A Dutch group led by Dr. Yvonne T. van der Schouw recently published a paper examining the link between vitamin K intake and heart attack (thanks Robert). They followed 16,057 women ages 49-70 years for an average of 8.1 years, collecting data on their diet and incidence of heart attack.
They found no relationship between K1 intake and heart attack incidence. K1 is the form found in leafy greens and other plant foods. They found that each 10 microgram increase in daily vitamin K2 consumption was associated with a 9% lower incidence of heart attack. Participants consumed an average of 29 micrograms K2 per day, with a range of 0.9 to 128 micrograms. That means that participants with the highest intake had a very much reduced incidence of heart attack on average. Vitamin K2 comes from animal foods (especially organs and pastured dairy)and fermented foods such as cheese, sauerkraut, miso and natto. Vitamin K is fat-soluble, so low-fat animal foods contain less of it. Animal foods contain the MK-4 subtype while fermentation produces longer menaquinones, MK-5 through MK-14.
There's quite a bit of evidence to support the idea that vitamin K2 inhibits and possibly reverses arterial calcification, which is possibly the best overall measure of heart attack risk. It began with the observations of Dr. Weston Price, who noticed an inverse relationship between the K2 MK-4 content of butter and deaths from coronary heart disease and pneumonia in several regions of the U.S. You can find those graphs in Nutrition and Physical Degeneration.
The 25% of participants eating the most vitamin K2 (and with the lowest heart attack risk) also had the highest saturated fat, cholesterol, protein and calcium intake. They were much less likely to have elevated cholesterol, but were more likely to be diabetic.
Here's where the paper gets strange. They analyzed the different K2 subtypes individually (MK-4 through MK-9). MK-7 and MK-6 had the strongest association with reduced heart attack risk per microgram consumed, while MK-4 had no significant relationship. MK-8 and MK-9 had a weak but significant protective relationship.
There are a few things that make me skeptical about this result. First of all, the studies showing prevention/reversal of arterial calcification in rats were done with MK-4. MK-4 inhibits vascular calcification in rats whereas I don't believe the longer menaquinones have been tested. Furthermore, they attribute a protective effect to MK-7 in this study, but the average daily intake was only 0.4 micrograms! You could get that amount of K2 if a Japanese person who had eaten natto last week sneezed on your food. I can't imagine that amount of MK-7 is biologically significant. That, among other things, makes me skeptical of what they're really observing.
I'm not convinced of their ability to parse the effect into the different K2 subtypes. They mentioned in the methods section that their diet survey wasn't very accurate at estimating the individual K2 subtypes. Combine that with the fact that the K2 content of foods varies quite a bit by animal husbandry practice and type of cheese, and you have a lot of variability in your data. Add to that the well-recognized variability inherent in these food questionnaires, and you have even more variabiltiy.
I'm open to the idea that longer menaquinones (K2 MK-5 and longer, including MK-7) play a role in preventing cardiovascular disease, but I don't find the evidence sufficient yet. MK-4 is the form of K2 that's made by animals, for animals. Mammals produce it in their breast milk and other animals produce it in eggs all the way down to invertebrates. I think we can assume they make MK-4, and not the longer menaquinones, for a reason.
MK-4 is able to play all the roles of vitamin K in the body, including activating blood clotting factors, a role traditionally assigned to vitamin K1. This is obvious because K2 MK-4 is the only significant source of vitamin K in the diet of infants before weaning. No one knows whether the longer menaquinones are able to perform all the functions of MK-4; it hasn't been tested and I don't know how you could ever be sure. MK-7 is capable of performing at least some of these functions, such as activating osteocalcin and clotting factors.
I do think it's worth noting that the livers of certain animals contain longer menaquinones, including MK-7. So it is possible that we're adapted to eating some of the longer menaquinones. Many cultures also have a tradition of fermented food (probably a relatively recent addition to the human diet), which could further increase the intake of longer menaquinones. The true "optimum", if there is one, may be to eat a combination of forms of K2, including MK-4 and the longer forms. But babies and healthy traditional cultures such as the Masai seem to do quite well on a diet heavily weighted toward MK-4, so the longer forms probably aren't strictly necessary.
Well if you've made it this far, you're a hero (or a nerd)! Now for some humor. From the paper:The concept of proposing beneficial effects to vitamin K2 seems to have different basis as for vitamin K1. Vitamin K1 has been associated with a heart-healthy dietary pattern in the earlier work in the USA and this attenuated their associations with CHD. Vitamin K2 has different sources and relate to different dietary patterns than vitamin K1. This suggests that the risk reduction with vitamin K2 is not driven by dietary patterns, but through biological effects.
They seem confused by the fact that people who ate foods high in saturated fat and cholesterol had less CHD, yet people consuming green vegetables didn't. Here's more:
Thus, although our findings may have important practical implications on CVD prevention, it is important to mention that in order to increase the intake of vitamin K2, increasing the portion vitamin K2 rich foods in daily life might not be a good idea. Vitamin K2 might be, for instance more relevant in the form of a supplement or in low-fat dairy. More research into this is necessary.
Translation: "People who ate the most cheese, milk and meat had the lowest heart attack rate, but be careful not to eat those things because they might give you a heart attack. Get your K2 from low-fat dairy (barely contains any) and supplements."
Vegetarians deserve our respect. They're usually thoughtful, conscientious people who make sacrifices for environmental and ethical reasons. I was vegetarian for a while myself, and I have no regrets about it.Vegetarianism and especially veganism can get pretty ideological sometimes. People who have strong beliefs like to think that their belief system is best for all aspects of their lives and the world, not just some aspects of it. Many vegetarians believe their way of eating is healthier than omnivory. One of the classic arguments for vegetarianism goes something like this: our closest living relatives, chimpanzees and bonobos, are mostly vegetarian, therefore that's the diet to which we're adapted as well. Here's the problem with that argument:
Where are chimps (Pan troglodytes) on this chart? They aren't on it, for two related reasons: they aren't in the genus Homo, and they diverged from us 5-7 million years ago. Homo erectus diverged from our lineage about 1.5 million years ago. I don't know if you've ever seen a Homo erectus skull, but 1.5 million years is clearly enough time to do some evolving. Homo erectus ate animals as a significant portion of its diet.If you look at the chart above, Homo rhodesiensis (often considered a variant of Homo heidelbergensis) is our closest ancestor, and our point of divergence with neanderthals (Homo neanderthalensis). Some archaeologists believe H. heidelbergensis was the same species as modern Homo sapiens. I haven't been able to find any direct evidence of the diet of H. heidelbergensis from bone isotope ratios, but the indirect evidence indicates that they were capable hunters who probably got a substantial proportion of their calories from meat. In Europe, they hunted now-extinct megafauna such as wooly rhinos. These things make modern cows look like chicken nuggets.H. heidelbergensis was a skilled hunter and very athletic. They were top predators in their ecosystems, judged by the fact that they took their time with carcasses, butchering them thoroughly and extracting marrow from bones. No predator or scavenger was capable of driving them away from a kill.Our closest recent relative was Homo neanderthalensis, the neanderthal. They died out around 30,000 years ago. There have been several good studies on the isotope ratios of neanderthal bones, all indicating that neanderthals obtained most of their protein from meat. They relied both on land and marine animals, depending on what was available. Needless to say, neanderthals are much more closely related to humans than chimpanzees, having diverged from us less than 500,000 years ago. That's less than one-tenth the time between humans and chimpanzees. I don't think this means humans are built to be carnivores, particularly since there is accumulating evidence of diverse plant consumption by neanderthals, but it certainly blows away the argument that we're built to be vegetarians. Historical human hunter-gatherers had very diverse diets, but on average were meat-heavy omnivores.
Ricardo just sent me a link to the British Heart Foundation statistics website. It's a goldmine. They have data on just about every aspect of health and lifestyle in the U.K. I find it very empowering to have access to this kind of information on the internet.I've just started sifting through it, but something caught my eye. The U.K. is experiencing an obesity epidemic similar to the U.S.:
Here's where it gets interesting. This should look familiar:
Hmm, those trends look remarkably similar. Just like in the U.S, the British are exercising more and getting fatter with each passing year. In fact, maybe exercise causes obesity. Let's see if there's any correlation between the two. I'm going to plot obesity on the X-axis and exercise on the Y-axis to see if there's a correlation. The data points only overlap on three years: 1998, 2003 and 2006. Let's take a look:
By golly, we've proven that exercise causes obesity! Clearly, the more people exercise, the fatter they get. The R-value is a measure of how closely the points fall on the best-fit line. 0.82 isn't bad for this type of data. If only we could get all British citizens to become couch potatoes, obesity would be a thing of the past! OK, I'm kidding. The obesity is obviously caused by something else. I'm illustrating the point that correlations can sometimes be misleading. Even if an association conforms to our preconceived notions of how the world works, that does not necessarily justify saying one factor causes another. Controlled experiments can often help us strengthen a claim of causality.
Health authorities tell us to eat more fiber for health, particularly whole grains, fruit and vegetables. Yet the Diet and Reinfarction Trial, which determined the effect of eating a high-fiber diet on overall risk of death, came up with this graph:
Oops! At two years, the group that doubled its fiber intake had a 27% greater chance of dying and a 23% greater chance of having a heart attack. The extra fiber was coming from whole grains. The difference wasn't statistically significant, so we can't make too much out of this. But at the very least, it doesn't support the idea that increasing grain fiber will extend your life. Why might fiber be problematic? I read a paper recently that gave a pretty convincing answer to that question: "Dietary Fibre and Mineral Bioavailability", by Dr. Barbara F. Hartland. By definition, fiber is indigestible. We can divide it into two categories: soluble and insoluble. Insoluble fiber is mostly cellulose and it's relatively inert, besides getting fermented a bit by the gut flora. Soluble fiber is anything that can be dissolved in water but not digested by the human digestive tract. It includes a variety of molecules, some of which are quite effective at keeping you from absorbing minerals. Chief among these is phytic acid, with smaller contributions from tannins (polyphenols) and oxalates. The paper makes a strong case that phytic acid is the main reason fiber prevents mineral absorption, rather than the insoluble fiber fraction. This notion was confirmed here. Whole grains would be a good source of minerals, if it weren't for their very high phytic acid content. Even though whole grains are full of minerals, replacing refined grains with whole grains in the diet (and especially adding extra bran) actually reduces the overall absorption of a number of minerals (free text, check out table 4). This has been confirmed repeatedly for iron, zinc, calcium, magnesium and phosphorus. Refining grains gets rid of the vitamins and minerals, but at least refined grains don't prevent you from absorbing the minerals in the rest of your food. Here's a comparison of a few of the nutrients in one cup of cooked brown vs. unenriched white rice (218 vs. 242 calories):
Brown rice would be quite nutritious if we could absorb all those minerals. There are a few ways to increase mineral absorption from whole grains. One way is to soak them in slightly acidic, warm water, which allows their own phytase enzyme to break down phytic acid. This doesn't seem to do much for brown rice, which doesn't contain much phytase. A more effective method is to grind grains and soak them before cooking, which helps the phytase function more effectively, especially in gluten grains and buckwheat. The most effective method by far, and the method of choice among healthy traditional cultures around the world, is to soak, grind and ferment whole grains. This breaks down nearly all the phytic acid, making whole grains a good source of both minerals and vitamins. The paper "Dietary Fibre and Mineral Bioavailability" listed another method of increasing mineral absorption from whole grains. Certain foods can increase the absorption of minerals from whole grains high in phytic acid. These include: foods rich in vitamin C such as fruit or potatoes; meat including fish; and dairy. Another point the paper made was that the phytic acid content of vegetarian diets is often very high, potentially leading to mineral deficiencies. The typical modern vegetarian diet containing brown rice and unfermented soy products is very high in phytic acid, and therefore it may make sense to ensure plentiful sources of easily absorbed minerals in the diet, such as dairy. The more your diet depends on plant sources for minerals, the more careful you have to be about how you prepare your food.
One of the things I've been noticing in my readings on grain processing and mineral bioavailability is that it's difficult to make whole grains into a good source of minerals. Whole grains naturally contain more minerals that milled grains where the bran and germ are removed, but most of the minerals are bound up in ways that prevent their absorption. The phytic acid content of whole grains is the main reason for their low mineral bioavailability. Brown rice, simply cooked, provides very little iron and essentially no zinc due to its high concentration of phytic acid. Milling brown rice, which turns it into white rice, removes most of the minerals but also most of the phytic acid, leaving mineral bioavailability similar to or perhaps even better than brown rice (the ratio of phytic acid to iron and zinc actually decreases after milling rice). If you're going to throw rice into the rice cooker without preparing it first, white rice may actually deliver an overall higher level of certain minerals than brown rice, though brown rice may have other advantages such as a higher feeling of fullness per calorie. Either way, the mineral availability of rice is low. Here's how Dr. Robert Hamer's group put it when they evaluated the mineral content of 56 varieties of Chinese rice:This study shows that the mineral bio-availability of Chinese rice varieties will be [less than] 4%. Despite the variation in mineral contents, in all cases the [phytic acid] present is expected to render most mineral present unavailable. We conclude that there is scope for optimisation of mineral contents of rice by matching suitable varieties and growing regions, and that rice products require processing that retains minerals but results in thorough dephytinisation.
It's important to note that milling removes most of the vitamin content of the brown rice, and most of the fiber, both of which could be disadvantageous depending on what your overall diet looks like. Potatoes and other tubers contain much less phytic acid than whole grains, which may be one reason why they're a common feature of extremely healthy cultures such as the Kitavans. I went on NutritionData to see if potatoes have a better mineral-to-phytic acid ratio than grains. They do have a better ratio than whole grains, although whole grains contain more total minerals. Soaking grains reduces their phytic acid content, but the extent depends on the grain. Gluten grain flours digest their own phytic acid very quickly when soaked, due to the presence of the enzyme phytase. Because of this, bread is fairly low in phytic acid, although whole grain yeast breads contain more than sourdough breads. Buckwheat flour also has a high phytase activity. The more intact the grain, the slower it breaks down its own phytic acid upon soaking. Some grains, like rice, don't have much phytase activity so they degrade phytic acid slowly. Other grains, like oats and kasha, are toasted before you buy them, which kills the phytase. Whole grains generally contain so much phytic acid that modest reductions don't free up much of the mineral content for absorption. Many of the studies I've read, including this one, show that soaking brown rice doesn't really free up its zinc or iron content. But I like brown rice, so I want to find a way to prepare it well. It's actually quite rich in vitamins and minerals if you can absorb them. One of the things many of these studies overlook is the effect of pH on phytic acid degradation. Grain phytase is maximally active around pH 4.5-5.5. That's slightly acidic. Most of the studies I've read soaked rice in water with a neutral pH, including the one above. Adding a tablespoon of whey, yogurt, vinegar or lemon juice per cup of grains to your soaking medium will lower the pH and increase phytase activity. Temperature is also an important factor, with approximately 50 C (122 F) being the optimum. I like to put my soaking grains and beans on the heating vent in my kitchen. I don't know exactly how much adding acid and soaking at a warm temperature will increase the mineral availability of brown rice (if at all), because I haven't found it in the literature. The bacteria present if you soak it in whey, unfiltered vinegar or yogurt could potentially aid the digestion of phytic acid. Another strategy is to add the flour of a high-phytase grain like buckwheat to the soaking medium. This works for soaking flours, perhaps it would help with whole grains as well?So now we come to the next problem. Phytic acid is a medium-sized molecule. If you break it down and it lets go of the minerals it's chelating, the minerals are more likely to diffuse out of the grain into your soaking medium, which you then discard because it also contains the tannins, saponins and other anti-nutrients that you want to get rid of. That seems to be exactly what happens, at least in the case of brown rice. So what's the best solution for maximal mineral and vitamin content? Do what traditional cultures have been doing for millenia: soak, grind and ferment whole grains. This eliminates nearly all the phytic acid, dramatically increasing mineral bioavailiability. Fermenting batter doesn't lose minerals because there's nowhere for them to go. In the West, we use this process to make bread. In Africa, they do it to make ogi, injera, and a number of other fermented grain dishes. In India, they grind rice and beans to make idli and dosas. In the Phillipines, they ferment ground rice to make puto. Fermenting ground whole grains is the most reliable way to improve their mineral bioavailability and nutritional value in general. But isn't having a rice cooker full of steaming brown rice so nice? I'm still working on finding a reliable way to increase its nutritional value.
Our story begins in East Africa in 1935, with two Bantu tribes called the Kikuyu and the Wakamba. Their traditional diets were mostly vegetarian and consisted of sweet potatoes, corn, beans, plantains, millet, sorghum, wild mushrooms and small amounts of dairy, small animals and insects. Their food was agricultural, high in carbohydrate and low in fat.Dr. Weston Price found them in good health, with well-formed faces and dental arches, and a dental cavity rate of roughly 6% of teeth. Although not as robust or as resistant to tooth decay as their more carnivorous neighbors, the "diseases of civilization" such as cardiovascular disease and obesity were nevertheless rare among them. South African Bantu eating a similar diet have a low prevalence of atherosclerosis, and a measurable but low incidence of death from coronary heart disease, even in old age.How do we reconcile this with the archaeological data showing a general decline in human health upon the adoption of agriculture? Humans did not evolve to tolerate the toxins, anti-nutrients and large amounts of fiber in grains and legumes. Our digestive system is designed to handle a high-quality omnivorous diet. By high-quality, I mean one that has a high ratio of calories to indigestible material (fiber). Our species is very good at skimming off the highest quality food in nearly any ecological niche. Animals that are accustomed to high-fiber diets, such as cows and gorillas, have much larger, more robust and more fermentative digestive systems.One factor that reconciles the Bantu data with the archaeological data is that much of the Kikuyu and Wakamba diet came from non-grain sources. Sweet potatoes and plantains are similar to the starchy wild plants our ancestors have been eating for nearly two million years, since the invention of fire (the time frame is debated but I think everyone agrees it's been a long time). Root vegetables and starchy fruit ted to have a higher nutrient bioavailibility than grains and legumes due to their lower content of anti-nutrients.The second factor that's often overlooked is food preparation techniques. These tribes did not eat their grains and legumes haphazardly! This is a factor that was overlooked by Dr. Price himself, but has been emphasized by Sally Fallon. Healthy grain-based African cultures often soaked, ground and fermented their grains before cooking, creating a porridge that's nutritionally superior to unfermented grains. The bran was removed from corn and millet during processing, if possible. Legumes were always soaked prior to cooking.These traditional food processing techniques have a very important effect on grains and legumes that brings them closer in line with the "paleolithic" foods our bodies are designed to digest. They reduce or eliminate toxins such as lectins and tannins, greatly reduce anti-nutrients such as phytic acid and protease inhibitors, and improve vitamin content and amino acid profile. Fermentation is particularly effective in this regard. One has to wonder how long it took the first agriculturalists to discover fermentation, and whether poor food preparation techniques or the exclusion of animal foods could account for their poor health.I recently discovered a paper that illustrates these principles: "Influence of Germination and Fermentation on Bioaccessibility of Zinc and Iron from Food Grains". It's published by Indian researchers who wanted to study the nutritional qualities of traditional fermented foods. One of the foods they studied was idli, a South Indian steamed "muffin" made from rice and beans. The amount of minerals your digestive system can extract from a food depends in part on the food's phytic acid content. Phytic acid is a molecule that traps certain minerals (iron, zinc, magnesium, calcium), preventing their absorption. Raw grains and legumes contain a lot of it, meaning you can only absorb a fraction of the minerals present in them.In this study, soaking had a modest effect on the phytic acid content of the grains and legumes examined. Fermentation, on the other hand, completely broke down the phytic acid in the idli batter, resulting in 71% more bioavailable zinc and 277% more bioavailable iron. It's safe to assume that fermentation also increased the bioavailability of magnesium, calcium and other phytic acid-bound minerals.Fermenting the idli batter also completely eliminated its tannin content. Tannins are a class of molecules found in many plants that are sometimes toxins and anti-nutrients. In sufficient quantity, they reduce feed efficiency and growth rate in a variety of species.Lectins are another toxin that's frequently mentioned in the paleolithic diet community. They are blamed for everything from digestive problems to autoimmune disease. One of the things people like to overlook in this community is that traditional processing techniques such as soaking, sprouting, fermentation and cooking, greatly reduce or eliminate lectins from grains and legumes. One notable exception is gluten, which survives all but the longest fermentation and is not broken down by cooking.Soaking, sprouting, fermenting, grinding and cooking are the techniques by which traditional cultures have been making the most of grain and legume-based diets for thousands of years. We ignore these time-honored traditions at our own peril.
I'm happy to say, it's time for a new installment of the "Paleolithic Diet Clinical Trials" series. The latest study was recently published in the European Journal of Clinical Nutrition by Dr. Anthony Sebastian's group. Dr. Sebastian has collaborated with Drs. Loren Cordain and Boyd Eaton in the past. This new trial has some major problems, but I believe it nevertheless adds to the weight of the evidence on "paleolithic"-type diets. The first problem is the lack of a control group. Participants were compared to themselves, before eating a paleolithic diet and after having eaten it for 10 days. Ideally, the paleolithic group would be compared to another group eating their typical diet during the same time period. This would control for effects due to getting poked and prodded in the hospital, weather, etc. The second major problem is the small sample size, only 9 participants. I suspect the investigators had a hard time finding enough funding to conduct a larger study, since the paleolithic approach is still on the fringe of nutrition science. I think this study is best viewed as something intermediate between a clinical trial and 9 individual anecdotes. Here's the study design: they recruited 9 sedentary, non-obese people with no known health problems. They were 6 males and 3 females, and they represented people of African, European and Asian descent. Participants ate their typical diets for three days while investigators collected baseline data. Then, they were put on a seven-day "ramp-up" diet higher in potassium and fiber, to prepare their digestive systems for the final phase. In the "paleolithic" phase, participants ate a diet of:Meat, fish, poultry, eggs, fruits, vegetables, tree nuts, canola oil, mayonnaise, and honey... We excluded dairy products, legumes, cereals, grains, potatoes and products containing potassium chloride...
Mmm yes, canola oil and mayo were universally relished by hunter-gatherers. They liked to feed their animal fat and organs to the vultures, and slather mayo onto their lean muscle meats. Anyway, the paleo diet was higher in calories, protein and polyunsaturated fat (I assume with a better n-6 : n-3 ratio) than the participants' normal diet. It contained about the same amount of carbohydrate and less saturated fat.There are a couple of twists to this study that make it more interesting. One is that the diets were completely controlled. The only food participants ate came from the experimental kitchen, so investigators knew the exact calorie intake and nutrient composition of what everyone was eating. The other twist is that the investigators wanted to take weight loss out of the picture. They wanted to know if a paleolithic-style diet is capable of improving health independent of weight loss. So they adjusted participants' calorie intake to make sure they didn't lose weight. This is an interesting point. Investigators had to increase the participants' calorie intake by an average of 329 calories a day just to get them to maintain their weight on the paleo diet. Their bodies naturally wanted to shed fat on the new diet, so they had to be overfed to maintain weight.On to the results. Participants, on average, saw large improvements in nearly every meaningful measure of health in just 10 days on the "paleolithic" diet. Remember, these people were supposedly healthy to begin with. Total cholesterol and LDL dropped. Triglycerides decreased by 35%. Fasting insulin plummeted by 68%. HOMA-IR, a measure of insulin resistance, decreased by 72%. Blood pressure decreased and blood vessel distensibility (a measure of vessel elasticity) increased. It's interesting to note that measures of glucose metabolism improved dramatically despite no change in carbohydrate intake. Some of these results were statistically significant, but not all of them. However, the authors note that:In all these measured variables, either eight or all nine participants had identical directional responses when switched to paleolithic type diet, that is, near consistently improved status of circulatory, carbohydrate and lipid metabolism/physiology.
Translation: everyone improved. That's a very meaningful point, because even if the average improves, in many studies a certain percentage of people get worse. This study adds to the evidence that no matter what your gender or genetic background, a diet roughly consistent with our evolutionary past can bring major health benefits. Here's another way to say it: ditching certain modern foods can be immensely beneficial to health, even in people who already appear healthy. This is true regardless of whether or not one loses weight.There's one last critical point I'll make about this study. In figure 2, the investigators graphed baseline insulin resistance vs. the change in insulin resistance during the course of the study for each participant. Participants who started with the most insulin resistance saw the largest improvements, while those with little insulin resistance to begin with changed less. There was a linear relationship between baseline IR and the change in IR, with a correlation of R=0.98, p less than 0.0001. In other words, to a highly significant degree, participants who needed the most improvement, saw the most improvement. Every participant with insulin resistance at the beginning of the study ended up with basically normal insulin sensitivity after 10 days. At the end of the study, all participants had a similar degree of insulin sensitivity. This is best illustrated by the standard deviation of the fasting insulin measurement, which decreased 9-fold over the course of the experiment.
Here's what this suggests: different people have different degrees of susceptibility to the damaging effects of the modern Western diet. This depends on genetic background, age, activity level and many other factors. When you remove damaging foods, peoples' metabolisms normalize, and most of the differences in health that were apparent under adverse conditions disappear. I believe our genetic differences apply more to how we react to adverse conditions than how we function optimally. The fundamental workings of our metabolisms are very similar, having been forged mostly in hunter-gatherer times. We're all the same species after all.
This study adds to the evidence that modern industrial food is behind our poor health, and that a return to time-honored foodways can have immense benefits for nearly anyone. A paleolithic-style diet may be an effective way to claim your genetic birthright to good health.
Paleolithic Diet Clinical Trials
Paleolithic Diet Clinical Trials Part II
One Last Thought
