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.

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The Fundamentals

I heard an interview of Michael Pollan yesterday on Talk of the Nation. He made some important points about nutrition that bear repeating. He’s fond of saying “don’t eat anything your grandmother wouldn’t recognize as food”. That doesn’t mean your grandmother specifically, but anyone’s grandmother, whether she was Japanese, American or African. The point is that commercial food processing has taken us away from the foods, and traditional food preparation methods, on which our bodies evolved to thrive. At this point, we don’t know enough about health to design a healthy synthetic diet. Diet and health are too complex for reductionism at our current level of understanding. For that reason, any departure from natural foods and traditional food processing techniques is suspect.

Mainstream nutrition science has repeatedly contradicted itself and led us down the wrong path. This means that traditional cultures still have something to teach us about health. Hunter-gatherers and certain other non-industrial cultures are still the healthiest people on Earth, from the perspective of non-communicable disease. Pollan used the example of butter. First we thought it was healthy, then we were told it contains too much saturated fat and should be replaced with hydrogenated vegetable margarine. Now we learn that trans fats are unhealthy, so we’re making new margarines that are low in trans fats, but are still industrially processed pseudo-foods. How long will it take to show these new fats are harmful? What will be the next industrial fat to replace them? This game can be played forever as the latest unproven processed food replaces the previous one, and it will never result in something as healthy as real butter.

The last point of Pollan’s I’ll mention is that the world contains (or contained) a diversity of different cultures, living in dramatically different ways, many of which do not suffer from degenerative disease. These range from carnivores like the Inuit, to plant-heavy agriculturalists like the Kitavans, to pastoralists like the Masai. The human body is adapted to a wide variety of foodways, but the one it doesn’t seem to like is the modern Western diet.

Pollan’s new book is In Defense of Food. I haven’t read it, but I think it would be a good introduction to the health, ethical and environmental issues that surround food choices. He’s a clear and accessible writer.

Merry Christmas, happy Hanukkah, and happy holidays to everyone!

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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.

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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.

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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, ¼ 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.

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