Researchers Uncover Treatment for Non Alcoholic Fatty Liver Disease
Nonalcoholic fatty liver disease (NAFLD), including nonalcoholic steatohepatitis (NASH), has reached epidemic proportions with no pharmacological therapy approved.
NAFLD is the most common cause of chronic liver disease in the Australian population, although precise estimates of prevalence are lacking. NAFLD may progress to liver fibrosis, cirrhosis, decompensated liver disease, and liver cancer and is becoming an increasingly common indication for liver transplantation in Australia.
Liver disease is a horrific condition that often goes unnoticed until it’s too late, often when it develops into cancer.
In 2012, there were 1,204 premature deaths due to liver disease in Australia. More than two-thirds (69%) of these deaths were among males. These deaths do not include those from liver cancer, which accounted for a further 889 premature deaths in 2012.
Lower circulating levels of the amino acid glycine is consistently reported in patients with NAFLD, but the causes for reduced glycine, its role as a causative factor, and its therapeutic potential remain unclear.
This study (1) was performed in late 2020 and recently released by the Michigan Medicine Frankel Cardiovascular Centre. The study demonstrates the strong protective effects of glycine, alone or in combination with the amino acid leucine, on preventing and treating various forms of fatty liver disease, as well as the obesity that often accompanies these conditions.
It is now known that, whereas most circulating amino acids are increased in NAFLD, glycine concentrations are decreased. Furthermore, lower circulating glycine is associated with higher prevalence of NAFLD comorbidities including obesity (2), Type 2 Diabetes (3), Metabolic Syndrome (4), Coronary Heart Disease, and Myocardial Infarction (5, 6), whereas higher glycine concentrations are associated with a favorable lipid (fat) profile (7).
Lead author Oren Rom, Ph.D., R.D., says,
"In particular, lower circulating glycine is consistently reported in patients with NAFLD and related comorbidities including diabetes, obesity and cardiovascular diseases. Our studies not only offer a metabolic explanation for defective glycine metabolism in NAFLD, but also uncover a potential glycine-based treatment."
According to the study, a daily human oral dose of 27mg/kg glycine is the minimum needed to produce the therapeutic effects on liver, excess weight and inflammation. This minimum therapeutic dose can be obtained from as little as 10g per day of hydrolysed collagen.
For the record, glycine and hydrolysed collagen have been used successfully in the past to treat bleeding ulcers, inflammatory bowel disease (IBD), and even diabetes type I. Check out this in-depth article (8).
Interestingly, the study found that a glycine-glycine-leucine tripeptide combination in a 1:1:1 ratio was even more effective than glycine on its own in reversing NAFLD/NASH, inflammation, obesity and other pathologies associated with the high polyunsaturated fat (PUFA) diet. That means adding some extra Leucine to the hydrolysed collagen may work even better!
The results of the study supports the literature that glycine is a semi-essential amino acid and that it should be taken as a nutritional supplement to guarantee a healthy metabolism.
So where do you get glycine from you ask?
Well besides your body naturally making some, you can get glycine from common foods we eat in our diet like meats, dairy, legumes, spinach, and seafood, however this does not provide enough for optimum health. The amount of glycine naturally synthesized by our body, about 3 g/day, together with that available from the diet, in the range 1.5 - 3.0 g/day, falls significantly short of the amount needed for all metabolic uses, including collagen synthesis, by about 10 g per day for a 70 kg person (9).
By far, the best supplement to take for optimal amounts of glycine is hydrolysed collagen and gelatin which can be purchased here (10).