More on Hydrogenated Fat

I stumbled on an interesting history of hydrogenated vegetable oil on the website Soy Info Center. It turns out, margarine was made out of animal fat before 1915. Hydrogenated vegetable shortening (Crisco) was introduced in 1911. Before that our intake of trans fat was very low, coming chiefly from dairy and meat (not the same as synthetic trans fats). Here's an excerpt from the website:

In 1909 Procter & Gamble in Cincinnati acquired the US rights to the Normann patent from Crosfield's and in 1911 they began marketing Crisco, the first hydrogenated shortening, which contained a large amount of cottonseed oil. In America, however, six other firms had been working since 1915 according to the patents of C.E. Kayser (1910) and Carleton Ellis (1912), and with a number of other processes, most of which were never published. After a long period of litigation, initiated by Procter & Gamble, for alleged infringement of patent rights, a US court decision held the 1915 Burchenal patent (US Patent 1,135,351), under whose broad claims P&G's shortening was then being made, to be invalid. This opened the way for a number of firms to begin manufacture of hydrogenated shortenings and, from 1915, margarines.

Hydrogenated vegetable oil wasn't widely eaten until 1920:

Before the use of hydrogenation, the production of shortening and margarine had been entirely dependent on animal fats as a source of raw materials. Increased demand soon caused these to grow scarce and expensive. Thus hydrogenation liberated shortening and margarine from their dependence on animal fats and made it possible for cooks to have products resembling lard and butter made from vegetable oils. Nevertheless it was not until after 1920 that hydrogenated vegetable oils were widely used in margarine and shortening. During the 1930s the use of hydrogenation worldwide took a quantum leap forward, as production increased greatly.

By the late 1970s roughly 60% of all edible oils and fats in the US were partially hydrogenated (Dutton, in Emken and Dutton 1979). And an estimated 75% of the soy oil used in the US was hydrogenated to make shortening and margarine, as well as large amounts of lightly hydrogenated soy cooking and salad oils (Kromer 1976).

Rizek et al. (1974) estimated that in the period from 1937 to 1972 per capita annual consumption of trans fatty acids increased by 81%, from 6.3-11.4 gm. During the same period per capita consumption of vegetable oils and fats increased by only 64% (from 36-59 gm).

Death from coronary heart disease was rare until 1925. It peaked in the 1950s, remaining high through the 1970s and diminishing only due to modern medical interventions. Coincidence? I don't know, but it's awfully suspicious.

Here is a description of the hydrogenation process. Makes my mouth water:

Typically, a mixture of refined oil and finely powdered nickel catalyst (comprising 0.05-0.1% of the weight of the oil) is pumped into a cylindrical pressure reactor of 5-20 tons capacity. It is heated by heating coils to 120-188°C (248-370°F) at 1-6 atmospheres pressure. Hydrogen is pumped into the bottom of the reactor and dispersed by a stirrer, continuously, as bubbles into the oil... After hydrogenation is completed to the desired degree, the oil is filtered to remove the catalyst (which may be reused) then pumped to a storage tank; it may later be blended with other harder or softer fats or oils to make margarine or shortening.

Who in his right mind would think this stuff is suitable for human consumption? Hydrogenated vegetable oil is ubiquitous in processed food, because of its low cost and long shelf life, although the amounts are diminishing since the FDA required it to be included on nutrition labels in 2006. The implication here is that consumers know it's unhealthy, but manufacturers aren't going to stop putting it in foods until someone shines a spotlight on them.

It will be interesting to see if CHD incidence drops with decreasing trans fat intake. The obesity epidemic does seem to be leveling off in the U.S. This also corresponds with other recent dietary improvements such as a small decrease in sugar, wheat and vegetable oil consumption (see this post).

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.

Leptin Resistance and Sugar

Leptin is a major hormone regulator of fat mass in vertebrates. It's a frequent topic on this blog because I believe it's central to overweight and modern metabolic disorders. Here's how it works. Leptin is secreted by fat tissue, and its blood levels are proportional to fat mass. The more fat tissue, the more leptin. Leptin reduces appetite, increases fat release from fat tissue and increases the metabolic rate. Normally, this creates a "feedback loop" that keeps fat mass within a fairly narrow range. Any increase in fat tissue causes an increase in leptin, which burns fat tissue at an accelerated rate. This continues until fat mass has decreased enough to return leptin to its original level.

Leptin was first identified through research on the "obese" mutant mouse. The obese strain arose by a spontaneous mutation, and is extremely fat. The mutation turned out to be in a protein investigators dubbed leptin. When researchers first discovered leptin, they speculated that it could be the "obesity gene", and supplemental leptin a potential treatment for obesity. They later discovered (to their great chagrin) that obese people produce much more leptin than thin people, so a defeciency of leptin was clearly not the problem, as it was in the obese mouse. They subsequently found that obese people scarcely respond to injected leptin by reducing their food intake, as thin people do. They are leptin resistant. This makes sense if you think about it. The only way a person can gain significant fat mass is if the leptin feedback loop isn't working correctly.

Another rodent model of leptin resistance arose later, the "Zucker fatty" rat. Zucker rats have a mutation in the leptin receptor gene. They secrete leptin just fine, but they don't respond to it because they have no functional receptor. This makes them an excellent model of complete leptin resistance. What happens to Zucker rats? They become obese, hypometabolic, hyperphagic, hypertensive, insulin resistant, and they develop blood lipid disturbances. It should sound familiar; it's the metabolic syndrome and it affects 24% of Americans (CDC NHANES III). Guess what's the first symptom of impending metabolic syndrome in humans, even before insulin resistance and obesity? Leptin resistance. This makes leptin an excellent contender for the keystone position in overweight and other metabolic disorders.

I've mentioned before that the two most commonly used animal models of the metabolic syndrome are both sugar-fed rats. Fructose, which accounts for 50% of table sugar and 55% of high-fructose corn syrup, is probably the culprit. Glucose, which is the remainder of table sugar and high-fructose corn syrup, and the product of starch digestion, does not have the same effects. I think it's also relevant that refined sugar contains no vitamins or minerals whatsoever. Sweetener consumption in the U.S. has increased from virtually nothing in 1850, to 84 pounds per year in 1909, to 119 pounds in 1970, to 142 pounds in 2005 (source).

In a recent paper, Dr. Philip Scarpace's group (in collaboration with Dr. Richard Johnson), showed that a high-fructose diet causes leptin resistance in rats. The diet was 60% fructose, which is extreme by any standards, but it caused a complete resistance to the effect of leptin on food intake. Normally, leptin binds receptors in a brain region called the hypothalamus, which is responsible for food intake behaviors (including in humans). This accounts for leptin's ability to reduce food consumption. Fructose-fed rats did not reduce their food intake at all when injected with leptin, while rats on a normal diet did. When subsequently put on a high-fat diet (60% lard), rats that started off on the fructose diet gained more weight.

I think it's worth mentionong that rodents don't respond to high-fat diets in the same way as humans, as judged by the efficacy of low-carbohydrate diets for weight loss. Industrial lard also has a very poor ratio of omega-6 to omega-3 fats (especially if it's hydrogenated), which may also contribute to the observed weight gain.

Fructose-fed rats had higher cholesterol and twice the triglycerides of control-fed rats. Fructose increases triglycerides because it goes straight to the liver, which makes it into fat that's subsequently exported into the bloodstream. Elevated triglycerides impair leptin transport from the blood to the hypothalamus across the blood-brain barrier, which separates the central nervous system from the rest of the body. Fructose also impaired the response of the hypothalamus to the leptin that did reach it. Both effects may contribute to the leptin resistance Dr. Scarpace's group observed.

Just four weeks of fructose feeding in humans (1.5g per kg body weight) increased leptin levels by 48%. Body weight did not change during the study, indicating that more leptin was required to maintain the same level of fat mass. This may be the beginning of leptin resistance.

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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