Non-Alcoholic Fatty Liver Disease and Disease Mongering

Wang and colleagues must be commended for showing evidence that cardiovascular health is the main issue with “non-alcoholic fatty liver disease (NAFLD)”. However, I would like to go further.

First, “fatty liver” is not a disease, only a symptom. There is no evidence yet that fatty liver per se leads to hepatitis or fibrosis. In a study of 50 non-selected subjects with morbid obesity, severe liver damage (16%) was consistently associated with alcohol intake or specific causes.

Second, several causes of liver diseases are underestimated and cause cardiovascular diseases. Accordingly, the threshold allowing 21 drinks/week (294 g of pure alcohol,14 g/US drink when using normalized glasses) for men to rule out alcohol as an etiology of non-alcoholic fatty liver disease is nonsense. Moreover, drinkers underestimate their consumption. Alcohol is most toxic: it is a class I (human) carcinogen beginning at one drink a day. No alcohol use is safe. In UK and France, the recommendation for those who choose to drink sets the “low-risk” threshold below 100 g/week. Smoking is significantly associated with NAFLD. Similarly, air pollution has deleterious effects on the liver. Although risks may be low, combination effects (cocktail effects) can have greater effect than individual substances added together.

The cornerstone of care as rightly stressed by Wang and colleagues must be healthy living: diet, physical activity, avoiding alcohol and tobacco. Life-style interventions are effective. Sadly, pilling may be the motto: a) there are more than 100 drugs currently going through phase II and III clinical trials for a symptom whose market is estimated to be $1.6bn (£1.2bn; €1.4bn) by 2020; b) the majority of authors of guidelines from the American College of Gastroenterology have financial conflicts of interest with the industry according to Medicaid Services Open Payments database (OPD) but only 34% of financial relationships evidenced by OPD were disclosed.