumption from these beverages was 46,627 kcal greater for children in the sugar-sweetened group than in the sucralose-sweetened group (5.8 × 77.3 × 104). In spite of this highly significant difference in calories consumed from the beverages, the total weight gain over this 18-mo study was only 1 kg greater for children in the sugar-sweetened group compared to sucralose group. No explanation was provided to account for the small difference in weight gain given the large difference in caloric consumption from the beverages. However, one possible explanation is that the children who consumed the sugar-sweetened beverages compensated by reducing their food intake. A control group that ingested water as a comparison was not included. Another study in adolescents showed no consistent reduction of weight gain at a 2-year follow-up when their families were supplied with artificially sweetened beverages in order to reduce their consumption of sugar-sweetened sodas ⁷¹.

Functional magnetic resonance (fMRI) imaging studies also indicate that the human brain signals distinguish caloric sweeteners (e.g., sucrose) from noncaloric sweeteners (e.g., sucralose and saccharin) ⁷². However, neuroimaging studies by Rudenga and Small ⁷³ revealed that routine use of high-potency sweeteners as a group altered brain responses to sucrose in the amygdala and insula as determined by fMRI scanning. These brain imaging studies in conjunction with epidemiological data that associate artificial sweetener use with weight gain suggest that high-potency sweeteners interfere with learned sweet–calorie relationships in humans as well as animals ⁶⁷.

Effect of Sucralose in Patients With Diabetes

A study of patients with diabetes ⁷⁴ reported no significant effect of sucralose on glycosylated hemoglobin (HbA1c) as a marker of the average plasma glucose concentrations over approximately 3 mo. Grotz et al. ⁷⁴ instructed patients with diabetes to self-administer capsules of sucralose twice daily over a 3-mo period; however, data on compliance with self-administration (e.g., urinary sucralose levels) and body weight changes were not reported. Daily supervision of capsule administration, rather than self-administration, is scientifically prudent for studies of patients with diabetes because noncompliance with treatment regimens is reportedly high in this population ⁷⁵. Further, no apparent information of dissolution characteristics of the capsule was provided; thus, it is unknown where sucralose was released in the GIT. Future studies of sucralose on diabetes management will require randomized trials that are carefully supervised and control for the variables involved.

Sucralose vs Aspartame

Aspartame is approved for use in food as a nutritive sweetener. Aspartame brand names include Nutrasweet®, Equal®, and Sugar Twin®. It does contain calories, aspartame, the only approved nutritive high-intensity sweetener, contains more than two percent of the calories in an equivalent amount of sugar, as opposed to non-nutritive sweeteners that contain less than two percent of the calories in an equivalent amount of sugar. But because it is about 200 times sweeter than table sugar, it is assumed that consumers are likely to use much less of it.

FDA approved aspartame in 1981 ⁷⁶ for uses, under certain conditions, as a tabletop sweetener, in chewing gum, cold breakfast cereals, and dry bases for certain foods (i.e., beverages, instant coffee and tea, gelatins, puddings, and fillings, and dairy products and toppings). In 1983 ⁷⁷, FDA approved the use of aspartame in carbonated beverages and carbonated beverage syrup bases, and in 1996, FDA approved it for use as a “general purpose sweetener” ⁷⁸.

• Aspartame is not heat stable and loses its sweetness when heated, so it typically isn’t used in baked goods.

Aspartame is one of the most exhaustively studied substances in the human food supply, with more than 100 studies supporting its safety.

FDA scientists have reviewed scientific data regarding the safety of aspartame in food and concluded that it is safe for the general population under certain conditions. However, people with a rare hereditary disease known as phenylketonuria have a difficult time metabolizing phenylalanine, a component of aspartame, and should control their intake of phenylalanine from all sources, including aspartame. Labels of aspartame-containing foods and beverages must include a statement that informs individuals with phenylketonuria that the product contains phenylalanine ².

Sucralose vs Stevia

Steviol glycosides (also referred to as Rebaudioside A, Reb-A, or rebiana) are natural constituents of the leaves of Stevia rebaudiana (Bertoni) Bertoni, a plant native to parts of South America and commonly known as Stevia. Highly purified extracts from the leaves of the Stevia rebaudiana are called “steviol glycosides.” They are non-nutritive sweeteners and are reported to be 200 to 400 times sweeter than table sugar ².

Stevia is found in many processed foods and drinks, such as desserts, chewing gum, baked goods, candy, and yogurt. It is also used as a tabletop sweetener. Stevia can be used as a substitute for sugar when you are baking. For best results, follow the package instructions for using it in your recipes.

FDA has received many “generally recognized as safe” GRAS Notices for the use of high-purity (95% minimum purity) steviol glycosides including Rebaudioside A (also known as Reb A), Stevioside, Rebaudioside D, or steviol glycoside mixture preparations with Rebaudioside A and/or Stevioside as predominant components. This means that qualified experts agree the available scientific evidence about this sugar substitute shows it is safe for use in foods and drinks. FDA has not questioned the notifiers’ GRAS determinations for these high-purity stevia derived sweeteners under the intended conditions of use identified in the GRAS notices submitted to FDA. FDA’s response letters on such high-purity steviol glycosides are available at FDA’s GRAS Notice Inventory website ⁷⁹.

• However, the use of stevia leaf and crude stevia extracts is not considered GRAS and their import into the United States is not permitted for use as sweeteners. For details, see Import Alert 45-06 ⁸⁰.

A lot of food manufacturers use the term “natural” to describe their products. But there is no industry-approved definition of the word, so its use is often meaningless ⁹. When it comes to non-nutritive sweeteners, “natural” usually refers to those that are made from a substance found in nature and/or without artificial or synthetic additives e.g. Stevia. Artificial sweeteners, on the other hand, are created in a laboratory e.g. Sucralose.

But there is no research to suggest that non-nutritive natural sweeteners are healthier or better for you in any way compared with their competitors ⁹.

Natural sweeteners can also refer to sweeteners with calories, such as maple syrup, molasses, barley malt and rice syrups, honey, agave nectar, coconut sugar, date sugar, and sucanat. These sweeteners are essentially less processed and arguably better for you than sugar because they contain some trace vitamins and minerals. But don’t get excited—sugar is really still sugar, and it’s far from a healthy food choice. A good goal: no more sugar from all sources than the equivalent of 6 teaspoons for women and 9 teaspoons for men each day ⁹.

References

1. U.S. Food and Drug Administration. CFR – Code of Federal Regulations Title 21. Sec. 172.831 Sucralose. https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/cfrsearch.cfm?fr=172.831
2. U.S. Food and Drug Administration. Additional Information about High-Intensity Sweeteners Permitted for use in Food in the United States. https://www.fda.gov/food/ingredientspackaginglabeling/foodadditivesingredients/ucm397725.htm
3. Biocatalytic synthesis of disaccharide high-intensity sweeterner sucralose via a tetrachlororaffinose intermediate. Bennett C, Dordick JS, Hacking AJ, Cheetham PS. Biotechnol Bioeng. 1992 Jan 20; 39(2):211-7. https://www.ncbi.nlm.nih.gov/pubmed/18600933/
4. Anderson M., Opawale F., Rao M., Delmarre D., Anyarambhatla G. Excipients for oral liquid formulations. In: Katdare A., Chaubal M. V., editors. Excipient development for pharmaceutical biotechnology, and drug delivery systems. New York, NY: Informa Healthcare USA; 2006. pp. 155–180.
5. Li X., Du Z., Huang X., Yuan W., Ying H. Solubility of sucralose in different solvents from (283.15 to 333.15) K. J. Chem. Eng. Data. 2010;55:2600–2602.
6. Sweeteners: state of knowledge review. Schiffman SS, Gatlin CA. Neurosci Biobehav Rev. 1993 Fall; 17(3):313-45. https://www.ncbi.nlm.nih.gov/pubmed/8272285/
7. Involvement of cytochrome P450 2E1 in the (omega-1)-hydroxylation of oleic acid in human and rat liver microsomes. Adas F, Berthou F, Picart D, Lozac’h P, Beaugé F, Amet Y. J Lipid Res. 1998 Jun; 39(6):1210-9. https://www.ncbi.nlm.nih.gov/pubmed/9643352/
8. EU Scientific Committee on Food. Sucralose in food. https://ec.europa.eu/jrc/en/interlaboratory-comparison/sucralose-food
9. American Diabetes Association. 5 Must-Know Facts About Sweeteners. http://www.diabetesforecast.org/2016/jan-feb/5-must-know-facts-about-sweeteners.html
10. Miller PE, Perez V. Low-calorie sweeteners and body weight and composition: a meta-analysis of randomized controlled trials and prospective cohort studies. The American Journal of Clinical Nutrition. 2014;100(3):765-777. doi:10.3945/ajcn.113.082826. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4135487/
11. American Diabetes Association. Not Completely Carbohydrate and Calorie-Free. http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/understanding-carbohydrates/artificial-sweeteners/not-completely-carbohydrate.html
12. Joint Expert Commission on Food Additives of the World Health Organization and the Food and Agriculture Organization. http://www.codexalimentarius.net/web/jecfa.jsp
13. American Diabetes Association. Using Sugar Substitutes in the Kitchen. http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/understanding-carbohydrates/artificial-sweeteners/using-sugar-substitutes.html
14. Schiffman SS, Rother KI. Sucralose, A Synthetic Organochlorine Sweetener: Overview of Biological Issues. Journal of Toxicology and Environmental Health Part B, Critical Reviews. 2013;16(7):399-451. doi:10.1080/10937404.2013.842523. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3856475/
15. Schiffman S. S. Rationale for further medical and health research on high-potency sweeteners. Chem. Senses. 2012;37:671–679. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3440882/
16. Schiffman S. S., Abou-Donia M. B. Sucralose revisited: Rebuttal of two papers about Splenda safety. Regul. Toxicol. Pharmacol. 2012;63:505–508. https://www.ncbi.nlm.nih.gov/pubmed/22579627
17. Sims J., Roberts A., Daniel J. W., Renwick A. G. The metabolic fate of sucralose in rats. Food Chem. Toxicol. 2000;38(suppl. 2):S115–S121. https://www.ncbi.nlm.nih.gov/pubmed/10882824
18. Roberts A., Renwick A. G., Sims J., Snodin D. J. Sucralose metabolism and pharmacokinetics in man. Food Chem. Toxicol. 2000;38(suppl. 2):S31–S41. https://www.ncbi.nlm.nih.gov/pubmed/10882816
19. Grice H. C., Goldsmith L. A. Sucralose—An overview of the toxicity data. Food Chem. Toxicol. 2000;38(suppl. 2):S1–S6. https://www.ncbi.nlm.nih.gov/pubmed/10882813
20. Molinary S. V., Quinlan M. E. Sucralose. In: Mitchell H., editor. Sweeteners and sugar alternatives in food technology. Oxford, UK: Blackwell; 2006. pp. 130–148.
21. Grotz V. L., Munro I. C. An overview of the safety of sucralose. Regul. Toxicol. Pharmacol. 2009;55:1–5. https://www.ncbi.nlm.nih.gov/pubmed/19464334
22. Hawkins D. R., Wood S. W., Waller A. R., Jordan M. C. Enzyme induction studies of TGS and TGS-HP in the rat. 1987. Unpublished report from Huntingdon Research Centre, Huntingdon, U.K. Submitted to the World Health Organization by Tate & Lyle. Referenced in WHO (World Health Organization). 1989. Trichlorogalactosucrose. In Toxicological evaluation of certain food additives and contaminants WHO Food Additives Series, no. 24. Cambridge University Press, 1989, no. 655. http://www.inchem.org/documents/jecfa/jecmono/v024je05.htm
23. Sasaki Y. F., Kawaguchi S., Kamaya A., Ohshita M., Kabasawa K., Iwama K., Taniguchi K., Tsuda S. The comet assay with 8 mouse organs: Results with 39 currently used food additives. Mutat. Res. 2002;519:103–119. https://www.ncbi.nlm.nih.gov/pubmed/12160896
24. Hutchinson S. A. The effect of pH, temperature and reactants on the thermal and non-thermal degradation of the high-intensity sweeteners: Alitame and sucralose. 1996. PhD dissertation. New Brunswick, NJ: Rutgers University.
25. Hutchinson S. A., Ho G. S., Ho C. T. Stability and degradation of the high-intensity sweeteners: Aspartame, alitame, and sucralose. Food Rev. Int. 1999;15:249–261.
26. Bannach G., Almeida R. R., Lacerda L. G., Schnitzler E., Ionashiro M. Thermal stability and thermal decomposition of sucralose. Ecl. Quím. São Paulo. 2009;34:21–26.
27. Rahn A., Yaylayan V. A. Thermal degradation of sucralose and its potential in generating chloropropanols in the presence of glycerol. Food Chem. 2010;118:56–61.
28. European Union. Directive 2003/115/EC of the European Parliament and of the Council of 22 December 2003 amending Directive 94/35/EC on sweeteners for use in foodstuffs. Off. J. Eur. Union. 2004;47(L24):65–71. http://eur-lex.europa.eu/legal-content/en/ALL/?uri=OJ:L:2004:024:TOC
29. National Cancer Institute at the National Institutes of Health. Artificial Sweeteners and Cancer. https://www.cancer.gov/about-cancer/causes-prevention/risk/diet/artificial-sweeteners-fact-sheet
30. Patel RM, Sarma R, Grimsley E. Headache. 2006 Sep;46(8):1303-4. Popular sweetner sucralose as a migraine trigger.
31. Young D. A., Bowen W. H. The influence of sucralose on bacterial metabolism. J. Dent. Res. 1990;69:1480–1484. https://www.ncbi.nlm.nih.gov/pubmed/2143512
32. Labare M. P., Alexander M. Microbial cometabolism of sucralose, a chlorinated disaccharide, in environmental samples. Appl. Microbiol. Biotechnol. 1994;42:173–178. https://www.ncbi.nlm.nih.gov/pubmed/7765816
33. Abou-Donia M. B., El-Masry E. M., Abdel-Rahman A. A., McLendon R. E., Schiffman S. S. Splenda alters gut microflora and increases intestinal P-glycoprotein and cytochrome P-450 in male rats. J. Toxicol. Environ. Health A. 2008;71:1415–1429. https://www.ncbi.nlm.nih.gov/pubmed/18800291
34. Prashant G. M., Patil R. B., Nagaraj T., Patel V. B. The antimicrobial activity of the three commercially available intense sweeteners against common periodontal pathogens: An in vitro study. J. Contemp. Dent. Pract. 2012;13:749–752. https://www.ncbi.nlm.nih.gov/pubmed/23403996
35. Jang H. J., Kokrashvili Z., Theodorakis M. J., Carlson O. D., Kim B. J., Zhou J., Kim H. H., Xu X., Chan S. L., Juhaszova M., Bernier M., Mosinger B., Margolskee R. F., Egan J. M. Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide-1. Proc. Natl. Acad. Sci. USA. 2007;104:15069–15074. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1986614/
36. Margolskee R. F., Dyer J., Kokrashvili Z., Salmon K. S. H., Ilegems E., Daly K., Maillet E. L., Ninomiya Y., Mosinger B., Shirazi-Beechey S. P. T1R3 and gustducin in gut sense sugars to regulate expression of Na+-glucose cotransporter 1. Proc. Natl. Acad. Sci. USA. 2007;104:15075–15080. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1986615/
37. Nakagawa Y., Nagasawa M., Yamada S., Hara A., Mogami H., Nikolaev V. O., Lohse M. J., Shigemura N., Ninomiya Y., Kojima I. Sweet taste receptor expressed in pancreatic ß-cells activates the calcium and cyclic AMP signaling systems and stimulates insulin secretion. PLoS One. 2009;4:e5106. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2663034/
38. Ren X., Zhou L., Terwilliger R., Newton S. S., de Araujo I. E. Sweet taste signaling functions as a hypothalamic glucose sensor. Front. Integr. Neurosci. 2009;3:12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706652/
39. Murphy KG, Bloom SR (2006). Gut hormones and the regulation of energy homeostasis. Nature 444, 854–859. https://www.nature.com/nature/journal/v444/n7121/full/nature05484.html
40. Ghatei MA, Uttenthal LO, Christofides ND, Bryant MG, Bloom SR (1983). Molecular forms of human enteroglucagon in tissue and plasma: plasma responses to nutrient stimuli in health and in disorders of the upper gastrointestinal tract. J Clin Endocrinol Metab 57, 488–495. https://www.ncbi.nlm.nih.gov/pubmed/6874888?dopt=Abstract
41. Adrian TE, Ferri GL, Bacarese-Hamilton AJ, Fuessl HS, Polak JM, Bloom SR (1985). Human distribution and release of a putative new gut hormone, peptide YY. Gastroenterology 89, 1070–1077. https://www.ncbi.nlm.nih.gov/pubmed/3840109?dopt=Abstract
42. Le Roux CW, Batterham RL, Aylwin SJ, Patterson M, Borg CM, Wynne KJ et al. (2006). Attenuated peptide YY release in obese subjects is associated with reduced satiety. Endocrinology 147, 3–8. https://www.ncbi.nlm.nih.gov/pubmed/16166213?dopt=Abstract
43. Freeman J. S. Role of the incretin pathway in the pathogenesis of type 2 diabetes mellitus. Cleve. Clin. J. Med. 2009;76(suppl. 5):S12–S19. https://www.ncbi.nlm.nih.gov/pubmed/19952298
44. Batterham RL, Cowley MA, Small CJ, Herzog H, Cohen MA, Dakin CL et al. (2002). Gut hormone PYY(3-36) physiologically inhibits food intake. Nature 418, 650–654. https://www.ncbi.nlm.nih.gov/pubmed/12167864?dopt=Abstract
45. Challis BG, Pinnock SB, Coll AP, Carter RN, Dickson SL, O’rahilly S (2003). Acute effects of PYY3-36 on food intake and hypothalamic neuropeptide expression in the mouse. Biochem Biophys Res Commun 311, 915–919. https://www.ncbi.nlm.nih.gov/pubmed/14623268?dopt=Abstract
46. Halatchev IG, Ellacott KL, Fan W, Cone RD (2004). Peptide YY3-36 inhibits food intake in mice through a melanocortin-4 receptor-independent mechanism. Endocrinology 145, 2585–2590. https://www.ncbi.nlm.nih.gov/pubmed/15016721?dopt=Abstract
47. Talsania T, Anini Y, Siu S, Drucker DJ, Brubaker PL (2005). Peripheral exendin-4 and peptide YY(3-36) synergistically reduce food intake through different mechanisms in mice. Endocrinology 146, 3748–3756. https://www.ncbi.nlm.nih.gov/pubmed/15932924?dopt=Abstract
48. Chelikani PK, Haver AC, Reeve Jr JR, Keire DA, Reidelberger RD (2006). Daily, intermittent intravenous infusion of peptide YY(3-36) reduces daily food intake and adiposity in rats. Am J Physiol Regul Integr Comp Physiol 290, R298–R305. https://www.ncbi.nlm.nih.gov/pubmed/16210414?dopt=Abstract
49. Flint A, Raben A, Astrup A, Holst JJ (1998). Glucagon-like peptide 1 promotes satiety and suppresses energy intake in humans. J Clin Invest 101, 515–520. https://www.ncbi.nlm.nih.gov/pubmed/9449682?dopt=Abstract
50. Gutzwiller JP, Goke B, Drewe J, Hildebrand P, Ketterer S, Handschin D et al. (1999). Glucagon-like peptide-1: a potent regulator of food intake in humans. Gut 44, 81–86. https://www.ncbi.nlm.nih.gov/pubmed/9862830?dopt=Abstract
51. Degen L, Oesch S, Casanova M, Graf S, Ketterer S, Drewe J et al. (2005). Effect of peptide YY3-36 on food intake in humans. Gastroenterology 129, 1430–1436. https://www.ncbi.nlm.nih.gov/pubmed/16285944?dopt=Abstract
52. Ford HE, Peters V, Martin NM, Sleeth ML, Ghatei MA, Frost GS, Bloom SR. Eur J Clin Nutr. 2011 Apr;65(4):508-13. doi: 10.1038/ejcn.2010.291. Epub 2011 Jan 19. Effects of oral ingestion of sucralose on gut hormone response and appetite in healthy normal-weight subjects. https://www.nature.com/ejcn/journal/v65/n4/full/ejcn2010291a.html
53. Pepino M. Y., Tiemann C. D., Patterson B. W., Wice B. M., Klein S. Sucralose affects glycemic and hormonal responses to an oral glucose load. Diabetes Care. 2013;36:2530–2535. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3747933/
54. American Heart Association. Artificial sweeteners may increase blood sugar. http://news.heart.org/artificial-sweeteners-may-increase-blood-sugar/
55. Nature doi:10.1038/nature13793. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. https://www.nature.com/nature/journal/vaop/ncurrent/pdf/nature13793.pdf
56. A Scientific Statement From the American Heart Association and the American Diabetes Association. Nonnutritive Sweeteners: Current Use and Health Perspectives. http://circ.ahajournals.org/content/circulationaha/126/4/509.full.pdf
57. Azad MB, Abou-Setta AM, Chauhan BF, et al. Nonnutritive sweeteners and cardiometabolic health: a systematic review and meta-analysis of randomized controlled trials and prospective cohort studies. CMAJ : Canadian Medical Association Journal. 2017;189(28):E929-E939. doi:10.1503/cmaj.161390. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5515645/
58. U.S. National Library of Medicine. Medline Plus. Could Artificial Sweeteners Raise Your Odds for Obesity ?. https://medlineplus.gov/news/fullstory_167249.html
59. Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain. Fowler SP, Williams K, Resendez RG, Hunt KJ, Hazuda HP, Stern MP. Obesity (Silver Spring). 2008 Aug; 16(8):1894-900. https://www.ncbi.nlm.nih.gov/pubmed/18535548/
60. Artificial sweetener use and one-year weight change among women. Stellman SD, Garfinkel L. Prev Med. 1986 Mar; 15(2):195-202. https://www.ncbi.nlm.nih.gov/pubmed/3714671/
61. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Dhingra R, Sullivan L, Jacques PF, Wang TJ, Fox CS, Meigs JB, D’Agostino RB, Gaziano JM, Vasan RS. Circulation. 2007 Jul 31; 116(5):480-8. https://www.ncbi.nlm.nih.gov/pubmed/17646581/
62. Dietary intake and the development of the metabolic syndrome: the Atherosclerosis Risk in Communities study. Lutsey PL, Steffen LM, Stevens J. Circulation. 2008 Feb 12; 117(6):754-61. https://www.ncbi.nlm.nih.gov/pubmed/18212291/
63. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. Yang Q. Yale J Biol Med. 2010 Jun; 83(2):101-8. https://www.ncbi.nlm.nih.gov/pubmed/20589192/
64. A role for sweet taste: calorie predictive relations in energy regulation by rats. Swithers SE, Davidson TL. Behav Neurosci. 2008 Feb; 122(1):161-73. https://www.ncbi.nlm.nih.gov/pubmed/18298259/
65. General and persistent effects of high-intensity sweeteners on body weight gain and caloric compensation in rats. Swithers SE, Baker CR, Davidson TL. Behav Neurosci. 2009 Aug; 123(4):772-80. https://www.ncbi.nlm.nih.gov/pubmed/19634935/
66. High-intensity sweeteners and energy balance. Swithers SE, Martin AA, Davidson TL. Physiol Behav. 2010 Apr 26; 100(1):55-62. https://www.ncbi.nlm.nih.gov/pubmed/20060008/
67. Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements. Swithers SE. Trends Endocrinol Metab. 2013 Sep; 24(9):431-41. https://www.ncbi.nlm.nih.gov/pubmed/23850261/
68. Patterns of weight change and their relation to diet in a cohort of healthy women. Colditz GA, Willett WC, Stampfer MJ, London SJ, Segal MR, Speizer FE. Am J Clin Nutr. 1990 Jun; 51(6):1100-5. https://www.ncbi.nlm.nih.gov/pubmed/2349925/
69. Inverse association between the effect of carbohydrates on blood glucose and subsequent short-term food intake in young men. Anderson GH, Catherine NL, Woodend DM, Wolever TM. Am J Clin Nutr. 2002 Nov; 76(5):1023-30. https://www.ncbi.nlm.nih.gov/pubmed/12399274/
70. A trial of sugar-free or sugar-sweetened beverages and body weight in children. de Ruyter JC, Olthof MR, Seidell JC, Katan MB. N Engl J Med. 2012 Oct 11; 367(15):1397-406. https://www.ncbi.nlm.nih.gov/pubmed/22998340/
71. A randomized trial of sugar-sweetened beverages and adolescent body weight. Ebbeling CB, Feldman HA, Chomitz VR, Antonelli TA, Gortmaker SL, Osganian SK, Ludwig DS. N Engl J Med. 2012 Oct 11; 367(15):1407-16. https://www.ncbi.nlm.nih.gov/pubmed/22998339/
72. Sucrose activates human taste pathways differently from artificial sweetener. Frank GK, Oberndorfer TA, Simmons AN, Paulus MP, Fudge JL, Yang TT, Kaye WH. Neuroimage. 2008 Feb 15; 39(4):1559-69. https://www.ncbi.nlm.nih.gov/pubmed/18096409/
73. Amygdala response to sucrose consumption is inversely related to artificial sweetener use. Rudenga KJ, Small DM. Appetite. 2012 Apr; 58(2):504-7. https://www.ncbi.nlm.nih.gov/pubmed/22178008/
74. Lack of effect of sucralose on glucose homeostasis in subjects with type 2 diabetes. Grotz VL, Henry RR, McGill JB, Prince MJ, Shamoon H, Trout JR, Pi-Sunyer FX. J Am Diet Assoc. 2003 Dec; 103(12):1607-12. https://www.ncbi.nlm.nih.gov/pubmed/14647086/
75. World Health Organization. Obesity and overweight 2016. Updated June 2016. http://www.who.int/mediacentre/factsheets/fs311/en/
76. U.S. Food and Drug Administration. Aspartame; Commissioner’s Final Decision. Friday 24 July, 1981. https://www.fda.gov/downloads/Food/IngredientsPackagingLabeling/FoodAdditivesIngredients/UCM404380.pdf
77. U.S. Food and Drug Administration. Aspartame. https://www.fda.gov/downloads/Food/IngredientsPackagingLabeling/FoodAdditivesIngredients/UCM404332.pdf
78. U.S. Food and Drug Administration. Aspartame. https://www.gpo.gov/fdsys/pkg/FR-1996-06-28/pdf/96-16522.pdf
79. U.S. Food and Drug Administration. GRAS Notices. https://www.accessdata.fda.gov/scripts/fdcc/?set=GRASNotices
80. U.S. Food and Drug Administration. Import Alert 45-06. https://www.accessdata.fda.gov/cms_ia/importalert_119.html

Health Benefits of Pomegranate

The pomegranate (Punica garanatum L.) fruit has a leathery rind (or husk) with many little pockets of edible seeds and juice inside. Researchers have studied all parts of the pomegranate for their potential health benefits. Those parts include the fruit, seed, seed oil, tannin-rich peel, root, leaf, and flower. The pomegranate has been used as a dietary supplement for many conditions including wounds, heart conditions, intestinal problems, and as a gargle for a sore throat.
Pomegranate is made into capsules, extracts, teas, powders, and juice products ¹.

Pomegranate is a long-lived and drought-tolerant plant. Arid and semiarid zones are popular for growing pomegranate trees. They are widely cultivated in Iran, India, and the Mediterranean countries such as Turkey, Egypt, Tunisia, Spain, and Morocco ². However, pomegranate is categorized as a berry but it belongs to its own botanical family, Punicaceae. The only genus is Punica, with one predominant species called P. granatum ³.

The pomegranate is an ancient fruit native to regions from the Himalayas in northern India to Iran. In recent years, however, cultivation of pomegranate has disseminated throughout many dry regions of the world, including parts of the United States. The trees can grow up to 30 feet in height. The leaves are opposite, narrow, oblong with 3-7 cm long and 2 cm broad. It has bright red, orange, or pink flowers, which are 3 cm in diameter with four to five petals. Edible pomegranate fruit has a rounded hexagonal shape, with 5-12 cm in diameter and weighing 200 g. The thick skin surrounds around 600 arils, which encapsulates the seeds ⁴.

Apart from fruit, pomegranate is available in various forms such as bottled juice (fresh or concentrated), powdered capsules, and tablets, which are derived from seed, fermented juice, peel, leaf and flower, gelatin capsules of seed oil extracts, dry or beverage tea from leaves or seeds, and other food productions such as jams, jellies, sauces, salad dressings, and vinegars. Anardana, which is the powdered form of pomegranate seed, is used as a form of spice ⁴.

Pomegranate nutrition facts

The 100 g edible portion of pomegranate contains water (77.93 g), protein (1.67 g), lipids (1.17 g), ash (0.53 g), carbohydrates (18.7 g), fiber (4 g) and sugars (13.67 g) (see Table 1).

Figure 1. Pomegranate rind and seed

Table 1. Pomegranate (Raw) Nutrition Content

Nutrient	Unit	Value per 100 g	cup arils (seed/juice sacs) 87 g	pomegranate (4″ dia) 282 g
Approximates
Water	g	77.93	67.8	219.76
Energy	kcal	83	72	234
Protein	g	1.67	1.45	4.71
Total lipid (fat)	g	1.17	1.02	3.3
Carbohydrate, by difference	g	18.7	16.27	52.73
Fiber, total dietary	g	4	3.5	11.3
Sugars, total	g	13.67	11.89	38.55
Minerals
Calcium, Ca	mg	10	9	28
Iron, Fe	mg	0.3	0.26	0.85
Magnesium, Mg	mg	12	10	34
Phosphorus, P	mg	36	31	102
Potassium, K	mg	236	205	666
Sodium, Na	mg	3	3	8
Zinc, Zn	mg	0.35	0.3	0.99
Vitamins
Vitamin C, total ascorbic acid	mg	10.2	8.9	28.8
Thiamin	mg	0.067	0.058	0.189
Riboflavin	mg	0.053	0.046	0.149
Niacin	mg	0.293	0.255	0.826
Vitamin B-6	mg	0.075	0.065	0.211
Folate, DFE	µg	38	33	107
Vitamin B-12	µg	0	0	0
Vitamin A, RAE	µg	0	0	0
Vitamin A, IU	IU	0	0	0
Vitamin E (alpha-tocopherol)	mg	0.6	0.52	1.69
Vitamin D (D2 + D3)	µg	0	0	0
Vitamin D	IU	0	0	0
Vitamin K (phylloquinone)	µg	16.4	14.3	46.2
Lipids
Fatty acids, total saturated	g	0.12	0.104	0.338
Fatty acids, total monounsaturated	g	0.093	0.081	0.262
Fatty acids, total polyunsaturated	g	0.079	0.069	0.223
Fatty acids, total trans	g	0	0	0
Cholesterol	mg	0	0	0
Other
Caffeine	mg	0	0	0

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ⁵]

Pomegranate Chemical Composition

46% weight per weight (w/w) of pomegranate is used as a juice, and the rest of it is considered to be waste. Pomegranate’s arils are depicted in Figure 1 as the edible red pulp that surrounds the seed that is used by juice manufacturing companies to produce pomegranate juice. The remaining solid waste from pomegranates, after juice extraction, the pomegranate rind and pomegranate seed contain various bioactive and nutritional components, such as flavonoids (e.g., anthocyanins), hydrolyzable tannins (e.g., punicalagin and ellagic acid), and fatty acids (e.g., punicic acid) ⁶. These components in pomegranate biowaste have various potential value addition applications in food and skin health ⁷. Table 2 shows some of the chemical properties of pomegranate rind and seed to help outline the various applications that add value to pomegranate’s biowaste as functional ingredients in food. For instance, pomegranate seed is a source of dietary fiber that has applications as a food additive in fiber-enriched products, including dough ⁸ and chicken nuggets ⁹.

The pomegranate rind is one of the waste components that comprises 43% w/w of the pomegranate fruit. Pomegranate seeds are another waste component of pomegranate and compose 11% w/w of the fruit. The oil content that is extracted from pomegranate seeds varies in weight percentages, depending on their cultivars, and it constitutes approximately 7.6–20% w/w of the pomegranate seed ¹⁰. The oil content of pomegranate varies depending on the climate of the growing region, the maturity of the fruit, cultivation practices, and storage conditions ¹¹.

Table 2. Chemical properties of pomegranate seed and rind by dry weight

Property	Seed Amount	Rind Amount
Moisture	10.44–12.86%	67.26–73.23%
Sugar	N/A	30.65–34.83%
Crude Oil	10.89–13.24%	N/A
Crude Protein	6.71–8.11%	3.96–7.13%
Crude Ash	1.61–2.29%	3.71–4.97%
Fiber	17.33–27.84%	28.10–33.93%
Pectin	N/A	6.8–10.1%

[Source ⁶ ]

Pomegranate seed

About 18% of dried and cleaned white pomegranate seeds are oil ¹². Figure 2 shows the five major fatty acid components found in pomegranate seed oil. There are 45 identified different fatty acids in pomegranate seed oil, with conjugated fatty acids making up over 80% weight/volume percentage (w/v%) of its composition ¹³. There are some phytoestrogen compounds in pomegranate seeds that have sex steroid hormones similar to those in humankind. The 17-alpha-estradiol is a mirror-image version of estrogen ⁴.

Punicic acid is the main fatty acid (~76%) in pomegranate seed oil, being followed closely by linoleic and oleic acids ¹⁴. Some studies show the health benefits of specific fatty acid components within the pomegranate seed oil, such as punicic acid’s role in preventing diabetes and related obesities ¹⁵. It has also been shown that punicic acid can inhibit skin cancer ¹⁶ and prevent type 2 diabetes in rats ¹⁷ and it possesses anti-diabetic, anti-obesity, anti-inflammatory, anticancer, and antioxidant properties ¹⁸. Similarly, a wide scope of applications for pomegranate seed oil extracts as a whole exist, including in food packaging, fat substitution, animal food production and functional ingredient, and antimicrobial agent and pharmaceutical capacities ¹³. There is an increasing demand and acceptance for pomegranate seed oil for consumers in the cosmetics, food, and pharmaceutical industries globally due to pomegranate seed oil’s valuable phytochemical composition and functional properties. The oil also has feasible extraction procedures, and it has applications in cosmetic products, especially in Europe ¹³.

Figure 2. Pomegranate seed oil major fatty acids

Figure 3. Punicic acid chemical structure

Pomegranate juice

Pomegranate juice is a good source of fructose, sucrose, and glucose ¹². Pomegranate juice also has some of the simple organic acids such as ascorbic acid, citric acid, fumaric acid, and malic acid. In addition, it contains small amounts of all amino acids, specifically proline, methionine, and valine. Both pomegranate juice and peel are rich in polyphenols. The largest classes include tannins and flavonoids that indicate pharmacological potential of pomegranate due to their strange antioxidative and preservative activities ⁴.

Ellagitannin is a type of tannins; it can be broken down into hydroxybenzoic acid such as ellagic acid. It is widely used in plastic surgeries, which prevents skin flap’s death due to its antioxidant activity ¹². Two other ellagitannins that are found in both pomegranate juice and peel are punicalagin and punicalin ¹². Several classes of pomegranate flavonoids include anthocyanins, flavan 3-ols, and flavonols. Pomegranate juice and peel have catechins with a high antioxidant activity. They are essential compounds of anthocyanin’s production with antioxidant and inflammatory role. Anthocyanins cause the red color of juice, which is not found in the peel. All pomegranate flavonoids show antioxidant activity with indirect inhibition of inflammatory markers such as tumor necrosis factor-alpha (TNF-α) ⁴.

Pomegranate rind

Pomegranate rind is the main non-edible portion that constitutes approximately 43% w/w of the fruit. Pomegranate rind is a source of bioactive compounds, including flavonoids, complex polysaccharides, minerals, and hydrolyzable tannins, such as punicalagin, ellagic, and gallic acid ⁷. Pomegranate rind has a variety of applications in wastewater treatment, including being used in the removal of phenolic compounds ¹⁹, in the removal of dye from wastewater by conversion of pomegranate rind to activated carbon ²⁰ and as renewable energy material sources ²¹. Pomegranate rind is a rich source of dietary fiber and pectin, as shown in Table 2. In one study, pomegranate rind powder was added to the diet of hypercholesteremic rats as a source of dietary fiber, and it has been shown to combat the risks that are associated with hypercholesterolemia such as lipid peroxidation ²². Pomegranate rind has also been supplemented in foods, such as cookies, to enhance its nutritional benefits ²³. Pomegranate rind’s phenolics assisted in improving oxidative stability during food storage in addition to significantly increasing the cookies’ dietary fiber content, which allows the product to be marketed towards health-conscious consumers ⁶. The phenolics in cookies also improve the antioxidant activity in the gastrointestinal tract at a 7.5% w/w of rind extract and regulates glucose metabolism by inhibiting alpha-glucosidase ²⁴. Alpha glucosidase enzymes catalyze hydrolysis of starch to produce glucose. In humans, these enzymes aid digestion of dietary carbohydrates and starches to produce glucose for intestinal absorption, which in turn, leads to increase in blood glucose levels. Inhibiting the function of these enzymes in patients with type-2 diabetes may reduce hyperglycemia. These findings suggest additional health benefits in the digestive tract, using pomegranate rind in bakery foods. In addition, pomegranate pectin has found food-related applications as a gelling agent ²⁵ and an emulsifier ²⁶. The properties and bioactive composition of pomegranate rind are what allows it to have several applications in skin health and food industries. Table 2 shows the chemical properties of the pomegranate seed and rind, which correspond to some of the potential uses of pomegranate biowaste in food additives.

Pomegranate bark and roots

The pomegranate tree’s bark and roots are rich sources of chemicals called alkaloids. They are carbon-based substances; they were used to treat worms in the human gastrointestinal tract in traditional medicine ⁴.

How to Eat a Pomegranate

Inside a pomegranate are those glistening red jewels – they are called arils (juice sacs). The arils are full of delicious, nutritious sweet juice that surround a small white crunchy seed. You can eat the whole arils including the fiber-rich seeds, or spit out the seeds if you prefer- it’s your choice. The rind and the white membranes surrounding the arils are bitter and we don’t suggest eating them- although some say even that part of the pomegranate has medicinal value.

How do you remove the seeds/arils?

To remove the seeds follow this simple 3 steps process:

Step 1. Cut the crown end off a pomegranate. Then cut the pomegranate in half vertically.

Step 2. Hold the pomegranate half, cut side down, over a deep bowl the roll out the arils with your fingers and discard everything else.

Step 3. Strain out the water. Then eat the succulent arils whole, seeds and all.

[Source: Pomegranate Council. ²⁷]

How do you juice a pomegranate ?

There are 3 main methods to get fresh squeezed juice:

• Juicer Method: Cut the fresh pomegranate in half as you would a grapefruit. The Pomegranate Council ²⁷ recommends using a hand-press juicer to juice a pomegranate. If you use an electric juicer, take care not to juice the membrane, so that the juice remains sweet. Strain the juice through a cheesecloth-lined strainer or sieve. Be cautious, as pomegranate juice can stain.

• Blender Method: Place 1 ½ to 2 cups seeds in a blender; blend until liquefied. Pour through a cheesecloth-lined strainer or sieve.

• Rolling Method: On a hard surface, press the palm of your hand against a pomegranate and gently roll to break all of the seeds inside (crackling stops when all seeds have broken open). Pierce the rind and squeeze out juice, or poke in a straw and press to release the juice. NOTE: Rolling can be done inside a plastic bag to contain any juice that may leak through the skin ²⁷.

Health effects of Pomegranate

Pomegranate has been heavily used in various ancient medicines, such as Ayurveda, for treatment of diabetes. As a result of its rapidly increasing production and consumption throughout the world, a considerable amount of recent research has explored the potential of pomegranate to fight for obesity and diabetes.

A study in male mice showed that consumption of pomegranate seed oil reduced weight gain, improved key markers that lead to the development of type-2 diabetes, and improved insulin sensitivity – all suggesting a diminished develpoment to type-2 diabetes ²⁸. Experiments in 3T3-L1 pre-adipocytes demonstrated that punicic acid, a conjugated linolenic acid found in pomegranate, activates peroxisome proliferator-activated receptor-gamma (PPAR-γ), an important target of insulin action and energy metabolism. Pucinic acid also augmented PPARγ downstream gene expression, and demonstrates an impaired ability to alleviate the pathogenesis of diabetes in PPARγ knockdown immune cells ²⁹. This suggests that pomegranate may be a natural complement to the synthetic thiazolidinediones (anti-diabetic drugs and PPAR-γ agonists), and alleviate pathogenesis of obesity and diabetes through a PPAR-γ mediated mechanism. In the Otsuka Long-Evans Tokushima Fatty rat model, pomegranate seed oil rich in punicic acid significantly decreased hepatic triacylglycerol contents and levels of monounsaturated fatty acid (MUFA) , which can be preventive for development of hepatic steatosis ³⁰. In obese rats, a model of metabolic syndrome, supplementation with pomegranate fruit extract and juice markedly decreased expression of vascular inflammatory markers such as thrombospondin and TGF-β ³¹. Also, a 4 week clinical trial administering 400 mg of pomegranate seed oil twice a day in hyperlipidemic subjects significantly improved the lipid profile as shown by a decreased triglyceride:HDL “good” cholesterol ratio ³².

Furthermore, pomegranate has shown dramatic antioxidant potential. It has been shown that pomegranate fruit extract, which is rich in polyphenolic antioxidants, represses the expression of oxidation-sensitive genes at the site of stress. More recently, studies show that pomegranate juice extract may prevent high blood pressure induced by Angiotensin II in diabetic rats by ameliorating oxidative stress and inhibiting Angiotensin-converting enzyme (ACE) activity ³³. Research is also heading towards development of a synergistic combination of various extracts. Recently, Fenercioglu et al ³⁴ demonstrated antagonizing effects on oxidative stress and lipid peroxidation of a supplement containing pomegranate extract, green tea extract, and absorbic acid in type 2 diabetic patients. All the above mentioned results clearly suggest that pomegranate can play an important role in the prevention of diabetes, obesity and their associated complication. Basis on these findings it can be suggested that pomegranate can considered as a rational complementary therapeutic agent to ameliorate obesity, diabetes and the resultant metabolic syndrome.

Pomegranate can induce its beneficial effects through its various metabolites. The antioxidant and antiatherosclerotic potentials of pomegranate are mainly relevant to the high polyphenol concentrations in pomegranate fruit such as ellagitannins and hydrolysable tannins ³⁵. COX-1 and COX-2 enzymes and IL-1 β activity can be inhibited by pomegranate fruit extract ³⁶.

It is suggested that pomegranate can antagonize the stimulation of mRNA of MMP-9 in THP-1/monocytes. The whole fruit and compounds inhibit TNF-induced MMP-9 promoter activity ³⁷. Urolithins are metabolites that are metabolized by the human intestinal microflora. These compounds decreased MMP-9 sretion and mRNA levels induced by HZ or TNF. It is suggested that ellagitannins are responsible for the control of excessive production of MMP-9, which could result in decreased production of noxious cytokine TNF ³⁸. TNF cytokines promote NFκB binding to target sequences while inducing transcription of several genes such as the MMP-9 gene ³⁹. Ellagitannins prevent NFκB promoter activity by blocking NFκB-driven transcription and affecting the entire cytokine cascade. Ellagitannins inhibit the activation of inflammatory pathways such as MAPK ⁴⁰. In addition, pomegranate compounds could inhibit angiogenesis through the downregulation of vascular endothelial growth factor in cancers ⁴¹.

Dietary fiber

Dietary fiber is found in fruits, vegetables, and whole grains. A high fiber diet helps to alleviate constipation, maintain healthy bowel movements, lower cholesterol levels, and control blood sugar levels ⁴². Pomegranate seed is shown to have a dietary fiber content of 17.33–27.84% w/w when six varieties of pomegranates from Turkey were tested (Table 2) ⁴³.

Pomegranate seed powder is a form of dietary fiber that can be used as a food additive. Pomegranate seed powder was used to replace a percentage of lean meat in the formulation of chicken nuggets in a study ⁹. The results showed that chicken nuggets had increased sensory attributes with a 3% w/w incorporation of pomegranate seed powder. There was also a significant increase in the crude fiber content of the nuggets with increasing levels of pomegranate seed powder. However, there was decreased emulsion stability as a result of decreased pH and water holding capacity and increased fat due to the abundance of fatty acids in pomegranate seeds ⁹. In a similar study on bread making, pomegranate seed flour was used to replace up to 5% w/w of the wheat flour without drastically changing the sensory qualities of the bread. The resulting bread was labeled as a good source of fiber with lower production costs ⁸. This is especially important because the bran and germ of wheat are taken out when wheat is milled, which causes a marked decrease in the dietary fiber content of the flour. When a portion of wheat flour was replaced with punicic acid-rich pomegranate seed powder, the bread’s dietary fiber, punicic acid, total polyphenol content, and radical scavenging activity were all increased ⁸. However, incorporating a 10% w/w level of pomegranate seed powder led to a slight decrease in the dough’s volume, crumb hardness, rheological properties, and sensory scores ⁴⁴. Pomegranate rind is also a source of dietary fiber and, when supplemented in cookies at an acceptable level of below 7.5% w/w, increases the crude fiber content by 80%. There was overall acceptability of the cookies, although this addition may have been attributed to the hardening of the cookies and a decline in sensory scores ²³.

Because fiber is an important nutrient needed to maintain healthy stool and bowel movements, the above studies show the merits of pomegranate in adding fiber to food products, such as chicken nuggets and dough, without drastically changing their sensory scores or quality. They also show the potential of pomegranate to be used as a source of fiber in other food products, such as granola bars. Pomegrain bars have been formulated in one study in optimized conditions with 55% w/w pomegranate seed powder.

Prostate cancer

After lung cancer, the second leading cause of male cancer death is prostate cancer worldwide. Its progress before onset of symptoms is slow; therefore, pharmacological and nutritional interventions could affect the quality of patient’s life by delaying its development ⁴⁵.

It was shown that pomegranate fruit could be used in the treatment of human prostate cancer because it could inhibit cell growth and induce apoptosis. It leads to induction of pro-apoptotic proteins (Bax and Bak) and downregulation of anti-apoptotic proteins (Bcl-xL and Bcl-2) ⁴⁶. Moreover, the presence of NFκB and cell viability of prostate cancer cell lines has been inhibited when using pomegranate fruit extract, because it blocks NFκB ⁴⁷. Polyphenols of fermented juice and pomegranate oil can inhibit the proliferation of LNCaP (epithelial cell line derived from a human prostate carcinoma), PC-3, and DU145 human prostate cancer cell lines. These effects were the result of changes in cell cycle distribution and apoptosis induction ⁴⁶. In addition, it is reported that pomegranate fruit extract oral administration in nude mice implanted with androgen-sensitive CWR22RV1 cells caused significant decrease in serum prostate-specific antigen (PSA) level and inhibited tumor growth ⁴⁷. Besides, the observed increase in NFκB activity during androgen dependence to androgen independence transition in the LAPC4 xenograft model was terminated ⁴⁸.

One small study ⁴⁹ from 2006 found that drinking a daily 227ml (8oz) glass of pomegranate juice significantly slowed the progress of prostate cancer in men with recurring prostate cancer. This was a well-conducted study, but more are needed to support these findings.

A more recent study ⁵⁰ from 2013 looked at whether giving men pomegranate extract tablets prior to surgery to remove cancerous tissue from the prostate would reduce the amount of tissue that needed to be removed. The results were not statistically significant, meaning they could have been down to chance.

Breast cancer

Fermented pomegranate juice has double the antiproliferative effect compared to fresh pomegranate juice in human breast cancer cell lines MCF-7 (breast cancer cell line isolated in 1970 from a 69-year-old Caucasian woman) and MB-MDA-231. In addition, pomegranate seed oil caused 90% prevention of proliferation of MCF-7 cells ⁵¹, ⁵².

Lung cancer

Pomegranate fruit extract can inhibit several signaling pathways, which can be used in the treatment of human lung cancer. Pathways include Mitogen-activated protein kinases (MAPK) PI3K/Akt and NFκB. In addition, there was a 4 day delay in the appearance of tumors (from 15 to 19 days) in mice implanted with A549 cells.[10] These studies indicate the chemopreventive effects of pomegranate fruit extract ⁴.

Colon cancer

Adams et al. ⁵³ have reported the anti-inflammatory effects of pomegranate juice on the signaling proteins in HT-29 human colon cancer cell line. Reduction in phosphorylation of the p65 subunit of NFκB, its binding to the NFκB response, and 79% inhibition in TNF-α protein expression have been observed with 50 mg/L concentration of pomegranate extract.

Skin cancer

It has been demonstrated that pomegranate oil has chemopreventive efficacy in mice. Reduced tumor incidence (7%), decrease in tumor numbers, reduction in ornithine decarboxylase activity (17%), significant inhibition in elevated Tissue plasminogen activator-mediated skin edema and hyperplasia, protein expression of ODC and COX-2, and epidermal ODC activity have been reported with pomegranate oil treatments ⁵⁴, ⁵⁵. Pomegranate extract in various concentrations (5-60 mg/L) was effective against UVA- and UVB-induced damage in SKU-1064 fibroblast cells of human, which was relevant in reducing NFκB transcription, downregulating proapoptotic caspase-3, and elevating the G0/G1 phase associated with deoxyribonucleic acid (DNA) repair ⁵⁶.

Cardiovascular diseases

Pomegranate juice is an affluent source of polyphenols with high antioxidative potential. Moreover, its antiatherogenic, antihypertensive, and anti-inflammatory effects have been shown in limited studies in human and murine models ³⁵.

Hypertension is the most common disease in primary care of patients. It is found in comorbidity with diabetes and cardiovascular disease, and the majority of patients do not tend to be medicated. Pomegranate juice prevents the activity of serum angiotensin-converting enzyme and reduces systolic blood pressure ⁵⁷. Angiotensin II acute subcutaneous administration causes increased blood pressure in diabetic Wistar rats. It has been shown that pomegranate juice administration (100 mg/kg) for 4 weeks could reduce the mean arterial blood pressure ⁵⁸. Pomegranate juice consumption resulted in 30% decrease in carotid intima-media thickness after 1 year. The patient’s serum paraoxonase 1 activity showed 83% increase, whereas both serum low dwnsity lipoprotein (LDL) basal oxidative state and LDL susceptibility to copper ion significantly decreased by 90% and 95%, respectively ⁵⁹.

Punicic acid, which is the main constituent of pomegranate seed oil, has antiatherogenic effects. In a study on 51 hyperlipidemic patients, pomegranate seed oil was administered twice a day (800 mg/day) for 4 weeks. There was a significant decrease in triglycerides (TG) and TG: High density lipoprotein (HDL) cholesterol ratio by 2.75 mmol/L and 5.7 mmol/L, respectively, whereas serum cholesterol, LDL-C, and glucose concentration remained unchanged ⁶⁰.

High plasma LDL concentration is the major risk factor for atherosclerosis. Therefore, LDL modifications, including oxidation, retention, and aggregation, play a key role in atherosclerosis as well. Studies have shown that consuming pomegranate juice for 2 weeks resulted in declined retention and aggregation of LDL susceptibility and increased activity of serum paraoxonase (a protective lipid peroxidation esterase related to HDL) by 20% in humans. Pomegranate juice administration in mice for 14 weeks showed reduced LDL oxidation by peritoneal macrophages by more than 90%, which was because of reduced cellular lipid peroxidation and superoxide release. The uptake of oxidized LDL showed 20% reduction in mice. The size of atherosclerotic lesions reduced by 44% after pomegranate juice supplementation ⁶¹. Moreover, pomegranate juice administration to apolipoprotein E-deficient mice with advanced atherosclerosis for 2 months reduced oxidized LDL (31%) and increased macrophage cholesterol efflux (39%) ⁶².

In cultured human endothelial cells and hypercholesterolemic mice, both pomegranate juice and fruit extract reduced the activation of ELK-1 and p-CREB (oxidation-sensitive responsive genes) and elevated the expression of endothelial nitric oxide synthase. It is suggested that polyphenolic antioxidant compounds in pomegranate juice are responsible for the reduction of oxidative stress and atherogenesis ⁶³.

In another study ⁶⁴, concentrated pomegranate juice was shown to reduce heart disease risk factors. Administration of concentrated pomegranate juice to 22 diabetic type 2 patients with hyperlipidemia could significantly reduce TC, LDL-C, LDL-C: HDL-C ratio, and TC: HDL-C ratio. However, it was unable to decrease serum TG and HDL-C concentrations.

Oral administration of pomegranate flower aqueous extract in streptozotocin-induced albino Wistar rats in both 250 mg/kg and 500 mg/kg doses for 21 days could significantly reduce fibrinogen (FBG), TC, TG, LDL-C, and tissue lipid peroxidation level and increased the level of HDL-C and glutathione content ⁶⁵.

Heart fibrosis increases among diabetics, which results in impairing cardiac function. Endothelin (ET)-1 and NFκB are interactive fibroblast growth regulators. It is suggested that pomegranate flower extract (500 mg/kg/day) in Zucker diabetic fatty rats could reduce the ratios of van Gieson-stained interstitial collagen deposit area to a total left ventricular area and perivascular collagen deposit areas to coronary artery media area in the heart and diminishes cardiac fibrosis in these rats. In addition, overexpressed cardiac fibronectin and collagen I and II messenger RNAs (mRNAs) were inhibited. It also decreased the upregulated cardiac mRNA expression of ET-1, ETA, inhibitor-κBβ, and c-jun. Pomegranate flower extract is a dual activator of peroxisome proliferator-activated receptor (PPAR)-α and γ and improves hyperlipidemia, hyperglycemia, and fatty heart in diabetic fatty Zucker rats ⁶⁶, ⁶⁷.

Punicic acid caused a dose-dependent increase in PPAR alpha and gamma reporter activity in 3T3-L1 cells. Dietary punicic acid reduced plasma glucose, suppressed NFκB activation and unregulated TNF-α expression and PPAR-α/γ responsive genes in adipose tissue and skeletal muscle ⁶⁸.

Pomegranate leaf extract was administered (400 and 800 mg/kg/day) to high-fat-diet-induced obese and hyperlipidemic mouse models for 5 weeks. The results indicated significant reduction in body weight, energy intake (based on food intake), serum total cholesterol (TC), TG, FBG, and TC/HDL-C ratio. Intestinal fat absorption was inhibited as well ⁶⁹.

The high fat diet (HFD) with 1% pomegranate seed oil (rich source of punicic acid) was administered for 12 weeks to induce obesity and insulin resistance in mice. The pomegranate seed oil-fed group exhibited lower body weight (4%) and body fat mass (3.1%) compared with only HFD-fed mice. A clear improvement was observed in peripheral insulin sensitivity (70%) in pomegranate seed oil-administered rats ⁷⁰.

Fatty liver is the most common abnormal liver function among diabetics. Pomegranate flower was examined for its antidiabetic effects on diabetic type II and obese Zucker rats. Rats fed with 500 mg/kg/day of pomegranate flower extract for 6 weeks showed decreased ratio of liver weight to tibia length, lipid droplets, and hepatic TG contents. In addition, it increased PPRA-α and Acyl-COA oxidase mRNA levels in HepG2 cells ⁷¹.

In a study by de Nigris et al. ⁷², they compared the influence of pomegranate fruit extract with pomegranate juice on nitric oxide and arterial function in obese Zucker rats. They have demonstrated that both pomegranate fruit extract and juice significantly reduced the vascular inflammatory markers expression, thrombospondin, and cytokine TGFP 1. Increased plasma nitrite and nitrate were observed with administration of either pomegranate fruit or juice.

Many studies have reported the anti-inflammatory potential of pomegranate extract. In a study on 30 Sprague-Dawley rats with acute inflammation due to myringotomy, it was observed that 100 μl/day of pomegranate extract could significantly reduce reactive-oxygen species (ROS) levels. The extract was administered 1 day before and 2 days after surgery. Reduced thickness of lamina propria and vessel density was reported as well ⁷³. Both ellagitannins and ellagic acid are the main components of pomegranate extract, which have anti-inflammatory properties. They are metabolized by gut microbiota to yield urolithins. It is suggested that urolithins are the main components responsible for the anti-inflammation properties of pomegranate. It is suggested that NFκB activation, MAPK downregulation of COX-2, and mPGES-1 expression were inhibited through a decrease in PGE2 production ⁷⁴. Neutrophils play key roles in inflammatory processes by releasing great amounts of ROS generated by NADPH-oxidase and myeloperoxidase. It is indicated that punicic acid exhibited a potent anti-inflammatory effect via prevention of TNF-α-induced priming of NADPH oxidase by targeting the p38MAPKinase/Ser 345-p 47 phox-axis and releasing MPO ⁷⁵. Hyperglycemia results in oxidative stress in diabetes mellitus, which is a major factor in the pathogenesis of cardiovascular disease. Results suggested that pomegranate extract, owing to its polyphenol-rich antioxidants (oleanolic, ursolic, and gallic acids), could prevent cardiovascular complications through decrease in LDL, increase in HDL, serum paraoxonase 1 stability and activity, and nitric oxide production ⁷⁶, ⁷⁷, ⁷⁸.

Anti-inflammatory effect

Pomegranate rind extract was tested on ex-vivo porcine skin for its anti-inflammatory effects. The punicalagin permeated the skin, thus downregulating COX-2, an inflammatory enzyme ⁷⁹. A hydrogel containing pomegranate rind extract and zinc sulfate was formulated by the same research team as a topical treatment for Herpes simplex virus (HSV) infection. The hydrogel exhibited virucidal and anti-inflammatory effects, with punicalagin permeating regions of the skin that are susceptible to infection ⁸⁰. This has relevance in the growing need for novel clinical products to combat HSV. Another study using the rind extract’s punicalagin with zinc (II) ions established virucidal and therapeutic effects against HSV infections, such as the common cold sore, in order to further emphasize this potential application ⁸¹.

In addition to bioactive components of pomegranate rind, pomegranate seed oil, when topically applied, alleviates oxidative and inflammatory stress brought on the skin by UV irradiation. A topical hydrogel that was formulated with silibinin-loaded pomegranate oil-based nanocapsules had an anti-inflammatory effect on mice skin damaged by UVB induced radiation ⁸². Furthermore, pomegranate seed oil nanoemulsions can provide photoprotection against UVB-induced damage of DNA in human keratinocyte HaCaT cells, which constitute most of the epidermis ⁸³. In another study on keratinocyte cells, pomegranate extract phenolics, including punicalagin, EA, and urolithin A, had protective effects against hydrogen peroxide-induced oxidative stress and cytotoxicity ⁸⁴. These studies demonstrate the existing potential of pomegranate extracts for use in sunscreen and cosmetics products. Furthermore, the topical application of pomegranate seed oil decreased skin tumor development and multiplicity, and it has shown applications as a chemo-preventive agent for skin cancer ¹⁶.

Osteoarthritis

The most common forms of arthritis are osteoarthritis and its major progressive degenerative joint disease, which could affect joint functions and quality of life in patients. It is mediated by proinflammatory cytokines such as IL-1 and TNF-α. MAPKs are important due to their inflammatory and cartilage damage regulation ⁸⁵. P38-MAPKs are responsible for regulating cytokine production, neutrophils activation, apoptosis, and nitric oxide synthesis. The MAPK family phosphorylates a number of transcription factors such as runt-related transcription factor-2 (RUNX-2) ⁸⁶.

Pomegranate extract, with its rich source of polyphenols, can inhibit IL-1 β-induced activation of MKK3, DNA-binding activity of RUNX-2 transcription factor, and p38 α-MAPK isoform ⁸⁵.

Rheumatoid arthritis

Rheumatoid arthritis is an autoimmune disease that affects 0.5-1% of people worldwide. Women are afflicted more than men. This inflammatory disease is characterized by inflammation and bone erosion ⁸⁵, ⁸⁶. Critical mediators in the pathogenesis of rheumatoid arthritis are TNF-α, IL-1 β, MCP1, Inducible nitric oxide synthase (iNOS), and COX-2-agents, which are stimulated by p38-MAPK and NFκB activation ⁸⁷, ⁸⁸.

The pomegranate has been used for centuries to treat inflammatory diseases, and people with rheumatoid arthritis sometimes take dietary supplements containing a pomegranate extract called POMx. However, little is known about the efficacy of POMx in suppressing joint problems associated with rheumatoid arthritis.

In a recent study, researchers from Case Western Reserve University and Aligarh (India) Muslim University used an animal model of rheumatoid arthritis—collagen-induced arthritis (CIA) in mice—to evaluate the effects of POMx. The animals received either POMx or water by stomach tube before and after collagen injection to induce arthritis. POMx significantly reduced the incidence and severity of CIA in the mice. The arthritic joints of the POMx-fed mice had less inflammation, and destruction of bone and cartilage were alleviated. Consumption of POMx, the researchers also concluded, selectively inhibited signal transduction pathways and cytokines critical to development and maintenance of inflammation in rheumatoid arthritis ⁸⁹. Severity of arthritis, joint inflammation, and IL-6 level were significantly reduced in pomegranate extract-fed mice ⁹⁰.

Although previous studies of POMx found cartilage-protective effects in human cell cultures, this is the first study to observe positive effects in a live model. The researchers note that the data from this study suggest the potential efficacy of POMx for arthritis prevention, but not for treatment in the presence of active inflammation; future studies will address disease-modifying effects of POMx. They also note that clinical trials are needed before POMx can be recommended as safe and effective for rheumatoid arthritis-related use in people ⁸⁹.

Antibacterial and antifungal effect

Since bacterial resistance to antimicrobial drugs is increasing, medicinal plants have been considered as alternative agents. Pomegranate has been widely approved for its antimicrobial properties ⁹¹, ⁹², ⁹³. It has been shown that dried powder of pomegranate peel has a high inhibition of Candida albicans ⁹⁴. In addition, antimicrobial effects of both methanol and dichloromethane pomegranate extracts have been demonstrated on the Candida genus yeast as pathogen-causing disease in immunosuppressive host ⁹⁵. Methicillin-resistant staphylococcus aureus (MRSA) and methicillin-sensitive staphylococcus aureus (MSSA) (multiple antibiotics resistant) produce panta valentine leukocidin (PVL) toxin, which can lead to higher levels of morbidity and mortality ⁹⁶, ⁹⁷. It is indicated that a combination of pomegranate peel extract with Cu (II) ions exhibit enhanced antimicrobial effects against isolated MSSA, MRSA, and PVL ⁹⁸. One of the leading etiological bacteria of urinary tract infections is Escherichia Coli. Strong antibacterial activity of ethanol extract against E. coli has been shown ⁹⁹.

Skin

Pomegranate rind and bioactive seed compounds can be integrated into skin health products, demonstrating the potential that biowaste can be converted into value-added products ⁶. Ellagic acid and punicalagin are both bioactive compounds of pomegranate rind that promote skin health by inhibiting tyrosinase and initiating anti-inflammatory and anti-fungal effects ⁷⁹. Pomegranate seed oil is rich in punicic acid, which gives it protective and anti-inflammatory characteristics to act against ultraviolet (UV)-induced radiation ¹⁰⁰. Solar ultraviolet (UV) radiations are the primary causes of many biological effects such as photoaging and skin cancer. These radiations resulted in DNA damage, protein oxidation, and matrix metalloproteinases induction. In one study, the effects of pomegranate juice, extract, and oil were examined against UVB-mediated damage. These products caused a decrease in UVB-induced protein expression of c-Fos and phosphorylation of c-Jun ¹⁰¹. On the other hand, production of proinflammatory cytokines IL-1 β and IL-6 was decreased by topical application of 10 micromol/L of ellagic acid. The inflammatory macrophages infiltration was blocked in the integuments of SKH-1 hairless UVB-exposed mice for 8 weeks ¹⁰². Furthermore, pomegranate seed oil can act as an inhibitor for aging-induced glycation, a process that negatively affects skin elasticity ¹⁰³.

Skin whitening

Pomegranate has one of the highest levels of ellagic acid among fruits and vegetables ⁶. Ellagic acid is a phenolic component that is used to protect skin against oxidative stress ¹⁰⁴. Ellagic acid is currently approved as a lightening ingredient for cosmetic formulations due to its ability to chelate copper ions that are present in tyrosinase enzymes, which are the main enzymes catalyzing the production of melanin ¹⁰⁵.

Ellagic acid that is found in pomegranate has advantageous treatment abilities for UVB-induced hyperpigmentation ¹⁰⁰. In one study, pomegranate rind extract containing 90% w/w ellagic acid was orally administered to UV irradiated guinea pigs to test its skin whitening effect. The extract taken orally had a comparable whitening effect to L-ascorbic acid (vitamin C), which is a known tyrosinase inhibitor on UV-induced pigmentation, and reduced the number of DOPA-positive melanocytes, whereas L-ascorbic acid did not ¹⁰⁶. Apart from its skin whitening effect, ellagic acid in pomegranate has more skin health applications that will be discussed in the next sections.

Skin wrinkling and skin aging

Pomegranate extract also has an anti-aging effect against skin wrinkling and it can increase skin elasticity. Pomegranate seed oil can improve the striae distensae skin condition, which is associated with a lack of skin elasticity. It was tested in an oil-in-water cream with Croton lechleri resin, which increased the thickness, hydration, and elasticity values of the dermis ¹⁰⁷. Another topical oil-in-water emulsion was formulated with pomegranate extract, donkey milk, and UV filters. In addition to an overall decrease in brown pigmentation, the emulsion had anti-aging effects on the skin, such as a decreased wrinkle count by 32.9%, decreased wrinkle length by 9.6%, and increased skin firmness and elasticity by 9.6%. This suggests that these effects are due to the synergistic potency of the ingredients of the formulation ¹⁰⁸. Pomegranate ellagic acid, in particular, has the ability to prevent UVB-induced thickening of the dermis, a process that can lead to skin wrinkling ¹⁰⁹.

Glycation, which is also known as the Maillard reaction, is a process that creates advanced glycation end products (AGEs), which is partly induced by aging ¹⁰³. It is also a non-enzymatic, irreversible reaction between reducing sugars and proteins ¹¹⁰. Skin glycation affects collagen in a way that results in the deterioration of skin elasticity. The anti-glycation property of a polysaccharide fraction from pomegranate extract was studied by evaluating the content of fructosamine, an early glycation product. The pomegranate extract acted as a glycation inhibitor due to both its free radical scavenging ability and its inhibition of fructosamine formation by modification of the amino or carbonyl groups in the Maillard reaction ¹⁰³. More recently, oral dosages of 100 mg/day pomegranate extract were given to post-menopausal healthy females. The results showed a decrease in glycative stress markers in those who had received the extract dosages ¹¹¹. Pomegranate extract was also found to be effective in firming skin after weight change or cosmetic surgery, as it increased the synthesis of glycosaminoglycans in the skin ¹¹². In another application, pomegranate extract from sterols with shale extract was used in a lip gloss formulation to treat rough, dry, or cracked lips and reduce the appearance of wrinkles ¹¹³. In short, pomegranate extract can be considered to be beneficial for eliminating wrinkles that are induced by skin aging and damage from UV.

Burn and wound healing

In addition to its skin whitening and anti-aging effects, ellagic acid from pomegranate rind extract has a protective effect on sunburns at low doses (100 mg/day ellagic acid) ¹¹⁴. Pomegranate extract with 40% w/w ellagic acid also has a healing effect on deep second-degree burn wounds in rats through the induction of collagen formation, which strengthens wounded tissue and speeds up the healing process ¹¹⁵. The same extract can also enhance the healing process for incision wounds on rats by increasing collagen content and angiogenesis while decreasing polymorphonuclear leukocytes infiltration, which causes tissue damage during inflammation ¹¹⁶. Furthermore, ellagic acid and pomegranate rind extract positively contribute to increasing tensile strength in rat incision wounds. Although a high dose of ellagic acid alone can inhibit polymorphonuclear leukocytes infiltration, it cannot produce significant amounts of collagen. This is an indication of the synergistic effect of pomegranate extract with ellagic acid on healing wounds ¹¹⁷.

Dental effects

The interbacterial coaggregations and these bacterial interactions with yeasts are related to the maintenance of oral microbiota. It is indicated that dried, powdered pomegranate peel shows a strong inhibition of C. albicans with a mean zone of 22 mm. In another study, the antiplaque effect of pomegranate mouth rinse has been reported ¹¹⁸. In addition, hydroalcoholic extract of pomegranate was very effective against dental plaque microorganisms (84% decrease (cfu/ml)) ¹¹⁹.

Reproductive system

One of the main constituents (16%) of the methanolic pomegranate seed extract is beta-sitosterol. It is suggested that the extract is a potent phasic activity stimulator in rat uterus, which happens due to the non-estrogenic effects of beta-sitosterol on inhibiting sarco-endoplasmic reticulum Ca2+ -ATPase (SERCA) and K channel, which resulted in contraction by calcium entry on L-type calcium channels and myosin light chain kinase (MLCK). It is demonstrated that pomegranate fruit extract has an embryonic protective nature against adrianycin-induced oxidative stress (adrianycin is a chemotherapeutic drug used in cancer treatment) ¹²⁰. Moreover, pomegranate juice consumption could increase epididymal sperm concentration, motility, spermatogenic cell density, diameter of seminiferous tubules and germinal cell layer thickness ¹²¹.

Alzheimer’s Disease

Hartman et al. ¹²² showed that mice treated by pomegranate juice have 50% less soluble Abeta 42 accumulation and amyloid deposition in the hippocampus, which could be considered for Alzheimer’s disease improvement.

Malaria

In the presence of pomegranate fruit rind, the induced MMP-9 mRNA levels by haemozoin or TNF was decreased, which may be attributed to the antiparasitic activity and the inhibition of the proinflammatory mechanisms responsible in the onset of cerebral malaria ¹²³, ¹²⁴.

HIV

The anti-HIV-1 microbicide of pomegranate juice blocks virus binding to CD4 and CXCR4/CCR5, thereby preventing infection by primary virus clades A to G and group O ¹²⁵.

Pomegranate safety

Many studies have been carried out on the different components derived from pomegranate but no adverse effects have been reported in the examined dosage. Histopathological studies on both sexes of OF-1 mice confirmed the non-toxic effects of the polyphenol antioxidant punicalagin. Besides, in a study on 86 overweight human subjects who received 1420 mg/day of pomegranate fruit extract in tablet form for 28 days, no side effects or adverse changes in urine or blood of individuals were reported ⁹¹, ¹²⁶.

Pomegranate Summary

Pomegranate is a potent antioxidant. This fruit is rich in flavonoids, anthocyanins, punicic acid, ellagitannins, alkaloids, fructose, sucrose, glucose, simple organic acids, and other components and has antiatherogenic, antihypertensive, and anti-inflammatory properties. Eventhough pomegranate can be used in the prevention and treatment of several types of cancer, cardiovascular disease, osteoarthritis, rheumatoid arthritis, and other diseases, mainly in laboratory animals and in petri dishes. We don’t have a lot of strong scientific evidence on the effects of pomegranate for people’s health. Many in vitro, animal and clinical trials have been carried out to examine and prove the therapeutic effects of these compounds, further human trials and studies are necessary to understand the therapeutic potentials of pomegranate ¹²⁷.

• A 2012 clinical trial of about 100 dialysis patients suggested that pomegranate juice may help ward off infections. In the study, the patients who were given pomegranate juice three times a week for a year had fewer hospitalizations for infections and fewer signs of inflammation, compared with patients who got the placebo.
• Pomegranate extract in mouthwash may help control dental plaque, according to a small 2011 clinical trial with 30 healthy participants.
• Pomegranate may help improve some signs of heart disease but the research isn’t definitive.

Lastly, Federal agencies have taken action against companies (POM Pomegranate) selling pomegranate juice and supplements for deceptive advertising and making drug-like claims about the products. For more on this, view the NCCIH Director’s Page entitled Excessive Claims ¹²⁸.

References

1. National Center for Complementary and Integrative Health. Pomegranate. https://nccih.nih.gov/health/pomegranate/at-a-glance
2. Genetic relationships among wild pomegranate (Punica granatum) genotypes from Coruh Valley in Turkey. Ercisli S, Gadze J, Agar G, Yildirim N, Hizarci Y. Genet Mol Res. 2011 Mar 15; 10(1):459-64. https://www.ncbi.nlm.nih.gov/pubmed/21425096/
3. Newman R. Sydney, Australia: Readhowyouwant; 2011. A wealth of phtochemicals. Pomegranate: The Most Medicinal Fruit p. 184.
4. Newman RA, Lansky EP, Block ML. Pomegranate: The Most Medicinal Fruit. Laguna Beach, California: Basic Health Publications; 2007. -A Wealth of Phytochemicals; p. 120.
5. United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. https://ndb.nal.usda.gov/ndb/
6. Ko, K., Dadmohammadi, Y., & Abbaspourrad, A. (2021). Nutritional and Bioactive Components of Pomegranate Waste Used in Food and Cosmetic Applications: A Review. Foods (Basel, Switzerland), 10(3), 657. https://doi.org/10.3390/foods10030657
7. Charalampia D., Koutelidakis A. From Pomegranate Processing By-Products to Innovative value added Func-tional Ingredients and Bio-Based Products with Several Applications in Food Sector. BAOJ Biotech. 2017;3:210.
8. Gül H., Şen H. Effects of pomegranate seed flour on dough rheology and bread quality. CyTA J. Food. 2017;15:622–628. doi: 10.1080/19476337.2017.1327461
9. Kaur S., Kumar S., Bhat Z.F. Utilization of pomegranate seed powder and tomato powder in the development of fi-ber-enriched chicken nuggets. Nutr. Food Sci. 2015;45:793–807. doi: 10.1108/NFS-05-2015-0066
10. Verardo V., Garcia-Salas P., Baldi E., Segura-Carretero A., Fernandez-Gutierrez A., Caboni M.F. Pomegranate seeds as a source of nutraceutical oil naturally rich in bioactive lipids. Food Res. Int. 2014;65:445–452. doi: 10.1016/j.foodres.2014.04.044
11. Viuda-Martos M, Fernández-López J, Pérez-Álvarez JA. Pomegranate and its Many Functional Components as Related to Human Health: A Review. Compr Rev Food Sci Food Saf. 2010 Nov;9(6):635-654. doi: 10.1111/j.1541-4337.2010.00131.x
12. Zarfeshany, A., Asgary, S., & Javanmard, S. H. (2014). Potent health effects of pomegranate. Advanced biomedical research, 3, 100. https://doi.org/10.4103/2277-9175.129371
13. Paul A., Radhakrishnan M. Pomegranate seed oil in food industry: Extraction, characterization, and applications. Trends Food Sci. Technol. 2020;105:273–283. doi: 10.1016/j.tifs.2020.09.014
14. Khoddami A., Man Y.B.C., Roberts T.H. Physico-chemical properties and fatty acid profile of seed oils from pomegranate (Punica granatum L.) extracted by cold pressing. Eur. J. Lipid Sci. Technol. 2014;116:553–562. doi: 10.1002/ejlt.201300416
15. Khajebishak Y., Payahoo L., Alivand M., Alipour B. Punicic acid: A potential compound of pomegranate seed oil in Type 2 diabetes mellitus management. J. Cell. Physiol. 2019;234:2112–2120. doi: 10.1002/jcp.27556
16. Hora J.J., Maydew E.R., Lansky E.P., Dwivedi C. Chemopreventive Effects of Pomegranate Seed Oil on Skin Tumor Development in CD1 Mice. J. Med. Food. 2003;6:157–161. doi: 10.1089/10966200360716553
17. Nekooeian A.A., Eftekhari M.H., Adibi S., Rajaeifard A. Effects of Pomegranate Seed Oil on Insulin Release in Rats with Type 2 Diabetes. Iran. J. Med. Sci. 2014;39:130–135.
18. Aruna P., Venkataramanamma D., Singh A.K., Singh R. Health Benefits of Punicic Acid: A Review. Compr. Rev. Food Sci. Food Saf. 2015;15:16–27. doi: 10.1111/1541-4337.12171
19. Ververi M., Goula A.M. Pomegranate peel and orange juice by-product as new biosorbents of phenolic compounds from olive mill wastewaters. Chem. Eng. Process. Process. Intensif. 2019;138:86–96. doi: 10.1016/j.cep.2019.03.010
20. Amin N.K. Removal of direct blue-106 dye from aqueous solution using new activated carbons developed from pomegranate peel: Adsorption equilibrium and kinetics. J. Hazard. Mater. 2009;165:52–62. doi: 10.1016/j.jhazmat.2008.09.067
21. Saadi W., Rodríguez-Sánchez S., Ruiz B., Souissi-Najar S., Ouederni A., Fuente E. Pyrolysis technologies for pomegranate (Punica granatum L.) peel wastes. Prospects in the bioenergy sector. Renew. Energy. 2019;136:373–382. doi: 10.1016/j.renene.2019.01.017
22. Hossin F.L.A. Effect of Pomegranate (Punica granatum) Peels and It’s Extract on Obese Hypercholesterolemic Rats. Pak. J. Nutr. 2009;8:1251–1257. doi: 10.3923/pjn.2009.1251.1257
23. Ismail T., Akhtar S., Riaz M., Ismail A. Effect of pomegranate peel supplementation on nutritional, organoleptic and stability properties of cookies. Int. J. Food Sci. Nutr. 2014;65:661–666. doi: 10.3109/09637486.2014.908170
24. Colantuono A., Ferracane R., Vitaglione P. In vitro bioaccessibility and functional properties of polyphenols from pom-egranate peels and pomegranate peels-enriched cookies. Food Funct. 2016;7:4247–4258. doi: 10.1039/C6FO00942E
25. Abid M., Yaich H., Hidouri H., Attia H., Ayadi M. Effect of substituted gelling agents from pomegranate peel on colour, textural and sensory properties of pomegranate jam. Food Chem. 2018;239:1047–1054. doi: 10.1016/j.foodchem.2017.07.006
26. Yang X., Nisar T., Hou Y., Gou X., Sun L., Guo Y. Pomegranate peel pectin can be used as an effective emulsifier. Food Hydrocoll. 2018;85:30–38. doi: 10.1016/j.foodhyd.2018.06.042
27. Pomegranate Council. http://www.pomegranates.org/index.php
28. Pomegranate seed oil consumption during a period of high-fat feeding reduces weight gain and reduces type 2 diabetes risk in CD-1 mice. McFarlin BK, Strohacker KA, Kueht ML. Br J Nutr. 2009 Jul; 102(1):54-9. https://www.ncbi.nlm.nih.gov/pubmed/19079947/
29. Activation of PPAR gamma and alpha by punicic acid ameliorates glucose tolerance and suppresses obesity-related inflammation. Hontecillas R, O’Shea M, Einerhand A, Diguardo M, Bassaganya-Riera J. J Am Coll Nutr. 2009 Apr; 28(2):184-95. https://www.ncbi.nlm.nih.gov/pubmed/19828904/
30. Dietary effect of pomegranate seed oil rich in 9cis, 11trans, 13cis conjugated linolenic acid on lipid metabolism in obese, hyperlipidemic OLETF rats. Arao K, Wang YM, Inoue N, Hirata J, Cha JY, Nagao K, Yanagita T. Lipids Health Dis. 2004 Nov 9; 3():24. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC534798/
31. The influence of pomegranate fruit extract in comparison to regular pomegranate juice and seed oil on nitric oxide and arterial function in obese Zucker rats. de Nigris F, Balestrieri ML, Williams-Ignarro S, D’Armiento FP, Fiorito C, Ignarro LJ, Napoli C. Nitric Oxide. 2007 Aug; 17(1):50-4. https://www.ncbi.nlm.nih.gov/pubmed/17553710/
32. Effect of pomegranate seed oil on hyperlipidaemic subjects: a double-blind placebo-controlled clinical trial. Mirmiran P, Fazeli MR, Asghari G, Shafiee A, Azizi F. Br J Nutr. 2010 Aug; 104(3):402-6. https://www.ncbi.nlm.nih.gov/pubmed/20334708/
33. Effect of pomegranate juice on Angiotensin II-induced hypertension in diabetic Wistar rats. Mohan M, Waghulde H, Kasture S. Phytother Res. 2010 Jun; 24 Suppl 2():S196-203. https://www.ncbi.nlm.nih.gov/pubmed/20020514/
34. The effects of polyphenol-containing antioxidants on oxidative stress and lipid peroxidation in Type 2 diabetes mellitus without complications. Fenercioglu AK, Saler T, Genc E, Sabuncu H, Altuntas Y. J Endocrinol Invest. 2010 Feb; 33(2):118-24. https://www.ncbi.nlm.nih.gov/pubmed/19834314/
35. Gil MI, Tomás-Barberán FA, Hess-Pierce B, Holcroft DM, Kader AA. Antioxidant activity of pomegranate juice and its relationship with phenolic composition and processing. J Agric Food Chem. 2000;48:4581–9. https://www.ncbi.nlm.nih.gov/pubmed/11052704
36. Tao X, Schulze-Koops H, Ma L, Cai J, Mao Y, Lipsky PE. Effects of Tripterygium wilfordii hook F extracts on induction of cyclooxygenase 2 activity and prostaglandin E2 production. Arthritis Rheum. 1998;41:130–8. https://www.ncbi.nlm.nih.gov/pubmed/9433878
37. Loeser RF, Erickson EA, Long DL. Mitogen-activated protein kinases as therapeutic targets in osteoarthritis. Curr Opin Rheumatol. 2008;20:581–6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892710/
38. Cerdá B, Cerón JJ, Tomás-Barberán FA, Espín JC. Repeated oral administration of high doses of the pomegranate ellagitannin punicalagin to rats for 37 days is not toxic. J Agric Food. 2003;51:3493–501. https://www.ncbi.nlm.nih.gov/pubmed/12744688
39. Prescott SM, Fitzpatrick FA. Cyclooxygenase-2 and carcinogenesis. Biochim Biophys Acta. 2000;1470:69–78. https://www.ncbi.nlm.nih.gov/pubmed/10722929
40. Kumar S, Votta BJ, Rieman DJ, Badger AM, Gowen M, Lee JC. IL-1- and TNF-induced bone resorption is mediated by p38 mitogen activated protein kinase. J Cell Physiol. 2001;187:294–303. https://www.ncbi.nlm.nih.gov/pubmed/11319753
41. Jurenka JS. Therapeutic applications of pomegranate (Punica granatum L.): A review. Altern Med Rev. 2008 13:128–44. USDA 2010. Pomegranates, Raw. United States Department of Agriculture. https://www.nal.usda.gov/
42. Dietary fiber: Essential for a healthy diet. https://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/fiber/art-20043983
43. Al Juhaimi F., Özcan M.M., Ghafoor K. Characterization of pomegranate (Punica granatum L.) seed and oils. Eur. J. Lipid Sci. Technol. 2017;119:1700074. doi: 10.1002/ejlt.201700074
44. Pamisetty A., Kumar K.A., Indrani D., Singh R.P. Rheological, physico-sensory and antioxidant properties of punicic acid rich wheat bread. J. Food Sci. Technol. 2020;57:253–262. doi: 10.1007/s13197-019-04055-3
45. Pomegranate fruit juice for chemoprevention and chemotherapy of prostate cancer. Malik A, Afaq F, Sarfaraz S, Adhami VM, Syed DN, Mukhtar H. Proc Natl Acad Sci U S A. 2005 Oct 11; 102(41):14813-8. https://www.ncbi.nlm.nih.gov/pubmed/16192356/
46. Rettig MB, Heber D, An J, Seeram NP, Rao JY, Liu H, et al. Pomegranate extract inhibits androgen-independent prostate cancer growth through a nuclear factor-kappaB-dependent mechanism. Mol Cancer Ther. 2008;7:2662–71. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2858627/
47. Albrecht M, Jiang W, Kumi-Diaka J, Lansky EP, Gommersall LM, Patel A, et al. Pomegranate extracts potently suppress proliferation, xenograft growth, and invasion of human prostate cancer cells. J Med Food. 2004;7:274–83. https://www.ncbi.nlm.nih.gov/pubmed/15383219
48. Kim ND, Mehta R, Yu W, Neeman I, Livney T, Amichay A, et al. Chemopreventive and adjuvant therapeutic potential of pomegranate (Punica granatum) for human breast cancer. Breast Cancer Res Treat. 2002;71:203–17. https://www.ncbi.nlm.nih.gov/pubmed/12002340
49. Phase II study of pomegranate juice for men with rising prostate-specific antigen following surgery or radiation for prostate cancer. Clin Cancer Res. 2006 Jul 1;12(13):4018-26. http://clincancerres.aacrjournals.org/content/12/13/4018.long
50. Freedland SJ, Carducci M, Kroeger N, et al. A Double Blind, Randomized, Neoadjuvant Study of the Tissue effects of POMx Pills in Men with Prostate Cancer Prior to Radical Prostatectomy. Cancer prevention research (Philadelphia, Pa). 2013;6(10):1120-1127. doi:10.1158/1940-6207.CAPR-12-0423. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3806642/
51. Mehta R, Lansky EP. Breast cancer chemopreventive properties of pomegranate (Punica granatum) fruit extracts in a mouse mammary organ culture. Eur J Cancer Prev. 2004;13:345–8. https://www.ncbi.nlm.nih.gov/pubmed/15554563
52. Khan N, Hadi N, Afaq F, Syed DN, Kweon MH, Mukhtar H. Pomegranate fruit extract inhibits prosurvival pathways in human A549 lung carcinoma cells and tumor growth in athymic nude mice. Carcinogenesis. 2007;28:163–73. https://www.ncbi.nlm.nih.gov/pubmed/16920736
53. Adams LS, Seeram NP, Aggarwal BB, Takada Y, Sand D, Heber D. Pomegranate juice, total pomegranate ellagitannins, and punicalagin suppress inflammatory cell signaling in colon cancer cells. J Agric Food Chem. 2006;54:980–5. https://www.ncbi.nlm.nih.gov/pubmed/16448212
54. Hora JJ, Maydew ER, Lansky EP, Dwivedi C. Chemopreventive effects of pomegranate seed oil on skin tumor development in CD1 mice. J Med Food. 2003;6:157–61. https://www.ncbi.nlm.nih.gov/pubmed/14585180
55. Syed DN, Malik A, Hadi N, Sarfaraz S, Afaq F, Mukhtar H. Photochemopreventive effect of pomegranate fruit extract on UVA-mediated activation of cellular pathways in normal human epidermal keratinocytes. Photochem Photobiol. 2006;82:398–405. https://www.ncbi.nlm.nih.gov/pubmed/16613491
56. Pacheco-Palencia LA, Noratto G, Hingorani L, Talcott ST, Mertens-Talcott SU. Protective effects of standardized pomegranate (Punica granatum L.) polyphenolic extract in ultraviolet-irradiated human skin fibroblasts. J Agric Food Chem. 2008;56:8434–41. https://www.ncbi.nlm.nih.gov/pubmed/18717570
57. Stowe CB. The effects of pomegranate juice consumption on blood pressure and cardiovascular health. Complement Ther Clin Pract. 2011;17:113–5. https://www.ncbi.nlm.nih.gov/pubmed/21457902
58. Mohan M, Waghulde H, Kasture S. Effect of pomegranate juice on Angiotensin II-induced hypertension in diabetic Wistar rats. Phytother Res. 2010;24:S196–203. https://www.ncbi.nlm.nih.gov/pubmed/20020514
59. Aviram M, Rosenblat M, Gaitini D, Nitecki S, Hoffman A, Dornfeld L, et al. Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation. Clin Nutr. 2004;23:423–33. https://www.ncbi.nlm.nih.gov/pubmed/15158307
60. Mirmiran P, Fazeli MR, Asghari G, Shafiee A, Azizi F. Effect of pomegranate seed oil on hyperlipidaemic subjects: A double-blind placebo-controlled clinical trial. Br J Nutr. 2010;104:402–6. https://www.ncbi.nlm.nih.gov/pubmed/20334708
61. Aviram M, Dornfeld L, Rosenblat M, Volkova N, Kaplan M, Coleman R, et al. Pomegranate juice consumption reduces oxidative stress, atherogenic modifications to LDL, and platelet aggregation: Studies in humans and in atherosclerotic apolipoprotein E-deficient mice. Am J Clin Nutr. 2000;71:1062–76. https://www.ncbi.nlm.nih.gov/pubmed/10799367
62. Kaplan M, Hayek T, Raz A, Coleman R, Dornfeld L, Vaya J, et al. Pomegranate juice supplementation to atherosclerotic mice reduces macrophage lipid peroxidation, cellular cholesterol accumulation and development of atherosclerosis. J Nutr. 2001;131:2082–9. https://www.ncbi.nlm.nih.gov/pubmed/11481398
63. de Nigris F, Williams-Ignarro S, Sica V, Lerman LO, D’Armiento FP, Byrns RE, et al. Effects of a pomegranate fruit extract rich in punicalagin on oxidation-sensitive genes and eNOS activity at sites of perturbed shear stress and atherogenesis. Cardiovasc Res. 2007;73:414–23. https://www.ncbi.nlm.nih.gov/pubmed/17014835
64. Esmaillzadeh A, Tahbaz F, Gaieni I, Alavi-Majd H, Azadbakht L. Cholesterol-lowering effect of concentrated pomegranate juice consumption in type II diabetic patients with hyperlipidemia. Int J Vitam Nutr Res. 2006;76:147–51. https://www.ncbi.nlm.nih.gov/pubmed/17048194
65. Bagri P, Ali M, Aeri V, Bhowmik M, Sultana S. Antidiabetic effect of Punica granatum flowers: Effect on hyperlipidemia, pancreatic cells lipid peroxidation and antioxidant enzymes in experimental diabetes. Food Chem Toxicol. 2009;47:50–4. https://www.ncbi.nlm.nih.gov/pubmed/18950673
66. Huang TH, Yang Q, Harada M, Li GQ, Yamahara J, Roufogalis BD, et al. Pomegranate flower extract diminishes cardiac fibrosis in Zucker diabetic fatty rats: Modulation of cardiac endothelin-1 and nuclear factor-kappaB pathways. J Cardiovasc Pharmacol. 2005;46:856–62. https://www.ncbi.nlm.nih.gov/pubmed/16306813
67. Huang TH, Peng G, Kota BP, Li GQ, Yamahara J, Roufogalis BD, et al. Pomegranate flower improves cardiac lipid metabolism in a diabetic rat model: Role of lowering circulating lipids. Br J Pharmacol. 2005;145:767–74. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1576197/
68. Hontecillas R, O’Shea M, Einerhand A, Diguardo M, Bassaganya-Riera J. Activation of PPAR gamma and alpha by punicic acid ameliorates glucose tolerance and suppresses obesity-related inflammation. J Am Coll Nutr. 2009;28:184–95. https://www.ncbi.nlm.nih.gov/pubmed/19828904
69. Lei F, Zhang XN, Wang W, Xing DM, Xie WD, Su H, DU LJ. Evidence of anti-obesity effects of the pomegranate leaf extract in high-fat diet induced obese mice. Int J Obes (Lond) 2007;31:1023–9. https://www.ncbi.nlm.nih.gov/pubmed/17299386
70. Vroegrijk IO, van Diepen JA, van den Berg S, Westbroek I, Keizer H, Gambelli L. Pomegranate Seed Oil, a rich source of Punicic Acid, prevents diet-induced obesity and insulin resistance in mice. Food Chem Toxicol. 2011;49:1426–30. https://www.ncbi.nlm.nih.gov/pubmed/21440024
71. Xu KZ, Zhu C, Kim MS, Yamahara J, Li Y. Pomegranate flower ameliorates fatty liver in an animal model of type 2 diabetes and obesity. J Ethnopharmacol. 2009;123:280–7. https://www.ncbi.nlm.nih.gov/pubmed/19429373
72. de Nigris F, Balestrieri ML, Williams-Ignarro S, D’Armiento FP, Fiorito C, Ignarro LJ, et al. The influence of pomegranate fruit extract in comparison to regular pomegranate juice and seed oil on nitric oxide and arterial function in obese Zucker rats. Nitric Oxide. 2007;17:50–4. https://www.ncbi.nlm.nih.gov/pubmed/17553710
73. Kahya V, Meric A, Yazici M, Yuksel M, Midi A, Gedikli O. Antioxidant effect of pomegranate extract in reducing acute inflammation due to myringotomy. J Laryngol Otol. 2011;1:370–5. https://www.ncbi.nlm.nih.gov/pubmed/21349238
74. González-Sarrías A, Larrosa M, Tomás-Barberán FA, Dolara P, Espín JC. NF-kappaB-dependent anti-inflammatory activity of urolithins, gut microbiota ellagic acid-derived metabolites, in human colonic fibroblasts. Br J Nutr. 2010;104:503–12. https://www.ncbi.nlm.nih.gov/pubmed/20338073
75. Boussetta T, Raad H, Lettéron P, Gougerot-Pocidalo MA, Marie JC, Driss F, et al. Punicic acid a conjugated linolenic acid inhibits TNFalpha-induced neutrophil hyperactivation and protects from experimental colon inflammation in rats. PLoS One. 2009;4:e6458. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2714468/
76. Katz SR, Newman RA, Lansky EP. Punica granatum: Heuristic treatment for diabetes mellitus. J Med Food. 2007;10:213–7. https://www.ncbi.nlm.nih.gov/pubmed/17651054
77. Rock W, Rosenblat M, Miller-Lotan R, Levy AP, Elias M, Aviram M. Consumption of wonderful variety pomegranate juice and extract by diabetic patients increases paraoxonase 1 association with high-density lipoprotein and stimulates its catalytic activities. J Agric Food Chem. 2008;56:8704–13. https://www.ncbi.nlm.nih.gov/pubmed/18759451
78. Fenercioglu AK, Saler T, Genc E, Sabuncu H, Altuntas Y. The effects of polyphenol-containing antioxidants on oxidative stress and lipid peroxidation in Type 2 diabetes mellitus without complications. J Endocrinol Invest. 2010;33:118–24. https://www.ncbi.nlm.nih.gov/pubmed/19834314
79. Houston D.M., Bugert J., Denyer S.P., Heard C.M. Anti-inflammatory activity of Punica granatum L. (Pomegranate) rind extracts applied topically to ex vivo skin. Eur. J. Pharm. Biopharm. 2017;112:30–37. doi: 10.1016/j.ejpb.2016.11.014
80. Houston D.M., Robins B., Bugert J.J., Denyer S.P., Heard C.M. In vitro permeation and biological activity of punicalagin and zinc (II) across skin and mucous membranes prone to Herpes simplex virus infection. Eur. J. Pharm. Sci. 2017;96:99–106. doi: 10.1016/j.ejps.2016.08.013
81. Houston D.M., Bugert J.J., Denyer S.P., Heard C.M. Potentiated virucidal activity of pomegranate rind extract (PRE) and punicalagin against Herpes simplex virus (HSV) when co-administered with zinc (II) ions, and antiviral activity of PRE against HSV and aciclovir-resistant HSV. PLoS ONE. 2017;12:e0179291
82. Marchiori M.C.L., Rigon C., Camponogara C., Oliveira S.M., Cruz L. Hydrogel containing silibinin-loaded pomegranate oil based nanocapsules exhibits anti-inflammatory effects on skin damage UVB radiation-induced in mice. J. Photochem. Photobiol. B Biol. 2017;170:25–32. doi: 10.1016/j.jphotobiol.2017.03.015
83. Baccarin T., Mitjans M., Ramos D., Lemos-Senna E., Vinardell M.P. Photoprotection by Punica granatum seed oil nanoemulsion entrapping polyphenol-rich ethyl acetate fraction against UVB-induced DNA damage in human keratinocyte (HaCaT) cell line. J. Photochem. Photobiol. B Biol. 2015;153:127–136. doi: 10.1016/j.jphotobiol.2015.09.005
84. Liu C., Guo H., DaSilva N.A., Li D., Zhang K., Wan Y., Gao X.H., Chen H.D., Seeram N.P., Ma H. Pomegranate (Punica granatum) phenolics ameliorate hydrogen peroxide-induced oxidative stress and cyto-toxicity in human keratinocytes. J. Funct. Foods. 2019;54:559–567. doi: 10.1016/j.jff.2019.02.015
85. Rasheed Z, Akhtar N, Haqqi TM. Pomegranate extract inhibits the interleukin-1b-induced activation of MKK-3, p38a-MAPK and transcription factor RUNX-2 in human osteoarthritis chondrocytes -Arthritis Res Ther. 2010;12:195. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2991031/
86. Lee JC, Laydon JT, McDonnell PC, Gallagher TF, Kumar S, Green D. A protein kinase involved in the regulation of inflammatory cytokine biosynthesis. Nature. 1994;372:739–46. https://www.ncbi.nlm.nih.gov/pubmed/7997261
87. Hayden MS, Ghosh S. Signaling to NF-B. Genes Dev. 2004;18:2195. https://www.ncbi.nlm.nih.gov/pubmed/15371334
88. Schieven GL. The biology of p38 kinase: A central role in inflammation. Curr Top Med Chem. 2005;5:921–8. https://www.ncbi.nlm.nih.gov/pubmed/16178737
89. Shukla M, Gupta K, Rasheed Z, et al. Consumption of hydrolyzable tannins-rich pomegranate extract suppresses inflammation and joint damage in rheumatoid arthritis. Nutrition. 2008;24(7–8):733–743. https://www.ncbi.nlm.nih.gov/pubmed/18490140
90. Shukla M, Gupta K, Rasheed Z, Khan KA, Haqqi TM. Bioavailable constituents/metabolites of pomegranate (Punica granatum L) preferentially inhibit COX2 activity ex vivo and IL-1beta-induced PGE2 production in human chondrocytes in vitro. J Inflamm (Lond) 2008;5:9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2438359/
91. Jurenka JS. Therapeutic applications of pomegranate (Punica granatum L.): A review. [Accessed September 2010];Altern Med Rev. 2008 13:128–44. USDA 2010.
92. Lansky E, Shubert S, Neeman I. Pharmacological and therapeutic properties of pomegranate. Israel: CIHEAM-Options Mediterraneennes; 2004;42:231–5.
93. Satish S, Mohana D, Ranhavendra M, Raveesha K. Antifungal activity of some plant extracts against important seed borne pathogens of Aspergillus sp. J Agric Sci Technol. 2007;3:109–19.
94. Mithun P, Prashant G, Murlikrishna K, Shivakumar K, Chandu G. Antifungal efficacy of Punica granatum, Acacia nilotica, Cuminum cyminum and Foeniculum vulgare on Candida albicans: An in vitro study. Indian J Dent Res. 2010;21:334–6. https://www.ncbi.nlm.nih.gov/pubmed/20930339
95. Höfling JF, Anibal PC, Obando-Pereda GA, Peixoto IA, Furletti VF, Foglio MA, Goncalves RB. Antimicrobial potential of some plant extracts against Candida species. Braz J Biol. 2010;70:1065–8. https://www.ncbi.nlm.nih.gov/pubmed/21180915
96. Ferrara AM. Treatment of hospital-acquired pneumonia caused by methicillin-resistant Staphylococcus aureus. Int J Antimicrob Agents. 2007;30:19–24. https://www.ncbi.nlm.nih.gov/pubmed/17475449
97. Wenzel RP, Bearman G, Edmond MB. Community-acquired methicillin-resistant staphylococcus aureus (MRSA): New issues for infection control. Int J Antimicrob Agents. 2007;30:210–2. https://www.ncbi.nlm.nih.gov/pubmed/17566712
98. Gould SW, Fielder MD, Kelly AF, Naughton DP. Anti-microbial activities of pomegranate rind extracts: Enhancement by cupric sulphate against clinical isolates of S. aureus, MRSA and PVL positive CA-MSSA. BMC Complement Altern Med. 2009;9:23. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2724405/
99. Sharma M, Li L, Celver J, Killian C, Kovoor A, Seeram NP. Effects of fruit ellagitannin extracts, ellagic acid, and their colonic metabolite, urolithin A, on Wnt signaling. J Agric Food Chem. 2010;58:3965–9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2850963/
100. Kanlayavattanakul M., Chongnativisit W., Chaikul P., Lourith N. Phenolic-rich Pomegranate Peel Extract: In Vitro, Cellular, and In Vivo Activities for Skin Hy-perpigmentation Treatment. Planta Med. 2020;86:749–759. doi: 10.1055/a-1170-7785
101. Afaq F, Zaid MA, Khan N, Dreher M, Mukhtar H. Protective effect of pomegranate-derived products on UVB-mediated damage in human reconstituted skin. Exp Dermatol. 2009;18:553–61. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3004287/
102. Bae JY, Choi JS, Kang SW, Lee YJ, Park J, Kang YH. Dietary compound ellagic acid alleviates skin wrinkle and inflammation induced by UV-B irradiation. Exp Dermatol. 2010;19:e182–90. https://www.ncbi.nlm.nih.gov/pubmed/20113347
103. Kumagai Y., Nakatani S., Onodera H., Nagatomo A., Nishida N., Matsuura Y., Kobata K., Wada M. Anti-Glycation Effects of Pomegranate (Punica granatum L.) Fruit Extract and Its Components in Vivo and in Vitro. J. Agric. Food Chem. 2015;63:7760–7764. doi: 10.1021/acs.jafc.5b02766
104. Mirsane S, Mirsane S. Benefits of ellagic acid from grapes and pomegranates against colorectal cancer. Caspian J Intern Med. 2017 Summer;8(3):226-227. doi: 10.22088/cjim.8.3.226
105. Turrini F., Malaspina P., Giordani P., Catena S., Zunin P., Boggia R. Traditional Decoction and PUAE Aqueous Extracts of Pomegranate Peels as Potential Low-Cost An-ti-Tyrosinase Ingredients. Appl. Sci. 2020;10:2795. doi: 10.3390/app10082795
106. Yoshimura M., Watanabe Y., Kasai K., Yamakoshi J., Koga T. Inhibitory Effect of an Ellagic Acid-Rich Pomegranate Extract on Tyrosinase Activity and Ultravio-let-Induced Pigmentation. Biosci. Biotechnol. Biochem. 2005;69:2368–2373. doi: 10.1271/bbb.69.2368
107. Bogdan C., Iurian S., Tomuta I., Moldovan M.L. Improvement of skin condition in striae distensae: Development, characterization and clinical efficacy of a cosmetic product containing Punica granatum seed oil and Croton lechleri resin extract. Drug Des. Dev. Ther. 2017;11:521–531. doi: 10.2147/DDDT.S128470
108. Baltazar D., Marto J., Berger T., Pinto P., Ribeiro H.M. The antiageing efficacy of donkey milk in combination with pomegranate extract and UV protection: A traditional ingredient in a modern formulation. Monogr. Spec. Issue Cosmet. Act. Ingred. H&PC Today Househ. Pers. Care Today. 2017;12:30–32.
109. Bae J.-Y., Choi J.-S., Kang S.-W., Lee Y.-J., Park J., Kang Y.-H. Dietary compound ellagic acid alleviates skin wrinkle and inflammation induced by UV-B irradiation. Exp. Dermatol. 2010;19:e182–e190. doi: 10.1111/j.1600-0625.2009.01044.x
110. Rout S., Banerjee R. Free radical scavenging, anti-glycation and tyrosinase inhibition properties of a polysaccharide frac-tion isolated from the rind from Punica granatum. Bioresour. Technol. 2007;98:3159–3163. doi: 10.1016/j.biortech.2006.10.011
111. Yagi M., Parengkuan L., Sugimura H., Shioya N., Matsuura Y., Nishida N., Nagatomo A., Yonei Y. Anti-glycation effect of pomegranate (Punica granatum L.) extract: An open clinical study. Glycative Stress Res. 2014;1:060–067
112. Castiel I., Gueniche A. Non-Therapeutic Cosmetic Use of at Least One Pomegranate Extract, as Agent for Firming Skin of a Subject, Who Has Weight Modification Prior to and/or After an Aesthetic Surgery and to Prevent and/or Treat Sagging Skin, in Espcenet. FR2967063A1. 2012 May 11
113. Wilson K. Lip Gloss. US 2012/0288319 A1. 2012 Nov 15
114. Kasai K., Yoshimura M., Koga T., Arii M., Kawasaki S. Effects of oral administration of ellagic acid-rich pomegranate extract on ultraviolet-induced pigmentation in the human skin. J. Nutr. Sci. Vitaminol. 2006;52:383–388. doi: 10.3177/jnsv.52.383
115. Lukiswanto B.S., Miranti A., Sudjarwo S.A., Primarizky H., Yuniarti W.M. Evaluation of wound healing potential of pomegranate (Punica granatum) whole fruit extract on skin burn wound in rats (Rattus norvegicus) J. Adv. Vet. Anim. Res. 2019;6:202–207. doi: 10.5455/javar.2019.f333
116. Yuniarti W.M., Primarizky H., Lukiswanto B.S. The activity of pomegranate extract standardized 40% ellagic acid during the healing process of incision wounds in albino rats (Rattus norvegicus) Vet. World. 2018;11:321–326. doi: 10.14202/vetworld.2018.321-326
117. Mo J., Panichayupakaranant P., Kaewnopparat N., Nitiruangjaras A., Reanmongkol W. Wound healing activities of standardized pomegranate rind extract and its major antioxidant ellagic acid in rat dermal wounds. J. Nat. Med. 2014;68:377–386. doi: 10.1007/s11418-013-0813-9
118. Bhadbhade SJ, Acharya AB, Rodrigues SV, Thakur SL. The antiplaque efficacy of pomegranate mouthrinse. Quintessence Int. 2011;42:29–36. https://www.ncbi.nlm.nih.gov/pubmed/21206931
119. Menezes SM, Cordeiro LN, Viana GS. Punica granatum (pomegranate) extract is active against dental plaque. J Herb Pharmacother. 2006;6:79–92. https://www.ncbi.nlm.nih.gov/pubmed/17182487
120. Promprom W, Kupittayanant P, Indrapichate K, Wray S, Kupittayanant S. The effects of pomegranate seed extract and beta-sitosterol on rat uterine contractions. Reprod Sci. 2010;17:288–96. https://www.ncbi.nlm.nih.gov/pubmed/19966214
121. Türk G, Sönmez M, Aydin M, Yüce A, Gür S, Yüksel M, et al. Effects of pomegranate juice consumption on sperm quality, spermatogenic cell density, antioxidant activity and testosterone level in male rats. Clin Nutr. 2008;27:289–96. https://www.ncbi.nlm.nih.gov/pubmed/18222572
122. Hartman RE, Shah A, Fagan AM, Schwetye KE, Parsadanian M, Schulman RN, et al. Pomegranate juice decreases amyloid load and improves behavior in a mouse model of Alzheimer’s disease. Neurobiol Dis. 2006;24:506–15. https://www.ncbi.nlm.nih.gov/pubmed/17010630
123. Dell’Agli M, Galli GV, Corbett Y, Taramelli D, Lucantoni L, Habluetzel A, et al. Antiplasmodial activity of Punica granatum L. fruit rind. J Ethnopharmacol. 2009;125:279–85. https://www.ncbi.nlm.nih.gov/pubmed/19577622
124. Dell’agli M, Galli GV, Bulgari M, Basilico N, Romeo S, Bhattacharya D, et al. Ellagitannins of the fruit rind of pomegranate (Punica granatum) antagonize in vitro the host inflammatory response mechanisms involved in the onset of malaria. Malar J. 2010;9:208. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2912927/
125. Neurath AR, Strick N, Li YY, Debnath AK. Punica granatum (pomegranate) juice provides an HIV-1 entry inhibitor and candidate topical microbicide. Ann N Y Acad Sci. 2005;1056:311–27. https://www.ncbi.nlm.nih.gov/pubmed/16387698
126. Vidal A, Fallarero A, Peña BR, Medina ME, Gra B, Rivera F, et al. Studies on the toxicity of Punica granatum L. (Punicaceae) whole fruit extracts. J Ethnopharmacol. 2003;89:295–300. https://www.ncbi.nlm.nih.gov/pubmed/14611895
127. Zarfeshany A, Asgary S, Javanmard SH. Potent health effects of pomegranate. Advanced Biomedical Research. 2014;3:100. doi:10.4103/2277-9175.129371. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4007340/
128. National Center for Complementary and Integrative Health. Excessive Claims. https://nccih.nih.gov/about/offices/od/2010-10.htm

Avocado

The avocado (Persea americana) originated in Mexico, Central or South America, and was first cultivated in Mexico as early as 500 BC ¹. The first English language mention of avocado was in 1696. In 1871, avocados were first introduced to the United States in Santa Barbara, California, with trees from Mexico. By the 1950s, there were over 25 avocado varieties commercially packed and shipped in California, with Fuerte accounting for about two-thirds of the production. As the large-scale expansion of the avocado industry occurred in the 1970s, the Hass avocado cultivar replaced Fuerte as the leading California variety and subsequently became the primary global variety ¹. The Hass avocado contains about 136 g of pleasant, creamy, smooth texture edible fruit covered by a thick dark green, purplish black, and bumpy skin. The avocado seed and skin comprise about 33% of the total whole fruit weight ². Avocados are a farm-to-market food; they require no processing, preservatives or taste enhancers. The avocado’s natural skin eliminates the need for packaging and offers some disease and insect resistance, which allows them to be grown in environmentally sustainable ways.

Although the U.S. Nutrition Labeling and Education Act defines the serving size of an avocado as one-fifth of a fruit, or 30 g (1 ounce), the National Health and Nutrition Examination Survey 2001–2006 finds that the average consumption is one-half an avocado (approximately 68 g) ³.

The nutrition and phytochemical composition of avocados is summarized in Table 1.

One-half an avocado is a nutrient and phytochemical dense food consisting of the following: dietary fiber (4.6 g), total sugar (0.2 g), potassium (345 mg), sodium (5.5 mg), magnesium (19.5 mg), vitamin A (5.0 μg RAE), vitamin C (6.0 mg), vitamin E (1.3 mg), vitamin K1 (14 μg), folate (60 mg), vitamin B-6 (0.2 mg), niacin (1.3 mg), pantothenic acid (1.0 mg), riboflavin (0.1 mg), choline (10 mg), lutein/zeaxanthin (185 μg), cryptoxanthin (18.5 μg), phytosterols (57 mg), and high-monounsaturated fatty acids (6.7 g) and 114 kcals or 1.7 kcal/g (after adjusting for insoluble dietary fiber), which may support a wide range of potential health effects ⁴. Avocados contain an oil rich in monounsaturated fatty acids (MUFA) in a water based matrix, which appears to enhance nutrient and phytochemical bioavailability and masks the taste and texture of the dietary fiber ⁵. Avocados are a medium energy dense fruit because about 80% of the avocado edible fruit consists of water (72%) and dietary fiber (6.8%) and has been shown to have similar effects on weight control as low-fat fruits and vegetables ⁶. An analysis of adult data from the NHANES 2001–2006 suggests that avocado consumers have higher high-density lipoprotein (HDL) cholesterol also known as the “good” cholesterol, lower risk of metabolic syndrome, and lower weight, BMI, and waist circumference than nonconsumers ⁷. One avocado fruit (136 g) has nutrient and phytochemical profiles similar to 1.5 ounces (42.5 g) of tree nuts (almonds, pistachios, or walnuts), which have qualified heart health claims ⁴ (Table 2).

Table 1. Avocado Calories – Carbs –  Protein – Fiber – Nutrition Content

Nutrient	Unit	Value per 100 g	cup, cubes 150 g	cup, pureed 230 g	cup, sliced 146 g	Avocado, Florida or California 201 g
Approximates
Water	g	73.23	109.84	168.43	106.92	147.19
Energy	kcal	160	240	368	234	322
Protein	g	2	3	4.6	2.92	4.02
Total lipid (fat)	g	14.66	21.99	33.72	21.4	29.47
Carbohydrate, by difference	g	8.53	12.79	19.62	12.45	17.15
Fiber, total dietary	g	6.7	10.1	15.4	9.8	13.5
Sugars, total	g	0.66	0.99	1.52	0.96	1.33
Minerals
Calcium, Ca	mg	12	18	28	18	24
Iron, Fe	mg	0.55	0.82	1.27	0.8	1.11
Magnesium, Mg	mg	29	44	67	42	58
Phosphorus, P	mg	52	78	120	76	105
Potassium, K	mg	485	728	1116	708	975
Sodium, Na	mg	7	10	16	10	14
Zinc, Zn	mg	0.64	0.96	1.47	0.93	1.29
Vitamins
Vitamin C, total ascorbic acid	mg	10	15	23	14.6	20.1
Thiamin	mg	0.067	0.101	0.154	0.098	0.135
Riboflavin	mg	0.13	0.195	0.299	0.19	0.261
Niacin	mg	1.738	2.607	3.997	2.537	3.493
Vitamin B-6	mg	0.257	0.386	0.591	0.375	0.517
Folate, DFE	µg	81	122	186	118	163
Vitamin B-12	µg	0	0	0	0	0
Vitamin A, RAE	µg	7	10	16	10	14
Vitamin A, IU	IU	146	219	336	213	293
Vitamin E (alpha-tocopherol)	mg	2.07	3.1	4.76	3.02	4.16
Vitamin D (D2 + D3)	µg	0	0	0	0	0
Vitamin D	IU	0	0	0	0	0
Vitamin K (phylloquinone)	µg	21	31.5	48.3	30.7	42.2
Lipids
Fatty acids, total saturated	g	2.126	3.189	4.89	3.104	4.273
Fatty acids, total monounsaturated	g	9.799	14.698	22.538	14.307	19.696
Fatty acids, total polyunsaturated	g	1.816	2.724	4.177	2.651	3.65
Fatty acids, total trans	g	0	0	0	0	0
Cholesterol	mg	0	0	0	0	0
Other
Caffeine	mg	0	0	0	0	0

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ²]

Table 2. Avocado compared to tree nut qualified health claims reference amount

Nutrient	Hass avocado 1 fruit (136 g)	Almonds 1.5 oz (42.5 g)	Pistachios 1.5 oz (42.5 g)	Walnuts 1.5 oz (42.5 g)
Water (g)	98.4	1.1	0.8	1.7
Calories (kcal)	227	254	240	278
Calories (kcal) (insoluble fiber adjusted)	201	239	235	269
Total fat (g)	21	22.1	19.1	27.7
Monounsaturated fat (g)	13.3	13.8	10.1	3.8
Polyunsaturated fat (g)	2.5	5.5	5.7	20
Saturated fat (g)	2.9	1.7	2.3	2.6
Protein (g)	2.7	9	9	6.5
Total Carbohydrate (g)	11.8	9	12.2	5.8
Dietary fiber (g)	9.2	4.6	4.2	2.9
Potassium (mg)	690	303	450	188
Magnesium (mg)	39	120	48	68
Vitamin C (mg)	12	0	1.4	0.6
Folate (mcg)	121	23	21	42
Vitamin B-6 (mg)	0.4	0.05	0.5	0.2
Niacin (mg)	2.6	1.5	0.6	0.5
Riboflavin (mg)	0.2	0.4	0.1	0.06
Thiamin (mg)	0.1	0.04	0.3	0.15
Pantothenic acid (mg)	2	0.1	0.2	0.2
Vitamin K (ug)	28.6	0	6.3	1.2
Vitamin E (α-Tocopherol) (mg)	2.7	10.1	0.9	0.3
γ-Tocopherol (mg)	0.44	0.3	9	8.9
Lutein + zeaxanthin (ug)	369	0	494	4.5
Total phytosterols (mg)	113	54	123	30

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ⁴]

How To Choose and Use Avocado

There are hundreds of types of avocados, but seven avocado varieties (Bacon, Fuerte, Gwen, Hass, Lamb Hass, Pinkerton, Reed and Zutano) are grown commercially in California. The Hass variety accounts for approximately 95 percent of the total crop each year – which runs from Spring to Fall.

Many varieties are available as certified organic fruit.

How to know when your avocado is ripe

• The best way to tell if an avocado is ripe and ready for immediate use is to gently squeeze the fruit in the palm of your hand. Ripe, ready-to-eat fruit will be firm yet will yield to gentle pressure.
• Color alone may not tell the whole story, because some avocado like the Hass avocado will turn dark green or black as it ripens, but some other avocado varieties retain their light-green skin even when ripe.
• Avoid fruit with dark blemishes on the skin or over-soft fruit.
• If you plan to serve the fruit in a few days, stock up on hard, unripened fruit.

How to Ripen your Avocados

• The easiest way to ripen an avocado is to place it on your counter or in your fruit bowl for a few days until it gives slightly to gentle squeezing in the palm of your hand.
• To speed up the process of ripening avocados, place the fruit in a plain brown paper bag and store at room temperature 65-75° F until ready to eat (usually two to five days).
• Including an apple or kiwifruit in the bag accelerates the process because these fruits give off natural ethylene gas, which will help ripen your avocados organically. Ethylene is a plant hormone that triggers the ripening process and is used commercially to help ripen bananas, avocados and other fruit. When placed in a paper bag, you are containing the ethylene and encouraging the fruit to ripen faster. For best results, use red or golden delicious apples. These old varieties produce more ethylene than newer varieties (e.g. Gala or Fuji) that have been bred to ripen slowly to maintain their crisp texture, and will be the most effective when it comes to ripening avocados ⁸.
• Tip: The more apples or kiwifruit you add, the quicker your avocados will ripen !
• Soft ripe fruit can be refrigerated until it is eaten, and should last for at least two more days.
• Refrigerate only ripe or soft avocados.
• Putting your avocado into the oven or microwave is not recommended. The avocado will soften, but it just won’t have the flavor or taste. It will actually taste like unripe avocado (because it is).

If you are cutting into an avocado and there are black spots, vascular bundles (stringiness) or bruises, discard those areas. Vascular bundles (stringiness or stringy avocado fibers running through the avocado pulp) are generally the result of fruit from younger trees, improper storage conditions or transitional times between origins (from one country to the next). Often times the fibers or strings will disappear or become less noticeable as the avocado season goes on and/or trees mature ⁸.

That being said, it’s very difficult to predict whether your avocados will have strings or not without cutting into them first.

Avocado and Weight Management

The availability and consumption of healthy foods, including vegetables and fruits, is associated with lower weight ⁹ and body mass index (BMI) ¹⁰. Over the last several decades, there has been the general perception that consuming foods rich in fat can lead to weight gain, and low-fat diets would more effectively promote weight control and reduce chronic disease risk ¹¹. However, a key large, randomized, long-term clinical trial found that a moderate fat diet can be an effective part of a weight loss plan and the reduction of chronic disease risk ¹². Strong and consistent evidence indicates that dietary patterns that are relatively low in energy density improve weight loss and weight maintenance among adults. Three randomized controlled weight loss trials found that lowering food-based energy density by increasing fruit and/or vegetable intake is associated with significant weight loss ¹⁰, ¹³, ¹⁴. The energy density of an entire dietary pattern is estimated by dividing the total amount of calories by the total weight of food consumed; low, medium, and high energy density diets contain 1.3 kcal, 1.7 kcal, and 2.1 kcal per g, respectively ¹⁵. Avocados have both a medium energy density of 1.7 kcal/g and a viscose water, dietary fiber and fruit oil matrix that appears to enhance satiety ¹⁶. This is consistent with research by Bes-Rastrollo et al. ⁹, which suggests that avocados support weight control similar to other fruits.

Several preliminary clinical studies suggest that avocados can support weight control. The first trial studied the effect of including one and a half avocados (200 g) in a weight loss diet plan. In this study, sixty-one healthy free-living, overweight, and obese subjects were randomly assigned into either a group consuming 200 g/d of avocados (30.6 g fat) substituted for 30 g of mixed fats, such as margarine and oil, or a control group excluding avocados for 6 weeks ¹⁷. Both groups lost similar levels of weight, body mass index (BMI), and percentage of body fat to confirm that avocados can fit into a weight loss diet plan. A randomized single blinded, crossover postprandial study of 26 healthy overweight adults suggested that one-half an avocado consumed at lunch significantly reduced self-reported hunger and desire to eat, and increased satiation as compared to the control meal ¹⁶. Additionally, several exploratory trials suggest that monounsaturated fatty acid (MUFA) rich diets help protect against abdominal fat accumulation and diabetic health complications ¹⁸, ¹⁹, ²⁰.

Avocado and Cardiovascular Health Benefits

Avocados provide nearly 20 essential nutrients, including a good source of fiber and folate, potassium, Vitamin E, B-vitamins, and folic acid.

Avocados are a potent source of nutrients as well as monounsaturated fatty acids (MUFAs). According to a recent study, adding an avocado a day to a heart-healthy diet can help improve LDL levels in people who are overweight or obese.

There are eight preliminary avocado cardiovascular clinical trials summarized in Table 3 ²¹, ²², ²³, ²⁴, ²⁵, ²⁶, ²⁷, ¹⁷.

Table 3. Avocado cardiovascular health clinical overview

Conclusions	Methods	Results	References
Daily addition of California avocados to the habitual diet showed a beneficial effect on total cholesterol (TC) and body weight control (Preliminary, uncontrolled study)	– Open label study for 4 weeks (n = 16) – Normal/hypercholesterolemic male patients in Veteran’s Administration Hospital – 27–72 yrs old – 0.5–1.5 California avocados per day in addition to habitual diet	– 1/2 subjects had significantly lowered total cholesterol (TC) by 9–43% – 1/2 subjects had unchanged total cholesterol – No subjects had increased total cholesterol – 3/4 of subjects lost weight or remained weight stable despite an increase intake of calories and fat – Generally the subjects had a more regular bowel movement pattern	Grant 28
An avocado enriched diet was more effective than the American Heart Association Diet in promoting heart healthy lipid profiles in women (Limited number of subjects and short duration)	– Randomized, crossover study for 3 weeks (n = 15) – Females w/ baseline total cholesterol (4–8 mm/L) – 37–58 years old – 66.8 ± 0.8 kg body weight – Two diets: (1) High monounsaturated fatty acid (MUFA) primarily avocado diet or (2) High in complex carbohydrates low-fat diet (American Heart Association Diet)	– Both diets decreased total cholesterol (TC) compared to baseline – Avocado diets were more effective in decreasing TC 8.2% vs. 4.9% – Low-density lipoprotein cholesterol (LDL-C also called “bad” cholesterol) decreased on avocado enriched diet but not American Heart Association Diet – High-density lipoprotein cholesterol (HDL-C also called “good” cholesterol) did not change on avocado enriched diet but decreased by 13.9% on the American Heart Association Diet	Colquhoun et al. 29
Avocado enriched diets can help avoid potential adverse effects of low-fat diets on HDL-C and triglycerides (Well designed study but limited number of subjects and short duration)	– Randomized, crossover study for 2 weeks (n = 16) – Healthy subjects baseline total cholesterol 4.2 ± 0.68 mm/L; mean age 26 years; mean BMI 22.9 – Four diets: (1) Control, typical diet (2) Monounsaturated fatty acid (MUFA) fat diets with avocado (75% from Hass Avocados) (RMF) (3) Habitual diet plus same level of Hass avocados as (2) (FME) (4) Low-saturated diet (LSF)	– Both RMF and LSF diets had similar reductions in total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C also called “bad” cholesterol) – Both habitual diet plus same level of Hass avocados (75% from Hass Avocados) and low-saturated fat diets had significantly lower total cholesterol, LDL-C and HDL-C – RMF and FME diets lowered triglycerides (TG) and the low-saturated fat diet had significantly increased triglycerides levels	Alvizouri-Munoz et al. 30
Partial replacement of avocados for other dietary fats in patients with type 2 diabetes favorably affected serum lipid profile and maintained adequate glycemic control (Well designed study but limited number of subjects)	– Randomized, crossover study for 4 weeks (n = 12) – Women with type 2 diabetes; mean 56 ± 8 years; BMI 28 ± 4 – Three diets (1) Control, American Diabetes Diet plan; 30% kcal from fat (ADA) (2) High MUFA diet with 1 avocado (Hass) and 4 teaspoons of olive oil; 40% kcal from fat (3) High in complex carbohydrates 20% Kcal from fat (High-Carb)	– Both high MUFA and high-Carb diets had a minor hypo-cholesterolemic effect with no changes in HDL-C – High MUFA diet was associated with a greater decrease in triglycerides (20 vs. 7% for High-Carb) – Glycemic control was similar for both High MUFA and High-Carb diets	Lerman-Garber et al. 31
Diets rich in avocados appear to help manage hyper-cholesterolemia (Well designed study but limited number of subjects and level of avocado consumption very high)	– Randomized crossover for study 4 weeks with a controlled diet (n = 16) – Hyper-cholesterolemic subjects with phenotype II and IV dyslipidemias – Two diets: (1) Avocado rich diet (75% fat from avocado) diet (2) Low-saturated fat diet	The Avocado diet had significantly lowered total cholesterol, LDL-C levels, and increased HDL-C with a mild decrease in triglycerides compared the low-saturated fat diet plan	Carranza et al. 32
Avocado-enriched diets had significantly improved lipoprotein and/or triglyceride profiles in normal and hyper-cholesterolemic subjects (Complex clinical design and very short duration)	– Randomized, controlled study for 7 days (n = 67) (1) Healthy normo-lipidemic subjects (< 200 mg/dL) (2) Mild hyper-cholesterolemia and type 2 diabetic patients (201–400 mg/dL)- Enriched avocado diet vs. isocaloric non-avocado diets. 300 g Hass Avocado substituted for other lipid sources (both diets contained about 50% kcal from fat	– Subjects with normal cholesterol had a 16% decrease in serum total cholesterol following avocado diets vs. an increase in total cholesterol with the control (p < 0.001) – Subjects with elevated cholesterol had significant decrease (p < 0.001) total serum cholesterol (17%), LDL-C (22%), triglycerides (22%), and a slight increase in HDL-C – No changes with the non-avocado habitual diet	Lopez-Ledesma et al. 33
Vegetarian diets with avocados promote healthier lipoprotein profiles compared to low-fat and vegetarian diets without avocados (Preliminary study with limited number of subjects)	– Randomized, prospective, transversal and comparative 4 week study and controlled diet (n = 13) – Dyslipidemic subjects with high blood pressure – Three vegetarian diets: (1) 70% carbohydrate, 10% protein and 20% lipids (2) 60% carbohydrates, 10% protein and 30% lipids (75% of the fat from Hass avocados) (3) Diet 2 w/o avocado	The avocado diet significantly reduced LDL-C, whereas high carbohydrate and non-avocado diets did not change LDL-C	Carranza-Madrigal et al. 34
The consumption of as much as 1 1/2 avocados within an energy-restricted diet does not compromise weight loss or lipoproteins or vascular function (Well designed study)	– Randomized, controlled, parallel study, free-living (n = 61) – Male (n = 13) and female (n = 48) adults with a age 40.8 ± 8.9 years; BMI 32 ± 3.9 – Energy restricted diet for 6 weeks at the rate of 30% kcal from fat – 200 g avocado/day (30.6 g fat) substituted for 30 g of mixed fat (e.g., margarine and vegetable oil) compared to a control diet without avocado	– There was no difference in body weight, BMI, and% body fat when avocados were substituted for mixed fats in an energy restricted diet – There was also no difference in serum lipids (total cholesterol, LDL-C, HDL-C, and triglycerides), fibrinogen, blood pressure, or blood flow when avocados were substituted for mixed fats in an energy-restricted diet	Pieterse et al. 35

[Source ³⁶]

The first exploratory avocado clinical study demonstrated that the consumption of 0.5–1.5 avocados per day may help to maintain normal serum total cholesterol in men ²¹. Half the subjects experienced a 9–43% reduction in serum total cholesterol and the other subjects (either diabetic or very hypercholesterolemic) experienced a neutral effect, but none of the subjects showed increased total cholesterol. Also, the subjects did not gain weight when the avocados were added to their habitual diet.

In the 1990s, a number of avocado clinical trials consistently showed positive effects on blood lipids in a wide variety of diets in studies on healthy, hypercholesterolemic, and type 2 diabetes subjects ²², ²³, ²⁴, ²⁵, ²⁶, ²⁷, ¹⁷. In hypercholesterolemic subjects, avocado enriched diets improved blood lipid profiles by lowering LDL-cholesterol and triglycerides and increasing HDL-cholesterol compared to high carbohydrate diets or other diets without avocado. In normolipidemic subjects, avocado enriched diets improved lipid profiles by lowering LDL-cholesterol without raising triglycerides or lowering HDL-cholesterol. These studies suggest that avocado enriched diets have a positive effect on blood lipids compared to low-fat, high carbohydrate diets or the typical American diet. However, since all these trials were of a small number of subjects (13–37 subjects) and limited duration (1–4 weeks), larger and longer term trials are needed to confirm avocado blood lipid lowering and beyond cholesterol health effects.

In a randomized crossover study of 12 women with type 2 diabetes, a monounsaturated fat diet rich in avocado was compared with a low-fat complex-carbohydrate-rich diet for effects on blood lipids ²⁴. After 4 weeks, the avocado rich diet resulted in significantly lowered plasma triglycerides and both diets maintained similar blood lipids and glycemic controls. Additionally, a preclinical study found that avocados can modify the HDL-C structure by increasing paraoxonase 1 activity, which can enhance lipophilic antioxidant capacity and help convert oxidized LDL-C back to its nonoxidized form ³⁷.

Avocado and Fatty Acids

Avocados can fit into a heart healthy dietary pattern such as the DASH (Dietary Approaches to Stop Hypertension) diet plan. Avocados contain a monounsaturated fatty acids (MUFA)-rich fruit oil with 71% MUFA, 13% polyunsaturated fatty acids (PUFA), and 16% saturated fatty acids (SFA). As the avocado fruit ripens, the saturated fat decreases and the monounsaturated oleic acid increases ³⁸. The use of avocado dips and spreads as an alternative to more traditional hard, saturated fatty acids rich spreads or dips can assist in lowering dietary saturated fatty acids intake ³⁹.

Table 4. Hass Avocado Spread and Dip Comparison

Spread and Dip Nutritional Comparison
	Fresh Avocado	Butter	Sour Cream	Margarine	Cheddar Cheese	Mayonnaise, Regular
Serving Size	50g (1/3 of a medium avocado)	1 Tbsp.	2 Tbsp.	1 Tbsp	1 oz. (1 slice)	1 Tbsp.
Calories	80	100	45	100	110	90
Total Fat (g)	8	12	4.5	11	9	10
Sat Fat (g)	1	7	3	2	5	1.5
Cholesterol (mg)	0	30	10	0	30	5
Sodium (mg)	0	90	10	95	180	90

Footnote: A 50g serving of fresh avocados contain 0mg of cholesterol, 0mg of sodium, 1g saturated fat. Nutritional values are for the item listed only; not as consumed with other foods or ingredients.

[Source Avocado Central. Hass Avocado Spread Comparison ³⁹]

Avocado and Dietary Fiber

Avocado fruit carbohydrates are composed of about 80% dietary fiber, consisting of 70% insoluble and 30% soluble fiber ⁴⁰. Avocados contain 2.0 g and 4.6 g of dietary fiber per 30 g and one-half fruit, respectively. Thus, moderate avocado consumption can help to achieve the adequate intake of 14 g dietary fiber per 1000 kcal as about one-third this fiber level can be met by consuming one-half an avocado.

Avocado and Sugars

Compared to other fruits, avocados contain very little sugar. One-half an avocado contains only about 0.2 g sugar (e.g., sucrose, glucose, and fructose). The primary sugar found in avocados is a unique seven-carbon sugar called D-mannoheptulose and its reduced form, perseitol, contributes about 2.0 g per one-half fruit but this is not accounted for as sugar in compositional database as it does not behave nutritionally as conventional sugar and is more of a unique phytochemical to avocados ⁴¹, ⁴². Preliminary D-mannoheptulose research suggests that it may support blood glucose control and weight management ⁴³. The glycemic index and load of an avocado is expected to be about zero due to its very low carbohydrate content.

Avocado and Potassium

Clinical evidence suggests that adequate potassium intake may promote blood pressure control in adults ⁴⁴. The mean intake of potassium by adults in the United States was approximately 3200 mg per day in men and 2400 mg per day in women, which is lower than the 4700 mg per day recommended intake ⁴⁵. Avocados contain about 152 mg and 345 mg of potassium per 30 g and one-half fruit, respectively. Also, avocados are naturally very low in sodium with just 2 mg and 5.5 mg sodium per 30 g and one-half fruit, respectively ². The health claim for blood pressure identifies foods containing 350 mg potassium and less than 140 mg of sodium per serving as potentially appropriate for this claim.

Avocado and Magnesium

Magnesium acts as a cofactor for many cellular enzymes required in energy metabolism, and it may help support normal vascular tone and insulin sensitivity ⁴⁶. Preliminary preclinical and clinical researches suggest that low magnesium may play a role in cardiac ischemia ⁴⁶. In the Health Professionals Follow-up Study, the results suggested that the intake of magnesium had a modest inverse association with risk of coronary heart disease in men ⁴⁷. Magnesium was shown to inhibit fat absorption to improve postprandial hyperlipidemia in healthy subjects ⁴⁸. Avocados contain about 9 and 20 mg magnesium per 30 g and one-half fruit, respectively ².

Avocado and Vitamins

• Antioxidant Vitamins

Avocados are one of the few foods that contain significant levels of both vitamins C and E. Vitamin C plays an important role in recycling vitamin E to maintain circulatory antioxidant protection such as potentially slowing the rate of LDL-cholesterol oxidation. Evidence suggests that vitamin C may contribute to vascular health and arterial plaque stabilization ⁴⁹. According to a recent review article, vitamin C might have greater cardiovascular disease protective effects on specific populations such as smokers, obese, and overweight people; people with elevated cholesterol, hypertension, and type 2 diabetics; and people over 55 years of age ⁵⁰. Avocado fruit contains 2.6 mg and 6.0 mg vitamin C per 30 g and one-half fruit, respectively ². Avocados contain 0.59 mg and 1.34 mg vitamin E (α-tocopherol) per 30 g and one-half avocado, respectively ². One randomized clinical study suggested that a combination of vitamin C and E may slow atherosclerotic progression in hypercholesterolemic persons ⁵¹.

• Vitamin K1 (phylloquinone)

Vitamin K1 functions as a coenzyme during synthesis of the biologically active form of a number of proteins involved in blood coagulation and bone metabolism ⁵². Phylloquinone (K1) from plant-based foods is considered to be the primary source of vitamin K in the human diet. Vitamin K1 in its reduced form is a cofactor for the enzymes that facilitate activity for coagulation ⁵³. The amount of vitamin K1 found in avocados is 6.3 μg and 14.3 μg per 30 g and one-half fruit, respectively ². Some people on anticoagulant medications are concerned about vitamin K intake; however, the avocado level of vitamin K1 per ounce is 150 times lower than the 1000 μg of K1 expected to potentially interfere with the anticoagulant effect of drugs such as warfarin (Coumadin) ⁵⁴, ⁵⁵.

• B-vitamins

Deficiencies in B-vitamins such as folate and B-6 may increase homocysteine levels, which could reduce vascular endothelial health and increase cardiovascular disease risk ⁵⁶. Avocados contain 27 μg folate and 0.09 mg vitamin B-6 per 30 g and 61 μg folate, respectively, and 0.20 mg vitamin B-6 per one-half fruit ².

Avocado and Phytochemicals

• Carotenoids

The primary avocado carotenoids are a subclass known as xanthophylls, oxygen-containing fat-soluble antioxidants ⁵⁷ (Table 1). Xanthophylls, such as lutein, are more polar than carotenes (the other carotenoid subclasses including β-carotene), so they have a much lower propensity for pro-oxidant activity ⁵⁸. Avocados have the highest lipophilic total antioxidant capacity among fruits and vegetables ⁵⁹. In a relatively healthy population, the DASH diet pattern clinical study reported reduced oxidative stress (blood ORAC and urinary isoprostanes) compared to a typical American diet ⁶⁰, which appears primarily due to the DASH diet providing significantly more serum carotenoids, especially the xanthophyll carotenoids lutein, β-cryptoxanthin, and zeaxanthin, as a result of increased fruit and vegetable consumption. Xanthophylls appear to reduce circulating oxidized LDL-C, a preliminary biomarker for the initiation and progression of vascular damage ⁶¹. The Los Angeles Atherosclerosis Study, a prospective study, findings suggest that higher levels of plasma xanthophylls were inversely related to the progression of carotid intima-media thickness, which may be protective against early atherosclerosis ⁶². Although this research is encouraging, more clinical studies are needed to understand the cardiovascular health benefits associated with avocado carotenoids.

The consumption of avocados can be an important dietary source of xanthophyll carotenoids ³⁸. Hass avocado carotenoid levels tend to significantly increase as the harvest season progresses from January to September ³⁸. In Hass avocados, xanthophylls lutein and cryptoxanthin predominate over the carotenes, contributing about 90% of the total carotenoids ³⁸. USDA reports lutein and zeaxanthin at 81 μg and 185 μg per 30 g and one half fruit, respectively, and cryptoxanthin at 44 μg and 100 μg per 30 g and one-half fruit, respectively ². However, a more comprehensive analysis of avocados including xanthophylls has found much higher levels ranging from 350–500 μg per 30 g to 800–1100 μg per one-half fruit at time of harvest ³⁸. The color of avocado flesh varies from dark green just under the skin to pale green in the middle section of the flesh to yellow near the seed ³⁸. The total carotenoid concentrations were found to be greatest in the dark green flesh close to peel ⁶³.

The intestinal absorption of carotenoids depends on the presence of dietary fat to solubilize and release carotenoids for transfer into the gastrointestinal fat micelle and then the circulatory system ⁶⁴, ⁶⁵. Avocado fruit has a unique unsaturated oil and water matrix naturally designed to enhance carotenoid absorption. For salads, a significant source of carotenoids, reduced fat or fat free salad dressings are common in the marketplace and these dressings have been shown to significantly reduce carotenoid absorption compared to full fat dressings ⁶⁶. Similar clinical research has demonstrated that adding avocado to salad without dressing, or with reduced fat/fat free dressing and serving avocados with salsa increases carotenoid bioavailability by 2–5 times ⁶⁷.

• Phenolics

Preliminary evidence suggests beneficial effects of fruit phenolics on reducing cardiovascular disease risk by reducing oxidative and inflammatory stress, enhancing blood flow and arterial endothelial health, and inhibiting platelet aggregation to help maintain vascular health ⁶⁸, ⁶⁹, ⁷⁰, ⁷¹. Avocados contain a moderate level of phenolic compounds contributing 60 mg and 140 mg gallic acid equivalents (GAE) per 30 g and one-half fruit, respectively. The avocado also has a total antioxidant capacity of 600 μmol Trolox Equilvalent (TE) per 30 g or 1350 μmol TE per one-half fruit ⁷². This places avocados in the mid-range of fruit phenolic levels. Avocados have the highest fruit lipophilic antioxidant capacity, which may be one factor in helping to reduce serum lipid peroxidation and promoting vascular health ⁷².

• Phytosterols

Avocados are the richest known fruit source of phytosterols ⁷³ with about 26 mg and 57 mg per 30 g and one half fruit, respectively ². Other fruits contain substantially less phytosterols at about 3 mg per serving ⁷³. Although the avocado’s phytosterol content is lower than that of fortified foods and dietary supplements, its unique emulsified fat matrix and natural phytosterol glycosides may help promote stronger intestinal cholesterol blocking activity than fortified foods and supplements ⁷⁴. A recent economic valuation in Canada of the potential health benefits from foods with phytosterols suggests that they may play a role in enhancing cardiovascular health and reducing associated health costs ⁷⁵.

Avovcado and Healthy Aging

• DNA Damage Protection

Several clinical studies suggest that xanthophylls, similar to those found in avocados, may have antioxidant and DNA protective effects with possible healthy aging protective effects. One study was conducted involving 82 male airline pilots and frequent air travelers who are exposed to high levels of cosmic ionizing radiation known to damage DNA, potentially accelerating the aging process ⁷⁶. There was a significant and inverse association between intake of vitamin C, beta-carotene, β-cryptoxanthin, and lutein-zeaxanthin from fruits and vegetables and the frequency of chromosome translocation, a biomarker of cumulative DNA damage. In another trial, lipid peroxidation (8-epiprostaglandin F2a) was correlated inversely with plasma xanthophyll levels ⁷⁷. In other studies, inverse correlations were found between lutein and oxidative DNA damage as measured by the comet assay, and in contrast to beta-carotene ⁷⁸, ⁷⁹. National Health and Nutrition Examination Survey analysis suggests that xanthophylls intake decreases with aging ⁸⁰.

• Osteoarthritis

Osteoarthritis (OA) is characterized by progressive deterioration of joint cartilage and function with associated impairment, and this affects most people as they age or become overweight or obese ⁸¹, ⁸². This joint deterioration may be triggered by oxidative and inflammation stress, which can cause an imbalance in biosynthesis and degradation of the joint extracellular matrix leading to loss of function ⁸¹. A cross-sectional study reported that fruits and vegetables rich in lutein and zeaxanthin (the primary carotenoids in avocados) are associated with decreased risk of cartilage defects (early indicator of osteoarthritis) ⁸³.

Avocado and soy unsaponifiables (ASU) is a mixture of fat soluble extracts in a ratio of about 1(avocado):2(soy). The major components of avocado and soy unsaponifiables (ASU) are considered anti-inflammatory compounds with both antioxidant and analgesic activities ⁸¹, ⁸⁴, ⁸⁵, ⁸⁶, ⁸⁷, ⁸⁸, ⁸⁹. In vitro studies found that pretreatment of chondrocytes with avocado and soy unsaponifiables blocked the activation of COX-2 transcripts and secretion of prostaglandin E2 (PGE2) to baseline levels after activation with lipopolysaccharide (LPS). Further study revealed that avocado and soy unsaponifiables can also block tumor necrosis factor-α (TNF-α), IL-1β, and iNOS expression to levels similar to those in nonactivated control cultures. Additional laboratory studies suggest that avocado and soy unsaponifiables (ASU) may facilitate repair of osteoarthritis cartilage through its effect on osteoblasts ⁸¹.

Clinical support for avocado and soy unsaponifiables in the management of hip and knee osteoarthritis comes from four randomized controlled trials ⁹⁰, ⁹¹, ⁹², ⁸⁹ and one meta-analysis ⁹³. All studies used 300 mg per day. The clinical trials were generally positive with three providing osteoarthritis support and one study showing no joint cartilage improvement compared to placebo.

• Eye Health

Lutein and zeaxanthin are selectively taken up into the macula of the eye (the portion of the eye where light is focused on the lens) ⁹⁴. Relative intakes of lutein and zeaxanthin decrease with age and the levels are lower in females than males ⁸⁰. Mexican Americans have the highest intake of lutein and zeaxanthin than any other ethnicity and they are among the highest consumers of avocados in the United States. Observational studies show that low dietary intake and plasma concentration of lutein may increase age-related eye dysfunction ⁹⁵. Research from the Women’s Health Initiative Observation Study found that MUFA rich diets were protective of age-related eye dysfunction ⁹⁶, ⁹⁷. Avocados may contribute to eye health since they contain a combination of MUFA and lutein/zeaxanthin and help improve carotenoid absorption from other fruits and vegetables ⁶⁷. Avocados contain 185 μg of lutein/zeaxanthin per one-half fruit, which is expected to be more highly bioavailable than most other fruit and vegetable sources.

• Skin Health

Skin often shows the first visible indication of aging. Topical application or consumption of some fruits and vegetables or their extracts such as avocado has been recommended for skin health ⁹⁸. The facial skin is frequently subjected to ongoing oxidative and inflammatory damage by exposure to ultraviolet (UV) and visible radiation and carotenoids may be able to combat this damage. A clinical study found that the concentration of carotenoids in the skin is directly related to the level of fruit and vegetable intake ⁹⁹. Avocado’s highly bioavailable lutein and zeaxanthin may help to protect the skin from damage from both UV and visible radiation ⁹⁸. Several small studies suggest that topical or oral lutein can provide photo-protective activity ¹⁰⁰, ¹⁰¹, ¹⁰².

A cross-sectional study examined the relationship between skin anti-aging and diet choices in 716 Japanese women ¹⁰³. After controlling for covariates including age, smoking status, BMI, and lifetime sun exposure, the results showed that higher intakes of total dietary fat were significantly associated with more skin elasticity. A higher intake of green and yellow vegetables was significantly associated with fewer wrinkles ¹⁰³. Several preclinical studies suggest that avocado components may protect skin health by enhancing wound healing activity and reducing UV damage ¹⁰³, ¹⁰⁴.

• Cancer

Avocados contain a number of bioactive phytochemicals including carotenoids, terpenoids, D-mannoheptulose, persenone A and B, phenols, and glutathione that have been reported to have anti-carcinogenic properties ¹⁰⁵. The concentrations of some of these phytochemicals in the avocado may be potentially efficacious (Jones et al., 1992). Currently, direct avocado anti-cancer activity is very preliminary with all data based on in vitro studies on human cancer cell lines.

Cancer of the larynx, pharynx, and oral cavity are the primary area of avocado cancer investigation. Glutathione, a tripeptide composed of three amino acids (glutamic acid, cysteine, and glycine) functions as an antioxidant ¹⁰⁶. The National Cancer Institute found that avocado’s glutathione levels of 8.4 mg per 30 g or 19 mg per one-half fruit is several fold higher than that of other fruits ¹⁰⁶. Even though the body digests glutathione down to individual amino acids when foods are consumed, a large population-based case controlled study showed a significant correlation between increased glutathione intakes and decreased risk of oral and pharyngeal cancer ¹⁰⁷. One clinical study found that plasma lutein and total xanthophylls but not individual carotenes or total carotenes reduced biomarkers of oxidative stress (urinary concentrations of both total F2-isoprostanes and 8-epi-prostaglandin) in patients with early-stage (in situ, stage I, or stage II) cancer of larynx, pharynx, or oral cavity ⁷⁸. Xanthophyll rich avocado extracts have been shown in preclinical studies to have anti-Helicobacter pylori activity for a potential effect on gastritis ulcers, which may be associated with gastric cancer risk.

Dietary carotenoids show potential breast cancer protective biological activities, including antioxidant activity, induction of apoptosis, and inhibition of mammary cell proliferation ⁷⁹. Studies examining the role of fruits and vegetables and carotenoid consumption in relation to breast cancer recurrence are limited and report mixed results ⁷⁹. In preclinical studies, total carotenoids and lutein appear to reduce oxidative stress, a potential trigger for breast cancer ¹⁰⁸. In women previously treated for breast cancer, a significant inverse association was found between total plasma carotenoid concentrations and oxidative stress ⁷⁹, but more clinical research is needed to confirm this finding.

Mammographic density is one of the strongest predictors of breast cancer risk ¹⁰⁹. The association between carotenoids and breast cancer risk as a function of mammographic density was conducted in a nested, case-control study consisting of 604 breast cancer cases and 626 controls with prospectively measured circulating carotenoid levels and mammographic density in the Nurses’ Health Study ¹⁰⁹. Overall, circulating total carotenoids were inversely associated with breast cancer risk. Among women in the highest tertile of mammographic density, elevated levels α-carotene, β-cryptoxanthin, lycopene, and lutein/zeaxanthin in the blood were associated with a 40–50% reduction in breast cancer risk . In contrast, there was no inverse association between carotenoids and breast cancer risk among women with low-mammographic density. These results suggest that plasma levels of carotenoids may play a role in reducing breast cancer risk, particularly among women with high mammographic density. There are no direct avocado breast cancer clinical studies.

Exploratory studies in prostate cancer cell lines suggest antiproliferative and antitumor effects of avocado lipid extracts ⁶³. Lutein is one of the active components identified. There are currently no human studies to confirm this potential lutein and prostate cancer relationship.

References

1. California Avocado Commission. California Avocado history. 2012. https://www.californiaavocado.com/
2. United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. https://ndb.nal.usda.gov/ndb/
3. Fulgoni V. L., Dreher M. L., Davenport A. J. Consumption of avocados in diets of US adults: NHANES 2011-2006. Boston, MA: American Dietetic Association; 2010a. Abstract #54.
4. USDA (U.S. Department of Agriculture) Avocado, almond, pistachio and walnut Composition. Nutrient Data Laboratory. USDA National Nutrient Database for Standard Reference, Release 24. Washington, DC: U.S. Department of Agriculture; 2011.
5. Unlu NZ, Bohn T, Clinton SK, Schwartz SJ. Carotenoid absorption from salad and salsa by humans is enhanced by the addition of avocado or avocado oil. J Nutr. 2005 Mar;135(3):431-6. doi: 10.1093/jn/135.3.431
6. Bes-Rastrollo M, van Dam RM, Martinez-Gonzalez MA, Li TY, Sampson LL, Hu FB. Prospective study of dietary energy density and weight gain in women. Am J Clin Nutr. 2008 Sep;88(3):769-77. doi: 10.1093/ajcn/88.3.769
7. Fulgoni V. L., Dreher M. L., Davenport A. J. Avocado consumption associated with better nutrient intake and better health indices in US adults: NHANES 2011-2006. Experimental Biology. 2010b. Abstract #8514. Anaheim, CA.
8. California Avocado Commission. How to Ripen an Avocado – the Definitive Guide. https://www.californiaavocado.com/blog/how-to-ripen-an-avocado
9. Prospective study of dietary energy density and weight gain in women. Bes-Rastrollo M, van Dam RM, Martinez-Gonzalez MA, Li TY, Sampson LL, Hu FB. Am J Clin Nutr. 2008 Sep; 88(3):769-77. https://www.ncbi.nlm.nih.gov/pubmed/18779295/
10. A low-energy-dense diet adding fruit reduces weight and energy intake in women. de Oliveira MC, Sichieri R, Venturim Mozzer R. Appetite. 2008 Sep; 51(2):291-5. https://www.ncbi.nlm.nih.gov/pubmed/18439712/
11. Is a low fat diet the optimal way to cut energy intake over the long-term in overweight people? Walker KZ, O’Dea K. Nutr Metab Cardiovasc Dis. 2001 Aug; 11(4):244-8. https://www.ncbi.nlm.nih.gov/pubmed/11831109/
12. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. Sacks FM, Bray GA, Carey VJ, Smith SR, Ryan DH, Anton SD, McManus K, Champagne CM, Bishop LM, Laranjo N, Leboff MS, Rood JC, de Jonge L, Greenway FL, Loria CM, Obarzanek E, Williamson DA. N Engl J Med. 2009 Feb 26; 360(9):859-73. https://www.ncbi.nlm.nih.gov/pubmed/19246357/
13. The impact of a long-term reduction in dietary energy density on body weight within a randomized diet trial. Saquib N, Natarajan L, Rock CL, Flatt SW, Madlensky L, Kealey S, Pierce JP. Nutr Cancer. 2008; 60(1):31-8. https://www.ncbi.nlm.nih.gov/pubmed/18444133/
14. Dietary energy density in the treatment of obesity: a year-long trial comparing 2 weight-loss diets. Ello-Martin JA, Roe LS, Ledikwe JH, Beach AM, Rolls BJ. Am J Clin Nutr. 2007 Jun; 85(6):1465-77. https://www.ncbi.nlm.nih.gov/pubmed/17556681/
15. Dietary energy density predicts women’s weight change over 6 y. Savage JS, Marini M, Birch LL. Am J Clin Nutr. 2008 Sep; 88(3):677-84. https://www.ncbi.nlm.nih.gov/pubmed/18779283/
16. Wien M., Haddad E., Sabate′ J. Effect of incorporating avocado in meals on satiety in healthy overweight adults. 2011. 11th European Nutrition Conference of the Federation of the European Nutrition Societies. October, 27. Madrid, Spain.
17. Substitution of high monounsaturated fatty acid avocado for mixed dietary fats during an energy-restricted diet: effects on weight loss, serum lipids, fibrinogen, and vascular function. Pieterse Z, Jerling JC, Oosthuizen W, Kruger HS, Hanekom SM, Smuts CM, Schutte AE. Nutrition. 2005 Jan; 21(1):67-75. https://www.ncbi.nlm.nih.gov/pubmed/15661480/
18. Differential effects of two isoenergetic meals rich in saturated or monounsaturated fat on endothelial function in subjects with type 2 diabetes. Tentolouris N, Arapostathi C, Perrea D, Kyriaki D, Revenas C, Katsilambros N. Diabetes Care. 2008 Dec; 31(12):2276-8. https://www.ncbi.nlm.nih.gov/pubmed/18835957/
19. Monounsaturated fat-rich diet prevents central body fat distribution and decreases postprandial adiponectin expression induced by a carbohydrate-rich diet in insulin-resistant subjects. Paniagua JA, Gallego de la Sacristana A, Romero I, Vidal-Puig A, Latre JM, Sanchez E, Perez-Martinez P, Lopez-Miranda J, Perez-Jimenez F. Diabetes Care. 2007 Jul; 30(7):1717-23. https://www.ncbi.nlm.nih.gov/pubmed/17384344/
20. A MUFA-rich diet improves posprandial glucose, lipid and GLP-1 responses in insulin-resistant subjects. Paniagua JA, de la Sacristana AG, Sánchez E, Romero I, Vidal-Puig A, Berral FJ, Escribano A, Moyano MJ, Peréz-Martinez P, López-Miranda J, Pérez-Jiménez F. J Am Coll Nutr. 2007 Oct; 26(5):434-44. https://www.ncbi.nlm.nih.gov/pubmed/17914131/
21. Influence of avocados on serum cholesterol. GRANT WC. Proc Soc Exp Biol Med. 1960 May; 104:45-7. https://www.ncbi.nlm.nih.gov/pubmed/13828982/
22. Comparison of the effects on lipoproteins and apolipoproteins of a diet high in monounsaturated fatty acids, enriched with avocado, and a high-carbohydrate diet. Colquhoun DM, Moores D, Somerset SM, Humphries JA. Am J Clin Nutr. 1992 Oct; 56(4):671-7. https://www.ncbi.nlm.nih.gov/pubmed/1414966/
23. Effects of avocado as a source of monounsaturated fatty acids on plasma lipid levels. Alvizouri-Muñoz M, Carranza-Madrigal J, Herrera-Abarca JE, Chávez-Carbajal F, Amezcua-Gastelum JL. Arch Med Res. 1992 Winter; 23(4):163-7. https://www.ncbi.nlm.nih.gov/pubmed/1308699/
24. Effect of a high-monounsaturated fat diet enriched with avocado in NIDDM patients. Lerman-Garber I, Ichazo-Cerro S, Zamora-González J, Cardoso-Saldaña G, Posadas-Romero C. Diabetes Care. 1994 Apr; 17(4):311-5. https://www.ncbi.nlm.nih.gov/pubmed/8026287/
25. Effects of avocado on the level of blood lipids in patients with phenotype II and IV dyslipidemias. Carranza J, Alvizouri M, Alvarado MR, Chávez F, Gómez M, Herrera JE. Arch Inst Cardiol Mex. 1995 Jul-Aug; 65(4):342-8. https://www.ncbi.nlm.nih.gov/pubmed/8561655/
26. Monounsaturated fatty acid (avocado) rich diet for mild hypercholesterolemia. López Ledesma R, Frati Munari AC, Hernández Domínguez BC, Cervantes Montalvo S, Hernández Luna MH, Juárez C, Morán Lira S. Arch Med Res. 1996 Winter; 27(4):519-23. https://www.ncbi.nlm.nih.gov/pubmed/8987188/
27. Effects of a vegetarian diet vs. a vegetarian diet enriched with avocado in hypercholesterolemic patients. Carranza-Madrigal J, Herrera-Abarca JE, Alvizouri-Muñoz M, Alvarado-Jimenez MR, Chavez-Carbajal F. Arch Med Res. 1997 Winter; 28(4):537-41. https://www.ncbi.nlm.nih.gov/pubmed/9428580/
28. GRANT WC. Influence of avocados on serum cholesterol. Proc Soc Exp Biol Med. 1960 May;104:45-7. doi: 10.3181/00379727-104-25722
29. Colquhoun DM, Moores D, Somerset SM, Humphries JA. Comparison of the effects on lipoproteins and apolipoproteins of a diet high in monounsaturated fatty acids, enriched with avocado, and a high-carbohydrate diet. Am J Clin Nutr. 1992 Oct;56(4):671-7. doi: 10.1093/ajcn/56.4.671
30. Alvizouri-Muñoz M, Carranza-Madrigal J, Herrera-Abarca JE, Chávez-Carbajal F, Amezcua-Gastelum JL. Effects of avocado as a source of monounsaturated fatty acids on plasma lipid levels. Arch Med Res. 1992 Winter;23(4):163-7.
31. Lerman-Garber I, Ichazo-Cerro S, Zamora-González J, Cardoso-Saldaña G, Posadas-Romero C. Effect of a high-monounsaturated fat diet enriched with avocado in NIDDM patients. Diabetes Care. 1994 Apr;17(4):311-5. doi: 10.2337/diacare.17.4.311
32. Carranza J, Alvizouri M, Alvarado MR, Chávez F, Gómez M, Herrera JE. Efectos del aguacate sobre los niveles de lípidos séricos en pacientes con dislipidemias fenotipo II y IV [Effects of avocado on the level of blood lipids in patients with phenotype II and IV dyslipidemias]. Arch Inst Cardiol Mex. 1995 Jul-Aug;65(4):342-8. Spanish.
33. López Ledesma R, Frati Munari AC, Hernández Domínguez BC, Cervantes Montalvo S, Hernández Luna MH, Juárez C, Morán Lira S. Monounsaturated fatty acid (avocado) rich diet for mild hypercholesterolemia. Arch Med Res. 1996 Winter;27(4):519-23.
34. Carranza-Madrigal J, Herrera-Abarca JE, Alvizouri-Muñoz M, Alvarado-Jimenez MR, Chavez-Carbajal F. Effects of a vegetarian diet vs. a vegetarian diet enriched with avocado in hypercholesterolemic patients. Arch Med Res. 1997 Winter;28(4):537-41.
35. Pieterse Z, Jerling JC, Oosthuizen W, Kruger HS, Hanekom SM, Smuts CM, Schutte AE. Substitution of high monounsaturated fatty acid avocado for mixed dietary fats during an energy-restricted diet: effects on weight loss, serum lipids, fibrinogen, and vascular function. Nutrition. 2005 Jan;21(1):67-75. doi: 10.1016/j.nut.2004.09.010
36. Dreher ML, Davenport AJ. Hass Avocado Composition and Potential Health Effects. Critical Reviews in Food Science and Nutrition. 2013;53(7):738-750. doi:10.1080/10408398.2011.556759. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3664913/
37. High-density lipoproteins (HDL) size and composition are modified in the rat by a diet supplemented with “Hass” avocado (Persea americana Miller). Pérez Méndez O, García Hernández L. Arch Cardiol Mex. 2007 Jan-Mar; 77(1):17-24. https://www.ncbi.nlm.nih.gov/pubmed/17500188/
38. California Hass avocado: profiling of carotenoids, tocopherol, fatty acid, and fat content during maturation and from different growing areas. Lu QY, Zhang Y, Wang Y, Wang D, Lee RP, Gao K, Byrns R, Heber D. J Agric Food Chem. 2009 Nov 11; 57(21):10408-13. https://www.ncbi.nlm.nih.gov/pubmed/19813713/
39. Avocado Central. Hass Avocado Spread Comparison: Spread on Nutrition with Hass Avocados. 2010. https://www.avocadocentral.com/nutrition/avocado-spread-comparison
40. Database and quick methods of assessing typical dietary fiber intakes using data for 228 commonly consumed foods. Marlett JA, Cheung TF. J Am Diet Assoc. 1997 Oct; 97(10):1139-48, 1151; quiz 1149-50. https://www.ncbi.nlm.nih.gov/pubmed/9336561/
41. Development of a rapid method for the sequential extraction and subsequent quantification of fatty acids and sugars from avocado mesocarp tissue. Meyer MD, Terry LA. J Agric Food Chem. 2008 Aug 27; 56(16):7439-45. https://www.ncbi.nlm.nih.gov/pubmed/18680299/
42. High-performance liquid chromatographic analysis of D-manno-heptulose, perseitol, glucose, and fructose in avocado cultivars. Shaw PE, Wilson CW 3rd, Knight RJ Jr. J Agric Food Chem. 1980 Mar-Apr; 28(2):379-62. https://www.ncbi.nlm.nih.gov/pubmed/7391374/
43. Roth G. Mannoheptulose glycolytic inhibitor and novel calorie restriction mimetic. 2009. Experimental Biology. Abstract # 553.1. New Orleans, LA.
44. American Heart Association. How Potassium Can Help Control High Blood Pressure. http://www.heart.org/HEARTORG/Conditions/HighBloodPressure/PreventionTreatmentofHighBloodPressure/Potassium-and-High-Blood-Pressure_UCM_303243_Article.jsp
45. American Heart Association. A Primer on Potassium. https://sodiumbreakup.heart.org/a_primer_on_potassium
46. IOM (Institute of Medicine) Chapter 6. Magnesium. Washington, DC: National Academies Press; 1997. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D and Fluoride; pp. 186–255.
47. Magnesium intake and risk of coronary heart disease among men. Al-Delaimy WK, Rimm EB, Willett WC, Stampfer MJ, Hu FB. J Am Coll Nutr. 2004 Feb; 23(1):63-70. https://www.ncbi.nlm.nih.gov/pubmed/14963055/
48. Effects of magnesium on postprandial serum lipid responses in healthy human subjects. Kishimoto Y, Tani M, Uto-Kondo H, Saita E, Iizuka M, Sone H, Yokota K, Kondo K. Br J Nutr. 2010 Feb; 103(4):469-72. https://www.ncbi.nlm.nih.gov/pubmed/19941679/
49. IOM (Institute of Medicine) Chapter 5. Vitamin C. Washington, DC: National Academies Press; 2000. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium and Carotenoids; pp. 95–122.
50. Vitamins and cardiovascular disease. Honarbakhsh S, Schachter M. Br J Nutr. 2009 Apr; 101(8):1113-31. https://www.ncbi.nlm.nih.gov/pubmed/18826726/
51. Six-year effect of combined vitamin C and E supplementation on atherosclerotic progression: the Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) Study. Salonen RM, Nyyssönen K, Kaikkonen J, Porkkala-Sarataho E, Voutilainen S, Rissanen TH, Tuomainen TP, Valkonen VP, Ristonmaa U, Lakka HM, Vanharanta M, Salonen JT, Poulsen HE, Antioxidant Supplementation in Atherosclerosis Prevention Study.. Circulation. 2003 Feb 25; 107(7):947-53. https://www.ncbi.nlm.nih.gov/pubmed/12600905/
52. Dietary reference intakes: vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Trumbo P, Yates AA, Schlicker S, Poos M. J Am Diet Assoc. 2001 Mar; 101(3):294-301. https://www.ncbi.nlm.nih.gov/pubmed/11269606/
53. Vitamin K, an example of triage theory: is micronutrient inadequacy linked to diseases of aging? McCann JC, Ames BN. Am J Clin Nutr. 2009 Oct; 90(4):889-907. https://www.ncbi.nlm.nih.gov/pubmed/19692494/
54. Low-dose oral vitamin K reliably reverses over-anticoagulation due to warfarin. Crowther MA, Donovan D, Harrison L, McGinnis J, Ginsberg J. Thromb Haemost. 1998 Jun; 79(6):1116-8. https://www.ncbi.nlm.nih.gov/pubmed/9657434/
55. Vitamin K content of nuts and fruits in the US diet. Dismore ML, Haytowitz DB, Gebhardt SE, Peterson JW, Booth SL. J Am Diet Assoc. 2003 Dec; 103(12):1650-2. https://www.ncbi.nlm.nih.gov/pubmed/14647095/
56. Homocysteine and coronary atherosclerosis: from folate fortification to the recent clinical trials. Antoniades C, Antonopoulos AS, Tousoulis D, Marinou K, Stefanadis C. Eur Heart J. 2009 Jan; 30(1):6-15. https://www.ncbi.nlm.nih.gov/pubmed/19029125/
57. Carotenoids and cardiovascular health. Voutilainen S, Nurmi T, Mursu J, Rissanen TH. Am J Clin Nutr. 2006 Jun; 83(6):1265-71. https://www.ncbi.nlm.nih.gov/pubmed/16762935/
58. Biologic activity of carotenoids related to distinct membrane physicochemical interactions. McNulty H, Jacob RF, Mason RP. Am J Cardiol. 2008 May 22; 101(10A):20D-29D. https://www.ncbi.nlm.nih.gov/pubmed/18474269/
59. Lipophilic and hydrophilic antioxidant capacities of common foods in the United States. Wu X, Beecher GR, Holden JM, Haytowitz DB, Gebhardt SE, Prior RL. J Agric Food Chem. 2004 Jun 16; 52(12):4026-37. https://www.ncbi.nlm.nih.gov/pubmed/15186133/
60. A dietary pattern that lowers oxidative stress increases antibodies to oxidized LDL: results from a randomized controlled feeding study. Miller ER 3rd, Erlinger TP, Sacks FM, Svetkey LP, Charleston J, Lin PH, Appel LJ. Atherosclerosis. 2005 Nov; 183(1):175-82. https://www.ncbi.nlm.nih.gov/pubmed/16216596/
61. Relationships of circulating carotenoid concentrations with several markers of inflammation, oxidative stress, and endothelial dysfunction: the Coronary Artery Risk Development in Young Adults (CARDIA)/Young Adult Longitudinal Trends in Antioxidants (YALTA) study. Hozawa A, Jacobs DR Jr, Steffes MW, Gross MD, Steffen LM, Lee DH. Clin Chem. 2007 Mar; 53(3):447-55. https://www.ncbi.nlm.nih.gov/pubmed/17234732/
62. Oxygenated carotenoid lutein and progression of early atherosclerosis: the Los Angeles atherosclerosis study. Dwyer JH, Navab M, Dwyer KM, Hassan K, Sun P, Shircore A, Hama-Levy S, Hough G, Wang X, Drake T, Merz CN, Fogelman AM. Circulation. 2001 Jun 19; 103(24):2922-7. https://www.ncbi.nlm.nih.gov/pubmed/11413081/
63. Inhibition of prostate cancer cell growth by an avocado extract: role of lipid-soluble bioactive substances. Lu QY, Arteaga JR, Zhang Q, Huerta S, Go VL, Heber D. J Nutr Biochem. 2005 Jan; 16(1):23-30. https://www.ncbi.nlm.nih.gov/pubmed/15629237/
64. Differential effect of dietary antioxidant classes (carotenoids, polyphenols, vitamins C and E) on lutein absorption. Reboul E, Thap S, Tourniaire F, André M, Juhel C, Morange S, Amiot MJ, Lairon D, Borel P. Br J Nutr. 2007 Mar; 97(3):440-6. https://www.ncbi.nlm.nih.gov/pubmed/17313704/
65. Pigments in avocado tissue and oil. Ashton OB, Wong M, McGhie TK, Vather R, Wang Y, Requejo-Jackman C, Ramankutty P, Woolf AB. J Agric Food Chem. 2006 Dec 27; 54(26):10151-8. https://www.ncbi.nlm.nih.gov/pubmed/17177553/
66. Carotenoid bioavailability is higher from salads ingested with full-fat than with fat-reduced salad dressings as measured with electrochemical detection. Brown MJ, Ferruzzi MG, Nguyen ML, Cooper DA, Eldridge AL, Schwartz SJ, White WS. Am J Clin Nutr. 2004 Aug; 80(2):396-403. https://www.ncbi.nlm.nih.gov/pubmed/15277161/
67. Carotenoid absorption from salad and salsa by humans is enhanced by the addition of avocado or avocado oil. Unlu NZ, Bohn T, Clinton SK, Schwartz SJ. J Nutr. 2005 Mar; 135(3):431-6. https://www.ncbi.nlm.nih.gov/pubmed/15735074/
68. Fruit polyphenols and CVD risk: a review of human intervention studies. Chong MF, Macdonald R, Lovegrove JA. Br J Nutr. 2010 Oct; 104 Suppl 3():S28-39. https://www.ncbi.nlm.nih.gov/pubmed/20955648/
69. Polyphenols and disease risk in epidemiologic studies. Arts IC, Hollman PC. Am J Clin Nutr. 2005 Jan; 81(1 Suppl):317S-325S. https://www.ncbi.nlm.nih.gov/pubmed/15640497/
70. Vascular action of polyphenols. Ghosh D, Scheepens A. Mol Nutr Food Res. 2009 Mar; 53(3):322-31. https://www.ncbi.nlm.nih.gov/pubmed/19051188/
71. Oxidative stress, endothelial dysfunction and atherosclerosis. Victor VM, Rocha M, Solá E, Bañuls C, Garcia-Malpartida K, Hernández-Mijares A. Curr Pharm Des. 2009; 15(26):2988-3002. https://www.ncbi.nlm.nih.gov/pubmed/19754375/
72. Wu X., Gu L., Holden J., Haytowitz D. B., Gebhardt S. E., Beecher G. R., Prior R. L. Development of a database for total antioxidant capacity in foods: A preliminary study. J. Food. Comp. Anal. 2007;17:407–422.
73. Avocado fruit is a rich source of beta-sitosterol. Duester KC. J Am Diet Assoc. 2001 Apr; 101(4):404-5. https://www.ncbi.nlm.nih.gov/pubmed/11320941/
74. Phytosterol glycosides reduce cholesterol absorption in humans. Lin X, Ma L, Racette SB, Anderson Spearie CL, Ostlund RE Jr. Am J Physiol Gastrointest Liver Physiol. 2009 Apr; 296(4):G931-5. https://www.ncbi.nlm.nih.gov/pubmed/19246636/
75. Economic valuation of the potential health benefits from foods enriched with plant sterols in Canada. Gyles CL, Carlberg JG, Gustafson J, Davlut DA, Jones PJ. Food Nutr Res. 2010 Oct 7; 54. https://www.ncbi.nlm.nih.gov/pubmed/20941328/
76. High dietary antioxidant intakes are associated with decreased chromosome translocation frequency in airline pilots. Yong LC, Petersen MR, Sigurdson AJ, Sampson LA, Ward EM. Am J Clin Nutr. 2009 Nov; 90(5):1402-10. https://www.ncbi.nlm.nih.gov/pubmed/19793852/
77. Plasma xanthophyll carotenoids correlate inversely with indices of oxidative DNA damage and lipid peroxidation. Haegele AD, Gillette C, O’Neill C, Wolfe P, Heimendinger J, Sedlacek S, Thompson HJ. Cancer Epidemiol Biomarkers Prev. 2000 Apr; 9(4):421-5. https://www.ncbi.nlm.nih.gov/pubmed/10794487/
78. Plasma Carotenoids and Biomarkers of Oxidative Stress in Patients with prior Head and Neck Cancer. Hughes KJ, Mayne ST, Blumberg JB, Ribaya-Mercado JD, Johnson EJ, Cartmel B. Biomark Insights. 2009 Mar 23; 4():17-26. https://www.ncbi.nlm.nih.gov/pubmed/19554200/
79. Plasma and dietary carotenoids are associated with reduced oxidative stress in women previously treated for breast cancer. Thomson CA, Stendell-Hollis NR, Rock CL, Cussler EC, Flatt SW, Pierce JP. Cancer Epidemiol Biomarkers Prev. 2007 Oct; 16(10):2008-15. https://www.ncbi.nlm.nih.gov/pubmed/17932348/
80. Intake of lutein and zeaxanthin differ with age, sex, and ethnicity. Johnson EJ, Maras JE, Rasmussen HM, Tucker KL. J Am Diet Assoc. 2010 Sep; 110(9):1357-62. https://www.ncbi.nlm.nih.gov/pubmed/20800129/
81. A potential role for avocado- and soybean-based nutritional supplements in the management of osteoarthritis: a review. DiNubile NA. Phys Sportsmed. 2010 Jun; 38(2):71-81. https://www.ncbi.nlm.nih.gov/pubmed/20631466/
82. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part I. Helmick CG, Felson DT, Lawrence RC, Gabriel S, Hirsch R, Kwoh CK, Liang MH, Kremers HM, Mayes MD, Merkel PA, Pillemer SR, Reveille JD, Stone JH, National Arthritis Data Workgroup. Arthritis Rheum. 2008 Jan; 58(1):15-25. https://www.ncbi.nlm.nih.gov/pubmed/18163481/
83. Effect of dietary lutein and zeaxanthin on plasma carotenoids and their transport in lipoproteins in age-related macular degeneration. Wang W, Connor SL, Johnson EJ, Klein ML, Hughes S, Connor WE. Am J Clin Nutr. 2007 Mar; 85(3):762-9. https://www.ncbi.nlm.nih.gov/pubmed/17344498/
84. Metabolic effects of avocado/soy unsaponifiables on articular chondrocytes. Lippiello L, Nardo JV, Harlan R, Chiou T. Evid Based Complement Alternat Med. 2008 Jun; 5(2):191-7. https://www.ncbi.nlm.nih.gov/pubmed/18604259/
85. Avocado soybean unsaponifiables (ASU) suppress TNF-alpha, IL-1beta, COX-2, iNOS gene expression, and prostaglandin E2 and nitric oxide production in articular chondrocytes and monocyte/macrophages. Au RY, Al-Talib TK, Au AY, Phan PV, Frondoza CG. Osteoarthritis Cartilage. 2007 Nov; 15(11):1249-55. https://www.ncbi.nlm.nih.gov/pubmed/17845860/
86. Avocado/soybean unsaponifiables prevent the inhibitory effect of osteoarthritic subchondral osteoblasts on aggrecan and type II collagen synthesis by chondrocytes. Henrotin YE, Deberg MA, Crielaard JM, Piccardi N, Msika P, Sanchez C. J Rheumatol. 2006 Aug; 33(8):1668-78. https://www.ncbi.nlm.nih.gov/pubmed/16832844/
87. Signaling transduction: target in osteoarthritis. Berenbaum F. Curr Opin Rheumatol. 2004 Sep; 16(5):616-22. https://www.ncbi.nlm.nih.gov/pubmed/15314504/
88. Avocado-soybean unsaponifiables (ASU) for osteoarthritis – a systematic review. Ernst E. Clin Rheumatol. 2003 Oct; 22(4-5):285-8. https://www.ncbi.nlm.nih.gov/pubmed/14576991/
89. Efficacy and safety of avocado/soybean unsaponifiables in the treatment of symptomatic osteoarthritis of the knee and hip. A prospective, multicenter, three-month, randomized, double-blind, placebo-controlled trial. Blotman F, Maheu E, Wulwik A, Caspard H, Lopez A. Rev Rhum Engl Ed. 1997 Dec; 64(12):825-34. https://www.ncbi.nlm.nih.gov/pubmed/9476272/
90. Structural effect of avocado/soybean unsaponifiables on joint space loss in osteoarthritis of the hip. Lequesne M, Maheu E, Cadet C, Dreiser RL. Arthritis Rheum. 2002 Feb; 47(1):50-8. https://www.ncbi.nlm.nih.gov/pubmed/11932878/
91. Symptoms modifying effect of avocado/soybean unsaponifiables (ASU) in knee osteoarthritis. A double blind, prospective, placebo-controlled study. Appelboom T, Schuermans J, Verbruggen G, Henrotin Y, Reginster JY. Scand J Rheumatol. 2001; 30(4):242-7. https://www.ncbi.nlm.nih.gov/pubmed/11578021/
92. Symptomatic efficacy of avocado/soybean unsaponifiables in the treatment of osteoarthritis of the knee and hip: a prospective, randomized, double-blind, placebo-controlled, multicenter clinical trial with a six-month treatment period and a two-month followup demonstrating a persistent effect. Maheu E, Mazières B, Valat JP, Loyau G, Le Loët X, Bourgeois P, Grouin JM, Rozenberg S. Arthritis Rheum. 1998 Jan; 41(1):81-91. https://www.ncbi.nlm.nih.gov/pubmed/9433873/
93. Symptomatic efficacy of avocado-soybean unsaponifiables (ASU) in osteoarthritis (OA) patients: a meta-analysis of randomized controlled trials. Christensen R, Bartels EM, Astrup A, Bliddal H. Osteoarthritis Cartilage. 2008 Apr; 16(4):399-408. https://www.ncbi.nlm.nih.gov/pubmed/18042410/
94. Associations between lutein, zeaxanthin, and age-related macular degeneration: an overview. Carpentier S, Knaus M, Suh M. Crit Rev Food Sci Nutr. 2009 Apr; 49(4):313-26. https://www.ncbi.nlm.nih.gov/pubmed/19234943/
95. Association between dietary fat intake and age-related macular degeneration in the Carotenoids in Age-Related Eye Disease Study (CAREDS): an ancillary study of the Women’s Health Initiative. Parekh N, Voland RP, Moeller SM, Blodi BA, Ritenbaugh C, Chappell RJ, Wallace RB, Mares JA, CAREDS Research Study Group. Arch Ophthalmol. 2009 Nov; 127(11):1483-93. https://www.ncbi.nlm.nih.gov/pubmed/19901214/
96. Fat consumption and its association with age-related macular degeneration. Chong EW, Robman LD, Simpson JA, Hodge AM, Aung KZ, Dolphin TK, English DR, Giles GG, Guymer RH. Arch Ophthalmol. 2009 May; 127(5):674-80. https://www.ncbi.nlm.nih.gov/pubmed/19433719/
97. Associations between age-related nuclear cataract and lutein and zeaxanthin in the diet and serum in the Carotenoids in the Age-Related Eye Disease Study, an Ancillary Study of the Women’s Health Initiative. Moeller SM, Voland R, Tinker L, Blodi BA, Klein ML, Gehrs KM, Johnson EJ, Snodderly DM, Wallace RB, Chappell RJ, Parekh N, Ritenbaugh C, Mares JA, CAREDS Study Group., Women’s Helath Initiative. Arch Ophthalmol. 2008 Mar; 126(3):354-64. https://www.ncbi.nlm.nih.gov/pubmed/18332316/
98. Lutein and zeaxanthin in eye and skin health. Roberts RL, Green J, Lewis B. Clin Dermatol. 2009 Mar-Apr; 27(2):195-201. https://www.ncbi.nlm.nih.gov/pubmed/19168000/
99. Effect of fruit and vegetable intake on skin carotenoid detected by non-invasive Raman spectroscopy. Rerksuppaphol S, Rerksuppaphol L. J Med Assoc Thai. 2006 Aug; 89(8):1206-12. https://www.ncbi.nlm.nih.gov/pubmed/17048431/
100. Skin aging. Puizina-Ivić N. Acta Dermatovenerol Alp Pannonica Adriat. 2008 Jun; 17(2):47-54. https://www.ncbi.nlm.nih.gov/pubmed/18709289/
101. Beneficial long-term effects of combined oral/topical antioxidant treatment with the carotenoids lutein and zeaxanthin on human skin: a double-blind, placebo-controlled study. Palombo P, Fabrizi G, Ruocco V, Ruocco E, Fluhr J, Roberts R, Morganti P. Skin Pharmacol Physiol. 2007; 20(4):199-210. https://www.ncbi.nlm.nih.gov/pubmed/17446716/
102. Role of topical and nutritional supplement to modify the oxidative stress. Morganti P, Bruno C, Guarneri F, Cardillo A, Del Ciotto P, Valenzano F. Int J Cosmet Sci. 2002 Dec; 24(6):331-9. https://www.ncbi.nlm.nih.gov/pubmed/18494887/
103. Association of dietary fat, vegetables and antioxidant micronutrients with skin ageing in Japanese women. Nagata C, Nakamura K, Wada K, Oba S, Hayashi M, Takeda N, Yasuda K. Br J Nutr. 2010 May; 103(10):1493-8. https://www.ncbi.nlm.nih.gov/pubmed/20085665/
104. Polyhydroxylated fatty alcohols derived from avocado suppress inflammatory response and provide non-sunscreen protection against UV-induced damage in skin cells. Rosenblat G, Meretski S, Segal J, Tarshis M, Schroeder A, Zanin-Zhorov A, Lion G, Ingber A, Hochberg M. Arch Dermatol Res. 2011 May; 303(4):239-46. https://www.ncbi.nlm.nih.gov/pubmed/20978772/
105. Selective induction of apoptosis of human oral cancer cell lines by avocado extracts via a ROS-mediated mechanism. Ding H, Han C, Guo D, Chin YW, Ding Y, Kinghorn AD, D’Ambrosio SM. Nutr Cancer. 2009; 61(3):348-56. https://www.ncbi.nlm.nih.gov/pubmed/19373608/
106. Dietary glutathione intake and the risk of oral and pharyngeal cancer. Flagg EW, Coates RJ, Jones DP, Byers TE, Greenberg RS, Gridley G, McLaughlin JK, Blot WJ, Haber M, Preston-Martin S. Am J Epidemiol. 1994 Mar 1; 139(5):453-65. https://www.ncbi.nlm.nih.gov/pubmed/8154469/
107. Anti-Helicobacter pylori activity of plants used in Mexican traditional medicine for gastrointestinal disorders. Castillo-Juárez I, González V, Jaime-Aguilar H, Martínez G, Linares E, Bye R, Romero I. J Ethnopharmacol. 2009 Mar 18; 122(2):402-5. https://www.ncbi.nlm.nih.gov/pubmed/19162157/
108. Chemopreventive characteristics of avocado fruit. Ding H, Chin YW, Kinghorn AD, D’Ambrosio SM. Semin Cancer Biol. 2007 Oct; 17(5):386-94. https://www.ncbi.nlm.nih.gov/pubmed/17582784/
109. Circulating carotenoids, mammographic density, and subsequent risk of breast cancer. Tamimi RM, Colditz GA, Hankinson SE. Cancer Res. 2009 Dec 15; 69(24):9323-9. https://www.ncbi.nlm.nih.gov/pubmed/19934322/

What is coconut sugar ?

Coconut sugar, sometimes called coconut palm sugar (also known as coco sugar, coco sap sugar or coconut blossom sugar), is made using the sap of cut flower buds of the coconut palm tree. Coconut sugar comes in crystal or granule form, block or liquid. It is essentially a two-step process. It starts with harvesting or “tapping” the blossoms of a coconut tree. Farmers make a cut on the spadix and the sap starts to flow from the cut. The sap is then collected in bamboo containers. The sap collected is then transferred into large woks and placed over moderate heat to evaporate the moisture content of the sap. The sap is translucent and is about 80% water. As the water evaporates, it starts to transform into a thick syrup-like substance known as a “toddy”. From this form, it is further reduced to crystal, block or soft paste form, or it remains in this form.

The major component of coconut sugar is sucrose (70–79%) followed by glucose and fructose (3–9%) each. Minor variations will occur due to differences in primary processing, raw material source, tree age and variety of coconut.

Many coconut sugar makers proudly boast coconut sugar’s ranking on the glycemic index (GI). However, if you are interested in learning and finding about the truth on coconut sugar glycemic index value, you can go to the official website for the glycemic index and international GI (glycemic index) database being maintained in the Boden Institute of Obesity, Nutrition, Exercise and Eating Disorders Centre at the University of Sydney here ¹: http://www.glycemicindex.com

What is Glycemic Index of Foods

The glycemic index (GI) is a ranking of carbohydrate foods from 0 to 100 based on how quickly and how much they raise blood sugar (glucose) levels after being eaten ¹. This is related to how quickly a carbohydrate containing food is broken down into glucose.

Foods with a high GI are those which are rapidly digested, absorbed and metabolised and result in marked fluctuations in blood sugar (glucose) levels. Low GI carbohydrates – the ones that produce smaller fluctuations in your blood glucose and insulin levels – is one of the secrets to long-term health, reducing your risk of type 2 diabetes and heart disease. It is also one of the keys to maintaining weight loss ¹.

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

The results from the Glycemic Index International Database ¹:

• Coconut sugar GI rating is 54.
• Compare that to regular table sugar, which has an average rating of 58.

As you can see eating coconut sugar has no difference on the glycemic index compared to sugar or eating a banana or pinto beans.

Furthermore, 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.

Why is the GI important ?

Considering the GI of carbohydrate foods can help with good diabetes management as:

• Lower GI foods produce lower, more stable blood sugar levels and therefore can help improve control of diabetes.
• Higher GI foods produce higher, faster rising blood sugar levels.
• Lower GI foods also help you to feel fuller for longer, which can help to control appetite and assist with weight management.

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.

Table 1. Coconut Sugar Nutrition Content

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ²]

Table 2. Natural Cane Sugar Nutrition Content

[Source: United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. ²]

When you compare the nutritional value of coconut sugar to your plain table sugar, both contain the same amount of calories per teaspoon ~ 15 calories or 375 calories per 100 gram.

Coconut sugar as substitute for sugar

Coconut palm sugar is a sugar substitute that seems to be gaining popularity in the market. The taste of pure coconut palm sugar is similar to brown sugar. For cooking purposes, it has a very low melt temperature and an extremely high burn temperature so it can be used baked products in place of sugar ³.

According to the American Diabetes Association ³, it is okay for people with diabetes to use coconut palm sugar as a sweetener, but they should not treat it any differently than regular sugar. It provides just as many calories and carbohydrates as regular sugar: about 15 calories and 4 grams of carbohydrate per teaspoon (see Table 1 and 2 above). So, you still need to account for it when planning meals.

Also, note that some coconut palm sugar on the market may be mixed with cane sugar and other ingredients. It is important to check nutrition labels and read the ingredient list on these products.

Is there difference between organic coconut sugar and non-organic coconut sugar ?

The only difference organic and non-organic is the way the coconut is grown and cultivated. Organic coconut and foods must be free of synthetic additives like pesticides, chemical fertilizers, and dyes, and must not be processed using industrial solvents. Simply stated, organic produce and other ingredients are grown without the use of pesticides, synthetic fertilizers, sewage sludge, genetically modified organisms, or ionizing radiation. Animals that produce meat, poultry, eggs, and dairy products do not take antibiotics or growth hormones. You may want to learn more about organic foods by going to “Are Organic foods healthier for you to eat ?”

Is coconut sugar good for you ?

Now you have a better understanding and knowledge on coconut sugar, this question is like asking “Is eating sugar good for you ?” or is eating sugar healthy ?

According to the latest Dietary Guidelines for Americans (designed to help Americans eat a healthier diet) published by the U.S. Department of Health and Human Services ⁴:

• Consume less than 10 percent of calories per day from added sugars ⁴

U.S. Department of Health and Human Services – Dietary Guidelines “limit calories from added sugars to less than 10 percent per day is a target based on food pattern modeling and national data on intakes of calories from added sugars that demonstrate the public health need to limit calories from added sugars to meet food group and nutrient needs within calorie limits. For most calorie levels, there are not enough calories available after meeting food group needs to consume 10 percent of calories from added sugars and 10 percent of calories from saturated fats and still stay within calorie limits.”

Perhaps you may be interested in another article we wrote on sugar by going to “The Truth About Sugar.”

Is coconut sugar paleo ?

A paleo diet (Caveman Diet) is a dietary plan based on foods similar to what might have been eaten during the Paleolithic era, which dates from approximately 2.5 million to 10,000 years ago. This diet consists of foods that are assumed to have been available to humans prior to the establishment of agriculture. The principal components of this diet are wild-animal source and uncultivated-plant source foods, such as lean meat, fish, vegetables, fruits, roots, eggs, and nuts. The diet excludes grains, legumes, dairy products, salt, refined sugar, and processed oils, all of which were unavailable before humans began cultivating plants and domesticating animals.

So the answer to that question, is coconut sugar is definitely no.

You can learn more about paleo and the paleo diet by going to “The Paleo Diet.”

References

1. Glycemic Index International Database, University of Sydney. http://www.glycemicindex.com
2. United States Department of Agriculture, Agriculture Research Service. USDA Food Composition Databases. https://ndb.nal.usda.gov/ndb/
3. American Diabetes Association. Coconut Palm Sugar. http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/making-healthy-food-choices/coconut-palm-sugar.html
4. U.S. Department of Health and Human Services. 2015–2020 Dietary Guidelines for Americans. https://health.gov/dietaryguidelines