Acne: Disease of Civilization

I often focus on the bigger facets of the disease of civilization. Things like cardiovascular disease and cancer, which are major killers and the subject of intensive research. But the disease of civilization is a spectrum of disorders that affects the body in countless ways, large and small.

I recently read an interesting paper written by an all-star cast, including Loren Cordain, Staffan Lindeberg and Boyd Eaton. It's titled "Acne Vulgaris: A Disease of Western Civilization". The paper presents data from two different groups, the Kitavans of Papua New Guinea and the Ache hunter-gatherers of Paraguay. Both were systematically examined by doctors trained to diagnose acne. Out of 1,200 Kitavans and 115 Ache of all ages, not a single case of acne was observed. Hunter-gatherers and other healthy non-industrial cultures have nice skin. I dare you to find a pimple in Nutrition and Physical Degeneration.

In Western societies, acne is a fact of life. The paper states that 79 to 95% of modern adolescents suffer from some degree of acne, along with about 50% of young adults. That's an enormous difference.

The paper presents a very Cordain-esque hypothesis to explain the high incidence of acne in Western societies. In sum, they state that the Western diet causes hyperinsulinemia, which is thought to promote acne. This is due to insulin's effects on skin cell proliferation, its interference with the retinoid (vitamin A) signaling pathway, and its effect on sebum production.

They then proceed to point the finger at the glycemic index/load of the Western diet as the culprit behind hyperinsulinemia. It's an unsatisfying explanation because the Kitavans eat a diet that has a high glycemic load due to its high carbohydrate content, low fat content, and relatively high-glycemic index foods. I think the answer is more likely to reside in the specific types of carbohydrate (processed wheat) rather than their speed of digestion, with possible contributions from refined vegetable oil and an excessive sugar intake.

Agave Syrup

Anna brought up agave syrup in a comment on the last post, so I thought I'd put up a little mini-post so everyone can benefit from what she pointed out.

Agave syrup is made from the heart of the agave plant, which is pressed to release a juice rich in inulin. Inulin is a polymer made of fructose molecules. The inulin is then broken down either by heat or by enzymatic processing. The result is a sweet syrup that is rich in fructose.

Agave syrup is marketed as a healthy, alternative sweetener. In fact, it's probably as bad or worse than high-fructose corn syrup (HFCS). They are both a refined and processed plant extract. Both are high in fructose, with agave syrup leading HFCS (estimates of agave syrup range up to 92% fructose by calories). Finally, agave syrup is expensive and inefficient to produce.

The high fructose content gives agave syrup a low glycemic index, because fructose does not raise blood glucose. Unfortunately, as some diabetics learned the hard way, using fructose as a substitute for sucrose (cane sugar) has negative long-term effects on insulin sensitivity.

In my opinion, sweeteners come with risks and there is no free lunch. The only solution is moderation.

How to Fatten Your Liver

Steatohepatitis is a condition in which the liver becomes inflamed and accumulates fat. It was formerly found almost exclusively in alcoholics. In the 1980s, a new condition was described called nonalcoholic steatohepatitis (NASH), basically steatohepatitis without the alcoholism. Today, NASH is thought to affect more than 2% of the adult American population. The liver has many important functions. It's not an organ you want to break.

This week, I've been reading about how to fatten your liver. First up: industrial vegetable oil. The study that initially sent me on this nerd safari was recently published in the Journal of Nutrition. It's titled "Increased Apoptosis in High-Fat Diet–Induced Nonalcoholic Steatohepatitis in Rats Is Associated with c-Jun NH2-Terminal Kinase Activation and Elevated Proapoptotic Bax". Quite a mouthful. The important thing for the purpose of this post is that the investigators fed rats a high-fat diet, which induced NASH.

Anytime a study mentions a "high-fat diet", I immediately look to see what they were actually feeding the animals. To my utter amazement, there was no information on the composition of the high-fat diet in the methods section, only a reference to another paper. Apparently fat composition is irrelevant. Despite the fact that a high-fat diet from coconut oil or butter does not produce NASH in rats. Fortunately, I was able to track down the reference. The only difference between the standard diet and the high-fat diet was the addition of a large amount of corn oil and the subtraction of carbohydrate (dextrin maltose).

Corn oil is one of the worst vegetable oils. You've eaten corn so you know it's not an oily seed. To concentrate the oil and make it palatable, manufacturers use organic solvents, high heat, and several rounds of chemical treatment. It's also extremely rich in n-6 linoleic acid. The consumption of corn oil and other n-6 rich oils has risen dramatically in the US in the last 30 years, making them prime suspects in NASH. They have replaced the natural (more saturated) fats we once got from meat and milk.

Next up: fructose. Feeding rats an extreme amount of fructose (60% of calories) gives them nonalcoholic fatty liver disease (NAFLD), NASH's younger sibling, even when the fat in their chow is lard. Given the upward trend of US fructose consumption (mostly from high-fructose corn syrup), and the refined sugar consumed everywhere else (50% fructose), it's also high on my list of suspects.

Here's my prescription for homemade foie gras: take one serving of soybean oil fried french fries, a basket of corn oil fried chicken nuggets, a healthy salad drenched in cottonseed oil ranch dressing, and wash it all down with a tall cup of soda. It's worked for millions of Americans!