What is a fatty liver disease ?

Fatty liver disease is a condition in which fat (triglycerides) builds up in your liver. Fatty liver or liver steatosis, is the accumulation of fat within liver cells, is a common histological finding in human liver biopsy specimens and affects 10–24% of the general population ¹. There are two main types of fatty liver disease ²:

Nonalcoholic fatty liver disease (NAFLD). Nonalcoholic fatty liver disease (NAFLD) is a type of fatty liver disease that is not related to heavy alcohol use. Nonalcoholic fatty liver disease (NAFLD) is the most common form of liver disease in the United States, affecting up to 30% of adults ³. There are two kinds of NAFLD ⁴:
1. Simple fatty liver also called nonalcoholic fatty liver (NAFL): Simple fatty liver is a form of nonalcoholic fatty liver disease (NAFLD) in which you have fat in your liver but little or no inflammation or liver cell damage. Simple fatty liver or nonalcoholic fatty liver (NAFL) is defined as 5% or greater hepatic steatosis without hepatocellular injury or fibrosis ³. Simple fatty liver typically does not progress to cause liver damage or complications ⁵.
2. Nonalcoholic steatohepatitis (NASH): Nonalcoholic steatohepatitis (NASH) is a form of nonalcoholic fatty liver disease (NAFLD) in which you have inflammation and liver cell damage, in addition to fat in your liver. Nonalcoholic steatohepatitis (NASH) is defined as 5% or greater hepatic steatosis plus hepatocellular injury and inflammation, with or without fibrosis ³. This form of liver injury carries a 20%-50% risk for progressive liver fibrosis, 30% risk for cirrhosis, and 5% risk for hepatocellular carcinoma (liver cancer) ⁶. Nonalcoholic steatohepatitis (NASH) may lead to cirrhosis or liver cancer ⁵.
Alcoholic fatty liver disease also called alcoholic steatohepatitis. Alcoholic fatty liver disease (alcoholic steatohepatitis) is due to heavy alcohol use. Your liver breaks down most of the alcohol you drink, so it can be removed from your body. But the process of breaking it down can generate harmful substances. These substances can damage liver cells, promote inflammation, and weaken your body’s natural defenses. The more alcohol that you drink, the more you damage your liver. Alcoholic fatty liver disease is the earliest stage of alcohol-related liver disease. The next stages are alcoholic hepatitis and cirrhosis.

Your liver is the largest organ inside your body and it is a vital organ that performs many essential functions. Your liver filters out harmful substances from your blood, makes bile to digest food, stores energy and nutrients, and manufactures hormones, proteins, and enzymes your body uses to function, remove poisons and ward off disease ⁷.

The fatty liver may or may not be inflamed. Inflammation of the liver due to fatty liver is called steatohepatitis. This inflammation may develop into scarring (fibrosis). Fibrosis often progresses to cirrhosis (scarring that distorts the structure of the liver and impairs its function).

Fatty liver (with or without fibrosis) due to any condition except consumption of large amounts of alcohol is called nonalcoholic fatty liver disease (NAFLD). NAFLD develops most often in people with at least one of the components of metabolic syndrome:

Excess body weight
High fat levels in the blood (triglyceride and cholesterol)
Insulin resistance

Inflammation of the liver due to NAFLD is called nonalcoholic steatohepatitis (NASH). This inflammation may develop into scarring (fibrosis) and cirrhosis.

People with fatty liver may feel tired or have mild abdominal discomfort but otherwise have no symptoms. Sometimes fatty liver causes advanced liver disease such as fibrosis and cirrhosis.

A liver biopsy may be needed to confirm the diagnosis and to determine the cause and extent of the damage.

There are no medicines to treat fatty liver disease. Treatment of fatty liver focuses on controlling or eliminating the cause of fatty liver. Treatment involves making changes to your lifestyle. This can improve the condition and even reverse it. Doctors focus on controlling or eliminating the cause of fatty liver, such as metabolic syndrome or consumption of large amounts of alcohol.

Fatty liver of pregnancy

Nonalcoholic fatty liver disease (NAFLD) is considered the liver manifestation of the metabolic syndrome, and is tightly linked with obesity and type 2 diabetes ⁸. The obesity epidemic has affected reproductive-aged women, with obesity present in over one third of U.S. women ages 20–39 years ⁹. Pregnancy itself is a relative insulin resistant state and concurrent maternal obesity further increases the risk for gestational diabetes ¹⁰.

In the U.S., a study was conducted from 2012 to 2016 on a total of 18.5 million pregnant women ¹¹. The aim was to find out how high certain pregnancy risks are in comparison groups ¹¹. In the evaluation, a distinction was made between 3 groups of pregnant women. The first group consisted of women without liver disease. The second group had chronic liver disease (n = 115,210). The third group were women with NAFLD (n = 5,640). It was shown that pregnant women with nonalcoholic fatty liver disease (NAFLD) have a higher risk of developing pregnancy-associated (gestational) diabetes compared to the control group (23 in 100 compared to 7-8 in 100) ¹¹. It was also found that pregnant women with NAFLD are also more frequently affected by severe pregnancy-induced increases in blood pressure (16 out of 100 compared to 4 out of 100 if there was no liver disease), of which the HELLP (hemolysis-elevated liver tests-low platelet count) syndrome is the most severe complication. HELLP syndrome is a rare life-threatening condition during pregnancy, the course of which is difficult to predict. This leads to a breakdown of the red blood cells, increased liver enzymes and a drop in red blood platelets. HELLP syndrome can result in immediate termination of pregnancy.

Your gynaecologist should contact the doctor treating your fatty liver disease and make an assessment of your possible individual risks of pregnancy. You should be informed in detail. In addition, physicians should support you in reducing metabolic risk factors, such as the existence of fatty liver, during a planned pregnancy.

Fatty liver symptoms

Fatty liver usually causes no symptoms. Some people may feel tired or generally unwell or have vague abdominal discomfort in the upper right part of their abdomen. The liver tends to enlarge and can be detected by doctors during a physical examination.

Causes of fatty liver

Fat accumulates in the liver for several reasons. Most commonly, fatty liver involves increased delivery of free fatty acids to the liver, increased synthesis of fatty acids in the liver, decreased oxidation of free fatty acid, or decreased synthesis or secretion of very-low-density lipoprotein (VLDL) ¹². Oxidative stress in the liver cells can activate stellate cells and lead to the production of collagen and inflammation ¹³.

The most common causes of fatty liver in the United States and other Western countries are ¹⁴:

Consumption of large amounts of alcohol
Obesity
Metabolic abnormalities, such as excess body weight, insulin resistance (as can occur in diabetes), and high levels of fats (triglycerides and cholesterol) in the blood
Exposure to some toxins
Certain drugs, including corticosteroids, tamoxifen, HIV treatment, estrogens, and certain chemotherapy drugs and others
Hereditary metabolic disorders called lipodystrophies, that cause your body to use or store fat improperly
Pregnancy

Other factors that may contribute to fatty liver disease include:

The use of medications (e.g., tamoxifen, amiodarone, methotrexate)
Metabolic abnormalities (e.g., glycogen storage disorders, homocystinuria)
Nutritional status (e.g., total parenteral nutrition, severe malnutrition, overnutrition, or a starvation diet)
Rapid weight loss or malnutrition
Rare genetic diseases like Wilson disease, celiac disease and hypobetalipoproteinemia.

The combination of excess body weight, insulin resistance, and high triglyceride levels is called metabolic syndrome. All of these conditions cause fat to accumulate in liver cells by causing the body to synthesize more fat or by processing (metabolizing) and excreting fat more slowly. As a result, fat accumulates and is then stored inside liver cells. Just consuming a high-fat diet does not result in fatty liver.

Rarely, fat accumulates in the liver during late pregnancy. This disorder, called fatty liver of pregnancy or microvesicular steatosis, is usually considered a different disorder from fatty liver.

Fatty liver prevention

The way to prevent non-alcoholic fatty liver disease (NAFLD) is to follow the same lifestyle advice given to people who already have the condition, including:

eating a healthy diet that is rich in fruit and vegetables, whole grains and healthy fats
maintaining a healthy weight
being physically active on most days of the week — check with your doctor first if you haven’t been exercising regularly.

Fatty liver disease complications

In many people, fatty liver by itself doesn’t cause too many problems. But in some people the fatty liver gets inflamed, causing a more serious condition called non-alcoholic steatohepatitis, or NASH. Ongoing inflammation may scar the liver, which can lead to cirrhosis. This is a serious illness. A few people who get cirrhosis of the liver develop liver cancer. Some people who develop severe cirrhosis of the liver need to have a liver transplant.

People with fatty liver have an increased risk of heart attack and stroke.

Fatty liver diagnosis

If your doctor suspects fatty liver, he may ask about your alcohol use. This information is crucial. Continued and excessive alcohol use can cause severe liver damage.

Your doctor will also ask about your diet and lifestyle factors that may make you more likely to develop non-alcoholic fatty liver disease (NAFLD), such as a lack of physical activity, eating a diet high in sugar, or drinking sugary beverages.

However, because fatty liver causes no symptoms in most cases, it frequently comes to medical attention when tests done for other reasons point to a liver problem. This can happen if your liver looks unusual on ultrasound or if you have an abnormal liver enzyme test.

Tests done to pinpoint the diagnosis and determine disease severity include:

Blood tests

Complete blood count
Liver enzyme and liver function tests. Your doctor may suspect you have NAFLD if your blood test shows increased levels of the liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST).
Tests for chronic viral hepatitis (hepatitis A, hepatitis C and others)
Celiac disease screening test
Fasting blood sugar
Hemoglobin A1C (HbA1c), which shows how stable your blood sugar is
Lipid profile, which measures blood fats, such as cholesterol and triglycerides

Your doctor may use the results of routine blood tests to calculate special scores, such as the FIB-4 or APRI. These scores can help doctors identify or rule out advanced liver fibrosis, or scarring.

Imaging procedures

Imaging procedures used to diagnose fatty liver include:

Abdominal ultrasound, which is often the initial test when liver disease is suspected.
Computerized tomography (CT) scanning or magnetic resonance imaging (MRI) of the abdomen. These techniques lack the ability to distinguish NASH from NAFLD, but still may be used.
Transient elastography, an enhanced form of ultrasound that measures the stiffness of your liver. Liver stiffness indicates fibrosis or scarring.
Magnetic resonance elastography, works by combining MRI imaging with sound waves to create a visual map (elastogram) showing the stiffness of body tissues.

Liver biopsy

If other tests are inconclusive, your doctor may recommend a procedure to remove a sample of tissue from your liver (liver biopsy). Liver biopsy is the only test that can prove a diagnosis of NASH and show clearly how severe the disease is. For liver biopsy, a doctor gives a local anesthetic to lessen any pain, then inserts a long hollow needle through the skin and into the liver to obtain a small piece of liver tissue for examination under a microscope. The tissue sample is examined in a laboratory to look for signs of inflammation and scarring.

A liver biopsy can be uncomfortable, and it does have small risks that your doctor will review with you in detail.

A liver biopsy can help determine whether fatty liver is present, whether it resulted from alcohol or certain other specific causes, and how severe the liver damage is.

Fatty liver treatment

There are no medicines to treat fatty liver disease. Treatment of fatty liver focuses on controlling or eliminating the cause of fatty liver. Lifestyle modifications and weight loss are the mainstays of the treatment ¹⁵. Treatment also involves glycemic (blood sugar) and lipid control. For patients with significant obesity, gastric bypass or other weight loss surgical modalities should be considered. Weight loss is proven to reduce fatty liver. Evidence available suggests that weight loss of 3% to 5% of body weight is necessary to notice an improvement in fatty liver, but a greater loss (up to 10%) is necessary to improve liver inflammation ¹⁶, ¹⁷.

Patients should also abstain from alcohol or hepatotoxic drugs.

If your fatty liver is caused by alcohol, then the most important thing to do is give up alcohol. This will prevent you from developing a more serious condition.

If you have non-alcoholic fatty liver disease (NAFLD), you will probably be advised to:

Drink no or very little alcohol
Follow a healthy diet and avoid sugar. Eat a healthy diet that’s rich in fruits, vegetables and whole grains, and keep track of all calories you take in.
Lose weight. If you’re overweight or obese, reduce the number of calories you eat each day and increase your physical activity in order to lose weight. Calorie reduction is the key to losing weight and managing this disease. If you have tried to lose weight in the past and have been unsuccessful, ask your doctor for help.
Exercise regularly. Aim for at least 30 minutes of exercise most days of the week. If you’re trying to lose weight, you might find that more exercise is helpful. But if you don’t already exercise regularly, get your doctor’s OK first and start slowly.
Control your blood sugar. Follow your doctor’s instructions to stay in control of your diabetes. Take your medications as directed and closely monitor your blood sugar.
Treat high cholesterol if you have it. A healthy plant-based diet, exercise and medications can help keep your cholesterol and your triglycerides at healthy levels.
Avoid medicines that can affect your liver
Quit smoking

Your doctor can help you. They may refer you to a dietitian, drug and alcohol counselor or specialist.

Avoiding all fat in your diet is not necessary. However, your doctor may recommend that you avoid certain foods, such as those that contain fructose (the sugar in fruit) and trans fats (a type of fat).

There is no specific medicine for fatty liver disease. However, depending on your situation, your doctor may advise that you take medicine to lower your lipid levels, or improve the way your body manages glucose.

No medicines have been approved to treat nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NASH) by the US Food and Drug Administration or by the European Medicines Agency. However, researchers are studying medicines that may improve these conditions. Medicine options include Metformin, Vitamin E, fish oil, Orlistat (an inhibitor of gastric and pancreatic lipase), and Sibutramine. It is important to notice that the evidence behind these pharmacological modalities is weak ¹³.

According to the European Association for the Study of the Liver guidelines ¹⁸, drug therapy should be reserved for: Progressive NASH (bridging fibrosis and cirrhosis); early-stage NASH at high risk for disease progression (age > 50 years, metabolic syndrome, diabetes mellitus or increased ALT) ¹⁹; active NASH with high necroinflammatory activities ²⁰. Similarly, in the American Association for the Study of Liver Diseases and Asian Pacific Association for the Study of the Liver guidelines, a pharmacological approach is recommended only for patients with NASH and fibrosis ⁸. In the National Institute for Health and Care Excellence guidance, just people with an advanced liver fibrosis (enhanced liver fibrosis [ELF] test > 10.51) are proposed for drug treatment ²¹. In the Italian Association for the Study of the Liver position paper, drug therapy is suggested for patients who are at high risk for disease progression²².

All guidelines acknowledge that any medicines prescribed explicitly for nonalcoholic fatty liver disease should be considered as an off-label treatment and that the decision should be discussed with the patient, carefully balancing the benefits and the safety. However, there are wide disagrement among the guidelines with regard to possibly helpful drugs (Table 4).

Metformin: Due to the evidence of its limited efficacy in improving the histological features of nonalcoholic fatty liver disease ²³, metformin is not recommended by any guidelines to specifically treat NAFLD ¹⁵.
Pioglitazone: Pioglitazone, a thiazolidinedione, is a peroxisome proliferator-activated receptor (PPAR) gamma agonist with insulin-sensitising effects. Treatment with pioglitazone improves insulin sensitivity, aminotransferases, steatosis, inflammation, and ballooning in patients with nonalcoholic steatohepatitis (NASH) and prediabetes or type 2 diabetes ²⁴. The PIVENS trial (a large multicenter randomized control trial) compared low dose pioglitazone (30 mg/d) vs vitamin E (800 UI/d) vs placebo for two years in patients without overt diabetes ²⁵. Pioglitazone improved all histological features (except for fibrosis) and achieved resolution of NASH more often than placebo ²⁵. The histological benefit occurred together with ALT improvement and partial correction of insulin resistance. The main side effects of glitazones are weight gain ²⁶ and bone fractures in women ²⁷. The use of pioglitazone for the treatment of NAFLD is endorsed both by the National Institute for Health and Care Excellence and American Association for the Study of Liver Diseases guidelines, with significant limitations. According to the National Institute for Health and Care Excellence, pioglitazone should be prescribed only in second and third level centers, after a careful evaluation ²¹. Whereas the American Association for the Study of Liver Diseases, pioglitazone is reserved for patients with biopsy-proven NASH ⁸. The European Association for the Study of the Liver guidelines are more cautious, generically suggesting to consider pioglitazone for the treatment of diabetes in patients with a concurrent NAFLD ¹⁸. Even the Asia-Pacific and the Italian guidelines acknowledge the potential benefits of pioglitazone, however, suggest that more evidence should be available before a firm recommendation can be made ²⁸, ²².
Vitamin E: Vitamin E is an anti-oxidant and has been investigated to treat nonalcoholic steatohepatitis (NASH). In the PIVENS trial, vitamin E at a dose of 800 IU/d of α-tocopherol for 96 wk was associated with a decrease in serum aminotransferases and histological improvement in steatosis, inflammation, and ballooning and resolution of steatohepatitis in adults with NASH ²⁵. Long-term safety of vitamin E is under dispute, with two different meta-analyses leading to conflicting results when analysing the all-cause mortality in patients treated with t doses of > 800 IU/d ²⁹, ²⁷. Similarly to pioglitazone, vitamin E is recommended by the National Institute for Health and Care Excellence and American Association for the Study of Liver Diseases guidelines (limited to biopsy-proven NASH in the latter case) ²¹, ⁸. Italian Association for the Study of the Liver and European Association for the Study of the Liver guidelines call for more evidence before any recommendation, while Asia-Pacific guidelines advice against the use of vitamin E which is described as not beneficial by the current evidence ²⁸.
Glucagon-like peptide-1 (GLP-1) analogues: Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist. Glucagon is an important hormone in the regulation of energy handling in your body. Glucagon-like peptide-1 (GLP-1) receptor agonists are a class of drugs that improve control of your blood sugar, cause weight loss and improve blood lipids. They also improve cardiovascular outcomes ³⁰. Therefore, they are approved for the treatment of diabetes and obesity. Liraglutide is one of these GLP-1 receptor agonists and has been tested in a randomized, placebo-controlled trial consisting of 52 patients with biopsy-proven NASH at a daily dose of 1.8 mg in 1-year study ³¹. NASH resolved significantly more frequently in liraglutide-treated patients than placebo-treated patients. Treatment with liraglutide also led to a trend in improvement of fibrosis stage. The same holds true for semaglutide, which was already shown to improve liver blood tests in patients with type 2 diabetes and obesity ³². Semaglutide was tested at several dose regimens for a treatment period of 1.5 years. NASH resolved significantly more frequently in patients treated with the higher doses of semaglutide than in patients that received placebo ³³. Fibrosis also tended to improve, but this result was not strong enough to be considered as a positive endpoint of the study. However, both the American Association for the Study of Liver Diseases and National Institute for Health and Care Excellence recommendations state that there is still too few evidence to support the use of GLP-1 analogues to specifically treat liver disease in patients with NAFLD ²¹, ⁸. The remaining guidelines also agree on this point, however also state that further evidence are needed to prove the efficacy of these drugs. In particular, the Asian Pacific Association for the Study of the Liver guidelines consider some more elements in their recommendations. On the one hand, glucagon-like peptide-1 (GLP-1) agonists appeared to reduce glycated hemoglobin more efficiently in Asian patients with type 2 diabetes mellitus ³⁴. On the other hand, there has been no study on Asian NASH patients, even if the pharmacokinetics of GLP-1 agonists do not appear to differ between Asian and non-Asian patients according to preliminary evidence ³⁵. You can consider using these drugs if you meet the diagnosis for which these drugs are approved by the regulatory authorities. For example, if you are living with type 2 diabetes, it could be worthwhile to consider including pioglitazone or glucagon-like peptide-1 (GLP-1) receptor agonists in the treatment of your type 2 diabetes, as they are also beneficial for your liver. This needs to be discussed with the doctors that treat your diabetes.
Statins: Historically, the use of statins in patients with chronic liver diseases has been considered as potentially troublesome due to the risk of hepatotoxicity. At the same time, a considerable portion of NAFLD patients usually receives statins because of their multiple cardiovascular risk factors. Consequently, the primary concern of the guidelines is the safety of statins. In this regard, a recent review underlined the safety of statin and their efficacy in reducing the associated cardiovascular morbidity in patients with NAFLD, including those with slightly elevated alanine transaminases (up to 3 × reference upper limit) ³⁶. All of the guidelines agree about the safety of prescribing statins (or continuing an ongoing statin therapy) in patients with NAFLD, even with compensated cirrhosis. However, routine prescription of a statin is not recommended in patients with decompensated cirrhosis and acute liver failure ³⁷.
Silymarin: Silymarinis a complex mixture of six major flavonolignans (silybins A and B, isosilybins A and B, silychristin, and silydianin), as well as other minor polyphenolic compounds ³⁸. In a randomized, double-blinded, placebo-controlled study on patients with biopsy-proven NASH, silymarin dosage of 700 mg three times daily for 48 wk resulted in a significantly higher percentage of fibrosis reduction compared with placebo (22.4% vs 6.0%) ³⁹. The dosage was safe and well tolerated ³⁹. Silymarin is mentioned as a potentially useful treatment for NASH in Asia-Pacific guidelines only. However, optimal dose and duration still require further studies before a full recommendation ²⁸.

For patients with advanced disease and cirrhosis, liver transplantation might have to be considered.

What food should I eat for healthy liver function?

Eating a healthy diet and being a healthy weight can often help avoid damage to your liver.

Eating the right types of food helps you and your liver stay healthy. So, try to eat a mix of:

Milk, yogurt and cheese
Meat and fish (fresh or tinned low salt) and/or eggs, tofu, nuts and seeds
Fruits (fresh or tinned low sugar)
Vegetables, beans and legumes (fresh or tinned low salt)
Grains (like breads, cereals, rice and pasta)
And drinking lots of water.

Nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is a condition in which fat builds up in your liver. This buildup of fat is not caused by heavy alcohol use. When heavy alcohol use causes fat to build up in the liver, this condition is called alcoholic liver disease ⁵.

There are two types of nonalcoholic fatty liver disease (NAFLD):

Simple fatty liver: Simple fatty liver, also called nonalcoholic fatty liver (NAFL), is a form of nonalcoholic fatty liver disease (NAFLD) in which you have fat in your liver but little or no inflammation or liver cell damage. Simple fatty liver or nonalcoholic fatty liver (NAFL) is defined as 5% or greater hepatic steatosis without hepatocellular injury or fibrosis ³. Simple fatty liver typically does not progress to cause liver damage or complications ⁵.
Nonalcoholic steatohepatitis (NASH): Nonalcoholic steatohepatitis (NASH) is a form of nonalcoholic fatty liver disease (NAFLD) in which you have inflammation and liver cell damage, in addition to fat in your liver. Nonalcoholic steatohepatitis (NASH) is defined as 5% or greater hepatic steatosis plus hepatocellular injury and inflammation, with or without fibrosis ³. This form of liver injury carries a 20%-50% risk for progressive liver fibrosis, 30% risk for cirrhosis, and 5% risk for hepatocellular carcinoma (liver cancer) ⁶. Nonalcoholic steatohepatitis (NASH) may lead to cirrhosis or liver cancer ⁵.

Simple fatty liver (Non-Alcoholic Fatty Liver or NAFL) and nonalcoholic steatohepatitis (NASH) are two separate conditions. Experts are not sure why some people with nonalcoholic fatty liver disease (NAFLD) have NASH while others have simple fatty liver (NAFL). People typically develop one type of NAFLD or the other, although sometimes people with one form are later diagnosed with the other form of nonalcoholic fatty liver disease (NAFLD). Research suggests that certain health conditions make you more likely to develop NAFLD or NASH.

It is important to note that Non-Alcoholic Fatty Liver (NAFL) is a spectrum, with NAFL being the mildest form and Non-Alcoholic Steatohepatitis (NASH) and cirrhosis being at the other end of the spectrum. NAFL (Non-Alcoholic Fatty Liver) or simply Steatosis and NASH (Non-Alcoholic Steatohepatitis) could only be distinguished with histology and liver biopsy ⁴⁰.

Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of liver disease in the United States. Between 30 and 40 percent of adults in the United States have nonalcoholic fatty liver disease (NAFLD) ³. Most people with nonalcoholic fatty liver disease have simple fatty liver also known as nonalcoholic fatty liver (NAFL). About 1.5% to 6.5% of U.S. adults have nonalcoholic steatohepatitis (NASH) ⁴¹.

Nonalcoholic fatty liver disease (NAFLD) is commonly associated with metabolic syndrome, obesity, diabetes, and hyperlipidemia. Nearly 80% of patients with metabolic syndrome have nonalcoholic fatty liver disease (NAFLD) ¹⁵.

Stages of non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) develops in 4 main stages. Most people will only ever develop the first stage, usually without realizing it. In a small number of cases, it can progress and eventually lead to liver damage if not detected and managed.

The main stages of nonalcoholic fatty liver disease (NAFLD) are:

Simple fatty liver (nonalcoholic fatty liver or NAFL) – a largely harmless build-up of fat in the liver cells that may only be diagnosed during tests carried out for another reason
Non-alcoholic steatohepatitis (NASH) – a more serious form of NAFLD, where the liver has become inflamed
Fibrosis – where persistent inflammation causes scar tissue around the liver and nearby blood vessels, but the liver is still able to function normally
Cirrhosis – the most severe stage, occurring after years of inflammation, where the liver shrinks and becomes scarred and lumpy; this damage is permanent and can lead to liver failure (where your liver stops working properly) and liver cancer

There are major differences in the way nonalcoholic fatty liver disease (NAFLD) develops and progresses between individuals ⁴². This is something scientists currently do not fully understand. This could be due to fluctuations in the severity of the metabolic risk factors as well as the impact of diverse (unhealthy) lifestyles, in addition to genetic factors ⁴³.

It can take years for fibrosis or cirrhosis to develop. In general, nonalcoholic fatty liver disease (NAFLD) fibrosis gets worse by one stage every 14 years ⁴⁴. Non-alcoholic steatohepatitis (NASH) fibrosis gets worse by one stage every seven years. These are only average figures. Progression is not linear and can be different according to the stage ⁴⁵. A recent analysis of patients in clinical trials showed that 20% of patients with fibrosis progressed to cirrhosis in two years, while 20% of patients with cirrhosis, but with good liver function and without complications of liver disease, developed more severe cirrhosis-related liver problems (decompensated liver cirrhosis) in two years ⁴⁶. These figures are called the 20% ‘rule’ ⁴⁷. In some cases, the liver can be damaged much faster than these average figures, and up to 1-in-5 patients with fibrosis progression are rapid progressors ⁴⁸.

It’s important to make lifestyle changes to prevent the condition getting worse.

Who gets nonalcoholic fatty liver disease?

Researchers do not know the cause of nonalcoholic fatty liver (NAFLD). They do know that it is more common in people who ⁴⁹:

Have type 2 diabetes and prediabetes
Are obese or overweight – particularly if you have a lot of fat around your waist (an “apple-like” body shape)
Smoke
Are middle aged or older (although children can also get it)
Have a condition that affects how your body uses insulin
Are insulin resistance, such as polycystic ovary syndrome (PCOS)
Are Hispanic, followed by non-Hispanic whites. It is less common in African Americans.
Have high levels of fats in the blood, such as cholesterol and triglycerides
Have high blood pressure
Take certain drugs, such as corticosteroids and some cancer drugs
Have certain metabolic disorders, including metabolic syndrome (a combination of diabetes, high blood pressure and obesity)
Have rapid weight loss
Have certain infections, such as hepatitis C
Have an underactive thyroid
Have been exposed to some toxins.

But nonalcoholic fatty liver disease (NAFLD) has been diagnosed in people without any of these risk factors, including young children. Research suggests that close to 10% of U.S. children ages 2 to 19 have NAFLD ⁵⁰. However, people are more likely to develop NAFLD as they age. Various studies show that more and more children are severely overweight and that fatty liver can develop in childhood ⁵¹. An unhealthy lifestyle, consisting of too little exercise and a high level of sugary and fatty foods in the daily diet also promotes the development of fatty liver in children. Even though it is recommended that children, just like adults, change their physical activity and nutritional behavior, there are nevertheless separate medical and therapeutic recommendations and measures that consider the specifics of children’s metabolic and physical development ⁵².

Nonalcoholic fatty liver disease (NAFLD) affects about 25 percent of people in the world. As the rates of obesity, type 2 diabetes, and high cholesterol are rising in the United States, so is the rate of nonalcoholic fatty liver disease (NAFLD). Nonalcoholic fatty liver disease is the most common chronic liver disorder in the United States ⁴⁹.

While NAFLD occurs in people of all races and ethnicities, it is most common among Hispanic individuals, followed by non-Hispanic whites and Asian Americans, including those of East Asian and South Asian descent ⁵³. Nonalcoholic fatty liver disease (NAFLD) is less common among non-Hispanic Blacks ⁵⁴. On average, Asian Americans with NAFLD have a lower BMI than non-Hispanic whites with NAFLD ⁵³. Experts think that genes may help explain some of the racial and ethnic differences in NAFLD.

Nonalcoholic fatty liver disease (NAFLD) is more common in people who have certain conditions, including obesity and conditions that may be related to obesity, such as type 2 diabetes. Researchers have found nonalcoholic fatty liver disease (NAFLD) in 40 to 80 percent of people who have type 2 diabetes and in 30 to 90 percent of people who are obese ⁵⁵. In research that tested for NAFLD in people who were severely obese and undergoing bariatric surgery, more than 90 percent of the people studied had NAFLD ⁵⁶.

Although nonalcoholic fatty liver disease (NAFLD) is very similar to alcohol-fatty liver disease, NAFLD is not caused by drinking too much alcohol. Alcoholic fatty liver disease only happens in people who are heavy drinkers, especially those who have been drinking for a long period of time. The risk is higher for heavy drinkers who are women, are obese, or have certain genetic mutations ⁴⁹.

Causes of non-alcoholic fatty liver disease (NAFLD)

Researchers do not know the cause of nonalcoholic fatty liver (NAFLD). Research suggests that certain health conditions, your genes, and diet and the digestive system may make you more likely to develop NAFLD. You are more likely to develop nonalcoholic fatty liver disease (NAFLD)—either simple fatty liver or NASH—if you:

are overweight or obese
have insulin resistance
have abnormal levels of fats in your blood, which may include:
- high levels of triglycerides,
- abnormal levels of cholesterol—high total cholesterol, high LDL cholesterol, or low HDL cholesterol
have metabolic syndrome or one or more traits of metabolic syndrome. Metabolic syndrome is a group of traits and medical conditions linked to overweight and obesity. People with metabolic syndrome are more likely to develop type 2 diabetes and heart disease. Experts think NAFLD may be closely linked to metabolic syndrome. Doctors define metabolic syndrome as the presence of any three of the following:
- large waist size,
- high levels of triglycerides in your blood,
- low levels of HDL cholesterol in your blood,
- high blood pressure,
- higher than normal blood glucose levels or a diagnosis of type 2 diabetes.
have type 2 diabetes.

Having more of these health conditions increases your chances of developing nonalcoholic steatohepatitis (NASH). Losing weight may cause NASH to switch to simple fatty liver (nonalcoholic fatty liver or NAFL), and regaining weight may cause simple fatty liver (nonalcoholic fatty liver or NAFL) to switch to nonalcoholic steatohepatitis (NASH).

Researchers have found that certain genes may make you more likely to develop NAFLD. These genes may help explain why NAFLD is more common in certain racial and ethnic groups. Experts are still studying the genes that may play a role in NAFLD.

Scientists have also examined the relationship between NAFLD and the microbiome—the bacteria in your digestive tract that help with digestion. Studies have found differences between the microbiomes of people who have NAFLD and those who don’t. Experts are still studying how the microbiome may affect NAFLD.

Researchers are studying whether diets high in fructose—a sugar that is part of table sugar and is also commonly added to sweeten drinks and foods—may increase the risk of NAFLD. Human studies and animal models suggest that dietary factors can affect fatty infiltration and lipid peroxidation in various types of liver disease including nonalcoholic fatty liver disease (NAFLD) ⁵⁷. More recently, increased ingestion of sugar sweetened beverages (e.g. soft drinks, fruit drinks, plus major sources of high fructose corn syrup) was found to be linked to nonalcoholic fatty liver disease (NAFLD) ⁵⁸ independent of metabolic syndrome, with NAFLD patients consuming 5 times the amount of carbohydrates from sugar sweetened beverages as compared to healthy persons ⁵⁹. Individuals consuming more than 1 sugar sweetened beverage daily showed a higher prevalence of metabolic syndrome than those consuming < 1 soft drink per day ⁶⁰.

Caramel is made by the carefully controlled heat treatment of carbohydrates, generally in the presence of acids and alkalis, in a process called caramelization. Soft drinks contain caramel coloring and sweetener, which is rich in advanced glycation end products which increase insulin resistance and inflammation ⁶¹, ⁶². The FDA has established 200 mg of caramel per kg body weight as an acceptable daily intake.

High fructose diets have induced fatty liver in rats and ducks ⁶³. Such diets have also caused increases in hepatic lipid peroxidation and activation of inflammatory pathways in the liver of rats ⁶⁴. The inborn error of metabolism known as hereditary fructose intolerance, a rare disease which results from a deficiency in the fructose metabolizing enzyme, aldolase B, has demonstrated that fructose consumption can cause progressive liver disease in humans ⁶⁵.

Recently, Stanphone demonstrated that consuming fructose-sweetened beverages, not glucose-sweetened beverages increases hepatic de-novo lipogenesis (fat production by the liver production), promotes dyslipidemia (abnormal blood cholesterol), decreases insulin sensitivity and increases visceral adiposity in overweight and obese adults ⁶⁶. One study of lean women found that 4 days of over feeding with a sucrose-sweetened (glucose + fructose) drink increased de-novo lipogenesis by 200%-300% ⁶⁷. Another feeding study showed that 2 day of high fructose intake (30% of kcal/d, consumed as sweetened beverage at every meal) resulted in decreased postprandial glucose concentration and insulin response and prolonged alimentary lipemia in women ⁶⁸. A recent clinical study indicates that NAFLD patients have a higher intake of soft drink and meat and a tendency towards a lower intake of fish rich in omega-3 ⁶⁹.

The extent to which excessive fructose might contribute to the high prevalence of NAFLD in Western societies has not been systematically investigated. It has been shown that consumption of sugar sweetened beverages is linked to obesity and results in an increased risk of metabolic syndrome. Individuals consuming > 1 soft drink per day had a higher prevalence of metabolic syndrome than those consuming < 1 drink per day ⁷⁰.

Research also suggests that certain genes may make you more likely to develop NAFLD. Experts are still studying the genes that may play a role in NAFLD ⁷¹.

In NAFLD, people have a buildup of fat in the liver that is not caused by alcohol use. If you have a history of heavy alcohol use and fat in your liver, your doctor may determine that you have alcoholic liver disease instead of NAFLD.

Table 1. Calories and sugar content in different soft drinks

Soft drinks: calorie content (number of calories)				Soft drinks: sugar content (numbers of teaspoons of sugar)
	12- oz. Can	20 oz. Bottle	64 oz. Big cup		12- oz. Can	20 oz. Bottle	64 oz. Big cup
Sunkist	190	325	1040	Orange slice	11.9	19.8	63.5
Mountain dew	165	275	880	Mint maid orange soda	11.2	18.7	59.7
Dr. Pepper	160	250	800	Mountain dew	11	18.3	58.7
Pepsi	150	250	800	Barq’s root beer	10.7	17.8	57.1
Coke classic	140	250	800	Pepsi	9.8	16.3	52.3
Sprite	140	250	800	Squirt	9.5	15.8	50.7
7-Up	140	250	800	Dr. Pepper	9.5	15.8	50.7
				7-Up	9.3	15.5	49.6
				Coke classic	9.3	15.5	49.6
				Sprite	9	15	48

[Source ⁷² ]

Causes of Nonalcoholic steatohepatitis (NASH)

Experts are not sure why some people with nonalcoholic fatty liver disease have NASH and others have simple fatty liver. Research suggests that certain genes may play a role.

People with nonalcoholic fatty liver disease are more likely to have NASH if they have one or more of the following conditions:

obesity, especially with a large waist size
high blood pressure
high levels of triglycerides or abnormal levels of cholesterol in their blood
type 2 diabetes
metabolic syndrome.

Less common causes of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NASH)

Less common causes of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NASH) include

disorders that cause your body to use or store fat improperly
rapid weight loss
certain infections, such as hepatitis C
certain medicines, such as amiodarone (Cordarone, Pacerone), diltiazem, glucocorticoids, highly active antiretroviral therapy, methotrexate (Rheumatrex, Trexall), synthetic estrogens, tamoxifen (Nolvadex, Soltamox), valproic acid
exposure to some toxins.

A study funded by the National Institute of Diabetes and Digestive and Kidney Diseases found that people who had surgery to remove their gallbladder were more likely to develop nonalcoholic fatty liver disease. More research is needed on the link between gallbladder removal and nonalcoholic fatty liver disease.

How you can prevent nonalcoholic fatty liver disease and NASH

You may be able to prevent nonalcoholic fatty liver disease and NASH by eating a healthy diet, limiting your portion sizes, and maintaining a healthy weight.

If you don’t have nonalcoholic fatty liver disease (NAFLD) or nonalcoholic steatohepatitis (NASH), you may be able to prevent these conditions by eating a healthy diet, limiting your portion sizes, and maintaining a healthy weight.

If you have nonalcoholic fatty liver disease or nonalcoholic steatohepatitis (NASH), your doctor may recommend gradually losing weight if you are overweight or obese.

Your doctor may suggest limiting your intake of fats to help prevent or treat nonalcoholic fatty liver disease or NASH. Fats are high in calories and increase your chance of becoming obese. Four types of fats are

Saturated fats, found in meat, poultry skin, butter, lard, shortening, and all milk and dairy products except fat-free versions.
Trans fats, found in foods that list hydrogenated or partially hydrogenated oil on the label, such as crackers and snack foods, commercially baked goods such as cookies and cakes, and fried foods such as doughnuts and french fries.
Monounsaturated fats, found in olive, peanut, and canola oils.
Polyunsaturated fats, found in greatest amounts in corn, soybean, and safflower oils, and many types of nuts. Omega-3 fatty acids are a type of polyunsaturated fat. Sources include oily fish such as salmon, walnuts, and flaxseed oil.

Replacing saturated fats and trans fats in your diet with monounsaturated fats and polyunsaturated fats, especially omega-3 fatty acids, may reduce your chance of heart disease if you have nonalcoholic fatty liver disease ⁷³.

Your doctor may suggest other dietary changes to help treat nonalcoholic fatty liver disease and NASH:

Eat more low-glycemic index foods—such as most fruits, vegetables, and whole grains. These foods affect your blood glucose less than high-glycemic index foods, such as white bread, white rice, and potatoes.
Avoid foods and drinks that contain large amounts of simple sugars, especially fructose. Fructose is found in sweetened soft drinks, sports drinks, sweetened tea, and juices.
Avoid heavy alcohol use, which can damage your liver. For men, experts define heavy alcohol use as more than 4 drinks per day or more than 14 drinks per week. For women, heavy alcohol use is more than 3 drinks per day or more than 7 drinks per week ⁵⁶.

Signs and symptoms of nonalcoholic fatty liver disease

Both nonalcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease are usually silent diseases with few or no symptoms ⁴⁹. If you do have symptoms, you may feel tired, have discomfort in the upper right side of your abdomen, have unexplained weight loss and weakness. If cirrhosis (the most advanced stage of nonalcoholic fatty liver disease) develops, you can get more severe symptoms, such as yellowing of the skin and the whites of the eyes (also known as jaundice), itchy skin, and swelling in the legs, ankles, feet or tummy (edema).

Because there are often no symptoms, it is not easy to find fatty liver disease. Your doctor may suspect that you have it if you get abnormal results on liver tests that you had for other reasons. To make a diagnosis, your doctor will use:

Your medical history
A physical exam
Various tests, including blood and imaging tests, and sometimes a biopsy

As part of the medical history, your doctor will ask if you have a history of health conditions that make you more likely to develop nonalcoholic fatty liver disease and NASH, such as:

overweight or obesity
insulin resistance
high levels of triglycerides or abnormal levels of cholesterol in your blood
metabolic syndrome
type 2 diabetes

Your doctor will ask about diet and lifestyle factors that may make you more likely to develop nonalcoholic fatty liver disease and NASH, such as a lack of physical activity or a habit of drinking beverages with added sugar.

Medical tests can’t show whether alcohol is the cause of fat in your liver. Your doctor will ask about your alcohol intake to find out whether fat in your liver is a sign of alcoholic liver disease or nonalcoholic fatty liver disease.

He or she will also ask which medicines you take, to try to determine whether a medicine is causing your nonalcoholic fatty liver disease.

During the physical exam, your doctor will examine your body and check your weight and height to calculate your body mass index (BMI). Your doctor will look for signs of fatty liver disease, such as

An enlarged liver
signs of insulin resistance such as darkened skin patches over your knuckles, elbows, and knees
Signs of cirrhosis, such as jaundice, a condition that causes your skin and whites of your eyes to turn yellow

You will likely have blood tests, including liver function tests and blood count tests. In some cases you may also have imaging tests, like those that check for fat in the liver and the stiffness of your liver. Liver stiffness can mean fibrosis, which is scarring of the liver. In some cases you may also need a liver biopsy to confirm the diagnosis, and to check how bad the liver damage is.

Nonalcoholic fatty liver disease complications

People with nonalcoholic fatty liver disease (NAFLD) may develop liver complications or other health problems.

Liver complications

People with simple fatty liver (nonalcoholic fatty liver or NAFL) typically don’t develop liver complications, although they have a higher risk for other health problems ⁴¹.
People with non-alcoholic steatohepatitis (NASH) can develop liver complications, such as cirrhosis and liver cancer. If cirrhosis leads to liver failure, you may need a liver transplant. People with NASH have an increased chance of dying from liver-related causes ⁸.

Other health problems

People with NAFLD have a higher risk for certain health problems, including:

cardiovascular disease, which is the most common cause of death in people who have nonalcoholic fatty liver disease (NAFLD) ⁸
type 2 diabetes
metabolic syndrome
conditions that may be part of metabolic syndrome, such as high blood pressure and abnormal levels of fats—cholesterol and triglycerides—in the blood.

Research shows that NAFLD increases the risk of developing type 2 diabetes, and if you already have type 2 diabetes, it makes controlling your type 2 diabetes more difficult ⁷⁴. Nonalcoholic fatty liver disease (NAFLD) also increases your risk of cardiovascular (heart) disease by damaging the walls of blood vessels ⁷⁵. NAFLD influences the build-up of mineral deposits or calcifications on the vessel walls, which is called atherosclerosis. It also causes damage to the heart, mainly the heart muscle and the system that regulates heart rhythm. NAFLD may also increase the risk of several types of cancer (including bowel cancer) ⁷⁶ and the development of kidney problems ⁷⁷.

It is still unclear whether all patients with NAFLD are at risk for all these serious problems, or if these complications are mainly restricted to patients with NASH ². Studies have shown that the severity of liver fibrosis is the most important predictor of what will happen to someone with NAFLD ⁷⁸. People with NAFLD who have more severe fibrosis were shown to have a higher chance of developing serious health problems or dying. These serious health issues obviously arise from liver disease, but also, and even more frequently, from non-liver-related diseases. Diseases of the heart and blood vessels (cardiovascular disease) are the most frequent problems encountered. Factors other than fibrosis (observed at the time of diagnosis) appear to be less predictive of health events later in life ⁷⁹. Liver fibrosis does not directly cause your heart to stop working. Having liver fibrosis is, however, a sign that your liver is not able to function in a highly effective way. This leads to long-term problems for the liver and/or other organs.

What tests do doctors use to diagnose nonalcoholic fatty liver disease and NASH ?

Doctors use blood tests, imaging tests, and sometimes liver biopsy to diagnose nonalcoholic fatty liver disease and NASH.

Blood tests

Complete blood count
Liver enzyme and liver function tests
Tests for chronic viral hepatitis (hepatitis A, hepatitis C and others)
Celiac disease screening test
Fasting blood sugar
Hemoglobin A1C (HbA1c), which shows how stable your blood sugar is
Lipid profile, which measures blood fats, such as cholesterol and triglycerides

A health care professional may take a blood sample from you and send the sample to a lab. Your doctor may suspect you have nonalcoholic fatty liver disease or NASH if your blood test shows increased levels of the liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Your doctor may perform additional blood tests to find out if you have other health conditions that may increase your liver enzyme levels.

Imaging tests

Your doctor may use the following imaging tests to help diagnose nonalcoholic fatty liver disease:

Ultrasound. Ultrasound uses a device called a transducer, which bounces safe, painless sound waves off your organs to create an image of their structure.
Transient elastography, an enhanced form of ultrasound that measures the stiffness of your liver. Liver stiffness indicates fibrosis or scarring.
Computerized tomography (CT) scans. CT scans use a combination of x-rays and computer technology to create images of your liver. For a CT scan, a health care professional may give you a solution to drink and an injection of a special dye, called contrast medium. Contrast medium makes the structures inside your body easier to see during the procedure. You’ll lie on a table that slides into a tunnel-shaped device that takes the x-rays.
Magnetic resonance imaging (MRI). MRI machines use radio waves and magnets to produce detailed images of your organs and soft tissues without using x-rays. A health care professional may give you an injection of contrast medium. With most MRI machines, you’ll lie on a table that slides into a tunnel-shaped device. Some machines allow you to lie in a more open space; examining the liver can be more difficult with these machines.
Magnetic resonance elastography, works by combining MRI imaging with sound waves to create a visual map (elastogram) showing the stiffness of body tissues.

A technician performs these tests in an outpatient center or a hospital. A technician can perform an ultrasound in a doctor’s office as well. A radiologist reads and reports on the images. You don’t need anesthesia , although you may receive light sedation during an MRI if you have a fear of confined spaces.

Imaging tests can show fat in your liver. These tests can’t show inflammation or fibrosis, so your doctor can’t use these tests to find out whether you have simple fatty liver or NASH. If you have cirrhosis, imaging tests may show nodules, or lumps, on your liver.

Liver biopsy

During a liver biopsy, a doctor will take a piece of tissue from your liver. A pathologist will examine the tissue under a microscope to look for signs of damage or disease.

A doctor performs a liver biopsy at a hospital or an outpatient center. A health care professional will tell you how to prepare for a liver biopsy. You may need to stop taking certain medicines to prepare. You may be asked not to eat or drink anything for 8 hours before the procedure. During the procedure, you may receive a local anesthetic, sedatives, and pain medicine.

During the biopsy, you’ll lie on a table with your right hand resting above your head. The doctor will numb the area where he or she will insert the biopsy needle with a local anesthetic and then use the needle to take a small piece of liver tissue.

A liver biopsy is the only way to detect liver inflammation and damage to diagnose NASH. Doctors don’t recommend this test for everyone with nonalcoholic fatty liver disease. Your doctor may recommend a liver biopsy if you are more likely to have NASH or if your other tests show signs of advanced liver disease or cirrhosis.

Table 2. Diagnostic criteria for non-alcoholic fatty liver disease according to the various guidelines

	European Association for the Study of the Liver (EASL)	National Institute for Health and Care Excellence (NICE)	Asian Pacific Association for the Study of the Liver	Italian Association for the Study of the Liver (AISF)	American Association for the Study of Liver Diseases (AASLD)
Required criteria	Steatosis in > 5% of hepatocytes by either imaging or histology	Excessive fat in the liver	Hepatic steatosis by either imaging or histology	Hepatic steatosis on either imaging or histology	Evidence of hepatic steatosis either by imaging or histology
	No other causes of steatosis	No other causes of steatosis	No other causes of steatosis	No other causes of steatosis	No other causes of steatosis
	Insulin resistance	No significant alcohol consumption	No significant alcohol consumption	No significant alcohol consumption	No significant alcohol consumption
					No coexisting chronic liver disease
Alcohol consumption threshold (men)	30 g/day	30 g/day	2 standard drink/day	30 g/day	21 standard drink/week
Alcohol consumption threshold (men)			140 g/week		294 g/week
Alcohol consumption threshold (women)	20 g/day	20 g/day	1 standard drink/day	20 g/day	14 standard drink/week
Alcohol consumption threshold (women)			70 g/week		196 g/week

[Source ¹⁵ ]

What are the treatments for fatty liver disease?

There are no medicines to treat fatty liver disease. Doctors recommend weight loss to treat nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Weight loss can reduce fat in the liver; inflammation; and fibrosis, or scarring ⁸⁰. If you are overweight or obese, losing weight by making healthy food choices, limiting portion sizes, and being physically active can improve nonalcoholic fatty liver disease and NASH. Losing at least 3 to 5 percent of your body weight can reduce fat in the liver. You may need to lose up to 10 percent of your body weight to reduce liver inflammation ⁵⁶.

If you have non-alcoholic fatty liver disease (NAFLD), you will probably be advised to:

drink no or very little alcohol
follow a healthy diet and avoid sugar
lose weight
exercise regularly
control your blood sugar
treat high cholesterol if you have it
avoid medicines that can affect your liver
quit smoking

Your doctor can help you. They may refer you to a dietitian, drug and alcohol counselor or specialist.

Doctors recommend gradually losing 7 percent of your body weight or more over the course of 1 year ⁸¹. Rapid weight loss through very low calorie diets or fasting—eating and drinking nothing except water—can make nonalcoholic fatty liver disease worse ⁸⁰.

If your doctor thinks that a certain medicine is the cause of your nonalcoholic fatty liver disease, you should stop taking that medicine. But check with your doctor before stopping the medicine. You may need to get off the medicine gradually, and you might need to switch to another medicine instead.

There are no medicines that have been approved to treat NAFLD. Studies are investigating whether a certain diabetes medicine or Vitamin E can help, but more studies are needed.

The most important part of treating alcohol-related fatty liver disease is to stop drinking alcohol. If you need help doing that, you may want to see a therapist or participate in an alcohol recovery program. There are also medicines that can help, either by reducing your cravings or making you feel sick if you drink alcohol.

Both alcoholic fatty liver disease and one type of nonalcoholic fatty liver disease (nonalcoholic steatohepatitis [NASH]) can lead to cirrhosis. Doctors can treat the health problems caused by cirrhosis with medicines, operations, and other medical procedures. If the cirrhosis leads to liver failure, you may need a liver transplant.

Patients should also abstain from alcohol or hepatotoxic drugs.

If your fatty liver is caused by alcohol, then the most important thing to do is give up alcohol. This will prevent you from developing a more serious condition.

What are some lifestyle changes that can help with fatty liver disease?

Lifestyle modification consisting of diet, exercise, and weight loss has been advocated to treat patients with nonalcoholic fatty liver disease (NAFLD) in all guidelines (Table 1) ¹⁵. Furthermore, weight loss has been reported as a keystone element in improving the histology features of nonalcoholic steatohepatitis (NASH) ⁸².

According to the Italian Association for the Study of the Liver position paper ²², the best therapeutic approach is an adequate lifestyle change focused on weight loss and achieved by physical activity (aerobic activities and resistance training) and healthy diet. In particular, a calorie restriction obtained with a low calorie (1200-1600 kcal/d), low fat (less than 10% of saturated fatty acid) and low carbohydrate diet (< 50% of total kcal) is suggested. A Mediterranean diet is recommended as the most effective dietary option to induce a weight loss together with beneficial effects on all cardio-metabolic risk factors associated with NAFLD ²².

The Asian Pacific Association for the Study of the Liver guidelines agree with a lifestyle intervention strategy for the treatment of NAFLD, focusing the attention on the timing of weight loss that should be gradual because of the deleterious effect of crash diets on NASH. Very low-calorie diets are considered unsustainable, and any specific regimen is preferred over the others ²⁸.

Also, the European Association for the Study of the Liver ¹⁸, National Institute for Health and Care Excellence ²¹ and American Association for the Study of Liver Diseases ⁸ guidelines recommend structured programmes aimed at lifestyle changes towards a healthy diet and habitual physical activity. According to all of these guidelines, a 7%-10% weight loss is the target of most lifestyle interventions.

If you have any types of fatty liver disease, there are some lifestyle changes that can help:

Eat a healthy diet, limiting salt and sugar, plus eating lots of fruits, vegetables, and whole grains
Get vaccinations for hepatitis A and B, the flu and pneumococcal disease. If you get hepatitis A or B along with fatty liver, it is more likely to lead to liver failure. People with chronic liver disease are more likely to get infections, so the other two vaccinations are also important.
Get regular exercise, which can help you lose weight and reduce fat in the liver
Talk with your doctor before using dietary supplements, such as vitamins, or any complementary or alternative medicines or medical practices. Some herbal remedies can damage your liver.

Table 3. Lifestyle changes to treat nonalcoholic fatty liver disease (NAFLD)

	European Association for the Study of the Liver (EASL)	National Institute for Health and Care Excellence (NICE)	Asian Pacific Association for the Study of the Liver	Italian Association for the Study of the Liver (AISF)	American Association for the Study of Liver Diseases (AASLD)
Dietary restrictions	500-1000 kcal deficit; weight loss of 500-1000 g/wk with a 7%-10% total weight loss	Main recommendations on diet of NICE’s obesity and preventing excess weight gain guidelines	500-1000 kcal deficit	1200-1600 kcal/d; fat-low (< 30% of total calories); carbohydrate-low (< 50% of total calories)	500-1000 kcal deficit
Physical activity	Aerobic and resistance training (150-200 min/wk in 3-5 sessions)	Main recommendation of on physical activity of NICE’s obesity and preventing excess weight gain guidelines	Aerobic and resistance training	Aerobic and resistance training	Aerobic and resistance training (> 150 min/wk)
Gold standard diet	Low-to-moderate fat and moderate-to-high carbohydrate intake	No specific suggestions	All, excluding very low-calorie diets	Mediterranean diet	No specific suggestions
	Low-carbohydrate ketogenic diets or high-protein
	Mediterranean diet

[Source ¹⁵ ]

Medicines

Metformin: Due to the evidence of its limited efficacy in improving the histological features of nonalcoholic fatty liver disease ²³, metformin is not recommended by any guidelines to specifically treat NAFLD ¹⁵.
Pioglitazone: Pioglitazone, a thiazolidinedione, is a peroxisome proliferator-activated receptor (PPAR) gamma agonist with insulin-sensitising effects. Treatment with pioglitazone improves insulin sensitivity, aminotransferases, steatosis, inflammation, and ballooning in patients with nonalcoholic steatohepatitis (NASH) and prediabetes or type 2 diabetes ²⁴. The PIVENS trial (a large multicenter randomized control trial) compared low dose pioglitazone (30 mg/d) vs vitamin E (800 UI/d) vs placebo for two years in patients without overt diabetes ²⁵. Pioglitazone improved all histological features (except for fibrosis) and achieved resolution of NASH more often than placebo ²⁵. The histological benefit occurred together with ALT improvement and partial correction of insulin resistance. The main side effects of glitazones are weight gain ²⁶ and bone fractures in women ²⁷. The use of pioglitazone for the treatment of NAFLD is endorsed both by the National Institute for Health and Care Excellence and American Association for the Study of Liver Diseases guidelines, with significant limitations. According to the National Institute for Health and Care Excellence, pioglitazone should be prescribed only in second and third level centers, after a careful evaluation ²¹. Whereas the American Association for the Study of Liver Diseases, pioglitazone is reserved for patients with biopsy-proven NASH ⁸. The European Association for the Study of the Liver guidelines are more cautious, generically suggesting to consider pioglitazone for the treatment of diabetes in patients with a concurrent NAFLD ¹⁸. Even the Asia-Pacific and the Italian guidelines acknowledge the potential benefits of pioglitazone, however, suggest that more evidence should be available before a firm recommendation can be made ²⁸, ²².
Vitamin E: Vitamin E is an anti-oxidant and has been investigated to treat nonalcoholic steatohepatitis (NASH). In the PIVENS trial, vitamin E at a dose of 800 IU/d of α-tocopherol for 96 wk was associated with a decrease in serum aminotransferases and histological improvement in steatosis, inflammation, and ballooning and resolution of steatohepatitis in adults with NASH ²⁵. Long-term safety of vitamin E is under dispute, with two different meta-analyses leading to conflicting results when analysing the all-cause mortality in patients treated with t doses of > 800 IU/d ²⁹, ²⁷. Similarly to pioglitazone, vitamin E is recommended by the National Institute for Health and Care Excellence and American Association for the Study of Liver Diseases guidelines (limited to biopsy-proven NASH in the latter case) ²¹, ⁸. Italian Association for the Study of the Liver and European Association for the Study of the Liver guidelines call for more evidence before any recommendation, while Asia-Pacific guidelines advice against the use of vitamin E which is described as not beneficial by the current evidence ²⁸.
Glucagon-like peptide-1 (GLP-1) analogues: Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist. Glucagon is an important hormone in the regulation of energy handling in your body. Glucagon-like peptide-1 (GLP-1) receptor agonists are a class of drugs that improve control of your blood sugar, cause weight loss and improve blood lipids. They also improve cardiovascular outcomes ³⁰. Therefore, they are approved for the treatment of diabetes and obesity. Liraglutide is one of these GLP-1 receptor agonists and has been tested in a randomized, placebo-controlled trial consisting of 52 patients with biopsy-proven NASH at a daily dose of 1.8 mg in 1-year study ³¹. NASH resolved significantly more frequently in liraglutide-treated patients than placebo-treated patients. Treatment with liraglutide also led to a trend in improvement of fibrosis stage. The same holds true for semaglutide, which was already shown to improve liver blood tests in patients with type 2 diabetes and obesity ³². Semaglutide was tested at several dose regimens for a treatment period of 1.5 years. NASH resolved significantly more frequently in patients treated with the higher doses of semaglutide than in patients that received placebo ³³. Fibrosis also tended to improve, but this result was not strong enough to be considered as a positive endpoint of the study. However, both the American Association for the Study of Liver Diseases and National Institute for Health and Care Excellence recommendations state that there is still too few evidence to support the use of GLP-1 analogues to specifically treat liver disease in patients with NAFLD ²¹, ⁸. The remaining guidelines also agree on this point, however also state that further evidence are needed to prove the efficacy of these drugs. In particular, the Asian Pacific Association for the Study of the Liver guidelines consider some more elements in their recommendations. On the one hand, glucagon-like peptide-1 (GLP-1) agonists appeared to reduce glycated hemoglobin more efficiently in Asian patients with type 2 diabetes mellitus ³⁴. On the other hand, there has been no study on Asian NASH patients, even if the pharmacokinetics of GLP-1 agonists do not appear to differ between Asian and non-Asian patients according to preliminary evidence ³⁵. You can consider using these drugs if you meet the diagnosis for which these drugs are approved by the regulatory authorities. For example, if you are living with type 2 diabetes, it could be worthwhile to consider including pioglitazone or glucagon-like peptide-1 (GLP-1) receptor agonists in the treatment of your type 2 diabetes, as they are also beneficial for your liver. This needs to be discussed with the doctors that treat your diabetes.
Statins: Historically, the use of statins in patients with chronic liver diseases has been considered as potentially troublesome due to the risk of hepatotoxicity. At the same time, a considerable portion of NAFLD patients usually receives statins because of their multiple cardiovascular risk factors. Consequently, the primary concern of the guidelines is the safety of statins. In this regard, a recent review underlined the safety of statin and their efficacy in reducing the associated cardiovascular morbidity in patients with NAFLD, including those with slightly elevated alanine transaminases (up to 3 × reference upper limit) ³⁶. All of the guidelines agree about the safety of prescribing statins (or continuing an ongoing statin therapy) in patients with NAFLD, even with compensated cirrhosis. However, routine prescription of a statin is not recommended in patients with decompensated cirrhosis and acute liver failure ³⁷.
Silymarin: Silymarinis a complex mixture of six major flavonolignans (silybins A and B, isosilybins A and B, silychristin, and silydianin), as well as other minor polyphenolic compounds ³⁸. In a randomized, double-blinded, placebo-controlled study on patients with biopsy-proven NASH, silymarin dosage of 700 mg three times daily for 48 wk resulted in a significantly higher percentage of fibrosis reduction compared with placebo (22.4% vs 6.0%) ³⁹. The dosage was safe and well tolerated ³⁹. Silymarin is mentioned as a potentially useful treatment for NASH in Asia-Pacific guidelines only. However, optimal dose and duration still require further studies before a full recommendation ²⁸.

For safety reasons, talk with your doctor before using dietary supplements, such as vitamins, or any complementary or alternative medicines or medical practices. Some herbal remedies can actually damage your liver.

For patients with advanced disease and cirrhosis, liver transplantation might have to be considered.

Table 4. Recommendations about drug treatment of non-alcoholic fatty liver disease (NAFLD)

	European Association for the Study of the Liver	National Institute for Health and Care Excellence	ASIA-PACIFIC	Italian Association for the Study of the Liver	American Association for the Study of Liver Diseases
Metformin	Insufficient evidence	Not beneficial	Not beneficial	Not mentioned	Not beneficial
Vitamin E	Insufficient evidence	Consider use regardless of diabetes	Not beneficial	Insufficient evidence	Consider use in non-diabetic, biopsy-proven NASH
PPAR-gamma agonists	Consider use in selected diabetic patients	Consider pioglitazone in adults regardless of diabetes	Insufficient evidence in Asian	Insufficient evidence, potentially useful	Pioglitazone indicated in biopsy-proven NASH (regardless of diabetes)
PUFA	Not beneficial	Insufficient evidence	Not beneficial	Not mentioned	Not beneficial
Pentoxifylline	Insufficient evidence	Not mentioned	Not beneficial	Not mentioned	Not mentioned
GLP-1 analogues	Insufficient evidence, potentially useful	Insufficient evidence	Insufficient evidence in Asian patients	Insufficient evidence, potentially useful	Insufficient evidence
UDCA	Not beneficial	Not beneficial	Not mentioned	Not mentioned	Not beneficial
Obetycolic acid	Scarce evidence	Not mentioned	waiting for ongoing RCT results	Waiting for ongoing RCT results	Insufficient evidence
Silymarin	Not mentioned	Not mentioned	insufficient evidence, potentially useful	Not mentioned	Not mentioned
Statins	Safe but not beneficial	Safe but not beneficial	Safe but not beneficial	Safe but not beneficial	Safe but not beneficial

Abbreviations: PPAR = Peroxisome proliferator-activated receptors; PUFA = Poly-unsaturated fatty acids; GLP-1 = Glucagon-like peptide-1

[Source ¹⁵ ]

How do doctors treat the complications of NASH?

If NASH leads to cirrhosis, doctors can treat the health problems caused by cirrhosis with medicines, operations, and other medical procedures. If cirrhosis leads to liver failure, you may need a liver transplant.

What is a liver transplant?

Your liver is the largest organ inside your body. It helps your body digest food, store energy, and remove poisons. You cannot live without a liver that works. If your liver fails, your doctor may put you on a waiting list for a liver transplant. Doctors do liver transplants when other treatment cannot keep a damaged liver working.

During a liver transplantation, the surgeon removes the diseased liver and replaces it with a healthy one. Most transplant livers come from a donor who has died ⁸³. Sometimes there is a living donor. This is when a healthy person donates part of his or her liver for a specific patient.

The most common reason for a transplant in adults is cirrhosis ⁸³. This is scarring of the liver, caused by injury or long-term disease. The most common reason in children is biliary atresia, a disease of the bile ducts.

If you have a transplant, you must take drugs the rest of your life to help keep your body from rejecting the new liver ⁸³.

Nonalcoholic steatohepatitis (NASH) is becoming the most common indication to liver transplantation in Western Countries ⁸⁴. Because of the high prevalence of obesity, sarcopenia, cardiovascular disease and chronic kidney disease among patients with NASH, there is a higher frequency of post-transplant complications and increased graft loss ⁸⁵. Because of the risk of prolonged ventilation, poor wound healing, higher rate of primary graft non-function, and increased infectious complications, patients with severe obesity (BMI > 40 kg/m²) may even be considered unﬁt for liver transplantation, unless efforts are made preoperatively to reduce body weight with individualized plans of lifestyle modiﬁcations ⁸⁶.

Bariatric surgery (weight loss surgery)

In patients unresponsive to lifestyle changes and pharmacotherapy, weight loss surgery or bariatric surgery is an option for reducing weight and metabolic complications, with stable results in the long-term ⁸⁷. Bariatric surgery can also improve liver histology, both regarding steatosis and ballooning ⁸⁸ and fibrosis ⁸⁹. However, the presence of established cirrhosis is associated with peri-operative risks. In particular, in the analysis performed from the Nationwide Inpatient Sample (1998-2007), mortality was higher in patients with compensated cirrhosis (0.9%) and much higher in those with decompensated cirrhosis (16.3%) ⁹⁰. No robust data on the comparative effects of different bariatric procedures on liver fat are available in the literature.

Based on the evidence as mentioned earlier, the European Association for the Study of the Liver guidelines consider bariatric surgery an option in patients unresponsive to lifestyle changes and pharmacotherapy, for reducing weight and metabolic complications ¹⁸. Guidance statements by the American Association for the Study of Liver Diseases also consider a role of foregut bariatric surgery in otherwise eligible obese individuals with NAFLD or NASH ⁸.

The Asia-Pacific recommendation limits the role of bariatric surgery only to patients with class 2 obesity (BMI > 32.5 kg/m² in Asians and 35 kg/m² in Caucasians) ²⁸. The Italian Association for the Study of the Liver and National Institute for Health and Care Excellence guidelines do not mention bariatric surgery.

What is alcoholic liver disease?

Alcoholic liver disease is damage to the liver and its function due to alcohol abuse ⁹¹. Your liver breaks down most of the alcohol you drink, so it can be removed from your body. But the process of breaking it down can generate harmful substances. These substances can damage liver cells, promote inflammation, and weaken your body’s natural defenses. The more alcohol that you drink, the more you damage your liver. Alcoholic fatty liver disease is the earliest stage of alcohol-related liver disease. The next stages are alcoholic hepatitis and cirrhosis.

Causes of alcoholic liver disease

Drinking too much alcohol, either on a single occasion – known as binge drinking – or drinking a lot over time, can take a serious toll on your health and well-being. In addition to injuring the liver, alcohol has many effects on your body including:

Lessening your ability to think clearly and move with coordination; it can change your mood and behavior.
Disrupting the processes involved in digestion, leading to malnutrition and weight loss.
Weakening your immune system and the ability to fight infections. Increasing your risk of developing certain cancers including cancers of the colon, liver, esophagus, mouth, and breast (for women).

Alcoholic liver disease occurs after years of heavy drinking. Over time, scarring and cirrhosis of the liver can occur. Cirrhosis is scarring of the liver and poor liver function. It is the last stage of chronic liver disease including alcoholic liver disease ⁹¹.

Alcoholic liver disease does not occur in all heavy drinkers. The chances of getting liver disease go up the longer you have been drinking and more alcohol you consume. You do not have to get drunk for the disease to happen ⁹¹.

Alcoholic liver disease seems to be more common in some families ⁹¹. Women may be more likely to have this problem than men ⁹¹.

What factors increase your risk for alcohol-related liver disease ?

The amount of alcohol you consume is the most important risk factor for developing alcohol-related liver disease ⁷. The risk increases with the length of time and amount of alcohol you drink. However, because many people who drink heavily or binge drink do not develop alcohol-related liver disease, we know there are other factors that affect a person’s susceptibility.

Additional risk factors that play a role in someone developing alcohol-related liver disease include:

Obesity: Obesity is a contributing factor to fatty liver disease. The combined effect of obesity and alcohol together is worse than the effect of either one of them alone.
Malnutrition: Many people who drink heavily are malnourished, either because they eat poorly due to loss of appetite and nausea or because alcohol and its toxic byproducts prevent the body from breaking down and absorbing nutrients. In both cases, the lack of nutrients contributes to liver cell damage.
Genetic factors: Genetics can influence how the body processes alcohol and may predispose someone to alcoholism and alcohol-related liver disease. Race and ethnicity: A higher risk of liver injury appears to be associated with one’s racial and ethnic heritage. For example, rates of alcoholic cirrhosis are higher in African-American and Hispanic males compared with Caucasian males.
Your sex: Women are more susceptible than men to the adverse effects of alcohol.
Pattern of drinking: It’s worse to drink outside of meal times and binge drink, defined as five drinks for men and four drinks for women in one sitting.
Chronic viral hepatitis, particularly hepatitis C: The combined effect of alcohol and viral hepatitis on the liver results in more advanced disease than either of them alone.

There are three main types of alcohol-related liver disease:

Fatty liver

Also called steatosis, this is the earliest stage of alcohol-related liver disease and the most common alcohol-related liver disorder ⁷. It is characterized by an excessive accumulation of fat inside liver cells, which makes it harder for the liver to function. Usually there are no symptoms, although the liver can be enlarged and you may experience upper abdominal discomfort on the right side. Fatty liver occurs fairly soon in almost all people who drink heavily. The condition will usually go away if you stop drinking.

Alcoholic hepatitis

This is an inflammation, or swelling, of the liver accompanied by the destruction of liver cells. Up to 35 percent of heavy drinkers develop alcoholic hepatitis, which can be mild or severe ⁷. Symptoms may include fever, jaundice, nausea, vomiting, abdominal pain and tenderness. In its mild form, alcoholic hepatitis can last for years and will cause progressive liver damage, although the damage may be reversible over time if you stop drinking. In its severe, acute form the disease may occur suddenly – after binge drinking for instance – and can quickly lead to life-threatening complications. Alcoholic cirrhosis: This is the most serious type of alcohol-related liver disease.

Cirrhosis

Cirrhosis refers to the replacement of normal liver tissue with nonliving scar tissue. Between 10 and 20 percent of heavy drinkers develop cirrhosis, usually after 10 or more years of drinking ⁷. Anything that damages the liver over many years can lead the liver to form scar tissue. Fibrosis is the first stage of liver scarring. When scar tissue builds up and takes over most of the liver, it’s referred to as cirrhosis. Research has shown that cirrhosis can be reversed, although this may not occur for all patients. Cirrhosis caused by alcohol can be a life-threatening disease ⁷.

How does alcohol-related liver disease progress ?

Many heavy drinkers will progress from fatty liver disease to alcoholic hepatitis to alcoholic cirrhosis over time. However, some heavy drinkers may develop cirrhosis without first having alcoholic hepatitis first ⁷. Others may have alcoholic hepatitis but never have symptoms. Additionally, alcohol consumption may worsen liver injury caused by non-alcoholic liver diseases such as chronic hepatitis C.

Since an individual’s susceptibility to the toxic effects of alcohol may vary by many factors including age, gender, genetics and coexistent medical conditions, it is reasonable for you to review alcohol use with your physician.

Symptoms of alcoholic liver disease

There may be no symptoms, or symptoms may come on slowly, depending on how well the liver is working. Symptoms tend to be worse after a period of heavy drinking.

Early symptoms include:

Fatigue and loss of energy
Poor appetite and weight loss
Nausea or belly pain
Small, red spider-like blood vessels on the skin.

As liver function worsens, symptoms may include:

Fluid buildup of the legs (edema) and in the abdomen (ascites)
Yellow color in the skin, mucous membranes, or eyes (jaundice)
Redness on the palms of the hands
In men, impotence, shrinking of the testicles, and breast swelling
Easy bruising and abnormal bleeding
Behavior changes and confusion or problems thinking
Pale or clay-colored stools

Alcoholic liver disease diagnosis

Your health care provider will do a physical exam to look for:

An enlarged liver or spleen
Excess breast tissue
Swollen abdomen, as a result of too much fluid
Reddened palms
Red spider-like blood vessels on the skin
Small testicles
Widened veins in the abdomen wall
Yellow eyes or skin (jaundice)

Tests you may have include:

Complete blood count (CBC)
Liver biopsy
Liver function tests
Coagulation studies

Tests to rule out other diseases include:

Abdominal CT scan
Blood tests for other causes of liver disease
Ultrasound of the abdomen

Treatment of alcoholic liver disease

Lifestyle Changes

Some things you can do to help take care of your liver disease are:

Abstinence: If you’ve been diagnosed with alcohol-related liver disease, the single most important thing you can do for yourself is to stop drinking. Abstinence is the only way of possibly reversing liver damage, or in more advanced cases, preventing it from becoming worse. Discuss treatment options with your healthcare provider; these can include counseling, medications, an outpatient treatment program or a residential inpatient stay. If you are physically addicted to alcohol, medical supervision in a detoxification (or detox) program may be required to safely reduce your alcohol levels. It can be dangerous to stop drinking very suddenly. A rapid reduction in alcohol can lead to withdrawal symptoms including anxiety, agitation, hallucinations and seizures. Your doctor can recommend a program that best meets your needs.
Nutrition therapy: Nutritional deficiencies are very common in people with alcohol-related liver disease. Your doctor will likely recommend a special diet, as well as vitamin and nutritional supplements, to combat the effects of malnutrition and help you gain weight if needed. You may be referred to a nutritionist who can assist you with meal planning. If you have trouble eating enough to get the vitamins and nutrients you need, your doctor may recommend giving you a special nutrient-rich liquid intravenously or via tube feeding. Eat a healthy diet that is low in salt.
Get vaccinated for diseases such as influenza, hepatitis A and hepatitis B, and pneumococcal pneumonia.
Talk to your doctor about all medicines you take, including herbs and supplements and over-the-counter medicines.

Medicines from your doctor

“Water pills” (diuretics) to get rid of fluid build-up
Vitamin K or blood products to prevent excess bleeding
Medicines for mental confusion
Antibiotics for infections
Depending on the severity of your disease, your doctor may recommend medications to help reduce liver inflammation. These drugs have shown some short-term benefit in increasing survival. Steroid treatment with prednisolone is usually the first-line medication, followed by pentoxifylline, if steroid therapy doesn’t work. No alternative medicine treatments have been found to cure alcoholic hepatitis.

Other Treatments

Endoscopic treatments for enlarged veins in the throat (bleeding varices)
Removal of fluid from the abdomen (paracentesis)
Placement of a transjugular intrahepatic portosystemic shunt (TIPS) to repair blood flow in the liver

When cirrhosis progresses to end-stage liver disease, a liver transplant may be needed.

Outlook (Prognosis) for alcoholic liver disease

Anyone with alcohol-related liver disease will improve their health and life expectancy if they stop drinking. People with fatty liver may be able to use alcohol moderately after their liver recovers. People with alcoholic hepatitis or alcoholic cirrhosis should stop drink completely.

For alcohol-related liver disease 10 people who do not stop drinking the outlook is poor. Continued excessive drinking can shorten your lifespan. Your risk for complications such as bleeding, brain changes, and severe liver damage go up. The outcome will likely be poor if you keep drinking.

Cirrhosis is caused by scarring of the liver. In most cases, the liver cannot heal or return to normal function once the damage is severe. Cirrhosis can lead to serious complications.

Possible Complications of alcoholic liver disease

Complications may include:

Bleeding disorders (coagulopathy)
Buildup of fluid in the abdomen (ascites) and infection of the fluid (bacterial peritonitis)
Enlarged veins in the esophagus, stomach, or intestines that bleed easily (esophageal varices)
Increased pressure in the blood vessels of the liver (portal hypertension)
Kidney failure (hepatorenal syndrome)
Liver cancer (hepatocellular carcinoma)
Mental confusion, change in the level of consciousness, or coma (hepatic encephalopathy).

References

Nonalcoholic fatty liver disease. Angulo P. N Engl J Med. 2002 Apr 18; 346(16):1221-31. https://www.ncbi.nlm.nih.gov/pubmed/11961152/
Francque, S. M., Marchesini, G., Kautz, A., Walmsley, M., Dorner, R., Lazarus, J. V., Zelber-Sagi, S., Hallsworth, K., Busetto, L., Frühbeck, G., Dicker, D., Woodward, E., Korenjak, M., Willemse, J., Koek, G. H., Vinker, S., Ungan, M., Mendive, J. M., & Lionis, C. (2021). Non-alcoholic fatty liver disease: A patient guideline. JHEP reports : innovation in hepatology, 3(5), 100322. https://doi.org/10.1016/j.jhepr.2021.100322
Nonalcoholic Fatty Liver Disease: Common Questions and Answers on Diagnosis and Management. Am Fam Physician. 2020 Nov 15;102(9):603-612. https://www.aafp.org/afp/2020/1115/p603.html
De Minicis S, Day C, Svegliati-Baroni G. From NAFLD to NASH and HCC: pathogenetic mechanisms and therapeutic insights. Curr Pharm Des. 2013;19(29):5239-49. DOI: 10.2174/1381612811319290006
The National Institute of Diabetes and Digestive and Kidney Diseases Health Information Center. Definition & Facts of NAFLD & NASH. https://www.niddk.nih.gov/health-information/liver-disease/nafld-nash/definition-facts
Expanding the natural history of nonalcoholic steatohepatitis: from cryptogenic cirrhosis to hepatocellular carcinoma. Bugianesi E, Leone N, Vanni E, Marchesini G, Brunello F, Carucci P, Musso A, De Paolis P, Capussotti L, Salizzoni M, Rizzetto M. Gastroenterology. 2002 Jul; 123(1):134-40. https://www.ncbi.nlm.nih.gov/pubmed/12105842/
American Liver Foundation. Alcohol-Related Liver Disease. http://www.liverfoundation.org/abouttheliver/info/alcohol/
Chalasani N, Younossi Z, Lavine JE, Charlton M, Cusi K, Rinella M, Harrison SA, Brunt EM, Sanyal AJ. The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2018 Jan;67(1):328-357. doi: 10.1002/hep.29367
Flegal KM, Carroll MD, Kit BK, Ogden CL. Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999-2010. JAMA. 2012 Feb 1;307(5):491-7. doi: 10.1001/jama.2012.39
Kim, S. Y., England, L., Wilson, H. G., Bish, C., Satten, G. A., & Dietz, P. (2010). Percentage of gestational diabetes mellitus attributable to overweight and obesity. American journal of public health, 100(6), 1047–1052. https://doi.org/10.2105/AJPH.2009.172890
Sarkar, M., Grab, J., Dodge, J. L., Gunderson, E. P., Rubin, J., Irani, R. A., Cedars, M., & Terrault, N. (2020). Non-alcoholic fatty liver disease in pregnancy is associated with adverse maternal and perinatal outcomes. Journal of hepatology, 73(3), 516–522. https://doi.org/10.1016/j.jhep.2020.03.049
Cleveland, E., Bandy, A., & VanWagner, L. B. (2018). Diagnostic challenges of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis. Clinical liver disease, 11(4), 98–104. https://doi.org/10.1002/cld.716
Antunes C, Azadfard M, Hoilat GJ, et al. Fatty Liver. [Updated 2021 Nov 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK441992
Fatty Liver. https://www.msdmanuals.com/en-au/home/liver-and-gallbladder-disorders/manifestations-of-liver-disease/fatty-liver
Leoni, S., Tovoli, F., Napoli, L., Serio, I., Ferri, S., & Bolondi, L. (2018). Current guidelines for the management of non-alcoholic fatty liver disease: A systematic review with comparative analysis. World journal of gastroenterology, 24(30), 3361–3373. https://doi.org/10.3748/wjg.v24.i30.3361
Loman BR, Hernández-Saavedra D, An R, Rector RS. Prebiotic and probiotic treatment of nonalcoholic fatty liver disease: a systematic review and meta-analysis. Nutr Rev. 2018 Nov 1;76(11):822-839. doi: 10.1093/nutrit/nuy031
von Schönfels W, Beckmann JH, Ahrens M, Hendricks A, Röcken C, Szymczak S, Hampe J, Schafmayer C. Histologic improvement of NAFLD in patients with obesity after bariatric surgery based on standardized NAS (NAFLD activity score). Surg Obes Relat Dis. 2018 Oct;14(10):1607-1616. doi: 10.1016/j.soard.2018.07.012
European Association for the Study of the Liver (EASL); European Association for the Study of Diabetes (EASD); European Association for the Study of Obesity (EASO). EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease. J Hepatol. 2016 Jun;64(6):1388-402. doi: 10.1016/j.jhep.2015.11.004
Adams LA, Sanderson S, Lindor KD, Angulo P. The histological course of nonalcoholic fatty liver disease: a longitudinal study of 103 patients with sequential liver biopsies. J Hepatol. 2005 Jan;42(1):132-8. doi: 10.1016/j.jhep.2004.09.012
Sanyal, A. J., Friedman, S. L., McCullough, A. J., Dimick-Santos, L., American Association for the Study of Liver Diseases, & United States Food and Drug Administration (2015). Challenges and opportunities in drug and biomarker development for nonalcoholic steatohepatitis: findings and recommendations from an American Association for the Study of Liver Diseases-U.S. Food and Drug Administration Joint Workshop. Hepatology (Baltimore, Md.), 61(4), 1392–1405. https://doi.org/10.1002/hep.27678
Non-alcoholic fatty liver disease (NAFLD): assessment and management. https://www.nice.org.uk/guidance/ng49/resources/nonalcoholic-fatty-liver-disease-nafld-assessment-and-management-pdf-1837461227461
Italian Association for the Study of the Liver (AISF). AISF position paper on nonalcoholic fatty liver disease (NAFLD): Updates and future directions. Dig Liver Dis. 2017 May;49(5):471-483. doi: 10.1016/j.dld.2017.01.147
Shields, W. W., Thompson, K. E., Grice, G. A., Harrison, S. A., & Coyle, W. J. (2009). The Effect of Metformin and Standard Therapy versus Standard Therapy alone in Nondiabetic Patients with Insulin Resistance and Nonalcoholic Steatohepatitis (NASH): A Pilot Trial. Therapeutic advances in gastroenterology, 2(3), 157–163. https://doi.org/10.1177/1756283X09105462
Belfort R, Harrison SA, Brown K, Darland C, Finch J, Hardies J, Balas B, Gastaldelli A, Tio F, Pulcini J, Berria R, Ma JZ, Dwivedi S, Havranek R, Fincke C, DeFronzo R, Bannayan GA, Schenker S, Cusi K. A placebo-controlled trial of pioglitazone in subjects with nonalcoholic steatohepatitis. N Engl J Med. 2006 Nov 30;355(22):2297-307. doi: 10.1056/NEJMoa060326
Sanyal, A. J., Chalasani, N., Kowdley, K. V., McCullough, A., Diehl, A. M., Bass, N. M., Neuschwander-Tetri, B. A., Lavine, J. E., Tonascia, J., Unalp, A., Van Natta, M., Clark, J., Brunt, E. M., Kleiner, D. E., Hoofnagle, J. H., Robuck, P. R., & NASH CRN (2010). Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. The New England journal of medicine, 362(18), 1675–1685. https://doi.org/10.1056/NEJMoa0907929
Cusi K, Orsak B, Bril F, Lomonaco R, Hecht J, Ortiz-Lopez C, Tio F, Hardies J, Darland C, Musi N, Webb A, Portillo-Sanchez P. Long-Term Pioglitazone Treatment for Patients With Nonalcoholic Steatohepatitis and Prediabetes or Type 2 Diabetes Mellitus: A Randomized Trial. Ann Intern Med. 2016 Sep 6;165(5):305-15. doi: 10.7326/M15-1774
Abner, E. L., Schmitt, F. A., Mendiondo, M. S., Marcum, J. L., & Kryscio, R. J. (2011). Vitamin E and all-cause mortality: a meta-analysis. Current aging science, 4(2), 158–170. https://doi.org/10.2174/1874609811104020158
Chitturi S, Wong VW, Chan WK, Wong GL, Wong SK, Sollano J, Ni YH, Liu CJ, Lin YC, Lesmana LA, Kim SU, Hashimoto E, Hamaguchi M, Goh KL, Fan J, Duseja A, Dan YY, Chawla Y, Farrell G, Chan HL. The Asia-Pacific Working Party on Non-alcoholic Fatty Liver Disease guidelines 2017-Part 2: Management and special groups. J Gastroenterol Hepatol. 2018 Jan;33(1):86-98. doi: 10.1111/jgh.13856
Miller ER 3rd, Pastor-Barriuso R, Dalal D, Riemersma RA, Appel LJ, Guallar E. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med. 2005 Jan 4;142(1):37-46. doi: 10.7326/0003-4819-142-1-200501040-00110
Pi-Sunyer X, Astrup A, Fujioka K, Greenway F, Halpern A, Krempf M, Lau DC, le Roux CW, Violante Ortiz R, Jensen CB, Wilding JP; SCALE Obesity and Prediabetes NN8022-1839 Study Group. A Randomized, Controlled Trial of 3.0 mg of Liraglutide in Weight Management. N Engl J Med. 2015 Jul 2;373(1):11-22. doi: 10.1056/NEJMoa1411892
Armstrong MJ, Gaunt P, Aithal GP, Barton D, Hull D, Parker R, Hazlehurst JM, Guo K; LEAN trial team, Abouda G, Aldersley MA, Stocken D, Gough SC, Tomlinson JW, Brown RM, Hübscher SG, Newsome PN. Liraglutide safety and efficacy in patients with non-alcoholic steatohepatitis (LEAN): a multicentre, double-blind, randomised, placebo-controlled phase 2 study. Lancet. 2016 Feb 13;387(10019):679-690. doi: 10.1016/S0140-6736(15)00803-X
Newsome, P., Francque, S., Harrison, S., Ratziu, V., Van Gaal, L., Calanna, S., Hansen, M., Linder, M., & Sanyal, A. (2019). Effect of semaglutide on liver enzymes and markers of inflammation in subjects with type 2 diabetes and/or obesity. Alimentary pharmacology & therapeutics, 50(2), 193–203. https://doi.org/10.1111/apt.15316
Newsome PN, Buchholtz K, Cusi K, Linder M, Okanoue T, Ratziu V, Sanyal AJ, Sejling AS, Harrison SA; NN9931-4296 Investigators. A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis. N Engl J Med. 2021 Mar 25;384(12):1113-1124. doi: 10.1056/NEJMoa2028395
Kim YG, Hahn S, Oh TJ, Park KS, Cho YM. Differences in the HbA1c-lowering efficacy of glucagon-like peptide-1 analogues between Asians and non-Asians: a systematic review and meta-analysis. Diabetes Obes Metab. 2014 Oct;16(10):900-9. doi: 10.1111/dom.12293
Ingwersen SH, Petri KC, Tandon N, Yoon KH, Chen L, Vora J, Yang W. Liraglutide pharmacokinetics and dose-exposure response in Asian subjects with Type 2 diabetes from China, India and South Korea. Diabetes Res Clin Pract. 2015 Apr;108(1):113-9. doi: 10.1016/j.diabres.2015.01.001
Cohen DE, Anania FA, Chalasani N; National Lipid Association Statin Safety Task Force Liver Expert Panel. An assessment of statin safety by hepatologists. Am J Cardiol. 2006 Apr 17;97(8A):77C-81C. doi: 10.1016/j.amjcard.2005.12.014
Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum CB, Eckel RH, Goldberg AC, Gordon D, Levy D, Lloyd-Jones DM, McBride P, Schwartz JS, Shero ST, Smith SC Jr, Watson K, Wilson PW, Eddleman KM, Jarrett NM, LaBresh K, Nevo L, Wnek J, Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH, DeMets D, Hochman JS, Kovacs RJ, Ohman EM, Pressler SJ, Sellke FW, Shen WK, Smith SC Jr, Tomaselli GF; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014 Jun 24;129(25 Suppl 2):S1-45. doi: 10.1161/01.cir.0000437738.63853.7a. Epub 2013 Nov 12. Erratum in: Circulation. 2014 Jun 24;129(25 Suppl 2):S46-8. Erratum in: Circulation. 2015 Dec 22;132(25):e396
Flora K, Hahn M, Rosen H, Benner K. Milk thistle (Silybum marianum) for the therapy of liver disease. Am J Gastroenterol. 1998 Feb;93(2):139-43. doi: 10.1111/j.1572-0241.1998.00139.x
Wah Kheong C, Nik Mustapha NR, Mahadeva S. A Randomized Trial of Silymarin for the Treatment of Nonalcoholic Steatohepatitis. Clin Gastroenterol Hepatol. 2017 Dec;15(12):1940-1949.e8. doi: 10.1016/j.cgh.2017.04.016
Nonalcoholic Fatty Liver Disease: Diagnosis and Management. Am Fam Physician. 2013 Jul 1;88(1):35-42. https://www.aafp.org/afp/2013/0701/p35.html
Younossi ZM, Koenig AB, Abdelatif D, Fazel Y, Henry L, Wymer M. Global epidemiology of nonalcoholic fatty liver disease—meta-analytic assessment of prevalence, incidence, and outcomes. Hepatology. 2016;64(1):73–84. doi:10.1002/hep.28431
Mazzotti A, Caletti MT, Sasdelli AS, Brodosi L, Marchesini G. Pathophysiology of Nonalcoholic Fatty Liver Disease: Lifestyle-Gut-Gene Interaction. Dig Dis. 2016;34 Suppl 1:3-10. doi: 10.1159/000447275
Eslam M, Valenti L, Romeo S. Genetics and epigenetics of NAFLD and NASH: Clinical impact. J Hepatol. 2018 Feb;68(2):268-279. doi: 10.1016/j.jhep.2017.09.003
Singh, S., Allen, A. M., Wang, Z., Prokop, L. J., Murad, M. H., & Loomba, R. (2015). Fibrosis progression in nonalcoholic fatty liver vs nonalcoholic steatohepatitis: a systematic review and meta-analysis of paired-biopsy studies. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 13(4), 643–e40. https://doi.org/10.1016/j.cgh.2014.04.014
Schuppan D, Surabattula R, Wang XY. Determinants of fibrosis progression and regression in NASH. J Hepatol. 2018 Feb;68(2):238-250. doi: 10.1016/j.jhep.2017.11.012
Sanyal AJ, Harrison SA, Ratziu V, Abdelmalek MF, Diehl AM, Caldwell S, Shiffman ML, Aguilar Schall R, Jia C, McColgan B, Djedjos CS, McHutchison JG, Subramanian GM, Myers RP, Younossi Z, Muir AJ, Afdhal NH, Bosch J, Goodman Z. The Natural History of Advanced Fibrosis Due to Nonalcoholic Steatohepatitis: Data From the Simtuzumab Trials. Hepatology. 2019 Dec;70(6):1913-1927. doi: 10.1002/hep.30664
Loomba, R., & Adams, L. A. (2019). The 20% Rule of NASH Progression: The Natural History of Advanced Fibrosis and Cirrhosis Caused by NASH. Hepatology (Baltimore, Md.), 70(6), 1885–1888. https://doi.org/10.1002/hep.30946
Friedman, S. L., Neuschwander-Tetri, B. A., Rinella, M., & Sanyal, A. J. (2018). Mechanisms of NAFLD development and therapeutic strategies. Nature medicine, 24(7), 908–922. https://doi.org/10.1038/s41591-018-0104-9
U.S. National Library of Medicine. Medline Plus. Fatty Liver Disease. https://medlineplus.gov/fattyliverdisease.html
Schwimmer JB, Deutsch R, Kahen T, Lavine JE, Stanley C, Behling C. Prevalence of fatty liver in children and adolescents. Pediatrics. 2006;118(4):1388–1393. doi: 10.1542/peds.2006-1212
Nobili V, Mantovani A, Cianfarani S, Alisi A, Mosca A, Sartorelli MR, Maffeis C, Loomba R, Byrne CD, Targher G. Prevalence of prediabetes and diabetes in children and adolescents with biopsy-proven non-alcoholic fatty liver disease. J Hepatol. 2019 Oct;71(4):802-810. doi: 10.1016/j.jhep.2019.06.023
Vos, M. B., Abrams, S. H., Barlow, S. E., Caprio, S., Daniels, S. R., Kohli, R., Mouzaki, M., Sathya, P., Schwimmer, J. B., Sundaram, S. S., & Xanthakos, S. A. (2017). NASPGHAN Clinical Practice Guideline for the Diagnosis and Treatment of Nonalcoholic Fatty Liver Disease in Children: Recommendations from the Expert Committee on NAFLD (ECON) and the North American Society of Pediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN). Journal of pediatric gastroenterology and nutrition, 64(2), 319–334. https://doi.org/10.1097/MPG.0000000000001482
Golabi P, Paik J, Hwang JP, Wang S, Lee HM, Younossi ZM. Prevalence and outcomes of non-alcoholic fatty liver disease (NAFLD) among Asian American adults in the United States. Liver International. 2019;39(4):748–757. doi:10.1111/liv.14038
Chalasani N, Younossi Z, Lavine JE, et al. The diagnosis and management of nonalcoholic fatty liver disease: practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2018;67(1):328–357. doi:10.1002/hep.29367
Brunt EM, Wong VW, Nobili V, et al. Nonalcoholic fatty liver disease. Nature Reviews Disease Primers. 2015;1:15080
Chalasani N, Younossi Z, Lavine JE, et al. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Association for the Study of Liver Diseases, American College of Gastroenterology, and the American Gastroenterological Association. Hepatology. 2012;55(6):2005–2023.
Dietary fat and alcoholic liver disease. Mezey E. Hepatology. 1998 Oct; 28(4):901-5. https://www.ncbi.nlm.nih.gov/pubmed/9755223/
Soft drink consumption linked with fatty liver in the absence of traditional risk factors. Assy N, Nasser G, Kamayse I, Nseir W, Beniashvili Z, Djibre A, Grosovski M. Can J Gastroenterol. 2008 Oct; 22(10):811-6. https://www.ncbi.nlm.nih.gov/pubmed/18925303/
Soft drink consumption is associated with fatty liver disease independent of metabolic syndrome. Abid A, Taha O, Nseir W, Farah R, Grosovski M, Assy N. J Hepatol. 2009 Nov; 51(5):918-24. https://www.ncbi.nlm.nih.gov/pubmed/19765850/
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/
Adverse effects of dietary fructose. Gaby AR. Altern Med Rev. 2005 Dec; 10(4):294-306. https://www.ncbi.nlm.nih.gov/pubmed/16366738/
Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy. Vlassara H, Cai W, Crandall J, Goldberg T, Oberstein R, Dardaine V, Peppa M, Rayfield EJ. Proc Natl Acad Sci U S A. 2002 Nov 26; 99(24):15596-601. https://www.ncbi.nlm.nih.gov/pubmed/12429856/
Effects of dietary fructose on liver steatosis in overfed mule ducks. Davail S, Rideau N, Bernadet MD, André JM, Guy G, Hoo-Paris R. Horm Metab Res. 2005 Jan; 37(1):32-5. https://www.ncbi.nlm.nih.gov/pubmed/15702436/
High dietary fructose induces a hepatic stress response resulting in cholesterol and lipid dysregulation. Kelley GL, Allan G, Azhar S. Endocrinology. 2004 Feb; 145(2):548-55. https://www.ncbi.nlm.nih.gov/pubmed/14576175/
Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Havel PJ. Nutr Rev. 2005 May; 63(5):133-57. https://www.ncbi.nlm.nih.gov/pubmed/15971409/
Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L, Havel PJ. J Clin Invest. 2009 May; 119(5):1322-34. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673878/
De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women. McDevitt RM, Bott SJ, Harding M, Coward WA, Bluck LJ, Prentice AM. Am J Clin Nutr. 2001 Dec; 74(6):737-46. http://ajcn.nutrition.org/content/74/6/737.long
Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. Teff KL, Elliott SS, Tschöp M, Kieffer TJ, Rader D, Heiman M, Townsend RR, Keim NL, D’Alessio D, Havel PJ. J Clin Endocrinol Metab. 2004 Jun; 89(6):2963-72. https://www.ncbi.nlm.nih.gov/pubmed/15181085/
Long term nutritional intake and the risk for non-alcoholic fatty liver disease (NAFLD): a population based study. Zelber-Sagi S, Nitzan-Kaluski D, Goldsmith R, Webb M, Blendis L, Halpern Z, Oren R. J Hepatol. 2007 Nov; 47(5):711-7. https://www.ncbi.nlm.nih.gov/pubmed/17850914/
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. http://circ.ahajournals.org/content/116/5/480.long
The National Institute of Diabetes and Digestive and Kidney Diseases Health Information Center. Symptoms & Causes of NAFLD & NASH. https://www.niddk.nih.gov/health-information/liver-disease/nafld-nash/symptoms-causes
Nseir W, Nassar F, Assy N. Soft drinks consumption and nonalcoholic fatty liver disease. World Journal of Gastroenterology : WJG. 2010;16(21):2579-2588. doi:10.3748/wjg.v16.i21.2579. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880768/
The National Institute of Diabetes and Digestive and Kidney Diseases Health Information Center. Eating, Diet, & Nutrition for NAFLD & NASH. https://www.niddk.nih.gov/health-information/liver-disease/nafld-nash/eating-diet-nutrition
Yki-Järvinen H. Non-alcoholic fatty liver disease as a cause and a consequence of metabolic syndrome. Lancet Diabetes Endocrinol. 2014 Nov;2(11):901-10. doi: 10.1016/S2213-8587(14)70032-4
Francque SM, van der Graaff D, Kwanten WJ. Non-alcoholic fatty liver disease and cardiovascular risk: Pathophysiological mechanisms and implications. J Hepatol. 2016 Aug;65(2):425-43. doi: 10.1016/j.jhep.2016.04.005
Mantovani A, Petracca G, Beatrice G, Csermely A, Tilg H, Byrne CD, Targher G. Non-alcoholic fatty liver disease and increased risk of incident extrahepatic cancers: a meta-analysis of observational cohort studies. Gut. 2021 Mar 8:gutjnl-2021-324191. doi: 10.1136/gutjnl-2021-324191
Targher G, Francque SM. A fatty liver leads to decreased kidney function? J Hepatol. 2017 Dec;67(6):1137-1139. doi: 10.1016/j.jhep.2017.08.018
Dulai, P. S., Singh, S., Patel, J., Soni, M., Prokop, L. J., Younossi, Z., Sebastiani, G., Ekstedt, M., Hagstrom, H., Nasr, P., Stal, P., Wong, V. W., Kechagias, S., Hultcrantz, R., & Loomba, R. (2017). Increased risk of mortality by fibrosis stage in nonalcoholic fatty liver disease: Systematic review and meta-analysis. Hepatology (Baltimore, Md.), 65(5), 1557–1565. https://doi.org/10.1002/hep.29085
Hagström H, Nasr P, Ekstedt M, Hammar U, Stål P, Hultcrantz R, Kechagias S. Fibrosis stage but not NASH predicts mortality and time to development of severe liver disease in biopsy-proven NAFLD. J Hepatol. 2017 Dec;67(6):1265-1273. doi: 10.1016/j.jhep.2017.07.027
The National Institute of Diabetes and Digestive and Kidney Diseases Health Information Center. Treatment for NAFLD & NASH. https://www.niddk.nih.gov/health-information/liver-disease/nafld-nash/treatment
Ahmed A, Wong RJ, Harrison SA. NAFLD review: diagnosis, treatment and outcomes. Clinical Gastroenterology and Hepatology. 2015;13(12):2062–2070.
Asrih M, Jornayvaz FR. Diets and nonalcoholic fatty liver disease: the good and the bad. Clin Nutr. 2014 Apr;33(2):186-90. doi: 10.1016/j.clnu.2013.11.003
U.S. National Library of Medicine. Liver Transplantation. https://medlineplus.gov/livertransplantation.html
Charlton MR, Burns JM, Pedersen RA, Watt KD, Heimbach JK, Dierkhising RA. Frequency and outcomes of liver transplantation for nonalcoholic steatohepatitis in the United States. Gastroenterology. 2011 Oct;141(4):1249-53. doi: 10.1053/j.gastro.2011.06.061
Tandon P, Ney M, Irwin I, Ma MM, Gramlich L, Bain VG, Esfandiari N, Baracos V, Montano-Loza AJ, Myers RP. Severe muscle depletion in patients on the liver transplant wait list: its prevalence and independent prognostic value. Liver Transpl. 2012 Oct;18(10):1209-16. doi: 10.1002/lt.23495
Hakeem AR, Cockbain AJ, Raza SS, Pollard SG, Toogood GJ, Attia MA, Ahmad N, Hidalgo EL, Prasad KR, Menon KV. Increased morbidity in overweight and obese liver transplant recipients: a single-center experience of 1325 patients from the United Kingdom. Liver Transpl. 2013 May;19(5):551-62. doi: 10.1002/lt.23618
Schauer, P. R., Bhatt, D. L., Kirwan, J. P., Wolski, K., Brethauer, S. A., Navaneethan, S. D., Aminian, A., Pothier, C. E., Kim, E. S., Nissen, S. E., Kashyap, S. R., & STAMPEDE Investigators (2014). Bariatric surgery versus intensive medical therapy for diabetes–3-year outcomes. The New England journal of medicine, 370(21), 2002–2013. https://doi.org/10.1056/NEJMoa1401329
Mathurin P, Hollebecque A, Arnalsteen L, Buob D, Leteurtre E, Caiazzo R, Pigeyre M, Verkindt H, Dharancy S, Louvet A, Romon M, Pattou F. Prospective study of the long-term effects of bariatric surgery on liver injury in patients without advanced disease. Gastroenterology. 2009 Aug;137(2):532-40. doi: 10.1053/j.gastro.2009.04.052
Lassailly G, Caiazzo R, Buob D, Pigeyre M, Verkindt H, Labreuche J, Raverdy V, Leteurtre E, Dharancy S, Louvet A, Romon M, Duhamel A, Pattou F, Mathurin P. Bariatric Surgery Reduces Features of Nonalcoholic Steatohepatitis in Morbidly Obese Patients. Gastroenterology. 2015 Aug;149(2):379-88; quiz e15-6. doi: 10.1053/j.gastro.2015.04.014
Bower G, Toma T, Harling L, Jiao LR, Efthimiou E, Darzi A, Athanasiou T, Ashrafian H. Bariatric Surgery and Non-Alcoholic Fatty Liver Disease: a Systematic Review of Liver Biochemistry and Histology. Obes Surg. 2015 Dec;25(12):2280-9. doi: 10.1007/s11695-015-1691-x
U.S. National Library of Medicine. Medline Plus. Alcoholic liver disease. https://medlineplus.gov/ency/article/000281.htm

What is a fatty liver disease ?

What is a fatty liver disease

Fatty liver of pregnancy

Fatty liver symptoms

Causes of fatty liver

Fatty liver prevention

Fatty liver disease complications

Fatty liver diagnosis

Blood tests

Imaging procedures

Liver biopsy

Fatty liver treatment

What food should I eat for healthy liver function?

Nonalcoholic fatty liver disease

Stages of non-alcoholic fatty liver disease

Who gets nonalcoholic fatty liver disease?

Causes of non-alcoholic fatty liver disease (NAFLD)

Table 1. Calories and sugar content in different soft drinks

Causes of Nonalcoholic steatohepatitis (NASH)

Less common causes of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis (NASH)

How you can prevent nonalcoholic fatty liver disease and NASH

Signs and symptoms of nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease complications

What tests do doctors use to diagnose nonalcoholic fatty liver disease and NASH ?

What are the treatments for fatty liver disease?

What are some lifestyle changes that can help with fatty liver disease?

Medicines

How do doctors treat the complications of NASH?

What is a liver transplant?

Bariatric surgery (weight loss surgery)

What is alcoholic liver disease?

Causes of alcoholic liver disease

What factors increase your risk for alcohol-related liver disease ?

There are three main types of alcohol-related liver disease:

Fatty liver

Alcoholic hepatitis

Cirrhosis

How does alcohol-related liver disease progress ?

Symptoms of alcoholic liver disease

Alcoholic liver disease diagnosis

Treatment of alcoholic liver disease

Outlook (Prognosis) for alcoholic liver disease

Possible Complications of alcoholic liver disease

The author Health Jade Team

you might also like