All those white bubbles are fat droplets.
I’m busier than a bumblebee right now, so unfortunately the high-fructose corn syrup post is going to have to wait till Tuesday. Today I’ll make a quick post about fatty liver disease.
Someone on the Facebook version of this blog posed the question, “How common is non-alcoholic fatty liver??”
The exact prevalence in the United States is not known, but surveys suggest that far too many Americans’ livers look like an Eskimo’s yummy dinner plate, stuffed with as much fat as the livers of Campbell’s protein-deficient, cancer-free rats.
Fatty liver is generally asymptomatic, but can prime a person to develop inflammation, cirrhosis, and in rare cases death. Most people who have it probably have no idea. One author used the prevalence of diabetes and obesity to estimate that about 40 million Americans have fatty liver. A survey of men and women in the multiracial urban population of Dallas County measured fatty liver directly and concluded that fully one third of the population had fatty liver.
Non-alcoholic fatty liver disease (NAFLD) was first described in adults in 1980 and was first described in children three years later. The rise of the NAFLD epidemic has paralleled the rise in obesity, but you do not have to be obese to have fatty liver. It’s more closely related to insulin resistance and leptin resistance, and some people can even be extra-skinny and have fatty liver. Over 40 percent of Americans have some form of pre-diabetes suggestive of insulin resistance. So the true incidence may be closer to 100 million Americans rather than 40 million.
What causes fatty liver? Dr. Robert Lustig makes an excellent case that fructose is the culprit in Sugar: The Bitter Truth. However, even as high-fructose corn syrup began replacing sucrose and total sweetener consumption increased, another change happened: the Great Doubling of PUFA consumption during the Oiling of America. Here’s a graph from Stephan Guyenet’s Whole Health Source Blog in his article “Have Seed Oils Caused a Multi-Generational Obesity Epidemic?”
I have written several blog posts on fatty liver in the past. If you missed them, you can check them out by following these two links:
In brief, corn oil, but not coconut oil or butter, induces fatty liver in animal experiments. In the alcoholic model, which according to Lustig’s hypothesis is the equivalent of a fructose- or sucrose-feeding model, palm oil is protective compared to fish oil; beef tallow or medium-chain fats from coconut oil are protective compared to corn oil; and cocoa butter is protective compared to corn oil. In fact, if animals consume 40% of their diet as cocoa butter, they can consume 30% of their calories as ethanol, and they might get mighty drunk but they don’t get fatty liver.
Why are PUFA’s so damaging? For a lengthy answer, check out my new article “Precious Yet Perilous — Understanding the Essential Fatty Acids.” If you’re not in the mood for a lengthy read, I describe the relationship between PUFA oxidation and atherosclerosis in my interview with Jimmy Moore. No reading required.
These deal mostly with heart disease, but the relationship to fatty liver is similar. Luckily, my obligate bumblebee busy-ness is mostly occupying me with 1) fructose and 2) fatty liver right now, so look forward to a number of blog posts on fatty liver in the next week or two. Suitable for a bumblebee, my next post will be about honey.