Fatty Liver and Misdirection

Drs. Anna Diehl and Chris Day wrote an article this November for the New England Journal of Medicine (NEJM) about non-alcoholic fatty liver. They include some alarming statistics. First, one in four Americans has this condition. It costs one-hundred billion dollars annually. It causes cirrhosis of the liver even without alcohol and can increase the lifetime risk of liver cancer significantly. So this is very dire news.

The review is a perfect example of a pharmaco-physiological review that seems to ignore the lifestyle determinants of a disease nearly completely. The cause of a disease is referred to in medicine as its pathogenesis. In the section on this topic, the authors state the following:

Evidence that multiple lipid intermediates are cytotoxic, combined with the numerous factors that might enhance or reduce vulnerability to each of these toxic moieties, suggests that nonalcoholic steatohepatitis may be the common manifestation of diverse disease processes. Characterizing these processes, developing approaches to detect their presence and intensity, and determining whether one or more pathogenic mechanisms predominate have become major foci for research because such knowledge is necessary for the development of effective interventions for preventing and treating nonalcoholic steatohepatitis.

Translating into English:

Many fats can kill liver cells, and lots of other things people do can make this worse, so fatty liver disease may be caused by a bunch of different things. Figuring out which fats actually play a major role in people getting fatty liver is important to figuring out how to prevent it and to treat it when it happens.

Imagine if someone said this:

Many different bullets can injure human beings, and lots of other things can make it worse. So gunshot wounds may be caused by a variety of actions. Figuring out which bullets actually damage people seriously is important in figuring out how to reduce gunshot wounds and treat them when they happen.

Both are technically true, but they are ignoring the most important determinant in whether or not someone gets the condition. If we acknowledge that without bullets, gunshot wounds vanish, what is so hard about acknowledging that diets low in total fat are effective in getting rid of the toxic effects of fat on the liver?

The authors then elucidate the genetic and epigenetic factors that lead to fatty liver before getting to their environmental factors. Here is where they talk about diet:

The intestinal microbiota influence host susceptibility to obesity, hepatic steatosis, nonalcoholic steatohepatitis, liver fibrosis, and primary liver cancer. Conversely, host factors (e.g., diet composition, adiposity, feeding frequency, and sleep–wake cycles) influence the intestinal microbiota.

Again in English:

Bacteria in the gut can influence obesity, fatty liver and its progression to cirrhosis and cancer. What individuals do (diet, overall body fat, eating often and sleeping well) influence the gut bacteria.

So the only mention of diet in this review of the causes of fatty liver that accepts as its basic facts that many different fats kill liver cells is a mention inside a parenthesis as it regards gut bacteria. There is one additional mention of what you put in your mouth, in a table of lifestyle interventions. It recommends weight loss, avoiding fructose-enhanced beverages, limiting alcohol and increasing coffee intake.

There you have it.

No mention of studies like this one published in 2003 in Hepatology that show saturated fat as a major dietary determinant of fatty liver disease and that diets very low in total fat were protective of the condition. It also showed that more fiber and plant-based antioxidants like ascorbate were associated with lower risk.

No mention of studies like this 2009 study from the American Journal of Clinical Nutrition, where they took actual patients with fatty liver, fed them a meal high in saturated fat and induced hormonal changes consistent with worsening fatty liver.

It’s bizarre. It’s almost as if the authors have a huge blind spot.

I wonder what that might be.


Look at the conflict of interest disclosure at the end of the article. Now I see. The primary author has taken money from:

“Pfizer, Novartis, and Lumena, participating in a clinical trial with Gilead Sciences, Conatus, Galmed, NGM Biopharmaceuticals, Bristol-Myers Squibb, Madrigal, Galectin Therapeutics, Exalenz Biosciences, Shire, Intercept, and Genfit, receiving grant support from and participating in a clinical trial with Immuron, receiving grant support for a research collaboration from Metabolon and Prometheus, receiving consulting fees from and participating in a clinical trial with Boehringer Ingelheim, receiving honoraria from and participating in a clinical trial with Allergan, receiving consulting fees and grant support for a research collaboration from Celgene, and holding a pending patent application for “Development of Novel Therapeutics to Treat Non-Alcoholic Steatohepatitis (NASH).” No other potential conflict of interest relevant to this article was reported.”

I wonder if a list of drug companies that the author didn’t take money from would be shorter.

This is personal to me.

I had fatty liver and was able to completely resolve the problem in less than a year by adopting a plant-based diet very low in fat. That alone solved the problem, with no need for help from Pfizer and Novartis, much less Immuron or Metabolon.

From the point of view of the authors, we have to talk about the variety of issues and challenges associated with this incredibly complex disease. If we make it simple and show people exactly what to do, there would be no market for “Novel Therapeutics.”

Please be clear, this isn’t a claim of conspiracy. It’s much more mundane. Upton Sinclair said it best, “It is difficult to get a man to understand something, when his salary depends upon his not understanding it!”

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