Observations from France

I recently got back from a trip to the UK and France visiting family and friends. It was great to see everyone, eat great food and even do some unexpected foraging (chestnuts, mushrooms, walnuts, blackberries). French people are in better general health than most industrialized nations. The obesity, diabetes and heart disease rates are all considerably lower than in the US, although still much higher than in non-industrial cultures. Here are a few of my observations about French food:

1. The French diet generally contains a lot of fat, mostly from traditional animal sources such as dairy and pork fat. Industrial seed oils have crept into the diet over the course of the 20th century, although not to the same degree as in most affluent nations. People seem to think that eating a lot of fat is unhealthy, particularly the younger generation, but they do it anyway. I had dinner with my family at a traditional restaurant in Lyon (a "bouchon Lyonnais" called Stepharo) last week. Before we ordered, they immediately brought out crispy fried chunks of pork skin and fat (I'm not claiming this is healthy!). The entree was a salad: a bed of lettuce piled high with chicken livers, herring, and "pig's feet". The pigs feet were essentially gobs of pork fat. It was a very good meal that I'll continue describing later in the post. I think it's worth pointing out that Lyon is in Southern France. Is this the "Mediterranean diet"?
   
2. French people eat organs. Yes, they never got the memo that muscle meat is the only edible tissue. A typical butcher or even grocery store will have liver, tripe, kidney and blood sausage on full display next to the meat. If you want to make a French person angry, try selling them a chicken or a rabbit without the liver, gizzard and heart. The main course at Stepharo was a large "andouilette", or tripe sausage, baked in mustard sauce. This was a typical traditional restaurant, not a hangout for gastronauts.
   
3. French people fiercely defend the quality of their food. Have you heard of the abbreviation AOC? It stands for "Appellation d�Origine Contr�l�e", or controlled designation of origin. A familiar example is Champagne, which has the AOC label. You can't call your sparkling wine Champagne unless it comes from the region Champagne. However, that's only half the story. AOC also designates a specific, traditional production method, in this case called the "m�thode champenoise." The AOC label can apply to a variety of food products, including wine, butter, cheese, honey, mustard and seafood, and is a guarantee of quality and tradition. 44 cheeses currently have the AOC designation, and these are commonly available in markets and grocery stores throughout the country (1). These are not fancy products that only the wealthy can afford-- many of them are quality foods that are accessible to nearly everyone. AOC defines many aspects of cheese production, often requiring a minimum amount of pasture time and specifying livestock breeds. The US has a few products that are regulated in a similar fashion, such as Bourbon whiskey, but generally we are far behind in assuring food quality and transparency.
4. French people cook. There is less outsourcing of food processing in France, for several reasons. One reason is that restaurants are generally expensive. That trend is changing however.

I don't think the French diet is optimal by any means. They eat a lot of white flour, some sugar, seed oils and other processed foods. But I do think the French diet has many good qualities, and it certainly poses a number of problems for the mainstream concept of healthy food. Hence the "French paradox."

Does Red Wine Protect the Cardiovascular System?

The 'French paradox' rears its ugly head again. The reasoning goes something like this: French people eat more saturated animal fat than any other affluent nation, and have the second-lowest rate of coronary heart disease (only after Japan, which has a much higher stroke rate than France). French people drink red wine. Therefore, red wine must be protecting them against the artery-clogging yogurt, beef and butter.

The latest study to fall into this myth was published in the AJCN recently (1). Investigators showed that 1/3 bottle of red wine per day for 21 days increased blood flow in forearm vessels of healthy volunteers, which they interpreted as "enhanced vascular endothelial function"*. The novel finding in this paper is that red wine consumption increases the migration of certain cells into blood vessels that are thought to maintain and repair the vessels. There were no control groups for comparison, neither abstainers nor a group drinking a different type of alcohol.

The investigators then went on to speculate that the various antioxidant polyphenols in red wine, such as the trendy molecule resveratrol, could be involved. Even though you have to give animals 500 bottles' worth of resveratrol per day to see any effect. But there's another little problem with this hypothesis...

Ethanol-- plain old alcohol. You could drink a 40 oz bottle of malt liquor every night and it would probably do the exact same thing.

No matter what the source, alcohol consumption is associated with a lower risk of cardiovascular disease out to about 3-4 drinks per day, after which the risk goes back up (2, 3)**. The association is not trivial-- up to a 62% lower risk associated with alcohol use. Controlled trials have shown that alcohol, regardless of the source, increases HDL cholesterol and reduces the tendency to clot (4).

Should we all start downing three drinks a day? Not so fast. Although alcohol does probably decrease heart attack risk, the effect on total mortality is equivocal. That's because it increases the risk of cancers and accidents. Alcohol is a drug, and my opinion is that like all drugs, overall it will not benefit the health of a person with an otherwise good diet and lifestyle. That being said, it's enjoyable, so I have no problem with drinking it in moderation. Just don't think you're doing it for your health.

So does red wine decrease the risk of having a heart attack? Yes, just as effectively as malt liquor. It's not the antioxidants and resveratrol, it's the ethanol. The reason the French avoid heart attacks is not because of some fancy compound in their wine that protects them from a high saturated fat intake. It's because they have preserved their diet traditions to a greater degree than most industrialized nations.

I do think it's interesting to speculate about why alcohol (probably) reduces heart attack risk. As far as I know, the mechanism is unknown. Could it be because it relaxes us? I'm going to ponder that over a glass of whiskey...


* It may well represent an improvement of endothelial function, but that's an assumption on the part of the investigators. It belongs in the discussion section, if anywhere, and not in the results section.

** The first study is really interesting. For once, I see no evidence of "healthy user bias". Rates of healthy behaviors were virtually identical across quintiles of alcohol intake. This gives me a much higher degree of confidence in the results.

Full-fat Dairy for Cardiovascular Health

I just saw a paper in the AJCN titled "Dairy consumption and patterns of mortality of
Australian adults". It's a prospective study with a 15-year follow-up period. Here's a quote from the abstract:

There was no consistent and significant association between total dairy intake and total or cause-specific mortality. However, compared with those with the lowest intake of full-fat dairy, participants with the highest intake (median intake 339 g/day) had reduced death due to CVD (HR: 0.31; 95% confidence interval (CI): 0.12�0.79; P for trend = 0.04) after adjustment for calcium intake and other confounders. Intakes of low-fat dairy, specific dairy foods, calcium and vitamin D showed no consistent associations.

People who ate the most full-fat dairy had a 69% lower risk of cardiovascular death than those who ate the least. Otherwise stated, people who mostly avoided dairy or consumed low-fat dairy had more than three times the risk of dying of coronary heart disease or stroke than people who ate the most full-fat diary.

Contrary to popular belief, full-fat dairy, including milk, butter and cheese, has never been convincingly linked to cardiovascular disease. In fact, it has rather consistently been linked to a lower risk, particularly for stroke. What has been linked to cardiovascular disease is milk fat's replacement, margarine. In the Rotterdam study, high vitamin K2 intake was linked to a lower risk of fatal heart attack, aortic calcification and all-cause mortality. Most of the K2 came from full-fat cheese. In my opinion, artisanal cheese and butter made from pasture-fed milk are the ultimate dairy foods.

From a 2005 literature review on milk and cardiovascular disease in the EJCN:

In total, 10 studies were identified. Their results show a high degree of consistency in the reported risk for heart disease and stroke, all but one study suggesting a relative risk of less than one in subjects with the highest intakes of milk.

...the studies, taken together, suggest that milk drinking may be associated with a small but worthwhile reduction in heart disease and stroke risk.

...All the cohort studies in the present review had, however, been set up at times when reduced-fat milks were unavailable, or scarce.

The fat is where the vitamins A, K2, E and D are. The fat is where the medium-chain triglycerides, butyric acid and omega-3 fatty acids are. The fat is where the conjugated linoleic acid is. So the next time someone admonishes you to reduce your dairy fat intake, what are you going to tell them??

The Lyon Diet-Heart Study: Implications

There's something ironic about the Mediterranean diet used in the Lyon diet heart study, the one that dramatically reduced participants' risk of heart attack and all-cause mortality relative to the prudent diet control group: it wasn't actually a Mediterranean diet.

The concept of the Mediterranean diet as protective against heart disease may have originated in Dr. Ancel Keys' Seven Countries study, in which he compared the food habits and cardiovascular mortality statistics both between and within seven European countries. Countries surrounding the Mediterranean, and in particular the Greek island of Crete, had the lowest cardiovascular death rates. The Cretan diet is high in monounsaturated fat, relatively low in saturated fat, low in omega-6, and high in omega-3 fatty acids, including fat from seafood and the plant omega-3 alpha-linolenic acid. It also includes abundant green vegetables. This became the inspiration for the modern American concept of the "Mediterranean diet". The part about low omega-6 tends to be omitted.

Of course, if you look at modern heart attack mortality statistics by country, France is the lowest in Europe. France is a Mediterranean country, yet happens to have a very high intake of saturated fat per capita. So the cardiologist-approved version of the Mediterranean diet isn't exactly accurate.

The Lyon study departs even further from the traditional Mediterranean diet. Neither the Cretan nor the French diet are low in fat, yet participants were encouraged to reduce their fat intake. The Cretan diet includes some animal fat and eggs, while Lyon participants were encouraged to avoid these. And finally, the margarine. You could be guillotined for using margarine instead of butter in France, and I'm sure the Cretans aren't too fond of it either. Yet the margarine used in the Lyon study was rich in omega-3 alpha-linolenic acid, a critical factor.

Previous intervention trials such as MRFIT, the Women's Health Initiative (WHI) dietary modification trial, and others, exhaustively tested the hypothesis that reducing total fat intake reduces cardiovascular mortality. It doesn't. A dozen trials have also tested the idea that reducing saturated fat reduces cardiovascular mortality. It doesn't. Increasing fiber doesn't, according to the DART trial. Increasing fruit and vegetables modestly doesn't, according to WHI.

So what's left that's unique about the Lyon trial? It was the only trial to dramatically reduce omega-6 consumption, to below 4% of calories, while increasing omega-3 consumption from plant and seafood sources. In my opinion, that combination is the only plausible explanation for the large reduction in heart attacks and total mortality. That combination also happens to be a consistent feature of the real Mediterranean diet. In both Crete and France, omega-6 intake is relatively low, and omega-3 intake is relatively high. They also eat more real food than processed food in general, a factor that I don't underestimate.

Where do we go from here? Obviously I'm not going to recommend eating omega-3 enriched margarine. Mediterranean countries don't need industrial goop to avoid a heart attack, and neither do you. Anyone who's been to France knows they don't deprive themselves over there. They eat real food and they enjoy it.

The way to preserve the essential elements of the Mediterranean diet without becoming an ascetic is to eat fats that are low in omega-6, and find a modest source of omega-3. That means eating full-fat dairy if you tolerate it, fatty meat if you enjoy it, organs, seafood, olive oil in moderation, coconut oil, butter, lard, and tallow. Along with a diet that is dominated by real, homemade food rather than processed food. Some people may also wish to supplement with small doses of high-vitamin cod liver oil, fish oil or flax. I consider the latter to be inferior to animal sources of omega-3, but it can be useful for vegetarians.

Eicosanoids and Ischemic Heart Disease, Part II

Here's where it gets more complicated and more interesting. The ratio of omega-6 to omega-3 matters, but so does the total amount of each. This is a graph from a 1992 paper by Dr. Lands:

Allow me to explain. These lines are based on values predicted by a formula developed by Dr. Lands that determines the proportion of omega-6 in tissue HUFA (highly unsaturated fatty acids; includes 20- to 22-carbon omega-6 and omega-3 fats), based on dietary intake of omega-6 and omega-3 fats. This formula seems to be quite accurate, and has been validated both in rodents and humans. As a tissue's arachidonic acid content increases, its EPA and DHA content decreases proportionally.

On the Y-axis (vertical), we have the proportion of omega-6 HUFA in tissue. On the X-axis (horizontal), we have the proportion of omega-6 in the diet as a percentage of energy. Each line represents the relationship between dietary omega-6 and tissue HUFA at a given level of dietary omega-3.

Let's start at the top. The first line is the predicted proportion of omega-6 HUFA in the tissue of a person eating virtually no omega-3. You can see that it maxes out around 4% of calories from omega-6, but it can actually be fairly low if omega-6 is kept very low. The next line down is what happens when your omega-3 intake is 0.1% of calories. You can see that the proportion of omega-6 HUFA is lower than the curve above it at all omega-6 intakes, but it still maxes out around 4% omega-6. As omega-3 intake increases, the proportion of omega-6 HUFA decreases at all levels of dietary omega-6 because it has to compete with omega-3 HUFA for space in the membrane.

In the U.S., we get a small proportion of our calories from omega-3. The horizontal line marks our average tissue HUFA composition, which is about 75% omega-6. We get more than 7% of our calories from omega-6. This means our tissue contains nearly the maximum proportion of omega-6 HUFA, creating a potently inflammatory and thrombotic environment! This is a very significant fact, because it explains three major observations:

1. The U.S has a very high rate of heart attack mortality.
2. Recent diet trials in which saturated fat was replaced with omega-6-rich vegetable oils didn't cause an increase in mortality, although some of the very first trials in the 1960s did.
3. Diet trials that increased omega-3 decreased mortality.

Observation number two is used by proponents of PUFA-rich vegetable oils, and it's a fair point. If omega-6 causes heart attacks, why hasn't that shown up in controlled trials? Here's the rebuttal. First of all, it did show up in two of the first controlled trials in the 1960s: Rose et al., and the unfortunately-named Anti-Coronary Club trial. In the first, replacing animal fat with corn oil caused a 4-fold increase in heart attack deaths and total mortality. In the second, replacing animal fat with polyunsaturated vegetable oil increased heart attack death rate, and total mortality more than doubled.

But the trend didn't continue into later trials. This makes perfect sense in light of the rising omega-6 intake over the course of the 20th century in the U.S. and other affluent nations. Once our omega-6 intake crossed the 4% threshold, more omega-6 had very little effect on the proportion of omega-6 HUFA in tissue. This may be why some of the very first PUFA diet trials caused increased mortality: there was a proportion of the population that was still getting less than 4% omega-6 in its regular diet at that time. By the 1980s, virtually everyone in the U.S. (and many other affluent nations) was eating more than 4% omega-6, and thus adding more did not significantly affect tissue HUFA or heart attack mortality.

If omega-3 intake is low, whether omega-6 intake is 5% or 10% doesn't matter much for heart disease. At that point, the only way to reduce tissue HUFA without cutting back on omega-6 consumption is to outcompete it with additional omega-3. That's what the Japanese do, and it's also what happened in several clinical trials including the DART trial.

This neatly explains why the French, Japanese and Kitavans have low rates of ischemic heart disease, despite the prevalence of smoking cigarettes in all three cultures. The French diet traditionally focuses on animal fats, eschews industrial vegetable oils, and includes seafood. They eat less omega-6 and more omega-3 than Americans. They have the lowest heart attack mortality rate of any affluent Western nation. The Japanese are known for their high intake of seafood. They also eat less omega-6 than Americans. They have the lowest heart attack death rate of any affluent nation. The traditional Kitavan diet contains very little omega-6 (probably less than 1% of calories), and a significant amount of omega-3 from seafood (about one teaspoon of fish fat per day). They have an undetectable incidence of heart attack and stroke.

In sum, this suggests that an effective way to avoid a heart attack is to reduce omega-6 consumption and ensure an adequate source of omega-3. The lower the omega-6, the less the omega-3 matters. This is a nice theory, but where's the direct evidence? In the next post, I'll discuss the controlled trial that proved this concept once and for all: the Lyon diet-heart trial.

The Coronary Heart Disease Epidemic: Possible Culprits Part I

In the last post, I reviewed two studies that suggested heart attacks were rare in the U.K. until the 1920s -1930s. In this post, I'll be discussing some of the diet and lifestyle factors that preceded and associated with the coronary heart disease epidemic in the U.K and U.S. I've cherry picked factors that I believe could have played a causal role. Many things changed during that time period, and I don't want to give the impression that I have "the answer". I'm simply presenting ideas for thought and discussion.

First on the list: sugar. Here's a graph of refined sugar consumption in the U.K. from 1815 to 1955, from the book The Saccharine Disease, by Dr. T. L. Cleave. Sugar consumption increased dramatically in the U.K. over this time period, reaching near-modern levels by the turn of the century, and continuing to increase after that except during the wars: Here's a graph of total sweetener consumption in the U.S. from 1909 to 2005 (source: USDA food supply database). Between 1909 and 1922, sweetener consumption increased by 40%:

If we assume a 10 to 20 year lag period, sugar is well placed to play a role in the CHD epidemic. Sugar is easy to pick on. An excess causes a number of detrimental changes in animal models and human subjects, including fatty liver, the metabolic syndrome, and small, oxidized low-density lipoprotein particles (LDL). Small and oxidized LDL associate strongly with cardiovascular disease risk and may be involved in causing it. These effects seem to be mostly attributable to the fructose portion of sugar, which is 50% of table sugar (sucrose), about 50% of most naturally sweet foods, and 55% of the most common form of high-fructose corn syrup. That explains why starches, which break down into glucose (another type of sugar), don't have the same negative effects as table sugar and HFCS.

Hydrogenated fat is the next suspect. I don't have any graphs to present, because no one has systematically tracked hydrogenated fat consumption in the U.S. or U.K. to my knowledge. However, it was first marketed in the U.S. by Procter & Gamble under the brand name Crisco in 1911. Crisco stands for "crystallized cottonseed oil", and involves taking an industrial waste oil (from cotton seeds) and chemically treating it using high temperature, a nickel catalyst and hydrogen gas (see this post for more information). Hydrogenated fats for human consumption hit markets in the U.K. around 1920. Here's what Dr. Robert Finlayson had to say about margarine in his paper "Ischaemic Heart Disease, Aortic Aneurysms, and Atherosclerosis in the City of London, 1868-1982":

...between 1909-13 and 1924-28, margarine consumption showed the highest percentage increase, whilst that of eggs only increased slightly and that of butter remained unchanged. Between 1928 and 1934, margarine consumption fell by one-third, while butter consumption increased by 57 percent: and increase that coincided with a fall of 48 percent in its price. Subsequently, margarine sales have burgeoned, and if one is correct in stating that the coronary heart disease epidemic started in the second decade of this century, then the concept of hydrogenated margarines as an important aetiological factor, so strongly advocated by Martin, may merit more consideration than hitherto.

Partially hydrogenated oils contain trans fat, which is truly new to the human diet, with the exception of small amounts found in ruminant fats including butter. But for the most part, natural trans fats are not the same as industrial trans fats, and in fact some of them, such as conjugated linoleic acid (CLA), may be beneficial. To my knowledge, no one has discovered health benefits of industrial trans fats. To the contrary, compared to butter, they shrink LDL size. They also inhibit enzymes that the body uses to make a diverse class of signaling compounds known as eicosanoids. Trans fat consumption associates very strongly with the risk of heart attack in observational studies. Which is ironic, because hydrogenated fats were originally marketed as a healthier alternative to animal fats. The Center for Science in the Public Interest shamed McDonald's into switching the beef tallow in their deep friers for hydrogenated vegetable fats in the 1990s. In 2009, even the staunchest opponents of animal fats have to admit that they're healthier than hydrogenated fat.

The next factor is vitamin D. When the industrial revolution became widespread in the late 19th century, people moved into crowded, polluted cities and vitamin D deficiency became rampant. Rickets was a scourge that affected more than half of children in some places. Dr. Edward Mellanby discovered that it's caused by severe vitamin D deficiency, milk was fortified with vitamin D2, and rickets was all but eliminated. However, it only takes a very small amount of vitamin D to avoid rickets, an amount that will not contribute significantly to optimum vitamin D status. Vitamin D modulates the body's inflammatory response, it's ability to resist calcium deposition in the arteries, and seems to be important for so many things I had to include it.

The rise of cigarettes was a major change that probably contributed massively to the CHD epidemic. They were introduced just after the turn of the century in the U.S. and U.K., and rapidly became fashionable (source):
If you look at the second to last graph from the previous post, you can see that there's a striking correspondence between cigarette consumption and CHD deaths in the U.K. In fact, if you moved the line representing cigarette consumption to the right by about 20 years, it would overlap almost perfectly with CHD deaths. The risk of heart attack is so strongly associated with smoking in observational studies that even I believe it probably represents a causal relationship. There's no doubt in my mind that smoking cigarettes contributes to the risk of heart attack and various other health problems.

Smoking is a powerful factor, but it doesn't explain everything. How is it that the Kitavans of Papua New Guinea, more than 3/4 of whom smoke cigarettes, have an undetectable incidence of heart attack and stroke? Why do the French and the Japanese, who smoke like chimneys (at least until recently), have the two lowest heart attack death rates of all the affluent nations? There's clearly another factor involved that trumps cigarette smoke. I have a guess, which I'll expand on in the next few posts.

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.

Vitamin K2, menatetrenone (MK-4)

Weston Price established the importance of the MK-4 isoform of vitamin K2 (hereafter, K2) with a series of interesting experiments. He showed in chickens that blood levels of calcium and phosphorus depended both on vitamin A and K2, and that the two had synergistic effects on mineral absorption. He also showed that chickens preferred eating butter that was rich in K2 over butter low in K2, even when the investigators couldn't distinguish between them. Young turkeys fed K2-containing butter oil along with cod liver oil (A and D) also grew at a much faster rate than turkeys fed cod liver oil alone.

He hypothesized that vitamin A, vitamin D and vitamin K2 were synergistic and essential for proper growth and subsequent health. He particularly felt that the combination was important for proper mineral absorption and metabolism. He used a combination of high-vitamin cod liver oil and high-vitamin butter oil to heal cavities, reduce oral bacteria counts, and cure numerous other afflictions in his patients. He also showed that the healthy non-industrial groups he studied had a much higher intake of these fat-soluble, animal-derived vitamins than more modern cultures.

Price found an inverse correlation between the levels of K2 in butter and mortality from cardiovascular disease and pneumonia in a number of different regions. A recent study examined the relationship between K2 (MK-4 through 10) consumption and heart attack risk in 4,600 Dutch men. They found a strong inverse association between K2 consumption and heart attack mortality risk. Men with the highest K2 consumption had a whopping 51% lower risk of heart attack mortality and a 26% lower risk of death from all causes compared to men eating the least K2! Their sources of K2 MK-4 were eggs, meats and dairy. They obtained MK-5 through MK-10 from fermented foods and fish. The investigators found no association with K1, the form found in plants.

Perigord, France is the world's capital of foie gras, or fatty goose liver. Good news for the bon vivants: foie gras turns out to be the richest known source of K2. Perigord also has the lowest rate of cardiovascular mortality in France, a country already noted for its low CVD mortality.

Rats fed warfarin, a drug that inhibits K2 recycling, develop arterial calcification. Feeding the rats K2 completely inhibits this effect. Mice lacking matrix Gla protein (MGP), a vitamin K-dependent protein that guards against arterial calcification, develop heavily calcified aortas and die prematurely. So the link between K2 and cardiovascular disease is a very strong one.

Mammals can synthesize K2 MK-4 from K1 to some degree, so dietary K1 and other forms of vitamin K may contribute to K2 MK-4 status. 

The synergism Weston Price observed between vitamins A, D and K2 now has a solid mechanism. In a nutshell, vitamins A and D signal the production of some very important proteins, and K2 is required to activate them once they are made. Many of these proteins are involved in mineral metabolism, thus the effects Price saw in his experiments and observations in non-industrialized cultures. For example, osteocalcin is a protein that organizes calcium and phosphorus deposition in the bones and teeth. It's produced by cells in response to vitamins A and D, but requires K2 to perform its function. This suggests that the effects of vitamin D on bone health could be amplified greatly if it were administered along with K2. By itself, K2 is already highly protective against fractures in the elderly. It works out perfectly, since K2 also protects against vitamin D toxicity.

I'm not going to go through all the other data on K2 in detail, but suffice it to say it's very very important. I believe that K2 is a 'missing link' that explains many of our modern ills, just as Weston Price wrote. Here are a few more tidbits to whet your appetite: K2 may affect glucose control and insulin release (1, 2). It's concentrated in the brain, serving an as yet unknown function.

Hunter-gatherers didn't have multivitamins, they had nutrient-dense food. As long as you eat a natural diet containing some vegetables and some animal products, and lay off the processed grains, sugar and vegetable oil, the micronutrients will take care of themselves.

Vitamin K2, MK-4 is only found in animal products. The best sources known are grass-fed butter from cows eating rapidly growing grass, and foie gras. K2 tends to associate with beta-carotene in butter, so the darker the color, the more K2 it contains (also, the better it tastes). Fish eggs, other grass-fed dairy, shellfish, insects and other organ meats are also good sources. Chris Masterjohn compiled a list of food sources in his excellent article on the Weston Price foundation website. I highly recommend reading it if you want more detail. K2 MK-7 is found abundantly in natto, a type of fermented soybean, and it may be partially converted to MK-4.

Finally, you can also buy K2 supplements. The best one is butter oil, the very same stuff Price used to treat his patients. I have used this one personally, and I noticed positive effects on my skin overnight. Thorne research makes a synthetic liquid K2 MK-4 supplement that is easy to dose drop-wise to get natural amounts of it. Other K2 MK-4 supplements are much more concentrated than what you could get from food so I recommend avoiding them. I am generally against supplements, but I've ordered the Thorne product for a little self-experimentation. I want to see if it has the same effect on my skin as the butter oil (update- it does).