Fatty liver is a silent disease that is commonly asymptomatic or may produce only vague upper right quadrant pain. Patients with metabolic syndrome, insulin resistance and/or type 2 diabetes, dyslipidemia, or obesity need to be screened for fatty liver. Screening for NAFLD (Nonalcoholic fatty liver disease) allows for interventions before the disease progresses to NASH (nonalcoholic steatohepatitis), cirrhosis, or hepatocellular carcinoma. Research is showing that an alarming % of patients with NASH develop hepatocellular carcinoma without ever progressing to cirrhosis.
There is a misconception that liver enzymes are a reliable predictor of fatty liver, but 50% of patients with NAFLD have shown liver enzymes within normal reference ranges. Gamma-glutamyltransferase (GGT) is one of the best predictors of cardiometabolic disease: GGT levels above 40 IU/L put a person at 20 times the risk for type 2 diabetes. There is not a lot written about this, but I consider elevated GGT to be a sensitive and specific test for fatty liver disease.
Both the American Association for the Study of Liver Diseases (AASLD), and the World Gastroenterology Organization (WGO) released guidelines in 2014 for providers in the United States to reference and follow these guidelines, while establishing the standard of care for the screening, diagnosis, and treatment of NAFLD and NASH. The recommended intervention for both include dietary caloric restriction coupled, with 3 hours a week of moderate exercise for 48 weeks. The goal here is a loss of 3-5% of body weight for those with NALFD, and a 10% loss in body weight for those with NASH, and achieving a BMI of 25. Weight loss should only be 1-2 pounds per week because rapid weight loss will promote steatosis (process describing the abnormal retention of lipids.
While I agree that exercise and diet are primary to the treatment of NAFLD, the changes essential for the reversal of NAFLD include, total elimination of trans fats, high fructose corn syrup and alcohol, as they have been shown to contribute to steatosis in the liver. Alcohol is an oxidant to hepatocytes (liver cells), and fructose consumption at >50 grams per day, leads directly to increased free fatty acid synthesis.
The Paleo-type diet, or a diet high in saturated fat are to be avoided by those with NASH. The diet shown to decrease steatosis was a standard Mediterranean diet, high in fiber, vegetables, fruits, whole grains, olive oil, nuts, fish, and modest amounts of pasture-fed meat.
Conditions that put a patient at highest risk for NAFLD include
obesity diabetes, metabolic syndrome. The link between obesity and NAFLD is so strong that 96% of morbidly obese patients and between 85% and 98% of patients undergoing bariatric surgery have NAFLD. As many as 70% of patients with type 2 diabetes show fatty infiltration on ultrasound. Older patients with diabetes are at particular risk. Half of patients with high triglycerides and low HDL have fatty liver. Nearly all patients with NAFLD have at least one feature of metabolic syndrome (hypertension, obesity, high cholesterol and insulin resistance) and about 30% have all of them. Men are twice as likely as women to have fatty liver. There is no explanation for this, but it is a pattern that is seen globally. Sleep apnea is associated with NAFLD because of its link to obesity and metabolic syndrome. Polycystic Ovarian Syndrome (PCOS), which is epidemic in young women, also increases risk for NAFLD. Vitamin D deficiency is linked to steatosis and fibrosis in the liver, along with increased insulin resistance.
One of the most overlooked etiological risk factors for Fatty Liver, is exposure to persistent organic pollutants such as; PCB, lead, mercury exposure, bisphenol (BPA) exposure, and glyphosate (most commonly used herbicide). Toxins create oxidative damage to liver cells, and mitochondria, and if the levels are high, these toxins can impair the methylation cycle, and production of s-adenosylmethionine (SAMe). The depletion of SAMe then contributes to inflammation, steatosis, and fibrosis of the liver.
There is a clear link between intestinal bacterial overgrowth, and liver damage. Small intestinal bacterial overgrowth (SIBO) is common with cirrhosis and has been detected in patients with NASH. Patients with SIBO are the ones who will become the patients with NASH because the dysbiosis accelerates the disease process. There is good research on the benefits of using a multi-strain probiotic providing >100 billion cfu/g.
S-adenosylmethionine (SAMe) is a prescription drug in Europe that is used to treat a variety of liver diseases, including NAFLD, but in the US it is only available over the counter, is expensive, and oxidizes easily. Betaine is an alternative that can support methylation, so in Germany it was tested in an 8 week trial for those with NASH that showed a 25% reduction in steatosis, while taking a syrup of betaine glucuronate. This research is important, but has gone essentially unrecognized in the United States. The syrup that is available here is dimethylglycine (DMG). Suggested dose 1 mL (1 gram) of DMG 4x/day.
Most of the patients with NASH will need to be treated for a minimum of 3 months prior to repeating blood work (liver enzymes including GGT and ferritin) and 6 months before repeating a liver biopsy or ultrasound.
To date, we have learned to start the process of liver tissue regeneration in cirrhosis, even at the F4 stage on the METAVIR scale.
We invite medical clinics, companies engaged in medical tourism and medical practitioners to cooperate.
We wrote letters of cooperation to more than 100 pharmaceutical companies, but no one answered.
Clinics can only stop liver cirrhosis and improve quality of life, but not reverse cirrhosis.
Our drug also has a positive effect on chronic hepatitis, including hepatitis B, C, B + D.