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Fatty Liver Add YEARS to your LIFE & LIFE to your YEARS!

Symptoms that may point toward fatty liver disease include:

  • Being overweight, especially around the abdomen
  • Pain and tenderness near the liver
  • Elevated liver enzymes (blood test)
  • Possible gall stones
  • High Cholesterol and/or blood triglycerides (blood test)
  • Difficulty losing weight. If you are having a difficult time taking off pounds, it may be because your fatty liver has reverted tostoring fat instead ofmetabolizing it.
  • A weakened immune system. This can open one up to a number of autoimmune and other harmful conditions.
  • Chronic fatigue. When the liver is not able to rid the body of excess fat and other waste products, one will likely feel sluggish most of the time.
  • Greater risk for diabetes. Fatty liver can result in insulin resistance, a key factor in diabetes. A recent study estimated that about 70% of individuals diagnosed with type-2 diabetes may also have fatty liver disease.
  • Syndrome X. Also known as Metabolic Syndrome X, this condition can also be a complication of fatty liver. Syndrome X involves a number of factors including abnormally high blood pressure and/or insulin levels, too much cholesterol, and excess body fat around the waistline. Metabolic Syndrome increases risk for diabetes, stroke, and cardiac disease.

Use this Natural Liver Detox 2 OZ daily for a week every 4 months to detox your liver & Gallbladder from TOXINS!

24 oz /700 ml apple cider vinegar (always use organic)
cup finely chopped garlic
cup finely chopped onion
2 fresh peppers, the hottest you can find (be careful with the cleaning wear gloves!!!)
cup grated ginger
2 tbsp grated horseradish
2 tbsp turmeric powder or 2 pieces of turmeric root

Scientists know that fat buildup in the liver is more common in people who are overweight, have type 2 diabetes, or drink excessive amounts of alcohol. But beyond that, not much about fatty liver disease is well understood. Does the diabetes or fatty liver come first? Do certain genes predispose people to fatty liver disease? How can the disease be detected early and treated? Do other diseases contribute to fat in the liver?

The pathogenesis of nonalcoholic fatty liver disease is not fully understood. One of the leading theories involves insulin resistance as a key mechanism leading to hepatic steatosis and perhaps also steatohepatitis. Another theory postulates that NAFLD is caused by oxidative stress secondary to steatohepatitis. Hepatic iron, leptin, antioxidant deficiencies,14 and intestinal bacterial have all been noted to be part of the pathogenesis of NAFLD.

Most individuals with NAFLD are asymptomatic, although some with NASH may complain of vague right upper abdominal discomfort, fatigue, and/or malaise.16 In clinical reality, NAFLD typically comes to the attention of the healthcare practitioner because laboratory testing reveals elevated liver aminotransferases. On physical exam, some patients may have hepatomegaly due to the fatty infiltration.7 Hepatic steatosis can also be detected incidentally on abdominal imaging.

Numerous therapies have been investigated for the NAFLD treatment. Weight loss is the only therapy with reasonable evidence suggesting it is beneficial and safe, although emerging data supports nutritional interventions. Conventionally, the following strategies are typically employed:
Weight loss for patients who are overweight or obese;
Hepatitis A and B vaccinations, except in those with serologic evidence of immunity21;
Treatment of risk factors for cardiovascular disease; and
Abstention from alcohol.

Pharmacological agents, such as pioglitazone, are not recommended. Numerous other drugs have been examined for the treatment of NASH. While some have shown initial promise, none have been sufficiently studied.

I have routinely screened my patients with high normal GGT levels, in isolation or in conjunction with high normal or elevated AST and/or ALT levels, with a liver ultrasound and have frequently seen evidence of NAFLD on the radiology report.

This is where nutritional and nutraceutical therapies have an enormous role to play. A diet rich in organic fruits and vegetables (the more varied the colors, the better) and avoidance of refined, processed, and charred foods are beneficial. I also recommend that my patients avoid trans fats and saturated fats,23 along with nitrates/nitrates and high fructose corn syrup. I recommend that they consume green tea, fresh fish, and liver-supportive foods. (Note of caution in regards to fish: Be aware of the mercury and other contaminants present in some fresh fish. The US Environmental Protection Agency is an excellent resource on safe fish consumption.) Liver-supportive foods include high sulfur foods like garlic and onions, as well as cruciferous vegetables28-30 like Brussels sprouts, cabbage, cauliflower, and broccoli. Other nutritious liver-supportive foods include artichokes, turmeric, beets, and green tea.

The following nutrients have shown the greatest clinical efficacy in addressing and even reversing the spectrum of NAFLD. In my practice, I have seen positive results in as little as 3 months, but typically it takes 9 to 12 months to see the most restoration and reversal of NAFLD.
Tocotrienols: 200 mg twice daily with food.34 Gamma-tocotrienol, but not alpha-tocopherol, attenuates triglycerides accumulation by regulating fatty acid synthase and carnitine palmitoyltransferase enzymes, leading to a reduction of hepatic inflammation and endoplasmic reticulum stress.
N-acetyl-cysteine (NAC): 600 mg twice daily, best taken on an empty stomach. NAC blocks the propagation of lipid peroxidation.

Avoid taking NSAID like Acetaminophen [Tylenol], ASA and Advil. Taking just 25 percent more of these drugs than the daily recommended dose the equivalent of just two extra strength pills per day can cause liver damage after just a couple of weeks of daily use.

When taken all at once, just under four times the maximum daily dose can be lethal! Previous research has also shown that taking just a little more than the recommended dose over the course of several days or weeks (referred to as staggered overdosing can be more risky than taking one large overdose.

In 2009, the FDA finally added a warning to acetaminophen containing drugs alerting consumers to its potential for causing liver damage. Using Tumeric, Ashwaganda and ginger is much safer natural anti inflammatory that will detox your liver.

The reason obesity might accelerate aging in your liver could have to do with an underlying cause of both weight gain and liver damage: fructose. You may already be aware that fructose, the sugar found in everything from high fructose corn syrup and fruit juice to agave syrup and honey, is harmful when consumed in excess.

This is precisely what most Americans do. However, you may be surprised to learn that fructose is, in many ways, very similar to alcohol in the damage that it can do to your body.

Foods that Detox Liver & Gallbladder:

1. Garlic

Just a small amount of this pungent white bulb has the ability to activate liver enzymes that help your body flush out toxins. Garlic also holds high amounts of allicin and selenium, two natural compounds that aid in liver cleansing.

2. Grapefruit

High in both vitamin C and antioxidants, grapefruit increases the natural cleansing processes of the liver. A small glass of freshly-squeezed grapefruit juice will help boost production of the liver detoxification enzymes that help flush out carcinogens and other toxins.

3. Beets and Carrots

Both are extremely high in plant flavonoids and beta-carotene; eating beets and carrots can help stimulate and improve overall liver function.

4. Green Tea

This liver loving beverage is full of plant antioxidants known as catechins, a compound known to assist liver function. Green tea is not only delicious, it is also a great way to improve your overall diet. Learn more about the benefits of green tea.

5. Leafy Green Vegetables

Leafy Greens
One of our most powerful allies in cleansing the liver, leafy greens can be eaten raw, cooked, or juiced. Extremely high in plant chlorophylls, greens suck up environmental toxins from the blood stream. With their distinct ability to neutralize heavy metals, chemicals and pesticides, these cleansing foods offer a powerful protective mechanism for the liver.

Try incorporating leafy greens such as bitter gourd, arugula, dandelion greens, spinach, mustard greens, and chicory into your diet. This will help increase the creation and flow of bile, the substance that removes waste from the organs and blood.

6. Avocados

This nutrient-dense super-food helps the body produce glutathione, a compound that is necessary for the liver to cleanse harmful toxins.

7. Apples

High in pectin, apples hold the chemical constituents necessary for the body to cleanse and release toxins from the digestive tract. This, in turn, makes it easier for the liver to handle the toxic load during the cleansing process.

8. Olive Oil

Cold-pressed organic oils such as olive, hemp and flax-seed are great for the liver, when used in moderation. They help the body by providing a lipid base that can suck up harmful toxins in the body. In this way, it takes some of the burden off the liver in terms of the toxic overload many of us suffer from.

9. Alternative Grains

You need alternative grains like quinoa, millet, and buckwheat in your diet.Your liver is your body filter for toxins, and grains that contain gluten are full of them. A study last year found that persons who experienced gluten sensitivities also had abnormal liver enzyme test results, and that is just one of many.

10. Cruciferous Vegetables

Eating broccoli and cauliflower will increase the amount of glucosinolate in your system, adding to enzyme production in the liver. These natural enzymes help flush out carcinogens, and other toxins, out of our body which may significantly lower risks associated with cancer.

11. Lemons & Limes

Lemons and Limes
These citrus fruits contain very high amounts of vitamin C, which aids the body in synthesizing toxic materials into substances that can be absorbed by water. Drinking freshly-squeezed lemon or lime juice in the morning helps stimulate the liver.

12. Walnuts

Holding high amounts of the amino acid arginine, walnuts aid the liver in detoxifying ammonia. Walnuts are also high in glutathione and omega-3 fatty acids, which support normal liver cleansing actions. Make sure you chew the nuts well (until they are liquefied) before swallowing.

13. Cabbage

Much like broccoli and cauliflower, eating cabbage helps stimulate the activation of two crucial liver detoxifying enzymes that help flush out toxins. Try eating more kimchi, coleslaw, cabbage soup and sauerkraut.

14. Turmeric

The liver favorite spice. Try adding some of this detoxifying goodness into your next lentil stew or veggie dish for an instant liver pick-me-up. Turmeric helps boost liver detox, by assisting enzymes that actively flush out dietary carcinogens.

15. Garcinia cambogia

The fruit of the Garcinia Cambogia plant is a small, green pumpkin and is used in many traditional Asian dishes for its sour flavor. The skin, or rind of the fruit contains a large amount of Hydroxycitric Acid (HCA), which is the active ingredient that has been known to aid with weight loss. Only buy Garcina Cambogia that has at least 60% HCA.

May aid in the reduction of fat cells forming*
May aid in increased weight loss*
May increase energy levels*
May help with fatty liver and uterine fibroids.

If you suspect you have fatty liver, ask your physician to do liver function test and complete the wellness IQ and this wellness assessment form to identify the cause for your fatty liver.
Health Assessment Form

Fatty Liver is More Dangerous than You Might Realize.

My doctor says I have a fatty liver and I should stay away from fat, writes this week house call. Are high-fat foods the culprit here? Any tips to help with a fatty liver?

Indeed, your doctor is right to feel concern: Fatty liver is a dangerous yet misunderstood disease. In America, it affects 90 million of us and 17 percent of our children.

Think about foie gras, the French delicacy made from duck or goose liver. It is made by force-feeding the animals a combination of sugar with corn and starch (a really sad, horrible practice), intentionally creating a fatty liver. Click here to read more.

Wishing you health and happiness,
Mark Hyman, MD

Nonalcoholic fatty liver is considered as a well-known disease which is catched by without using alcohol. There is high prevalence of nonalcoholic fatty liver in the community and this condition potentially can progress to hepatic cirrhosis and hepatic defect (1-3). In developed country, it is estimated that 20% to 30% of adult populations are developed to nonalcoholic fatty liver (4-8). 50% of diabetic people and approximately 80% of obese people with morbidity obesity are developed to nonalcoholic fatty liver (6-9-10). To prevalence of nonalcoholic fatty liver in western countries is likely concurrent with epidemic obesity and also it is associated with metabolic disorders (5-11-14). Patients with nonalcoholic fatty liver usually have insulin resistance (14-19). The prevalence of nonalcoholic fatty liver has been increased in individuals who have normal body mass index (BMI). However, these people have central obesity and latent insulin resistance (17-18-20-21). In epidemiologic studies, these patients with suitable weight have unhealthy diet (22-24).
The effectiveness and immunity of medication therapy is unclear in treatment of nonalcoholic fatty liver (25). Obesity has the most correlation to nonalcoholic fatty liver (26). Therefore, to modify the lifestyle is the first line treatment for nonalcoholic fatty liver. Managing the nonalcoholic fatty liver includes the gradually decreasing the weight and increasing the physical activity (27-33).
Studies did not determine which material or micronutrient in the diets potentially increases the risk of developing to nonalcoholic fatty liver; however, it is obvious that keeping the low weight will be difficult in long term (34). To change the diet composition without decreasing the rate of calorie will be a practical and realistic variation for treatment of nonalcoholic fatty liver. Therefore, it is very important to evaluate the relationship between particular micronutrients and compounds of diet to nonalcoholic fatty liver.
This review study has been performed on epidemiological studies which evaluated the relationship between nonalcoholic fatty liver to diet compounds, weight loss, and physical activity.

Three main sources are available for increasing the TG (triglyceride) concentration in liver. These sources include increased inflow of free fatty acids from internal tissues to liver, increased intra-hepatic lipogenesis and increased received of fatty diet. The recent human studies suggested that high amount of fat in diet is removed by liver (35-36). Therefore, postprandial high changes in the rate of fat metabolism may be observed in patients with nonalcoholic fatty liver. In a study on 15 patients with nonalcoholic fatty liver and 15 healthy people, the total rate of TG and VLDL (very low density lipoprotein) was higher in individuals with nonalcoholic fatty liver after receiving the single oral fat. The rate of ApoB48 and ApoB100 did not change after receiving fat by patients with nonalcoholic fatty liver. These findings suggested that increased removing of TG in the postprandial period was associated with decreased secretion of VLDL which in turn increases the rate of hepatic steatosis (37). The relationship between total fat of diet and the content of liver fat has been studied directly in the human studies. In a cross-sectional study, 10 obese women received two types of diets with the equal rate of calories during two weeks. The rate of fat in one diet was 16% and it was 56% in the other one. The rate of fatty liver was measured by spectroscopy. The rate of liver content was decreased up to 20% by using of low fat diet; however, it is increased up to 35% by using of high fat diet. The rate of changes in fatty liver was concurrent to changes in the rate of fasting plasma insulin. These changes are considered very important because people did not change their weight during the study (36). In the other study, the bariatric surgery was performed on 74 patients with morbidity obesity (90% developed to nonalcoholic fatty liver). The diet of these patients was evaluated through a 24-hours recall. The rate of consuming the meals was compared to liver histological data. There was not any meaningful correlation between the rates of received calorie or proteins to steatosis, fibrosis and hepatitis. Nevertheless, taking the high carbohydrate (approximately 56%) had significantly correlation to the rate of inflammation. However, the rate of taking the fat had reverse correlation to the rate of inflammation. The findings of this study determine neither the correlation between each kind of dietary fats to nonalcoholic fatty liver nor the correlation between each kind of simple or complex carbohydrate to the rate of inflammation and histological findings in the patients with nonalcoholic fatty liver (41). The correlation between carbohydrate and nonalcoholic fatty liver was evaluated in one study. The diet of 28 patients with nonalcoholic steatohepatitis was compared to 18 patients with simple steatosis. This study determined that receiving carbohydrate in group with nonalcoholic steatohepatitis was much more than the other group. Especially, the rate of taking simple carbohydrate was higher in the group with nonalcoholic steatohepatitis.
It is reasonable that fat and carbohydrate should be used according to recommendable rates (according to the recommendations of the American Heart Institute). Therefore, it is emphasized that the components of fat and the kind of carbohydrates (simple and complex) should be changed in the diet of patients with nonalcoholic fatty liver.
The type of the fat in the diet and other micronutrients:
Contrary to metabolic and cardiovascular diseases, there are sparse epidemiologic studies that evaluate the correlation between the types of fat in diet to the rate of fatty liver (5). One study has been performed with low number of samples but the diet was evaluated accurately (based on 7 days of recording the food intake). 25 patients with nonalcoholic steatohepatitis were compared to the control group in terms of their diets. The diet of patients with nonalcoholic fatty liver was rich of saturated fat and cholesterol, but the content of PUFA (poly unsaturated fatty acid), fiber, ascorbic acid and tocopherol were very low in their diet (37). The results of this study were supported by the other study and ratio of the receiving the unsaturated fatty acid to saturated fatty acid in the both groups of nonalcoholic steatohepatitis and fatty liver were lower than control group (42). The relationship between the kind of fat in the diet to the oxidative stress markers was evaluated in patients with nonalcoholic fatty liver. Diet analysis has been done by using of Food frequency Questionnaire in 43 people with nonalcoholic steatohepatitis and 33 healthy people. There was negative relationship between saturated fat and total received fat to the ratio of glutathione with oxidized glutathione of plasma to fiber, carbohydrate, MUFA and PUFA (45-46).
Several kinds of fats can have protective effect on nonalcoholic fatty liver. It is proved that omega 3 improves nonalcoholic fatty liver. The lab studies demonstrated that the diet rich of omega 3 increased the insulin sensitivity in rats (44). In addition, it decreases the rate of intrahepatic TG and also it improves steatohepatitis (45-46).
Two observational studies determined that the rate of omega 3 consumption is low in patients with nonalcoholic fatty liver. In the first study which was performed as case-control study, 45 patients with nonalcoholic fatty liver were adjusted to 856 people in control group in the terms of age and sex (45). The history of diet was evaluated through FFQ. The results of study demonstrated that intake of omega 6 and the ratio of omega 6 to omega 3 was higher in the patients with nonalcoholic fatty liver. These results suggested that the quality and quantity of the received fat is more likely higher than the rate of calorie in patients with nonalcoholic fatty liver.
The second cross-sectional study was performed on 349 volunteers. The history of diet was assessed by FFQ. The results of the study indicated that the patients with nonalcoholic fatty liver consumed more red meat and less fish (rich of omega 3). The red meat is rich of omega 6 in the terms of fatty acid. Therefore, data suggested that receiving higher red meat increases the ratio of omega 6 to omega 3 in patients with nonalcoholic fatty liver (47). Two clinical trials suggested the protective role of omega 3 in patients with nonalcoholic fatty liver. The first study as nonrandomized controlled study evaluated the effect of receiving one year complementary dose of 1000 mg/day omega 3 (EPA, DHA) by 42 patients with nonalcoholic fatty liver compared to 14 people as control group. PUFA supplement significantly improved the serum enzymes (ALT, AST, and GGT) and it decreased the rate of fat in liver (48). The second non-control clinical trial was performed on 23 patients with nonalcoholic fatty liver. These patients received 2700 mg EPA/per day for one year. The level of serum ALT has been improved meaningfully. 7 subjects were under hepatic biopsy after treatment. The sampling demonstrated that the rate of inflammation, steatosis and fibrosis has been improved (49). In the both clinical trials, the body weight did not change.
There are sparse studies about the relationship between trans-fatty acids and MUFA to nonalcoholic fatty liver. So, further investigations should be performed on fatty liver and trans-fatty acids as well as MUFA.
Trans- fatty acids:
The quantitative studies have been performed for the role of trans-fatty acids in the development of the nonalcoholic fatty liver. To consume the trans-fatty acids increases the risk of developing to insulin resistance and cardiovascular diseases.
In a study which was performed on Syria rats, one group was given PUFA and the other group was given trans-fatty acids. A group who received trans-fatty acids developed to impaired glucose tolerance. In addition, the rate of insulin resistance has been increased in these rats (52). In one study, the effect of western lifestyle was tested on Syria rats. The rate of liver steatosis significantly increased in rats which were received trans-fatty acids associated with beverages rich of fructose (53). Therefore, the role of trans-fatty acids should be evaluated in progress of the nonalcoholic fatty liver.
Oleic acid is consumed as the main source of MUFA in the diet. Olive oil is the most important source of oleic acid (other sources are avocado and seeds). MUFA decreases the blood lipid indices, and it reduces the ratio of LDL and total cholesterol to HDL as well.
In one meta-analysis study, the effect of various diets on lipid and glycemic indices has been evaluated. The result of this meta-analysis indicated that diets rich of monounsaturated fatty acids decreases TG concentration and blood cholesterol 19% and 22%, respectively. Also, it increases the rate of HDL but it does not affect LDL (55).
In one study, rats received the MCD diet (lack of colin and methionine) associated with monounsaturated fatty acids. Olive oil decreased the rate of TG concentration in liver up to 30% compared to the other rats that received only MCD diet. Olive oil improves the rate of insulin resistance, increases the rate of hepatic secretion of TG, and decreases the TG flow from the peripheral organs to liver (56). The rate of hepatosteatosis was improved in the rats that received olive oil associated with balanced diet (57). Contrary to polyunsaturated oil, olive oil prevents progression of hepatic fibrosis (58). Nevertheless, it is unclear whether the patients with nonalcoholic fatty liver have received olive oil or MUFA less than healthy people. The role of MUFA in development or improvement of nonalcoholic fatty liver is not fully understood.
The observational studies for cholesterol indicated controversial results. Some studies concluded that there is not any difference between the rate of intake cholesterol in patients with nonalcoholic fatty liver and control group (47-59). Nevertheless, Moso et al. in a study showed that people with nonalcoholic fatty liver intake higher cholesterol. Also, a recent study advocated the role of cholesterol of diet in the development of nonalcoholic fatty liver. In this study, 12 subjects with normal weight who developed to nonalcoholic fatty liver were compared to 44 obese subjects with nonalcoholic fatty liver. It should be considered that the rate of intake cholesterol in first group was very higher than second group; however, the rate of intake unsaturated fatty acids was very lower in first group. Therefore, this difference in consuming the cholesterol and PUFA likely is associated with progress of nonalcoholic fatty liver in people with normal weight (24). In one study on the non-obese animal models, it was showed that diet rich of cholesterol causes nonalcoholic fatty liver (60). Increased cholesterol in diet results in increasing the synthesis of fatty acids in hepatic cells (24). Eventually, further investigations are required to determine the effect of various diets with different fats and the effect of these fats on progression or improvement of nonalcoholic fatty liver.
The relationship between sweetened beverages and nonalcoholic fatty liver:
The sweetened beverages have increased the sugar consumption throughout the world (61). In the recent decades, to consume the sweetened beverages has elevated in the world (62). The recent studies (2005-2006) demonstrated that children and adults intake 172 and 175 Kcal/day, respectively due to drinking the sweetened beverages (63). To consume the sweetened beverages is associated with the risk of developing to obesity, diabetes, metabolic syndrome, fatty liver, and related cardiac diseases result from increased intake of calorie as well as very rapid absorption of the available sugar in these beverages (59.64.69).
The diets rich of sucrose increase the TG synthesis in the liver. It is evident that the rats and human who intake diet rich of fructose and sucrose are developed to fatty liver. Therefore, it is reasonable the patients with nonalcoholic fatty liver to use lower fructose (71). In addition, the sweetened beverages such as cola have caramel dye and they are rich of AGES (advanced glycation end products). These compounds increase the insulin and inflammation resistance (61). In the recent years, some studies confirmed the relationship between nonalcoholic fatty liver and consumption of sweetened beverages (22-59-72-73). In a study, 31 people with normal weight that developed to nonalcoholic fatty liver were compared to 30 healthy subjects. The patients with nonalcoholic fatty liver significantly consumed sweetened beverages (43% more) and juices (8% more) (22). In the other study, patients with nonalcoholic fatty liver were compared to control group. The patients with fatty liver received sweetened beverages twofold than control group (72).
In one study after adjusting for age, sex and calorie intake on 427 participants with nonalcoholic fatty liver, it was demonstrated that intake the daily fructose meaningfully was associated with hepatic fibrosis (74).
Generally, it should be considered that the sweetened beverages play a significant role in developing to nonalcoholic fatty liver. The physician should ask the patient questions about the history of drinking the sweetened beverages.
The pattern of western diet and fast food
To evaluate the pattern of diet can realistically determine the correlation between fatty liver and components of diet. The meals have different kind of food materials and the compound of food materials can have synergistic effect on each other or they can interfere (75). The investigators consider western diet as diet with higher fructose, sweetened beverages (22. 59. 72), red meat (47, 59), cholesterol, saturated fatty acids (47-59) and lower fiber (47), and vegetables and fruits (23). This diet has direct correlation to development of nonalcoholic fatty liver.
In human, fast food consumption has a direct correlation to increased insulin resistance. In CARDIA study, the results of the prospective study during 15 years on 3031 participants with nonalcoholic fatty liver demonstrated that people who eat more fast food (more than 2 times in week) are overweight (> 4.5 kg) and have insulin resistance twofold than people who eat fast food less than once a week (76). In an animal trial, a diet similar to fast food results in impaired hepatic cells (53). In one study on 18 healthy students, they had received fast food 2 times a day for 4 weeks. The rate of taking energy and weight of these people increased and the rate of insulin resistance became twofold. Also, the rate of serum TG and ALT increased in these people (77). These foods are rich of energy, saturated fatty acids and trans-fatty acids, simple carbohydrates, and fructose, but they have little fiber. As a result, they increase the fatty acids in liver and they produce local inflammation (78).
Weight loss
In the past decades, during the clinical trials three types of diet have been prescribed for reducing the weight of the patient with nonalcoholic fatty liver. The first diet is very low calorie diet (VLCD) that significantly decreases the weight. The second diet in clinical trials is the balanced diet associated with physical activity and behavior therapy. The third diet is associated with the lifestyle modification.
The examples from first diet includes the number of clinical trials in decades of 1970 and 1960 (79-80), a low calorie diet (1500 Kcal) and/or fasting that significantly decreased weight. Steatosis had been decreased in all patients; however, it damaged liver, increased the hepatic necrosis and fibrosis in people with abruptly decreased weight.
In one study which was performed by Anderson et al. in 1991, 41 subjects with mortality obesity received a diet associated with formula including 400 Kcal. The rate of steatosis was improved but it increased 24% inflammation in hepatic duct and increased hepatic fibrosis (81). In the other study, VLCD diet with more low weight or equal to 10% normalized hepatic enzymes (82). Two studies with small sample evaluated the effect of a standard diet associated with graduate decreasing weight on histology of liver (83). In a study, after three months treatment there was significantly improvement in the rate of steatosis as well as hepatic inflammation and fibrosis.
In a study on 15 participants with fatty liver, these persons received a standard diet along with behavior therapy. The weight of 9 subjects among 15 reduced up to 7% and as a result it improved the rate of nonalcoholic fatty liver; however, in 6 subjects the weight and also the rate of fat concentration in liver did not change (84).
In the other study, 32 patients with nonalcoholic fatty liver divided to two groups randomly. One group only received education about lifestyle modification (control group) and the other group received a weight loss diet and physical activity (case group). The rate of steatosis in the case group significantly improved than control group. The participants with more than 7% weight loss demonstrated meaningfully improvement in the rate of steatosis and hepatic duct inflammation.
In a clinical trial, Erlistat was used for decreasing the weight in patients with nonalcoholic fatty liver, and 9% weight loss imporved steatosis in these patients (86). In the other study, the lifestyle of participants with nonalcoholic fatty liver and diabetes type II was modified. These patients were given a weight loss diet associated with increased physical activity for 12 months. The control group received some recommendations about improved nutrition and physical activity. After 12 months the case group had more weight loss (approximately 8.5%) than control group and the rate of hepatic steatosis was improved (87).
In a clinical trial by Suzuki et al., 348 participants with increased ALT received a instructional brochure for weight loss diet. After three months, these persons were evaluated. The rate of serum ALT improved in subjects with more than 5% weight loss, and also the rate of serum ALT in 136 subjects reached to normal rate (89). In a clinical trial, 152 participants with increased liver enzymes divided to two groups randomly. One group had more lifestyle modification but the other group had less one (nutrition and physical activity). At the end of the study, the rate of reduction in the hepatic enzymes was higher in the group with more modification in the lifestyle than other group (88). 67 individuals with fatty liver participated in a study. Once a month, they were visited by practitioner and also once every three months they were consulted by nutritionist. In addition, they had equal lifestyle modification (increased physical activity and they received a weight loss diet). At the end of six months, the interference of hepatic enzymes and the ratio of liver to spleen improved in these people (90). Determining the therapeutic effect of weight loss in the clinical trial has two restrictions as follow: the first restriction is due to the little number of samples in the study and the second one is to determine the effect of weight loss on liver histology because liver biopsy is performed in the studies due to ethical considerations. The liver biopsy is essential for evaluating the effect of weight loss on hepatic steatosis. This is important because some diets apparently decrease the hepatic enzymes, but they cause damage of liver. The noninvasive methods should be used for evaluating the histological features of liver and they determine the real effect of weight loss on liver. Nevertheless, in the reviewed studies the weight loss improved the liver function. Weight loss has been confirmed as therapeutic method.
Physical activity
Higher physical activity is beneficial for people. It decreases the risk of developing to diabetes type II, insulin resistance, blood pressure, dyslipidemia, impaired glucose tolerance and metabolic syndrome (91-95). The studies demonstrated that physical activity play key role in treatment of patients with nonalcoholic fatty liver. Several observational studies showed that there is reverse correlation between prevalence of fatty liver to the time of physical activity. In one study with more samples (349), individuals with fatty liver spent less time for physical activity (aerobic and resistance exercises) (95). In the other study with 218 participants, there was reverse correlation between physical fitness and developing to fatty liver (97). In one study on 37 persons with nonalcoholic fatty liver, hepatic biopsy demonstrated that patients with lower physical activity had higher steatosis in liver (98). The useful effects of physical activity have been supported by recent clinical trials. In a clinical trial on 141 participants with nonalcoholic fatty liver, the subjects were given instruction for physical activity during 3 months. After three months, the weight of persons with physical activity> 60 minuets/week significantly decreased (mean 2.4 kg), and also their insulin resistance and hepatic enzymes reduced (99). In the other clinical trial, the aerobic physical activity along with a low energy diet helped to normalizing the level of hepatic enzymes (100). Therefore, it is appear that increased physical activity improves the level of hepatic enzymes. In a clinical trial on 19 subjects with obesity, the short time effect of aerobic physical activity on liver, blood, visceral fats and muscular lipid was evaluated by using of MRI. Cycling for four weeks (three sessions per week for 30 to 45 minutes) meaningfully decreased the rate of plasma TG up to 4%, the rate of visceral fats up to 12%, and the rate of hepatic TG up to 21%. It should be considered that these changes were produced without weight loss (101). For three months, a study has been done on 12 obese subjects with fatty liver. They received the resistance exercise program including two one-hour sessions per week. The physical activity increased the strength and muscularity in participants. Although the rate of fatty liver did not change, but the rate of insulin resistance was increased without weight loss (103). The more physical activity causes weight loss and it likely results in increased insulin resistance and glucose homeostasis (104). Physical activity increases insulin receptors in muscles. As a result, the rate of glucose inflow into the muscles is elevated (105). Also, physical activity has beneficial effect on fatty acids oxidation by increasing the rate of oxidation (106). TG concentration will be decreased by higher physical activity (107). The rate of removal of free fatty acids in plasma is decreased in athletes than non- athletes people (108). The similar findings in monozygote twins defined that increased physical activity in one of them (due to the lack of genetic impairment effect) decreases the fatty acids removal by liver (106). In the recent years, there is great attention to resistance exercises for increasing the physical activity (109-110). A study demonstrated that resistance exercises significantly reduce the rate of visceral fat and also it increases the lipid indices (112). A randomized clinical trial showed the effect of aerobic and resistance exercises on cardiovascular diseases. Resistance exercises not only increase the rate of lean body mass but also decrease the rate of total fat of body (113). In one meta-analysis study, the aerobic and resistance exercises were compared and the resistance exercise increased the lean body mass than aerobic one (114). Increased the volume of muscle through increasing the area of reserving glucose reduces the required insulin for normalizing the level of glucose (115). The US Centers of Prevention and Control of Diseases recommend that healthy people do more than 30 minutes moderate to severe activity, all days per week, and also they should do resistance exercises more than 3 times a week for > 20 minutes in each session. However, these instructions extensively have been recommended, only 27.7% American adults do the moderate to vigorous physical activity and 29.2% do not have any regular activity (116-117). In addition, the prevalence of physical activity in adults with diabetes is very less than non-diabetic people (118). People with diabetes less likely perform the recommendations related to physical activity (119). In one study, the time of sedentary life of persons was measured. The sedentary time had direct correlation to the rate of fasting insulin (121). Environmental factors such as driving by car instead of walking, sedentary activity and watching TV reduce physical activity (122).
Dietary supplements
Vitamin E
Vitamin therapy with high dose vitamin E supplement as 1000-300 IU/day (recommended as approximately 30 IU/daily) has been associated with conflict results. In the uncontrolled clinical trials, receiving the vitamin E was associated with reduced hepatic enzymes (133); however, simultaneously using of vitamin E, lifestyle modification, diet and physical activity in controlled trials did not show the therapeutic effects of vitamin E (124-125). In randomized clinical trial, 247 patients with nonalcoholic fatty liver randomly divided to three groups: the first group was given 30mg/day pigolitazone, the second group was given 800 IU/day vitamin E, and the third group received placebo. The duration of this study was 2 years. There was significantly improvement in nonalcoholic fatty liver by Vitamin E therapy compare to placebo. Vitamin E and pigolitazone reduced ALT, AST and the rate of steatosis than placebo, but the rate of hepatic fibrosis did not change (126). Nevertheless, some clinical trials demonstrated that using high dose vitamin E causes stroke and death due to different reasons (127-128).
Vitamin D
Many studies have suggested than vitamin D potentially play key role in decreasing the development of diabetes type 2, hypertension, and cardiovascular diseases (129-131). The level of vitamin D of serum independently is related to the beta cells functions and insulin sensitivity in patients with diabetes type II (132). In one study, the level of serum vitamin D was low in patients with nonalcoholic fatty liver (133). In a study, Targer et al. compared 60 patients with nonalcoholic fatty liver 60 healthy individuals in terms of the level of serum vitamin D. the level of serum vitamin D in the group with nonalcoholic fatty liver was very lower than healthy individuals. In patients with nonalcoholic fatty liver, the level of serum vitamin D was related to the level of steatosis, inflammation and hepatic fibrosis (133). In one study, the relationship between vitamin D of serum, fatty liver and cardiac diseases was evaluated. In this study, 670 patients with nonalcoholic fatty liver were compared to 30 healthy individuals. Patients with nonalcoholic fatty liver had very lower level of serum vitamin D than control group (134). Eventually, further investigations are required for evaluating the correlation between the level of serum vitamin D, nonalcoholic fatty liver and the therapeutic effects of serum vitamin D on nonalcoholic fatty liver.
Nonalcoholic fatty liver not only is a chronic hepatic disease but also it predisposed to development of diabetes type II (133-137). Also, in some studies the nonalcoholic fatty liver is related to cardiovascular diseases (138-144). It is important to know the risk factors which result in nonalcoholic fatty liver, because prevention of these risk factors can reduce the risk of nonalcoholic fatty liver. The relationship between nutrition to nonalcoholic fatty liver in human and animal has been confirmed (22, 36, 47, 65, 73, 85, 143). Nevertheless, most observational and retrospective studies have been done in this field. Therefore, the nutritional studies relate to dietary recall have some restrictions such as more or less estimation for taking the food. For removing these restrictions, various recalls should be obtained from patient with nonalcoholic fatty liver. Also, the large prospective studies and more clinical trials shall be performed for determining the correlation between nonalcoholic fatty liver and nutrition. Today, there is not any stable recommendation as therapeutic strategy for patients with nonalcoholic fatty liver (due to the lack of qualified studies about nonalcoholic fatty liver). With regard to the available data, the weight loss more than 5-10% results in the decreased level of steatosis (146). In addition, the healthy nutrition is very important in these diseases. Therefore, these patients should be instructed about the way of healthy nutrition. The patients should be recommended that not only decrease the rate of consumption the trans and saturated fatty acids but also they should increase intake of the poly unsaturated fatty acids, specially omega 3. Patients with nonalcoholic fatty liver should decrease drinking the sweetened beverages and also they should increase consuming the vegetables and fruits rich of fiber. They should reduce to consume the red meat and fast foods; however, eating the fish should be increased. Physical activity should be considered as a part of treatment. Increasing the duration of physical activity causes significantly improvement in nonalcoholic fatty liver (148). The treatment team for patients with this disease should be consisted of dietician, psychology, and expert of physical exercise (150-151) so as to achieve the therapeutic purposes.

Non-Alcoholic Fatty Liver disease (NAFLD). NAFLD causes serious liver problems. It results in painful swelling and scarring that can lead to cirrhosis, liver failure and even death.

I blame our modern food supply for this new epidemic. Industrial foods are drenched in Big Agra’s high-fructose corn syrup. It’s in everything from Oreos to salad dressings to sodas.

That is a disaster. Let me explain

Fructose isn’t like other sugars. Most of it goes straight to your liver instead of going into your muscles and tissues for energy. It promotes the formation of new triglyceride fat molecules. It triggers your liver cells to store this fat where it doesn’t belong. At the same time, it blocks the breakdown of old fats. It stimulates free radical production and promotes insulin resistance. All of that results in inflammation and NAFLD.

You could have NAFLD and not even know it. Up to 30% of Americans do. You see, NAFLD is a sneaky disease. In the early stages, the only signs are some fatigue and maybe a dull pain in the right upper quadrant of your abdomen.

But there is good news. Recently a study in the Journal of the American College of Nutrition reported that coenzyme Q10 (CoQ10) can help treat NAFLD.1

The randomized, double-blind trial included 41 people with mild to moderate NAFLD.Researchers gave half the patients 100 milligrams of CoQ10 every day. The other half got a placebo. After 12 weeks, all of the signs of NAFLD were lower in the CoQ10 group.

In addition, the researchers graded the NAFLD cases by the percentage of liver cells containing fat droplets before and after treatment. No patients had a normal grade at the start of the trial but four patients returned to normal liver function after the CoQ10 treatment. Only one patient on the placebo group returned to normal.

CoQ10 also boosted levels of adiponectin, a protein linked to weight loss, better insulin sensitivity and lower levels of inflammation.

I’m not surprised by these results. I’ve been recommending CoQ10 to my patients for decades for heart health. It’s a powerful antioxidant and anti-inflammatory.

You can get CoQ10 from food, especially beef, sardines, mackerel, peanuts, and organ meats like liver and kidney. But the amounts in food won’t be enough to protect your heart and to stop NAFLD.

And if you’ve been taking Big Pharma’s statin drugs, your levels of CoQ10 are likely to be very low. You see, statins deplete your body’s supply of CoQ10 by about 20 percent.2

That’s why I recommend taking a supplement.

Most CoQ10 supplements you find in the drugstore contain ubiquinone. Your body has to reduce ubiquinone to ubiquinol in order to use it.But as you get older, your body’s ability to make that conversion drops off.

If you’re over 40, you need the ubiquinol form of CoQ10. It may cost you a little more but it’s worth the price. That’s because ubiquinol is FAR more effective. One study found that taking 450 mg of ubiquinol was almost three times as effective as the same dose of CoQ10.3

I recommend taking 100 to 300 milligrams of ubiquinol per day (divided into two doses). Don’t go overboard. Very large doses (1000 mg or more per day) may cause restlessness and insomnia.

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