Butter, Margarine and Heart Disease

Shortly after World War II, margarine replaced butter in the U.S. food supply. Margarine consumption exceeded butter in the 1950s. By 1975, we were eating one-fourth the amount of butter eaten in 1900 and ten times the amount of margarine. Margarine was made primarily of hydrogenated vegetable oils, as many still are today. This makes it one of our primary sources of trans fat. The consumption of trans fats from other sources also likely tracked closely with margarine intake.


Coronary heart disease (CHD) resulting in a loss of blood flow to the heart (heart attack), was first described in detail in 1912 by Dr. James B. Herrick. Sudden cardiac death due to CHD was considered rare in the 19th century, although other forms of heart disease were diagnosed regularly by symptoms and autopsies. They remain rare in many non-industrial cultures today. This could not have resulted from massive underdiagnosis because heart attacks have characteristic symptoms, such as chest pain that extends along the arm or neck. Physicians up to that time were regularly diagnosing heart conditions other than CHD. The following graph is of total heart disease mortality in the U.S. from 1900 to 2005. It represents all types of heart disease mortality, including 'heart failure', which are non-CHD disorders like arrhythmia and myocarditis.

The graph above is not age-adjusted, meaning it doesn't reflect the fact that lifespan has increased since 1900. I couldn't compile the raw data myself without a lot of effort, but the age-adjusted graph is here. It looks similar to the one above, just a bit less pronounced. I think it's interesting to note the close similarity between the graph of margarine intake and the graph of heart disease deaths. The butter intake graph is also essentially the inverse of the heart disease graph.

Here's where it gets really interesting. The U.S. Centers for Disease Control has also been tracking CHD deaths specifically since 1900. Again, it would be a lot of work for me to compile the raw data, but it can be found here and a graph is in Anthony Colpo's book The Great Cholesterol Con. Here's the jist of it: there was essentially no CHD mortality until 1925, at which point it skyrocketed until about 1970, becoming the leading cause of death. After that, it began to fall due to improved medical care. There are some discontinuities in the data due to changes in diagnostic criteria, but even subtracting those, the pattern is crystal clear.

The age-adjusted heart disease death rate (all forms of heart disease) has been falling since the 1950s, largely due to improved medical treatment. Heart disease incidence has not declined substantially, according to the Framingham Heart study. We're better at keeping people alive in the 21st century, but we haven't successfully addressed the root cause of heart disease.

Was the shift from butter to margarine involved in the CHD epidemic? We can't make any firm conclusions from these data, because they're purely correlations. But there are nevertheless mechanisms that support a protective role for butter, and a detrimental one for margarine. Butter from pastured cows is one of the richest known sources of vitamin K2. Vitamin K2 plays a central role in protecting against arterial calcification, which is an integral part of arterial plaque and the best single predictor of cardiovascular death risk. In the early 20th century, butter was typically from pastured cows.

Margarine is a major source of trans fat. Trans fat is typically found in vegetable oil that has been hydrogenated, rendering it solid at room temperature. Hydrogenation is a chemical reaction that is truly disgusting. It involves heat, oil, hydrogen gas and a metal catalyst. I hope you give a wide berth to any food that says "hydrogenated" anywhere in the ingredients. Some modern margarine is supposedly free of trans fats, but in the U.S., less than 0.5 grams per serving can be rounded down so the nutrition label is not a reliable guide. Only by looking at the ingredients can you be sure that the oils haven't been hydrogenated. Even if they aren't, I still don't recommend margarine, which is an industrially processed pseudo-food.

One of the strongest explanations of CHD is the oxidized LDL hypothesis. The idea is that LDL lipoprotein particles ("LDL cholesterol") become oxidized and stick to the vessel walls, creating an inflammatory cascade that results in plaque formation. Chris Masterjohn wrote a nice explanation of the theory here. Several things influence the amount of oxidized LDL in the blood, including the total amount of LDL in the blood, the antioxidant content of the particle, the polyunsaturated fat content of LDL (more PUFA = more oxidation), and the size of the LDL particles. Small LDL is considered more easily oxidized than large LDL. Small LDL is also associated with elevated CHD mortality. Trans fat shrinks your LDL compared to butter.

In my opinion, it's likely that both the decrease in butter consumption and the increase in trans fat consumption contributed to the massive incidence of CHD seen in the U.S. and other industrial nations today. I think it's worth noting that France has the highest per-capita dairy fat consumption of any industrial nation, along with a comparatively low intake of hydrogenated fat, and also has the second-lowest rate of CHD, behind Japan.

U.S. Weight, Lifestyle and Diet Trends, 1970- 2007

For this post, I compiled statistics on U.S. weight, health and lifestyle trends, and graphed them as consistently as possible. They span the period from 1970 to 2007, during which the obesity rate doubled. The data come from the National Health and Nutrition Examination Survey (NHANES), the Behavioral Risk Factor Surveillance System (BRFSS), and the U.S. Department of Agriculture (USDA). Some of the graphs are incomplete, either because the data don't exist, or because I wasn't able to find them. Obesity is defined as a body mass index (BMI) of 30+; overweight is a BMI of 25+. Yes, it's frightening. It has affected adults and children (NHANES).
The percentage of Americans who report exercising in their spare time has actually increased since 1988 (BRFSS).
We're eating about 250 more calories per day, according to NHANES.
The 250 extra calories are coming from carbohydrate (NHANES).

We're eating more vegetables and fruit (USDA).
We're eating more meat by weight, although calories from meat have probably gone down because the meat has gotten leaner (USDA). This graph represents red meat, fish and poultry. The increase comes mostly from poultry. Boneless, skinless chicken breasts anyone?
We're eating more sugar (USDA). The scale of the graph doesn't allow you to fully appreciate that sweetener consumption had increased by a full 100 calories per day by 1999, although it has dropped a bit since then. This is based on food disappearance data. In other words, the amount consumed is estimated using the amount sold domestically, minus a percentage that approximates waste. High-fructose corn syrup has seized nearly 50% of the sweetener market since 1970.
Again, the scale of the graph doesn't allow you to fully appreciate the magnitude of the change here. In 2000, we ate approximately 2.5 ounces, or 280 calories, more processed grains per day than in 1970 (USDA). That has since decreased slightly (34 calories). You might be saying to yourself right now "hey, that plus the 100 calories from sugar adds up to more of an increase than the NHANES data show!" Yes, and I think that points to the fact that the data sets are not directly comparable. NHANES data are self-reported whereas USDA data are collected from vendors. Regardless of the absolute numbers, our processed grain consumption has gone way up since 1970.

Wheat is still king. Although we grow a lot of corn in this country, most of it gets fed to animals. We prefer eating wheat without first feeding it to an intermediary. In absolute quantity, wheat consumption has increased more than any other grain (not including corn syrup).
Bye bye whole milk. Hello skim milk (USDA).

This graph represents "added fats", as opposed to fats that occur naturally in meat or milk (the USDA does not track the latter). Added fats include salad oil, cooking oil, deep fry oil, butter, lard, tallow, etc. We are eating a lot more vegetable oil than we were in 1970. It comes chiefly from the industrial, omega-6 rich oils such as soybean, corn and canola. Added animal fats have increased slightly, but it's pretty insignificant in terms of calories.

There is an artifact in this graph that I have to point out. In 2000, the USDA changed the way it gathered vegetable oil data. This led to an abrupt, apparent increase in its consumption that is obvious on the graph. So it's difficult to make any quantitative conclusions, but I think it's clear nevertheless that vegetable oil intake has increased considerably.

Between 1970 and 1980, something changed in the U.S. that caused a massive increase in obesity and other health problems. Some combination of factors reached a critical mass that our metabolism could no longer tolerate. The three biggest changes in the American diet since 1970:

• An increase in cereal grain consumption, particularly wheat.
• An increase in sweetener consumption
• The replacement of meat and milk fat with industrial vegetable oils, with total fat intake remaining the same.

Mainstream America has done to itself what it did to native American and other indigenous cultures worldwide, with the same result.

Peripheral vs. Ectopic Fat

I went to an interesting presentation the other day by Dr. George Ioannou of the University of Washington, on obesity and liver disease. He made an interesting distinction between the health effects of two types of body fat. The first is called subcutaneous fat (or peripheral fat). It accumulates right under the skin and is evenly distributed over the body's surface area, including extremities. The second is called ectopic fat. Ectopic means "not where it's supposed to be". It accumulates in the abdominal region (beer belly), the liver, muscle tissue including the heart, the pancreas, and perhaps in lipid-rich deposits in the arteries. Subcutaneous fat can be measured by taking skinfold thickness in different places on the body, or sometimes by measuring arm or leg circumference. Ectopic fat can be measured by taking waist circumference.

It's an absolutely critical distinction, because ectopic fat associates with poor health outcomes while subcutaneous fat does not. In this recent study, waist circumference was associated with increased risk of death while arm and leg circumference were associated with a reduced risk of death. I think the limb circumference association in this particular study is probably confounded by muscle mass, but other studies have also shown a strong, consistent association between ectopic fat and risk of death, but not subcutaneous fat. The same goes for dementia and a number of other diseases. I think it's more than an epidemiological asssociation. Surgically removing the abdominal fat from mice prevents insulin resistance and prolongs their lifespan.

People with excess visceral fat are also much more likely to have fatty liver and cirrhosis. It makes sense if you think of them both as manifestations of ectopic fat. There's a spectrum of disorders that goes along with excess visceral fat and fatty liver: it's called the metabolic syndrome, and it affects a quarter of Americans (NHANES III). We already have a pretty good idea of what causes fatty liver, at least in lab animals: industrial vegetable oils and sugar. What's the most widely used animal model of metabolic syndrome? The sugar-fed rat. What are two of the main foods whose consumption has increased in recent decades? Vegetable oil and sugar. Hmm... Fatty liver is capable of causing insulin resistance and diabetes, according to a transgenic mouse that expresses a hepatitis C protein in its liver.

You want to keep your liver happy. All those blood tests they do in the doctor's office to see if you're healthy-- cholesterol levels, triglycerides, insulin, glucose-- reflect liver function to varying degrees.

Abdominal fat is a sign of ectopic fat distribution throughout the body, and its associated metabolic consequences. I think we know it's unhealthy on a subconscious level, because belly fat is not attractive whereas nicely distributed subcutaneous fat can be. If you have excess visceral fat, take it as a sign that your body does not like your current lifestyle. It might be time to think about changing your diet and exercise regime. Here are some ideas.

Polyunsaturated Fat Intake: What About Humans?

Now we know how to raise a healthy pig or rat: balance omega-6 linoleic acid (LA) and omega-3 alpha-linolenic acid (LNA) and keep both relatively low. LA and LNA are the most basic (and shortest) forms of omega-6 and omega-3 fats. They are the only fats the body can't make on its own. They're found in plant foods, and animal foods to a lesser extent. Animals convert them to longer-chain fats like arachidonic acid (AA; omega-6), EPA (omega-3) and DHA (omega-3). These long-chain, animal PUFA are involved in a dizzying array of cellular processes. They participate directly as well as being further elongated to form eicosanoids, a large class of very influential signaling molecules.

AA is the precursor of a number of inflammatory eicosanoids, while omega-3-derived eicosanoids tend to be less inflammatory and participate in long-term repair processes. A plausible explanation for the negative health effects of LA-rich vegetable oils is the fact that they lead to an imbalance in cellular signaling by increasing the formation of AA and decreasing the formation of EPA and DHA. Both inflammatory and anti-inflammatory signaling are necessary in the proper context, but they must be in balance for optimal function. Many modern diseases involve excess inflammation. LA also promotes oxidative and nitrosative damage to organs, as explained in the last post. This is an enormous oversimplification, but I'll skip over the details (most of which I don't know) because they could fill a stack of textbooks.

How do we raise a healthy human? Although I think pigs are a decent model organism for studying diet and health as it relates to humans, they don't have as much of a carnivorous history as we do. You would expect them to be more efficient at converting plant nutrients to their animal counterparts: carotenes to vitamin A, vitamin K1 to K2, and perhaps short-chain polyunsaturated fats (PUFA) to long-chain fats like AA, EPA and DHA. I mention it simply to point out that what goes for a pig may not necessarily go for a human when it comes to fatty acid conversion.

I've dug up a few papers exploring this question. I don't intend this post to be comprehensive but I think it's enough to get a flavor of what's going on. The first paper is an intervention trial comparing the effect of flax oil and fish oil supplementation on the fat composition of red blood cells. Investigators gave volunteers either 1.2 g, 2.4 g or 3.6 g (one teaspoon) flax oil per day; or 0.6 g or 1.2 g fish oil per day. The volunteers were U.S. firefighters, who otherwise ate their typical diet rich in omega-6. Flax oil supplementation at the two higher doses increased EPA, but did not increase DHA or decrease AA significantly. This suggests that humans can indeed convert some ALA to long-chain omega-3 fats, but adding ALA to a diet that is already high in omega-6 does not reduce AA or increase the all-important DHA.

The fish oil supplement, even at one-sixth the highest flax oil dose, increased EPA and DHA to a greater extent than flax oil, and also decreased AA. This shows that fish oil has a greater effect than flax oil on the fat profile of red blood cells in the context of a diet rich in omega-6. Another study also found that ALA intake is not associated with EPA or DHA in blood plasma. This could suggest either that humans aren't very good at converting ALA to longer n-3 fats, that the pathways are blocked by excessive LA or some other factor (a number of things block conversion of omega-3 fats), or that our bodies are already converting sufficient omega-3 and fish oil is overkill.

What happens when you reduce omega-6 consumption while increasing omega-3? In one study, participants were put on a "high LA" or "low LA" (3.8% of calories) diet. The first had an omega-6 : omega-3 ratio of 10.1, while the second had a ratio of 4.0. As in the previous intervention study, EPA was higher on the low LA diet. Here's where it gets interesting: DHA levels fell precipitously throughout the study, regardless of which diet the participants were eating. This has to do with a special requirement of the study diet: participants were not allowed to eat seafood. This shows that most of the DHA in the blood is obtained by eating DHA from animal fat, rather than elongating it from ALA such as flax oil. This agrees with the finding that strict vegetarians (vegans) have a low level of DHA in blood plasma.

In another intervention study, researchers achieved a better omega-6 : omega-3 ratio, with participants going from a baseline ratio of 32.2 to an experimental ratio of 2.2 for 10 weeks. The change in ratio was mostly from increasing omega-3, rather than decreasing omega-6. This caused an increase in serum EPA and DHA, although the DHA did not quite reach statistical significance (p= 0.06). In this study, participants were encouraged to eat fish 3 times per week, which is probably the reason their DHA rose. Participants saw a metabolic shift to fat burning, and an increase in insulin sensitivity that was on the cusp of statistical significance (p= 0.07).

I think what the data suggest is that humans can convert short-chain omega-3 (ALA) to EPA, but we don't efficiently elongate it to DHA. At least in the context of a high LA intake. Another thing to keep in mind is that serum PUFA are partially determined by what's in fat tissue. Modern Americans have an abnormally high proportion of LA in their fat tissue, sometimes over 20%. This contributes to a higher proportion of omega-6 and its derivatives in all tissues. "Wild" humans, including our paleolithic ancestors, would probably have values in the lower single digits. LA in fat tissue has a half-life of about 2 years, so restoring balance is a long-term process. Omega-3 fats do not accumulate to the same degree as LA, typically comprising about 1% of fat tissue. At this point, one could rightly ask: we know how diet affects blood polyunsaturated fats, but what's the relevance to health? There are multiple lines of evidence, all of which point in generally the same direction in my opinion.

There are associations between omega-6 intake (from vegetable oils), low omega-3 intake, and a number of health and psychiatric problems. Another line of evidence comes from intervention trials. The Lyon diet-heart study was one of the most successful intervention trials of all time. The experimental group increased their intake of fish, poultry, root vegetables, green vegetables, bread and fruit, while decreasing intake of red meat and dairy fat. A key difference between this study and other intervention trials is that participants were encouraged to eat a margarine rich in omega-3 ALA. In sum, participants decreased their total PUFA intake, decreased omega-6 intake and increased intake of ALA and long-chain omega-3s. After an average of 27 months, total mortality was 70% lower in the intervention group than in the control group eating the typical diet! This effect was not seen in trials that encouraged vegetable and grain consumption, discouraged red meat and dairy fat consumption, but didn't alter PUFA intake or the omega-6 : omega-3 ratio, such as the Women's Health Initiative.

As usual, the most important line of evidence comes from healthy non-industrial cultures that did not suffer from modern non-communicable diseases. They invariably consumed very little omega-6 LA (3% of calories or less), ate a roughly balanced amount of omega-6 and omega-3, and had a source of long-chain (animal) omega-3. They did not eat much omega-3 from plant sources (such as flax), as concentrated sources are rare in nature. Dr. Weston Price observed that cultures throughout the world sought out seafood if available, sometimes going to great lengths to obtain it. Here's an exerpt from Nutrition and Physical Degeneration about Fiji islanders:

Since Viti Levu, one of the islands of this group, is one of the larger islands of the Pacific Ocean, I had hoped to find on it a district far enough from the sea to make it necessary for the natives to have lived entirely on land foods. Accordingly, with the assistance of the government officials and by using a recently opened government road I was able to get well into the interior of the island by motor vehicle, and from this point to proceed farther inland on foot with two guides. I was not able, however, to get beyond the piles of sea shells which had been carried into the interior. My guide told me that it had always been essential, as it is today, for the people of the interior to obtain some food from the sea, and that even during the times of most bitter warfare between the inland or hill tribes and the coast tribes, those of the interior would bring down during the night choice plant foods from the mountain areas and place them in caches and return the following night and obtain the sea foods that had been placed in those depositories by the shore tribes. The individuals who carried these foods were never molested, not even during active warfare. He told me further that they require food from the sea at least every three months, even to this day. This was a matter of keen interest, and at the same time disappointment since one of the purposes of the expedition to the South Seas was to find, if possible, plants or fruits which together, without the use of animal products, were capable of providing all of the requirements of the body for growth and for maintenance of good health and a high state of physical efficiency.

Price searched for, but did not find, vegetarian groups that were free of the diseases of civilization. What he found were healthy cultures that put a strong emphasis on nutrient-dense animal foods, particularly seafoods when available. I think all this information together suggests that the optimum, while being a fairly broad range, is a low intake of omega-6 LA (less than 3% of calories) and a modest intake of animal omega-3 for DHA.

I believe the most critical element is reducing omega-6 LA by eliminating industrial vegetable oils (soybean, corn, cottonseed, etc.) and the foods that contain them from the diet. Fats from pasture-raised ruminants (butter, beef, lamb etc.) and wild fish are naturally balanced. We no longer commonly eat the most concentrated land source of DHA, brain, so I think it's wise to eat seafood sometimes. According to the first study I cited, 1/4 teaspoon of fish oil (or cod liver oil) per day is enough to elevate plasma DHA quite significantly. This amount of omega-3 could be obtained by eating seafood weekly.

Polyunsaturated Fat Intake: Effects on the Heart and Brain

I'm revisiting the topic of the omega-6/omega-3 balance and total polyunsaturated fat (PUFA) intake because of some interesting studies I've gotten a hold of lately (thanks Robert). Two of the studies are in pigs, which I feel are a decent model organism for studying the effect of diet on health as it relates to humans. Pigs are omnivorous (although more slanted toward plant foods), have a similar digestive system to humans (although sturdier), are of similar size and fat composition to humans, and have been eating grains for about the same amount of time as humans.

In the last post on the omega-6/omega-3 balance, I came to the conclusion that a roughly balanced but relatively low intake of omega-6 and omega-3 fats is consistent with the diets of healthy non-industrial cultures. There were a few cultures that had a fairly high long-chain omega-3 intake from seafood (10% of calories), but none ate much omega-6.

The first study explores the effect of omega-6 and omega-3 fats on heart function. Dr. Sheila Innis and her group fed young male pigs three different diets:

1. An unbalanced, low PUFA diet. Pig chow with 1.2% linoleic acid (LA; the main omega-6 plant fat) and 0.06% alpha linolenic acid (ALA; the main omega-3 plant fat).
   
2. A balanced, low PUFA diet. Pig chow with 1.4% LA and 1.2% ALA.
3. An unbalanced, but better-than-average, "modern diet". Pig chow with 11.6% LA and 1.2% ALA.

After 30 days, they took a look at the pigs' hearts. Pigs from the first and third (unbalanced) groups contained more "pro-inflammatory" fats (arachidonic acid; AA) and less "anti-inflammatory" fats (EPA and DHA) than the second group. The first and third groups also experienced an excessive activation of "pro-inflammatory" proteins, such as COX-2, the enzyme inhibited by aspirin, ibuprofen and other NSAIDs.

The most striking finding of all was the difference in lipid peroxidation between groups. Lipid peroxidation is a measure of oxidative damage to cellular fats. In the balanced diet hearts, peroxidation was half the level found in the first group, and one-third the level found in the third group! This shows that omega-3 fats exert a powerful anti-oxidant effect that can be more than counteracted by excessive omega-6. Nitrosative stress, another type of damage, tracked with n-6 intake regardless of n-3, with the third group almost tripling the first two. I think this result is highly relevant to the long-term development of cardiac problems, and perhaps cardiovascular disease in general.

In another study with the same lead author Sanjoy Ghosh, rats fed a diet enriched in omega-6 from sunflower oil showed an increase in nitrosative damage, damage to mitochondrial DNA, and a decrease in maximum cardiac work capacity (i.e., their hearts were weaker). This is consistent with the previous study and shows that the mammalian heart does not like too much omega-6! The amount of sunflower oil these rats were eating (20% food by weight) is not far off from the amount of industrial oil the average American eats.

A third paper by Dr. Sheila Innis' group studied the effect of the omega-6 : omega-3 balance on the brain fat composition of pigs, and the development of neurons in vitro (in a culture dish). There were four diets, the first three similar to those in the first study:

1. Deficient. 1.2% LA and 0.05% ALA.
2. Contemporary. 10.7% LA and 1.1% ALA.
   
3. Evolutionary. 1.2% LA and 1.1% ALA.
4. Supplemented. The contemporary diet plus 0.3% AA and 0.3% DHA.

The first thing they looked at was the ability of the animals to convert ALA to DHA and concentrate it in the brain. DHA is critical for brain and eye development and maintenance. The evolutionary diet was most effective at putting DHA in the brain, with the supplemented diet a close second and the other three lagging behind. The evolutionary diet was the only one capable of elevating EPA, another important fatty acid derived from ALA. If typical fish oil rather than isolated DHA and AA had been given as the supplement, that may not have been the case. Overall, the fatty acid composition of the brain was quite different in the evolutionary group than the other three groups, which will certainly translate into a variety of effects on brain function.

The researchers then cultured neurons and showed that they require DHA to develop properly in culture, and that long-chain omega-6 fats are a poor substitute. Overall, the paper shows that the modern diet causes a major fatty acid imbalance in the brain, which is expected to lead to developmental problems and probably others as well. This can be partially corrected by supplementing with fish oil.

Together, these studies are a small glimpse of the countless effects we are having on every organ system, by eating fats that are unfamiliar to our pre-industrial bodies. In the next post, I'll put this information into the context of the modern human diet.

Real Food X: Roasted Marrow Bones

Bone marrow is a food that has been prized throughout history-- from hunter-gatherer tribes to haute cuisine chefs. It's not hard to understand why, once you've tasted it. It's delicate, meaty and fatty. It's also rich in fat-soluble vitamins, including vitamins K1 and K2, although this will depend on what the animal has eaten.

Roasted marrow bones make a simple appetizer. Beef bones are the best because of their size. Select wide bones that are cut about three inches long. They should be from the femur or the humerus, called the "shank bones". These are sometimes available in the frozen meats section of a grocery store, otherwise a butcher can procure them. If you have access to a farmer's market that sells meats, vendors will typically have bones cut for you if you request it.

Recipe

1. Preheat oven to 450 F (230 C).
2. Place bones, cut side up, in a baking dish or oven-proof skillet.
3. Bake for about 15 minutes, until the marrow begins to separate from the bone, but not much longer because it will turn to mush.
4. Scoop out and eat the marrow by itself, on sourdough rye toast or however you please.
5. Make soup stock from the leftover bones.

Vitamin K2 in Marrow

I'm always on the lookout for foods rich in vitamin K2 MK-4, because it's so important and so rare in the modern food system. I heard some internet rumors that marrow might be rich in fat-soluble vitamins. Google let me down, so I decided to look through the rat studies on K2 MK-4 in which they looked at its tissue distribution.

I found one that looked at the K2 MK-4 content in different tissues of rats fed vitamin K1. Marrow was rich in K2, along with testes. It contains 10-20 times more MK-4 than liver by weight, and more than any of the other organs they tested (serum, liver, spleen, kidney, heart, testes, marrow, brain) except testes. They didn't include values for salivary gland and pancreas, the two richest sources.

If we assume beef marrow has the same amount of MK-4 as rat marrow per weight (I have no idea if this is really the case, but it's probably in the ballpark), two ounces of beef marrow would contain about 10 micrograms MK-4. Not a huge source, but significant nevertheless.

Bone marrow was a prized food in many hunter-gatherer societies. Let's see what Dr. Weston Price has to say about it (from Nutrition and Physical Degeneration):

For the Indians living inside the Rocky Mountain Range in the far North of Canada, the successful nutrition for nine months of the year was largely limited to wild game, chiefly moose and caribou. During the summer months the Indians were able to use growing plants. During the winter some use was made of bark and buds of trees. I found the Indians putting great emphasis upon the eating of the organs of the animals, including the wall of parts of the digestive tract. Much of the muscle meat of the animals was fed to the dogs. It is important that skeletons are rarely found where large game animals have been slaughtered by the Indians of the North. The skeletal remains are found as piles of finely broken bone chips or splinters that have been cracked up to obtain as much as possible of the marrow and nutritive qualities of the bones. These Indians obtain their fat-soluble vitamins and also most of their minerals from the organs of the animals. An important part of the nutrition of the children consisted in various preparations of bone marrow, both as a substitute for milk and as a special dietary ration.

Here's a bit more about these same groups, also from Nutrition and Physical Degeneration:

The condition of the teeth, and the shape of the dental arches and the facial form, were superb. Indeed, in several groups examined not a single tooth was found that had ever been attacked by tooth decay. In an examination of eighty-seven individuals having 2,464 teeth only four teeth were found that had ever been attacked by dental caries. This is equivalent to 0.16 per cent. As we came back to civilization and studied, successively, different groups with increasing amounts of contact with modern civilization, we found dental caries increased progressively, reaching 25.5 per cent of all of the teeth examined at Telegraph Creek, the point of contact with the white man's foods. As we came down the Stikine River to the Alaskan frontier towns, the dental caries problem increased to 40 per cent of all of the teeth.

Evidently, the traditionally-living groups were doing something right.

Google Flu Trends

I just discovered a wonderful new tool from Google.org, Google Flu Trends. Google.org is the philanthropic branch of Google. Flu Trends gives you real-time data on flu incidence in your U.S. state, as well as for the country as a whole. Here's how it works:

We've found that certain search terms are good indicators of flu activity. Google Flu Trends uses aggregated Google search data to estimate flu activity in your state up to two weeks faster than traditional flu surveillance systems.

Each week, millions of users around the world search for online health information. As you might expect, there are more flu-related searches during flu season, more allergy-related searches during allergy season, and more sunburn-related searches during the summer.

Google's data match up well with U.S. Centers for Disease Control and Prevention (CDC) data on flu incidence, but are available 1-2 weeks before CDC data. Here's a comparison of Flu Trends and CDC data for previous years. Plus, Google makes the information easily accessible and user-friendly.

I think this a fantastic use of the massive amount of raw information on the internet. It's amazing what a person can do with a brain and an internet connection these days.

Can Vitamin K2 Reverse Arterial Calcification?

It certainly can in rats. In April 2007, Dr. Cees Vermeer and his group published a paper on the effect of vitamin K on arterial calcification (the accumulation of calcium in the arteries). As I mentioned two posts ago, arterial calcification is tightly associated with the risk of heart attack and death. Warfarin-treated rats are an established model of arterial calcification. Warfarin also causes calcification in humans. The drug is a "blood thinner" that inhibits vitamin K recycling, and inhibits the conversion of vitamin K1 (phylloquinone) to K2 MK-4 (menaquinone-4). This latter property turns out to be the critical one in the calcification process.

Rats are able to convert vitamin K1 to K2 MK-4, whereas humans don't seem to convert well. Conversion efficiency varies between species. Dr. Vermeer's group treated rats with warfarin for 6 weeks, during which they developed extensive arterial calcification. They also received vitamin K1 to keep their blood clotting properly. At 6 weeks, the warfarin-treated rats were broken up into several groups:

• One continued on the warfarin and K1 diet
• One was placed on a diet containing a normal amount of K1 (no warfarin)
  
• One was placed on a high K1 diet (no warfarin)
• The last was placed on a high K2 MK-4 diet (no warfarin)
  

After 6 more weeks, the first two groups developed even more calcification, while the third and fourth groups lost about 40% of their arterial calcium. The high vitamin K groups also saw a decrease in cell death in the artery wall, a decrease in uncarboxylated (inactive) MGP, and an increase in arterial elasticity. They also measured the vitamin K content of aortas from each group. The group that received the 12-week warfarin treatment had a huge amount of K1 accumulation in the aorta, but no K2 MK-4. This is expected because warfarin inhibits the conversion of K1 to K2 MK-4. It's notable that when conversion to K2 was blocked, K1 alone was totally ineffective at activating MGP and preventing calcification.

In the group fed high K1 but no warfarin, there was about three times more K2 MK-4 in the aortas than K1, suggesting that they had converted it effectively and that vascular tissue selectively accumulates K2 MK-4. A high K1 intake was required for this effect, however, since the normal K1 diet did not reverse calcification. The rats fed high K2 MK-4 had only K2 MK-4 in their aortas, as expected.

What does this mean for us? K2 MK-4 appears to be the form of vitamin K that arteries prefer (although not enough is known about the longer menaquinones, such as MK-7, to rule out a possible effect). Humans don't seem to be very good at making the conversion from K1 to K2 MK-4 (at normal intakes; there are suggestions that at artificially large doses we can do it). That means we need to ensure an adequate K2 MK-4 intake to prevent or reverse arterial calcification; eating K1-rich greens won't cut it. It's worth noting that the amounts of K1 and K2 used in the paper were very large, far beyond what is obtainable through food. But the regression took only 6 weeks, so it's possible that a smaller amount of K2 MK-4 over a longer period could have the same effect in humans.

K2 MK-4 (and perhaps other menaquinones like MK-7) may turn out to be an effective treatment for arterial calcification and cardiovascular disease in general. It's extremely effective at preventing osteoporosis-related fractures in humans. That's a highly significant fact. Osteoporosis and arterial calcification often come hand-in-hand. Thus, they are not a result of insufficient or excessive calcium, but of a failure to use the available calcium effectively. In the warfarin-treated rats described above, the serum (blood) calcium concentration was the same in all groups. Osteoporosis and arterial calcification are two sides of the same coin, and the fact that one can be addressed with K2 MK-4 means that the other may be as well.

Both osteoporosis and arterial calcification may turn out to be symptoms of vitamin K2 deficiency, resulting from the modern fear of animal fats and organs, and the deterioration of traditional animal husbandry practices. So eat your pastured dairy, organs, fish roe and shellfish! And if you have arterial calcification, as judged by a heart scan, you may want to consider supplementing with additional K2 MK-4 (also called menaquinone-4 and menatetrenone).

The osteoporosis studies were done with 45 milligrams per day, which was well tolerated but seems excessive to me. Smaller doses were not tested. From the limited information available on the K2 content of foods, 1 milligram of K2 MK-4 per day seems like the upper limit of what you can get from food. That's about 40 times more than the average person eats. Anything more and you're outside your body's operating parameters. Make sure you're getting adequate vitamin D3 and A if you supplement with K2. Vitamin D3 in particular increases the secretion of MGP, so the two work in concert.

Cardiovascular Disease and Vitamin K2

Vitamin K2 is intimately involved in calcium metabolism. Matrix Gla-protein (MGP) is a vitamin K-dependent protein that is secreted in cartilage, lung, heart, kidney and arteries. MGP prefers the MK-4 form of vitamin K2, the type that occurs almost exclusively in animal foods. Mice lacking MGP develop extensive arterial and soft tissue calcification (accumulation of calcium, as in bone). Same for humans with naturally occurring mutations in MGP (Keutel syndrome). It also happens in rats treated with warfarin, which inhibits vitamin K recycling. Let's hear what Dr. Cees Vermeer and his group have to say about MGP:

Among the proteins involved in vascular calcium metabolism, the vitamin K-dependent matrix Gla-protein (MGP) plays a dominant role. Although on a molecular level its mechanism of action is not completely understood, it is generally accepted that MGP is a potent inhibitor of arterial calcification. Its pivotal importance for vascular health is demonstrated by the fact that there seems to be no effective alternative mechanism for calcification inhibition in the vasculature. An optimal vitamin K intake is therefore important to maintain the risk and rate of calcification as low as possible.

So why do we care about vessel calcification? It associates strongly with the risk of heart attack and total mortality, better than traditional markers like the Framingham risk index*. That's because it's actually a measure of the disease process, rather than a marker with an unclear connection to it.

In my post on vitamin K2, I mentioned the Rotterdam study, which found that vitamin K2 intake is strongly associated with a lower risk of cardiovascular and total mortality. Vitamin K1, which is the type found in plants, was not associated with reduced mortality. I just came across another study in women selected from the PROSPECT cohort that showed something similar. Women with the highest K2 intake had the lowest level of coronary calcification. There was no association with K1. This suggests, yet again, that humans aren't very good at making the conversion from K1 to K2 MK-4. This is probably because during evolution, we always had a ready source of K2, so efficient conversion became unnecessary. Vitamin K2 MK-4 is found almost exclusively in animal foods.

Notably absent from the main text body is a discussion of where the K2 is coming from. It's tucked away in one sentence of the methods section: "cheese contributed 54%, milk products 22% and meat 15% of menaquinone intake." Oops! These are the foods that are supposed to cause heart disease! And do you remember where the K2 is? In the fat-- double oops! Yet another important nutrient that's found in animal fat.

Keep in mind that these Dutch women have an intake of K2 that is probably lower than what we would have eaten as hunter-gatherers. Most people in modern societies are verifiably K2 deficient. A focus on the organs (brain, pancreas) and fats of wild animals, shellfish, fish eggs and insects would have assured hunter-gatherers a high intake of vitamin K2 MK-4. This is precisely what Weston Price found in Nutrition and Physical Degeneration. He refers to vitamin K2 MK-4 as "activator X" in the book. In modern times, our most readily available source of vitamin K2 MK-4 is actually not a paleolithic food at all, it's butter from pasture-raised cows. It's how we can get away with not eating brain, pancreas and bugs.


*I plugged my numbers into this Framingham risk index calculator and it gave me the message "Please go back and enter an HDL value in the range of 20-100."!! I can imagine if you follow NCEP dietary guidelines your HDL would never break 100 mg/dL!

Winterize Your Diet

As winter approaches, there are steps you can take to preserve your health and well-being. Here's a list of things I find useful:

-Eat in season. Root vegetables like beets, turnips, rutabagas and potatoes are in season and make a satisfying dish. Try baked beets with raw garlic, sage and butter. Winter squash are tasty, nutritious and colorful. They make excellent soups and mashes, and can be baked or steamed. My favorite varieties are butternut, kabochas, delicata and gold nugget. They pair well with sage or nutmeg. In some places, hardy greens such as kale and collards are available in winter. Many fruits such as apples, pears and citrus are in season during the winter (or stored from fall).

-Prepare soup stocks. There's nothing like a long-simmered bone broth to drive away the winter chill. They are also rich in minerals and gelatin, which aids digestion and soothes the digestive tract.

-Make sauerkraut or other fermented vegetables. Fermentation was once used as a means to preserve flavor and nutrition for the winter. Fermented vegetables are a powerful digestive aid. After the first frost, cabbage is at its sweetest. Sweet cabbage makes the best kraut.

-Keep your vitamin D level high. This may protect against the typical winter ills, including flu and seasonal depression. Unless you live in a warm climate and spend time outside in the winter regularly, it's wise to seek out vitamin D. High-vitamin cod liver oil, pasture-raised animal fats, shellfish and fatty fish are good sources. Some people may wish to supplement with vitamin D3.

DART: Many Lessons Learned

The Diet and Reinfarction Trial (DART), published in 1989, is one of the most interesting clinical trials I've had the pleasure to read about recently. It included 2,033 British men who had already suffered from an acute myocardial infarction (MI; heart attack), and tested three different strategies to prevent further MIs. Subjects were divided into six groups:

• One group was instructed to reduce total fat to 30% of calories (from about 35%) and replace saturated fat (SFA) with polyunsaturated fat (PUFA).


• The second group was told to double grain fiber intake.


• The third group was instructed to eat more fatty fish or take fish oil if they didn't like fish.


• The remaining three were control groups that were not advised to change diet; one for each of the first three.
  

Researchers followed the six groups for two years, recording deaths and MIs. The fat group reduced their total fat intake from 35.0 to 32.3% of calories, while doubling the ratio of PUFA to SFA (to 0.78). After two years, there was no change in all-cause or cardiac mortality. This is totally consistent with the numerous other controlled trials that have been done on the subject. Here's the mortality curve:

Here's what the authors have to say about it:

Five randomised trials have been published in which a diet low in fat or with a high P/S [polyunsaturated/saturated fat] ratio was given to subjects who had recovered from MI. All these trials contained less than 500 subjects and none showed any reduction in deaths; indeed, one showed an increase in total mortality in the subjects who took the diet.

So... why do we keep banging our heads against the wall if clinical trials have already shown repeatedly that total fat and saturated fat consumption are irrelevant to heart disease and overall risk of dying? Are we going to keep doing these trials until we get a statistical fluke that confirms our favorite theory? This DART paper was published in 1989, and we have not stopped banging our heads against the wall since. The fact is, there has never been a properly controlled clinical trial that has shown an all-cause mortality benefit for reducing total or saturated fat in the diet (without changing other variables at the same time). More than a dozen have been conducted to date.

On to fish. The fish group tripled their omega-3 intake, going from 0.6 grams per week of EPA to 2.4 g (EPA was their proxy for fish intake). This group saw a significant reduction in MI and all-cause deaths, 9.3% vs 12.8% total deaths over two years (a 27% relative risk reduction). Here's the survival chart:

Balancing omega-6 intake with omega-3 has consistently improved cardiac risk in clinical trials. I've discussed that here.

The thing that makes the DART trial really unique is it's the only controlled trial I'm aware of that examined the effect of grain fiber on mortality (without simultaneously changing other factors). The fiber group doubled their grain fiber intake, going from 9 to 17 grams by eating more whole grains. This group saw a non-significant trend toward increased mortality and MI compared to its control group. Deaths went up from 9.9% to 12.1%, a relative risk increase of 18%. I suspect this result was right on the cusp of statistical significance, judging by the numbers and the look of the survival curve:

You can see that the effect is consistent and increases over time. At this rate, it probably would have been statistically significant at 2.5 years.

I think the problem with whole grains is that the bran and germ contain a disproportionate amount of toxins, such as the mineral-binding phytic acid.  The bran and germ also contain a disproportionate amount of nutrients. To have your cake and eat it too, soak, sprout or ferment grains. This reduces the toxin load but preserves or enhances nutritional value. Wheat may be a problem whether it's treated this way or not.

Subjects in the studies above were eating grain fiber that was not treated properly, and so they were increasing their intake of some pretty nasty toxins while decreasing their nutrient absorption. Healthy non-industrial cultures would never have made this mistake. Grains must be treated with respect, and whole grains in particular.

We're Starting to Get It

I just read an interesting post on the Food is Love blog.

According to the USDA (admittedly not always the most reliable source of accurate information, but we’ll go with it for the moment), the number of farmers markets in the US has risen significantly in the last ten years, from 2,746 in 1998 to 4,685 in 2008. If we get another 580 markets, an increase possible in the next year or two if trends continue, we’ll have tripled the number of recorded markets since 1994.

Furthermore,

Plenty of farmers markets don’t get tallied in official lists, of course. Valereee, over at Cincinnati Locavore, points out that the USDA database only lists a quarter of the markets in her hometown. I see a few missing on the Seattle list as well.

People are slowly starting to get it. We're realizing that the processed food industry does not look out for our best interests. We're realizing that the frailty of modern children as well as our own health problems are due to the outsourcing of agriculture and food preparation. We're realizing that local farms and markets build strong communities.

We're realizing that a return to traditional, wholesome food is the only path to whole health and well-being.


Further reading:
My Real Food manifesto.

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...

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.

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 with 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. 

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.

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.

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.