Extensive build-up of fat in the liver is responsible for a range of diseases including simple steatosis , Non-Alcoholic Fatty Liver Disease (NAFLD), obesity and diabetes, which are now considered to have reached epidemic proportions. How can you know if you are at risk of fatty Liver? By testing the function of your PEMT gene and your diet, see our Dirty Gene Finder™ test below.
Steps to Reversing Fatty Liver
1. Consume lots more organic, non GMO Cruciferous vegetables, increase saturated fats, significantly lower or eliminate carbs. See Mega Greens. Adding more toxic chemicals in the liver will worsening a fatty liver, the capacity for your liver to detoxify is dependent on L-Glutathione (GSH) see LIPO-GSH, which allows your liver to turn poisons into harmless particles (this can detoxify pesticides). This is in garlic, onion, radish and cruciferous vegetables. Selenium is also a co-factor.
2. Lower insulin – this includes alcohol) Insulin makes fat which deposits in your liver. Watch: Why Insulin Resistance Causes Fatty Liver
3. Choline – this is in egg yolks, cruciferous foods, beef/veal liver(pate), wild cod, free range eggs, chicken, red meat, beetroot, soy-lecithin, whey protein, turkey, shiitake dried Mushrooms. Lesser sources: Asparagus, Broccoli, brussel sprouts, cauliflower, lentils, flax seed, mung beans, spinach, green peas. Choline supplements: Alpha GPC, choline bitartrate and CDP-choline, soy-lecithin capsules. See our LivMagic™ capsules with Choline & Cruciferous veggies.
4. Use Intermittent Fasting to keep insulin low for most of the day (12 to 18 hours), avoid snacking especially at night. Watch: Keto and Intermittent Fasting: the Big Overview for Beginners
5. To help increase Bile and Enzymes before eating, take Digestive Bitters.
The Common misconception that eating fat will make your liver fat
It’s actually and mainly the carbohydrates that are the cause, in particular the fructose or High Fructose Corn Syrup (HFCS). It’s worth reading about insulin resistance and hyperinsulinemia, as well as the metabolism of fructose, to really understand why (Carbohydrate intake and NAFLD: fructose as a weapon of mass destruction. High fructose corn syrup (HFCS)-containing beverages were associated with metabolic abnormalities, and contributed to the development of NAFLD in human trials. Ingested carbohydrates are a major stimulus for hepatic de novo lipogenesis (DNL) and are more likely to directly contribute to NAFLD than dietary fat. Substrates used for the synthesis of newly made fatty acids by DNL are primarily glucose, fructose, and amino acids. (Ref.)
Dirty PEMT Gene is Linked to Fatty Liver
Non-alcoholic fatty liver disease – steatohepatitis – is an increasingly common chronic form of hepatitis. Researchers at Okayama University Graduate School of Medicine explain in a recent report, “Although obesity is undoubtedly one of the main risk factors for the development of non-alcoholic fatty liver disease, many clinical observations demonstrated the presence of lean NAFLD patients with normal body mass index (BMI).” The team’s latest work shows that absence of the enzyme phosphatidylethanolamine N-methyltransferase (PEMT), while protecting from diet-induced obesity and diabetes, leads to the prominent development of fatty liver disease and tumours in response to a high-fat high-sucrose diet.
PEMT catalyses methylation of phosphatidylethanolamine (PE) to phosphatidylcholine (PC) in liver cells using S-adenosyl methionine as a methyl donor. The ratio of PE to PC is known to be crucial to cell membrane integrity and resistance to endoplasmic reticulum stress and the infiltration of the liver with fat.
The team fed mice lacking the PEMT enzyme a high-fat high-sucrose diet for up to 90 weeks. They monitored the fat accumulation and insulin resistance before examining their livers. The researchers noted enhanced apoptosis and cell proliferation in the liver, which they explain through transactivation of the protein p53, which is inhibited in the presence of PEMT. The researchers also note a similarity in the response of the PEMT knock-out mice to that of lean human patients suffering from non-alcoholic steatohepatitis. (Ref.)
Dirty Gene Finder™ Report
When your PEMT gene function is weak you can be more susceptible to fatty liver and also SIBO which is a result of poor bile flow. You can test for the function of your PEMT gene and others by taking our Question-based test.
Choline deficiency and Lean Fatty Liver Disease (NAFLD)
Mice fed a methionine and choline-deficient diet (MCD) are a widely used mouse models for research. An absence of obesity and insulin resistance has been observed in both MCD mice and PEMT knockout mice fed high-fat high-sucrose diets.
PC is synthesized from choline, and a balance in PE and PC levels is thought to be important for maintaining cell membrane integrity, stabilising lipid droplets and the normal distribution of fat. Disrupting this balance appears to cause accumulation of fat in the liver.
PEMT catalyses methylation of PE, which also produces PC. The similar effects – lack of obesity and prominent steatohepatitis – is also observed in PEMT knock-out mice and human NAFLD patients with low levels of PEMT.