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??

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18.30 | 0 comments

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.

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10.52 | 0 comments

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 the single best 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.

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20.23 | 0 comments

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.

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17.00 | 0 comments