Dietary Fats and Heart Disease – Exposing the Villain

“I would only argue that Senators don’t have the luxury that the research scientist does, of waiting until every last shred of evidence is in.”

These words were spoken by Senator George McGovern 35 years ago when confronted by Dr. Robert Olson from St. Louis University. Senator McGovern’s Select Committee on Nutrition and Human Needs went ahead and published their famous report, “Dietary goals for the United States” in 1977.

Dietary Fats and Heart Disease - Exposing the Villain

The committee’s members acknowledged that their recommendations relied on epidemiological and observational data at best. There were no prospective randomized studies available to support their recommendations.

Dr. D.M. Hegsted, professor of nutrition at Harvard School of Public Health, who assisted in the preparation of the report wrote: “The question to be asked, therefore, is not why should we change our diet but why not. What are the risks associated with eating less meat, less fat, less saturated fat, less cholesterol, less sugar, less salt and more fruits, vegetables, unsaturated fat and cereal products – especially whole grain cereals. There are none that can be identified and important benefits can be expected”.

What the committee’s members probably did not realize however, was that their report laid the foundation for worldwide dietary guidelines for the next 35 years. Ever since , “eat less saturated fat and cholesterol…” , has been the cornerstone recommendation from medical professionals, for patients with heart disease or those who want to reduce their risk of heart attack.

Although the McGovern committee’s report turned out to be  influential, several other important expert panels had already provided similar recommendations. The advise  to limit saturated fats was already alive in the 1950s. In 1957 the American Heart Association suggested that a decreased consumption of saturated fats might reduce  the risk of heart disease.

The Inter-Society Commission for Heart Disease Resources and The American Heart Association had already in the early 1970s suggested a reduction in dietary cholesterol to less than 300 mg a day.

However, the experts did not agree. In October 1977, the Canadian Department of National Health and Welfare concluded that: “Evidence is mounting that dietary cholesterol may not be  important to the great majority of people… Thus a diet restricted in cholesterol would not be necessary for the general population”.

But  the wheels were turning fas, and food manufacturers were already adopting new strategies. Low-fat food varieties of all possible kinds spread throughout the world. Butter consumption decreased, and vegetable oils became popular. Cholesterol and saturated fat were to be  eliminated from our dishes. The villains had been exposed  and had to be  taken care of.

Trans Fat Joins the Villains

The French scientist Paul Sabatier developed the hydrogenation process in the 1890s. In 1902, Wilhelm Normann found that liquid oils could be hydrogenated to form trans fatty acids. This turned out to be the first man made fat.

During the second world war, the use of trans fats rose because of the increased use of margarine. In the early 1980s there was a strong campaign by consumer advocacy groups against using saturated fat for frying in fast-food restaurants. In response, most fast-food companies began using partially hydrogenated oils containing trans  fat instead of beef tallow and tropical oils high in saturated fats.

A lot of evidence indicates that the fear of saturated fats during the 1950s through the 1980s, lead to an increased use of trans fats.

In the 1990s it became clear however that trans fats might be harmful. Numerous research studies during the 1990’s revealed correlations between trans fatty acids and increased LDL-cholesterol and a higher incidence of heart disease.

In 1993 health advocacy groups started calling for fast-food restaurants to stop using partially hydrogenated oils in their deep fryers. Trans fat was the new villain.

In 2003, Denmark was the first country in the world to limit the use of trans fats by law. Trans fat labeling became mandatory in the United States in 2006. The same year, The American Heart Association became the first major health organization to specify a daily limit:  less than 1 percent of calories from trans fat. Later in the year, New York became the first U.S. city to pass a regulation limiting trans fat in restaurants.  Multiple cities and states have since proposed similar regulations.

Is Polyunsaturated Fat (PUFA) a Healthier Option than Saturated Fat?

The recommendation to substitute PUFA for saturated fat was one of the main goals of the McGovern report in 1977.

This probably originated from the research of the influential Minnesota epidemiologist, Ancel Keys. Keys is often acknowledged as the father of the diet-heart hypothesis. He published many studies in the 1960′, and 70’s demonstrating higher cholesterol levels among patients with heart disease. His studies also showed higher cholesterol levels among people who consumed food rich in saturated fat and cholesterol.

From his famous “Seven Countries Study” Keys concluded that dietary fat was the single most important cause of heart disease because it elevates blood cholesterol. However, the study has been criticized for the method in which populations were selected for the study, and the way that the population (ecologic) correlations were carried out. Keys believed, like so many others, that a Mediterranean-style diet low in animal fat and rich in PUFA protected against heart disease.

Advice to replace animal fats rich in saturated fats by vegetable oils rich in PUFA  has been a cornerstone of worldwide dietary guidelines for half a century.

However, when the advice originated fifty years ago, PUFAs were regarded as single molecular category with one highly relevant biological effect – to reduce blood levels of cholesterol. At that time, omega-6 (linoleic acid) was the best known PUFA. Since then, it has been recognized that PUFAs comprise multiple species of omega-3 and omega 6, each with unique biochemical properties, and perhaps different cardiovascular effects.

What was the evidence behind recommending decreased consumption of saturated fat and increased consumption of PUFA?

Interestingly, there were three prospective studies performed during the 1960’s and 70’s comparing the effects of these two types of fats. The studies involving a total of 1300 men with heart disease in England, Norway, and Australia used diets with high ratios of PUFAs  to saturated fats, limited dietary cholesterol, and low levels of monounsaturated fat.

The trials lasted five years, and despite achieving lower cholesterol levels, people on the experimental diet did not do any better than their counterparts did on the control diet. Therefore, these studies did not support the hypothesis that substituting PUFA for saturated fat was beneficial. Somehow, the medical community did not seem to take notice. Interestingly, one of these studies, The Sydney Diet Heart Study was recently recovered, reevaluated and published in the British Medical Journal. The results have received huge attention.

Linoleic Acid (Omega – 6) –  The New Villain

Fat and heart disease - exposing the villain

The Sidney Diet Heart Study was a randomized trial conducted from 1966 – 1973. It tested the effect of replacing saturated fat with linoleic acid (omega-6) from safflower oil.

Safflower oil is a concentrated source of linoleic acid, containing no other PUFAs. The study population consisted of 458 men aged 30-59 years with a recent history of heart attack (acute myocardial infarction or acute coronary insufficiency). The men were randomized to an intervention group (n=221) and a control group (n=237).

The intervention group received instruction to increase their PUFA  intake to about 15% of food energy, and to reduce their intake of saturated fat and dietary cholesterol to less than 10% of food energy and 300 mg per day, respectively.

To achieve these targets, intervention participants were provided with liquid safflower oil and safflower oil polyunsaturated margarine (“Miracle” brand, Marrickville Margarine). Liquid safflower oil was substituted for animal fats, common margarines, and shortenings in cooking oils, salad dressings, baked goods, and other products, and was also taken as a supplement. Safflower oil polyunsaturated margarine was used in place of butter and common margarine. The control group received no specific dietary instruction. However, some participants began substituting polyunsaturated margarine for butter after their coronary event.

The results of the study were quite striking. Compared with the control group, the intervention group had an increased risk of all-cause mortality (17.6% vs. 11.8%),  cardiovascular mortality (17.2% vs. 11.0%) and mortality from coronary heart disease (15.3% vs. 10.1%). This difference existed despite the fact that total serum cholesterol decreased more in the intervention group than in the control group (13.3% vs. 5.5%).

These unfavorable effects of omega-6 are consistent with two other randomized controlled trials, in which saturated fats were replaced  with omega-6 and common margarines were replaced  with corn oil.

By reanalyzing  the original Sidney Diet Heart Study data, the authors were able to include the study into their previous  meta-analysis. The meta-analysis  covers secondary prevention studies where saturated  fats were replaced, either by omega-6 selective PUFA  interventions or a combination of omega-6 and omega-3.

In short; replacing saturated fats with PUFAs containing mainly omega-6 fatty acids appears to increase coronary heart disease mortality, while replacing saturated fats with a combination of omega-3 and omega-6 decreases coronary heart disease mortality. This may explain why a diet rich in omega-3, such as the Mediterranean diet appears to positively affect the risk of heart disease.

Omega-6 is the most abundant fatty acid in low-density lipoprotein (LDL) particles. Oxidized linoleic acid metabolites (OXLAMs) are the most abundant oxidized fatty acids in oxidized LDL. The authors of the British Medical Journal paper suggest that a diet-induced increase in the production of bioactive OXLAMs may contribute to atherosclerosis and cardiovascular disease pathogenesis. This hypothesis supports the possibility that atherosclerosis may occur through mechanisms that are very distantly related to plasma cholesterol.

Is It All Due to the Trans Fats?

Australia’s National Heart Foundation has claimed the recent Sidney Diet Heart Study is misguided. Dr Robert Grenfell who is National Health Director at the Heart Foundation points out that “in the 60s and 70s margarine still contained trans fats which we now know are extremely harmful to heart health. Replacing saturated fat with a product that was high in trans fat would never be recommended now.”

Bill Shrapnel, the Deputy Chairman of the Sidney University Nutrition Research Foundation agrees that “the study was not objective because margarine no longer contains the trans fatty acids it did at the time of the trials”. He adds: When the study began, Miracle margarine contained approximately 15 per cent trans fatty acids which have the worst effect on heart disease risk of any fat. The adverse effects of the intervention in this study was almost certainly due to the increase in trans fatty acids in the diet.”

The authors of the recent British Medical Journal article have a completely different view on the trans fat issue. In their discussion of the results they point out that the trans fatty acid content of the participant’s diets was not recorded. On the other hand they argue that the restriction of common margarines and shortenings (major sources of trans fatty acids) in the intervention group would be expected to substantially reduce consumption of trans fatty acids compared with the control group.

Thus, the consumption of trans fatty acids may indeed have been higher among the control patients than the intervention patients. Trans fatty acids are known to raise cholesterol levels. The fact that cholesterol levels decreased more in the intervention group than in the control group does not indicate that the intervention group had more trans fatty acids in their diet.

Dietary Fats and Heart Disease – Exposing the Villain

When it comes to crime novel, Agatha Christie is the master of twists and turns. You never know until the last page who is the villain. In one chapter you are led to believe it was the gardener or the butler. In the next chapter you definitively suspect the beautiful widow. The two things you could be certain of was that there were always going to be more twists and turns, and the end would take you by surprise. I somehow have a similar feeling about fat and heart disease. There will be  more twists and turns before we know the truth. For the time being though, it appears that the doomed outlaw, saturated fat may not be the worst villain. Indeed, the evidence against it is fairly weak.

At least, saturated fat appears more innocent than trans fat and omega-6.   I wonder, could Ancel Keys have been studying an effect of trans fat instead of saturated fat in his epidemiological research. Since he never separated these two, we will probably never know.

19 thoughts on “Dietary Fats and Heart Disease – Exposing the Villain”

  1. Doc,

    it’s rather unfortunate that you do even bother to conduct decent investigation. This reminds of Richard Dawkins who diclosed how sad it is that the creationist do not posses even the rudimentary information over the topic they so much criticize. Think about it, if you read the last page of a novel would you have any clue what actually happened?

    The holy nonsense manthra and new gospel is that Ancel Keys cherry picked the data. The skeptics cannot even tell the difference between a data set produced by the F.A.O and mortality statistics of WHO which Keys compared in 1953. The fact that Keys chose six countries out of the data set of 22 was simple done because only 6 countries showed reliable and vital statistics that were relatively reliable. Mexico f.e had not even developed a death certificate system in the 1950s. Moreover Keye did not even think the Finnish statistics, the best target for diet-heart, were reliable for his use.The data by the F.A.O had nothing do with the seven countries study which is prospective cohort study that continues even today. You went deep on the nonsense while claiming that the seven countries reported that dietary fat per se was deemed as bad. Those who criticize Keys are nothing short from the creationist online. This nonsense over Keys is simple not tolerable.

    The whole Keys story is documented here:

    It would have helped if you had read this excellent review by Pedersen et al 2011:

    “The amount and type of dietary fat to a large extent determines the number of circulating LDL particles and blood levels of total cholesterol. Moreover, SFA with 12–16 carbon atoms are the most potent LDL- or total-cholesterol-raising fatty acids(21)”.,

    “Recent critics of the role of SFA have questioned the rigour of the early dietary trials of CVD prevention and questioned current public health policy on limiting the intake of SFA (8) they suggest that more attention should be paid to increased intake of PUFA (9). The trials demonstrate unequivocally that replacing SFA, largely from dairy and meat fats (but in the Leren trial also with some TFA), by PUFA reduces serum cholesterol levels and CHD risk (9). That replacement of SFA by a variety of carbohydrate-containing foods also reduces CHD risk may be inferred from ecological studies, e.g. in Finland. CHD was also almost non-existent in rural China when mean cholesterol levels were approximately 3·5 mmol/l (1350 mg/l), with total fat intakes only about 15 % of energy and extremely low intakes of SFA (10,11). These observations, replicated in many other countries, should not be ignored even if meta-analyses of prospective cohort studies suggest no independent associations of SFA intake with CHD risk (2). The null results of the latter studies (2) probably reflect measurement error, residual confounding, over-adjustment by covariates on the causal pathway and large variations in plasma cholesterol compared to variations in intake of dietary fat (3,12–15). The role of SFA risks may also be overlooked, given the strong emphasis on TFA (16) and the incorrect proposition that the CHD epidemic in affluent societies has been primarily linked to a high consumption of TFA(17)”.,

    I have a challenge for you Doc, please read through the editorial by Stamler in regards to Siri-Tarino meta-analysis, and pay close attention to it:

    “…To neglect this fact in a review about humans is to imply that the Darwinian foundation of biomedical research is invalid and/or that there is a body of substantial contrary evidence in humans. Neither is the case. Dietary cholesterol (as well as SFA) adversely influences human serum lipid concentrations, per cited equations”.

    Based on the same material than Siri-Tarino used, Stamler calculated that saturated fats increase the risk of heard fatal CHD by 32% despite over-adjustement for lipids, regression dilution bias and sick-quitter effect. This is a massive RR and cannot be neglected by anyone who interested in lipids and their affect on long-term health. It was unfortunate that Siri-Tarino et al did not even look at this crucial end-point. Moreover, Stamler showed that the out of 16 studies used only 5 used legitimate, modern and valid dietary assesment methods (multiday food record, dietary history) RR was >1.00 for saturated fats in all 5 studies, even though 3 were adjusted for serum or dietary lipids

    • @Richard. Thanks for sharing your thoughts. I admire your interest and knowledge on the subject. Your opinion is indeed shared by many of my colleagues. I have looked into the links you provided, they´re interesting. In fact I found the Keys story very intriguing.

      I have huge respect for Ancel Keys and his research. It is a misinterpretation if you believe it was my intention to discredit him in any way. Regarding your words “You went deep on the nonsense while claiming that the seven countries reported that dietary fat per se was deemed as bad”: These were not my words. Keys believed that dietary fat played a key role for heart disease, mainly because it elevated plasma cholesterol. That´s all I said. I did not say that Keys believed “dietary fat per se was bad”. Indeed I finished the same paragraph by these words: “Keys believed, like so many others, that a Mediterranean-style diet low in animal fat and rich in PUFA protected against heart disease.”

      I agree that the Sidney Diet Heart Study was a small trial. However, that does not mean the results can be ignored. The metaanalysis provided by the authors indeed supports the results of the study.

      The control group was allowed to use commercial margarine, and they did. So there is no proof that trans fat consumption was higher in the intervention group.

      I believe, as you do, that LDL-cholesterol plays a role in atherogenesis. LDL-cholesterol is one of the best risk markers available. However, it has not been proven that the atherogenicity of low density lipoprotein is due to the cholesterol it carries. Indeed cholesterol rich particles may be less atherogenic than particles that carry small amounts of cholesterol. There are so many other substances and mechanisms involved in atherogenesis. People have heart attacks without elevated LDL- cholesterol, and many people with high cholesterol never have heart attacks. Obviously we still don´t know the whole story. It is likely that mechanisms distantly related to cholesterol may play a role in atherosclerosis. If you read through may blog you may see that I have had lots of thoughts on this. I will continue to keep an open mind.

  2. Actually, saturated fats have little effect on cholesterol levels compared to other dietary factors. Excerpt:

    A diet rich in foods with proven heart-healthy benefits is significantly better than a diet low in saturated fat for reducing LDL-cholesterol levels in patients with hyperlipidemia, according to the results of a new study [1]. The “dietary portfolio” of cholesterol-lowering foods reduced LDL-cholesterol levels by 26 mg/dL, nearly as large a reduction as was observed in some of the earliest statin trials, according to researchers.

    Research also indicates that lowering total and LDL cholesterol may be problematic for preserving muscle mass. Excerpt from a 2011 press release:

    The so-called “bad cholesterol” – low-density lipoprotein commonly called LDL – may not be so bad after all, shows a Texas A&M University study that casts new light on the cholesterol debate, particularly among adults who exercise. Steve Riechman, a researcher in the Department of Health and Kinesiology, says the study reveals that LDL is not the evil Darth Vader of health it has been made out to be in recent years and that new attitudes need to be adopted in regards to the substance. His work, with help from colleagues from the University of Pittsburgh, Kent State University, the Johns Hopkins Weight Management Center and the Northern Ontario School of Medicine, is published in the Journal of Gerontology. Riechman and colleagues examined 52 adults from ages to 60 to 69 who were in generally good health but not physically active, and none of them were participating in a training program. The study showed that after fairly vigorous workouts, participants who had gained the most muscle mass also had the highest levels of LDL (bad) cholesterol, “a very unexpected result and one that surprised us. “It shows that you do need a certain amount of LDL to gain more muscle mass. There’s no doubt you need both – the LDL and the HDL — and the truth is, it (cholesterol) is all good. You simply can’t remove all the ‘bad’ cholesterol from your body without serious problems occurring.

    The prejudice against LDL cholesterol runs wide and deep; worldwide in fact. But mortality figures do not suggest any health benefit for cholesterol levels below 200 because the lowest all cause mortality lies in the 200 to 240 range.

    And consuming a diet rich in saturated fats while limiting omega-6 and carbohydrate intake is a good way to lower triglycerides. Excerpt:

    One of the more remarkable results from Jeff Volek’s laboratory in the past few years was the demonstration that when the blood of volunteers was assayed for saturated fatty acids, those who had been on a low carbohydrate diet had lower levels than those on an isocaloric low-fat diet. This, despite the fact that the low-carbohydrate diet had three times the amount of saturated fat as the low-fat diet. How is this possible? What happened to the saturated fat in the low-carbohydrate diet? Well, that’s what metabolism does. The saturated fat in the low-carbohydrate arm was oxidized while (the real impact of the study) the low-fat arm is making new saturated fatty acid.

    In this excerpt from an article published in a 2012 South African Medical Journal article, Dr. Timothy Noakes briefly sums up the problem we face:

    The evidence is tenuous for the related diet/heart hypothesis, which holds that a diet full of ‘artery-clogging saturated fat causes an elevation of blood lipid concentrations, thus promoting coronary atherosclerosis and ultimately heart attack. I argue that the evidence is essentially non-existent. Opposing this is that coronary heart disease (CHD) is, like obesity and diabetes, an inflammatory disorder caused by abnormal carbohydrate metabolism in those eating a diet low in omega-3 polyunsaturated fats and high in trans fatty acids and omega-6 polyunsaturated fats.

    One thing I don’t understand is that while everyone now agrees that trans fats are a health hazard, nobody mentions the fact that a lot of trans fats are omega-6 trans fats. And some are omega-9 trans fats.

  3. Davebrown,

    The first study you quoted was that by Jenkins. The diet he prescribed was a vegan diet with soy-products and canola margharine. Not really something I see promoted by the low-carb echo-chamber. Yes, his diet worked better that the “low-saturated” fat diet that is commonly prescribed in hospitals and which includes plenty of animal protein. Although, the Jenkins diet did not work as well as Ornish low-fat vegan diet which has been documented to produce 40% drops in LDL cholesterol in just 12-weeks. This is equivalent to high-dose statin theraphy.

    Rural-Central Africans are one of the most musculus people on the planet, yet they have traditionally had very low cholesterol levels (TC cholesterol between 3-3,5mmol/l) thanks to their starch-heavy diet (sorghum, maize, legumes). I think the scare of loosing muscle mass should not be top priority next to low LDL levels and long-term benefits they provide.

    The mortality data is nonsense. Who would not know that the cholesterol levels of sick Western people start to plummet rapidly after the age of 60. This is due to metabolic changes in the intestine induced by senile devitalization. Some cancers suck up the circulating LDL cholesterol as well. Low-blood pressure and low BMI are both associated with higher mortality. J-curve phenomenon.Just like cholesterol, BMI is great predictor for quality of life all the way to the 60s. After that, the relationship with mortality and BMI is cofounded by comorbidities.

  4. Doc,

    In regards to the Sydney-trial; the TC cholesterol in the intervention arm after the 12-month follow-up was 6.3mmol/ (vs. 6.9 among the controls). No additional information was provided. The cholesterol levels, despite being lower in the intervention, was way enough what is required to keep up the disease process going at a full pace.

    I think professor Peter Clifton provided very informative insights;

    This is a very small study with only 63 total deaths. The 5.8% difference between groups for total mortality represents a difference of 10 deaths between groups (p=0.051) computed from the % deaths which does not meet conventional statistical significance. Figure 1 though only shows a difference in 6 deaths between groups. Certainly there is no evidence of benefit but the evidence of harm is relatively weak.

    Although dismissed by the authors trans fats are likely to be responsible for the lack of benefit. The margarine would have contained at least 20% trans fatty acids and if the participants were eating 25g/day of margarine then they would be consuming 5g of trans which might represent about 2% of calories. From the Nurses Health study this could reduce heart disease by 40-50% which would almost completely remove the apparent increased risk from the N6 margarines.The more margarine eaten the greater the risk. The test margarine would have mostly supplanted butter rather than other margarines. The fall in total cholesterol seen not only reflects a fall in LDL cholesterol but also a trans induced fall in HDL cholesterol.

    The fact that an increase in PUFA in the control group (90% of which would have been N6) was not associated with harm suggests the findings in the intervention group are confounded by the trans fats.”

  5. An excellent review Axel. Two additional points: Ancel Keys followed the Mediterranean Diet and lived to be almost 101 years old. In addition, the Lyon Diet Heart Trial achieved significant reductions in total mortality, CV mortality and recurrent MI in heart attack survivors randomized to the Western “prudent” diet or the Mediterranean Diet despite levels of LDL-cholesterol far above current guidelines (4.23 mmol/L in controls versus 4.17 mmol/L in Mediterranean Diet). It’s important to emphasize that IT’S NOT ALL ABOUT THE LDL!

    • @bhrdoc. Thanks Barbara. I agree with you on the Mediterranean diet. If there was a “heart healthy diet” contest I would definitively vote for the Mediterranean diet. It emphasizes healthy fats (PUFAs with high proportion of omega-3) and healthy carbohydrates, lots of fish, not to much red meat, lots of vegetable. Recent studies also show that this diet is also one of the best choices for type-2 diabetics.

    • @ Jeffry. Thanks Jeff. Actually me and Kris at Authority Nutrition keep on touch all the time. Iceland is a small country and we have common interests. Kris knows more than anybody about the secrets of the internet, so I try to get advice from him when I can.

  6. Few seem to realize that any dietary change that reduces omega-6 intake furnishes at least some protection from heart disease and other chronic inflammatory conditions. Most Paleo enthusiasts know to stop consuming industrial seed oils and replace them with traditional fats such as butter, lard, beef tallow, and coconut oil. Low-fat enthusiasts accomplish much the same thing. By restricting total fat intake, they inadvertently reduce their daily intake of omega-6s. An intermediate approach is the Mediterranean diet which is high in omega-9 monounsaturated fatty acids. Here’s an excerpt from an 2009 article about Dietary fat quality and heart disease. “The only long-term trial that reduced n-6 LA intake to resemble a traditional Mediterranean diet (but still higher than preindustrial LA intake) reduced CHD events and mortality by 70% [31]. Although this does not prove that LA intake has adverse consequences, it clearly indicates that high LA intake is not necessary for profound CHD risk reduction.” (Google – PDF Dietary fat quality and heart disease).

    When one starts digging into the subject matter, the omega-6 research paints a grim picture. Excerpts:

    “Southampton researchers have demonstrated that mothers who have higher levels of n-6 polyunsaturated fatty acids (PUFAs), which are found in cooking oils and nuts, during pregnancy have fatter children.”

    “While a diet rich in saturated fat and polyunsaturated fats from olives, nuts and fish is still thought to benefit overall health, excessive amounts of omega-3 fats, especially with omega-6 fats already concentrated in the body, could trigger inflammation responses in tissues.”

    “A recent study suggests a close association between dietary omega-6 and the development of overweight and obesity. Omega-6 is a type of fat found in certain vegetable oils which is present in large amount in processed and junk food. New results from experiments using animal models show that a high intake of omega-6 led to overproduction of signalling compounds that stimulate the appetite, with the result that the animals ate more and developed obesity.”

    Circumstantially, the global increase in omega-6 industrial seed oil consumption correlates strongly with increases in obesity and the entire spectrum of chronic inflammatory diseases. Excerpts:

    “If you lived in a village or urban-slum area in China or Mexico or Egypt 25 years ago, you were unlikely to have electricity or pumped water. You certainly did not know what television was; you walked to work or rode a cart linked to an animal; and your work was physically very strenuous. Your diet was monotonous and was based on rice or wheat products with possibly a few vegetables and/or beans, and few condiments and no cooking oil. If you go back to those same villages or slum areas today, people have electricity and television, their transportation is often via a bus or gas-powered vehicle, and their work utilizes some type of gas-powered engine. And their diet includes a lot of vegetable oil and some processed-food products that contain added sugar. Some animal-source foods — be they chicken, beef, pork, goat or fish products — are consumed, as well…

    Today we find from one of my studies in process that, of 38 countries from the developing world for which we have nationally representative data, in all except four there are more overweight problems and obesity among adult women than there are those dealing with being underweight. Worldwide today, the number of obese people far exceeds the number of undernourished ones. This is a startling development that requires some explanation. What is happening to the diets of the world?

    Again, imagine how bland and healthful the diets of Mexicans might have been. When at their best, rice, beans, tortillas and a little citrus juice produce a well-balanced diet that is low in oil and sugar and high in fiber and many critical nutrients.
    But the modern food-processing industry and added consumer income, urbanization, improved transportation, TV, food advertising and other changes have led to diets that are much higher in fat and added sugar. Healthful fruits and vegetables are not increasing much in people’s diets, while they are more likely to consume sugared water in some soft drinks or fruit drinks and add a lot of vegetable oil to their dishes. And they consume more meat.

    A revolution has occurred. For instance, in the early 1980s, no adults in China consumed what we call a high-fat diet with more than 30 percent of their calories from fat. Today, over half of Chinese adults consume such a diet. In China, dietary shifts are very quickly occurring. Rice and flour intake is down, and animal-source foods such as pork and poultry and fish are way up, and the steepest increase is in the use of edible vegetable oils for cooking. People are eating more diverse and tasty meals; in fact, edible oil is a most-important ingredient in enhancing the texture and taste of dishes…The edible-oil increase is found throughout Asia and Africa and the Middle East as a major source of change.”

    To me, the most horrifying aspect of excessive omega-6 intake is what it does to the brains of children. Excerpt:

    “It thus seems possible that the high n−6/n−3 ratio in the American diet might contribute to the relatively low ranking of American children in international testing (NCES, 2005) compared to children in countries with lower n−6/n−3 ratios, like Japan.”

    With evidence of this sort available, one wonders how much longer the Harvard School of Public Health and the American Heart Association can continue to recommend Americans up their intake of omega-6s. Excerpts:

    “For polyunsaturated fats, the American Heart Association has set 8 to 10 percent of calories as a prudent target; there is evidence, though, that eating more polyunsaturated fat—on the order of 15 percent of daily calories—in place of saturated fat can lower heart disease risk.”

    “The British Medical Journal study is interesting, but not conclusive. It is offset by a large body of scientific evidence that continues to show cardiovascular benefits associated with eating mono- and poly-unsaturated fat, rich in Omega-6 linoleic acids, in place of saturated fats,” said Penny Kris-Etherton, Ph.D., R.D., American Heart Association spokesperson and distinguished professor of nutrition at Pennsylvania State University.”

  7. Dr. Mary Enig points out that it was the CSPI that “forced” restaurants to switch from natural saturated fats to trans fats proclaiming its safety. Then, they lobbied to against the use of trans fats when the safety evidence mounted against.

    It may instructive to point out that fatty acids supply more ATP than glucose.

    “The oxidation of fatty acids yields significantly more energy per carbon atom than does the oxidation of carbohydrates. The net result of the oxidation of one mole of oleic acid (an 18-carbon fatty acid) will be 146 moles of ATP (2 mole equivalents are used during the activation of the fatty acid), as compared with 114 moles from an equivalent number of glucose carbon atoms.”

    Therefore, fatty acids have to be the preferred evolutionary fuel. Natural selection will optimize on the high quality fuel. It’s unlikely that we would have evolved on a high quality fuel only for it to kill us.

  8. @BHRDOC

    CV mortality and recurrent MI in heart attack survivors randomized to the Western “prudent” diet or the Mediterranean Diet despite levels of LDL-cholesterol far above current guidelines (4.23 mmol/L in controls versus 4.17 mmol/L in Mediterranean Diet). It’s important to emphasize that IT’S NOT ALL ABOUT THE LDL!

    I see the role of cholesterol to CHD in terms of the so-called causal exposure model (Sniderman et al 2012). Against this background, the above comments seem somewhat odd to me. I have three particular problems with this line of reasoning!

    1) Age; Lyon was a secondary prevention made-up of old people. Age is a risk factor, but its relationship to cholesterol is not straightforward. Cholesterol levels start to generally plummet in Western people after the age 60. As I wrote, this is due to senile devitalization and metabolic changes in the intestine that lead to weakened cholesterol absorption and synthesis. Blood-pressure and BMI are often also quite low on older people, at a time when strokes and heart-attacks are most expected.

    2) Lipid-lowering agents; 34% of the controls were on statins as opposed to 26,5% compared to the intervention arm.

    3) Recurrence of an event; as the authors of Lyon-diet trial stated:

    “..and each increase of 1 mmol/L of total cholesterol increased the risk of recurrence by 20% to 30%. Epidemiological studies have consistently shown a positive correlation between plasma cholesterol levels and the incidence of (and mortality from) CHD in various populations.24,25 Thus, our population does not appear to be different from other low-risk populations. 25,26 In other words, the data indicate that neither the Mediterranean dietary pattern nor any major bias has altered the usual and expected relationships between the major risk factors of CHD and recurrence”

    Lyon-trial does not change the well-established evidence that people who’ve maintained low cholesterol levels throughout the life rarely get strokes or heart-attacks.

  9. Similar to Richard’s opinion I feel that this article is misleading. By the time of the McGovern report in 1977 there was much more data than just “epidemiological and observational data”. By 1977 there were dozens of rigorously controlled metabolic ward experiments clearly demonstrating that dietary cholesterol and saturated fat elevate serum cholesterol. Furthermore most of the 17 diet and drug trials included in Sir Richard Peto’s meta-analysis presented at the 1984 NIH consensus (published previously in 1981) had already been published by 1977. Peto demonstrated that pooling either the diet or drug trials that successfully lowered serum cholesterol resulted in a statistically significant decreased risk of coronary heart disease.

    Also, it had already been demonstrated by this time in hundreds of experiments in mammalian and avian species- herbivores, omnivores, carnivores and about one dozen different species of nonhuman primates that dietary cholesterol and saturated fat are a primary cause of atherosclerosis.

    Another point that is greatly misleading is your attempt to refute Dr. Grenfell’s opinion that the intervention group in the Sydney Diet Heart Study consumed more trans-fat in their diet is part by stating that “Trans fatty acids are known to raise cholesterol levels. The fact that cholesterol levels decreased more in the intervention group than in the control group does not indicate that the intervention group had more trans fatty acids in their diet.”
    Indeed it has been demonstrated in randomized controlled trials that replacing carbohydrates, polyunsaturated fats or monounsaturated fats with trans-fats significantly raises serum cholesterol. However as you obviously already know, it has also been demonstrated that when saturated fat, especially for lauric, myristic and palmitic acids are replaced with trans-fat serum cholesterol actually decreases, and this is partly due to a decrease in HDL cholesterol. As the focus of this experiment was on replacing saturated fats with a margarine assumed to be rich in polyunsaturated fats, a decline in serum cholesterol would have actually been the expected result had the experimental group consumed a significantly larger amount of trans-fat.

    As Peter Clifton pointed out, the observed decline in serum cholesterol in the experimental group could be partly be explained by “a trans induced fall in HDL cholesterol”. The decline in serum cholesterol could also be partly explained by the observed decline in caloric intake and a slight drop in BMI.

    There is an enormous body of evidence from a vast number of animal species including over a dozen experiments carried out on a variety of nonhuman primate species demonstrating that replacing linoleic acid with saturated fat significantly accelerates atherosclerosis. These experiments cast great doubt on the biologically plausibility of this linoleic acid hypothesis and provides confidence for the findings form prospective cohort studies and other studies cited by American Heart Association which support the hypothesis that replacing saturated fat with linoleic acid confers benefit. Furthermore a recent systematic review of 15 randomized controlled trials also cast doubt on the hypothesis that linoleic acids increases markers of inflammation.

    This does not necessarily mean that replacing saturated fat with largely empty calories in the form of seed oils is the most optimal method to achieve more favourable blood lipids. A more appropriate approach maybe to replace foods rich in saturated fats with nuts and seeds which are rich in antioxidants that may mitigate any potential PUFA induced oxidization.

  10. The bottom line is, that whether LA or TFA was killing people in Sydney, the patients were using this product because of faith in the lipid hypothesis.
    @richard has many good arguments but none explains the lack of correlation between SFA and CHD or total mortality.
    Most recently in Finland with very high upper intake (KIHD).
    EFAs are essential nutrients so of course they are protective in proper amounts and ratios, but they can replace bread as well as butter to get this effect, and it seems to plateau at around 5%E, not 15%.
    You need to look at all-cause mortality as well as CHD mortality – differences in dietary fats do not affect all-cause mortality. Death is the more reliable diagnosis.

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  12. Excellent writing. I am confused by the statement, “Trans fatty acids are known to raise cholesterol levels. The fact that
    cholesterol levels decreased more in the intervention group than in the
    control group does not indicate that the intervention group had more
    trans fatty acids in their diet”

    Someday we will not use the term “cholesterol”. LDLc is very different from LDLp or apo B. More HDLc increases total cholesterol. However it may be HDLp that is more important. Trying to form policy even today on poor lab data.

  13. Hello Dr Sigurdson,

    I am an internal medicine physician and I have been looking for sound, evidence-based approach to provide dietary counseling to my patients. I have found a lot of evidence in support of low carb diets that are also rich in natural fats. In light of the rise in PUFA-rich seed and vegetable oil in our diets and the continued caution from AHA regarding saturated fats, I have the following questions:

    1- How do you interpret the results of “Circulating Omega-6 Polyunsaturated Fatty Acids and Total and Cause-Specific Mortality” study in Circulation, in 2014? It seems to be a robust piece of evidence in support of more linoleic acid in our diets.

    2- How can we reconcile this with the plausible role of oxidized linoleic acid in atherosclerosis, as described in article titled “Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis” in Open Heart BMJ in 2018?



    links to above references:


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