One Last Thought

In Dr. Lindeberg's paleolithic diet trial, subjects began with ischemic heart disease, and glucose intolerance or type II diabetes. By the end of the 12-week study, on average their glucose control was approaching normal and every subject had normal fasting glucose. Glucose control and fasting glucose in subjects following the "Mediterranean diet" did not change significantly. He didn't report changes in cardiovascular risk factors.

Why was the paleolithic diet so effective at restoring glucose control, while the Mediterranean diet was not? I believe the reason is that the Mediterranean diet did not eliminate the foods that were causing the problem to begin with: processed grains, particularly wheat. The paleolithic diet was lower in carbohydrate than the Mediterranean diet (40% vs 52%), although not exceptionally so. The absolute difference was larger since the paleolithic dieters were eating fewer calories overall (134 g vs 231 g). When they analyzed the data, they found that "the effect of the paleolithic diet on glucose tolerance was independent of carbohydrate intake". In other words, paleolithic dieters saw an improvement in glucose tolerance even if they ate as much carbohydrate as the average for the Mediterranean group.

This study population is not representative of the general public. These are people who suffered from an extreme version of the "disease of civilization". But they are examples of a process that I believe applies to nearly all of us to some extent. This paper adds to the evidence that the modern diet is behind these diseases.

A quick note about grains. Some of you may have noticed a contradiction in how I bash grains and at the same time praise Nutrition and Physical Degeneration. I'm actually not against grains. I think they can be part of a healthy diet, but they have to be prepared correctly and used in moderation. Healthy non-industrial cultures almost invariably soaked, sprouted or sourdough-fermented their grains. These processes make grains much more nutritious and less irritating to the digestive tract, because they allow the seeds to naturally break down their own toxins such as phytic acid, trypsin inhibitors and lectins.

Gluten grains are a special case. 12% of the US public is though to be gluten sensitive, as judged by anti-gliadin antibodies in the bloodstream. Nearly a third have anti-gliadin antibodies in their feces [update- these two markers may or may not indicate gluten sensitivity. SJG 2011]. Roughly 1% have outright celiac disease, in which the gut lining degenerates in response to gluten. All forms of gluten sensitivity increase the risk of a staggering array of health problems. There's preliminary evidence that gluten may activate the innate immune system in many people even in the absence of antibodies. From an anthropological perspective, wherever wheat flour goes, so does the disease of civilization. Rice doesn't have the same effect. It's possible that properly prepared wheat, such as sourdough, might not cause the same problems, but I'm not taking my chances. I certainly don't recommend quick-rise bread, and that includes whole wheat. Whole wheat seemed to be enough to preserve glucose intolerance in Lindeberg's study...

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Paleolithic Diet Clinical Trials Part II

There were a number of remarkable changes in both trials. I'll focus mostly on Dr. Lindeberg's trial because it was longer and better designed. The first thing I noticed is that caloric intake dropped dramatically in both trials, -36% in the first trial and a large but undetermined amount in Dr Lindeberg's. The Mediterranean diet group ended up eating 1,795 calories per day, while the paleolithic dieters ate 1,344. In both studies, participants were allowed to eat as much as they wanted, so those reductions were purely voluntary.

This again agrees with the theory that certain neolithic or industrial foods promote hyperphagia, or excessive eating. It's the same thing you see in low-carbohydrate diet trials, such as this one, which also reduce grain intake. The participants in Lindeberg's study were borderline obese. When you're overweight and your body resets its fat mass set-point due to an improved diet, fatty acids come pouring out of fat tissue and you don't need as many calories to feel satisfied. Your diet is supplemented by generous quantities of lard. Your brain decreases your calorie intake until you approach your new set-point.

That's what I believe happened here. The paleolithic group supplemented their diet with 3.9 kg of their own rump fat over the course of 12 weeks, coming out to 30,000 additional calories, or 357 calories a day. Not quite so spartan when you think about it like that.

The most remarkable thing about Lindeberg's trial was the fact that the 14 people in the paleolithic group, 2 of which had moderately elevated fasting blood glucose and 10 of which had diabetic fasting glucose, all ended up with normal fasting glucose after 12 weeks. That is truly amazing. The mediterranean diet worked also, but only in half as many participants.

If you look at their glucose tolerance by an oral glocose tolerance test (OGTT), the paleolithic diet group improved dramatically. Their rise in blood sugar after the OGTT (fasting BG subtracted out) was 76% less at 2 hours. If you look at the graph, they were basically back to fasting glucose levels at 2 hours, whereas before the trial they had only dropped slightly from the peak at that timepoint. The mediterranean diet group saw no significant improvement in fasting blood glucose or the OGTT. Lindeberg is pretty modest about this finding, but he essentially cured type II diabetes and glucose intolerance in 100% of the paleolithic group.

Fasting insulin, the insulin response to the OGTT and insulin sensitivity improved in the paleolithic diet whereas only insulin sensitivity improved significantly in the Mediterranean diet. Fasting insulin didn't decrease as much as I would have thought, only 16% in the paleolithic group.

Another interesting thing is that the paleolithic group lost more belly fat than the Mediterranean group, as judged by waist circumference. This is the most dangerous type of fat, which is associated with, and contributes to, insulin resistance and the metabolic syndrome. Guess what food belly fat was associated with when they analyzed the data? The strongest association was with grain consumption (probably mostly wheat), and the association remained even after adjusting for carbohydrate intake. In other words, the carbohydrate content of grains does not explain their association with belly fat because "paleo carbs" didn't associate with it. The effect of the paleolithic diet on glucose tolerance was also not related to carbohydrate intake.

So in summary, the "Mediterranean diet" may be healthier than a typical Swedish diet, while a diet loosely modeled after a paleolithic diet kicks both of their butts around the block. My opinion is that it's probably due to eliminating wheat, substantially reducing refined vegetable oils and dumping the processed junk in favor of real, whole foods. Here's a zinger from the end of the paper that sums it up nicely (emphasis mine):

The larger improvement of glucose tolerance in the Paleolithic group was independent of energy intake and macronutrient composition, which suggests that avoiding Western foods is more important than counting calories, fat, carbohydrate or protein. The study adds to the notion that healthy diets based on whole-grain cereals and low-fat dairy products are only the second best choice in the prevention and treatment of type 2 diabetes.

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Paleolithic Diet Clinical Trials

If Dr. Ancel Keys (of diet-heart hypothesis fame) had been a proponent of "paleolithic nutrition", we would have numerous large intervention trials by now either confirming or denying its ability to prevent health problems. In this alternate reality, public health would probably be a lot better than it is today. Sadly, we have to settle for our current reality where the paleolithic diet has only been evaluated in two small trials, and medical research spends its (our) money repeatedly conducting failed attempts to link saturated fat to every ill you can think of. But let's at least take a look at what we have.

Both trials were conducted in Sweden. In the first one, lead by Dr. Per Wändell, 14 healthy participants (5 men, 9 women) completed a 3-week dietary intervention in which they were counseled to eat a "paleolithic diet". Calories were not restricted, only food categories were. Participants were told to eat as much as they wanted of fruit, vegetables, fish, lean meats, nuts, flax and canola oil, coffe and tea (without dairy). They were allowed restricted quantities of dried fruit, potatoes (2 medium/day) salted meat and fish, fat meat and honey. They were told not to eat dairy, grain products, canned food, sugar and salt.

After three weeks, the participants had:

• Decreased their caloric intake from 2,478 to 1,584 kcal
• Increased their percentage protein and fat, while decreasing carbohydrate
• Decreased saturated fat, increased dietary cholesterol, decreased sodium intake, increased potassium
  
• Lost 2.3 kg (5 lb)
• Decreased waist circumference, blood pressure and PAI-1

Not bad for a 3-week intervention on healthy subjects. This study suffered from some serious problems, however. #1 is the lack of a control group as a means for comparison. Ouch. #2 is the small study size and resulting lack of statistical power. I consider this one encouraging but by no means conclusive.

The second study was conducted by the author of the Kitava study, Dr. Staffan Lindeberg. The study design was very interesting. He randomly assigned 29 men with ischemic heart disease, plus type II diabetes or glucose intolerance, to either a "Mediterranean diet" or a "paleolithic diet". Neither diet was calorie-restricted. Here's the beauty of the study design: the Mediterranean diet was the control for the paleo diet. The reason that's so great is it completely eliminates the placebo effect. Both groups were told they were being assigned to a healthy diet to try to improve their health. Each group was educated on the health benefits of their diet but not the other one. It would have been nice to see a regular non-intervention control group as well, but this design was adequate to see some differences.

Participants eating the Mediterranean diet were counseled to focus on whole grains, low-fat dairy, potatoes, legumes, vegetables, fruit, fatty fish and vegetable oils rich in monounsaturated fats and alpha-linolenic acid (omega-3). I'm going to go on a little tangent here. This is truly a bizarre concept of what people eat in the Mediterranean region. It's a fantasy invented in the US to justify the mainstream concept of a healthy diet. My father is French and I spent many summers with my family in southern France. They ate white bread, full-fat dairy at every meal, legumes only if they were smothered in fatty pork, sausages and lamb chops. In fact, full-fat dairy wasn't fat enough sometimes. Many of the yogurts and cheeses we ate were made from milk with extra cream added. Want to get a lecture from Grandmere? Try cutting the fat off your pork chop!

The paleolithic group was counseled to eat lean meat, fish, fruit, leafy and cruciferous vegetables, root vegetables (including moderate amounts of potatoes), eggs and nuts. They were told to avoid dairy, grain products, processed food, sugar and beer.

Both groups were bordering on obese at the beginning of the study. All participants had cardiovascular disease and moderate to severe glucose intolerance (i.e. type II diabetes). After 12 weeks, both groups improved on several parameters. That includes fat mass and waist circumference. But the paleolithic diet trumped the Mediterranean diet in many ways:

• Greater fat loss in the the midsection and a trend toward greater weight loss
  
• Greater voluntary reduction in caloric intake (total intake paleo= 1,344 kcal; Med= 1,795)
  
• A remarkable improvement in glucose tolerance that did not occur significantly in the Mediterranean group
• A decrease in fasting glucose
  
• An increase in insulin sensitivity (HOMA-IR)
  

Overall, the paleolithic diet came out looking very good. But I haven't even gotten to the best part yet. At the beginning of the trial, 12 out of the 14 people in the paleo group had elevated fasting glucose. At the end, every single one had normal fasting glucose. In the Mediterranean group, 13 out of 15 began with elevated glucose and 8 out of 15 ended with it. This clearly shows that a paleolithic diet is an excellent way to restore glucose control to a person who still has beta cells in their pancreas.

This post is getting long, so I think I'll save the interpretation for the next post.

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Acne Anecdotes

Thanks for all the interesting comments on the last post. Here are some highlights:

Methuselah:

I had bad acne as a teenager and although the worst of it did clear up for as I got older (this seems to be the pattern, so presumably there are hormones other than insulin involved,) I still had spotty skin into my 20s and 30s. When I went onto a Paleo diet my skin cleared up totally.

Neil:

I am lucky enough to have reasonable skin already, but reducing carbs and vegetable oils has at the least coincided with a notable improvement

Jeff:

I used to get... 2-3 pimples most months. Since I have gone Paleo I have had not a single pimple in 8 months.

Itsthewoo:

I had terrible acne that lasted from 9 yrs right up until 20 years - the same week I started the atkins diet. Then it stopped.

I see the skin as a barometer of health. A truly healthy person's skin is smooth, free of acne and has a gentle blush in the cheeks. Unhealthy skin is pale, puffy, pasty, dry, oily, or excessively red in the cheeks and face. It's no coincidence that what we perceive as attractive also happens to indicate health.

I'll add one more anecdote, from myself. In high school, my friends called me "the ghost" because my skin was so pale. I had mild but persistent acne and difficulty tanning. Over the past few years, as I've improved my diet, my skin has smoothed, I've regained the color in my cheeks, I've regained my ability to tan well and my acne has disappeared.

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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.

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Got Breast Milk?: Interspecies Suckling

Would You Drink Breast Milk Ice Cream?
Not long ago, Hans Locher, the landlord of the Swiss restaurant Storchen, announced he intended to serve soup, sauces, and even antelope steak in a glaze that contained up to 75% human breast-milk content. The idea came to him 35 years before when he experimented cooking with his wife’s surplus milk. Locher offered US$14.50 for a liter of human milk, but his aspirations were squashed by the Swiss government: "Humans are not on the list of authorised milk suppliers such as cows or sheep."

In response to the international news on Locher’s proposal, People for the Ethical Treatment of Animals (PETA), sent out a letter to Ben & Jerry’s, requesting that they begin to integrate human milk into their product. (Using human milk for human food isn’t the newest idea). Ben & Jerry’s then sent PETA a letter of their own. They wrote: "We applaud PETA's novel approach to bringing attention to an issue, but we believe a mother's milk is best used for her child." A woman who was later interviewed at the Ben & Jerry’s factory was grossed out by the suggestion, especially after having to deal with nursing her own children: “The (breast) pumps just weren't that much fun. You really do feel like a cow.”

In all the buzz, Americans really didn’t understand PETA’s intentions. The letter was in jest, a clever way of getting the press to not only inform the public on the perils of drinking cow’s milk, but also to rattle some awareness into people that “cow’s milk is for baby cows.” Ben & Jerry’s letter summarized PETA’s point to the tee: “Mother’s milk is best used for her child.” In other words, stop making ice cream with the milk of mother cows; calves should be drinking cow’s milk, not human adults!Read more »

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Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is milder form of NASH, in which the liver becomes enlarged and accumulates fat. Ready for a shocker? The prevalence of NAFLD is thought to be between 20 and 30 percent in the Western world, and rising. It's typically associated with insulin resistance and often with the metabolic syndrome. This has lead some researchers to believe it's caused by insulin resistance. It's a chicken and egg question, but I believe it's the other way around if anything.

There are certain animal models of human disease that are so informative I keep coming back to them again and again. One of my favorites is the LIRKO mouse, or liver-specific insulin receptor knockout mouse. The LIRKO mouse is missing its insulin receptor in the liver only, so it is a model of severe insulin resistance of the liver. It accumulates a small amount of fat in its liver in old age, but nothing that resembles NAFLD. So liver insulin resistance doesn't lead to NAFLD or NASH, at least in this model.

What else happens to the LIRKO mouse? It develops severe whole-body insulin resistance, impaired glucose tolerance, high fasting blood glucose and hyperinsulinemia (chronically elevated insulin). So insulin resistance in the liver is sufficient to cause whole-body insulin resistance, hyperinsulinemia and certain other hallmarks of the metabolic syndrome, while liver and whole-body insulin resistance are not sufficient to cause NAFLD or NASH. This is consistent with the fact that nearly everyone with NAFLD is insulin resistant, while many who are insulin resistant do not have NAFLD.

In all fairness, there are reasons why NAFLD is believed to be caused by insulin resistance. For example, insulin-sensitizing drugs improve NAFLD. However, that doesn't mean the initial metabolic 'hit' wasn't in the liver. One could imagine a scenario in which liver insulin resistance leads to insulin resistance in other tissues, which creates a positive feedback that aggravates NAFLD. Or perhaps NAFLD requires two 'hits', one to peripheral insulin sensitivity and another directly to the liver.

In any case, I feel that the most plausible mechanism for NAFLD goes something like this: too much n-6 from polyunsaturated vegetable oil (along with insufficient n-3), plus too much fructose from sweeteners, combine to cause NAFLD. The liver becomes insulin resistant at this point, leading to whole-body insulin resistance, hyperinsulinemia, impaired glucose tolerance and general metabolic havoc.

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