we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least, and were the most physically active.
With a comment and a like, the fats article is rapidly becoming my most popular article ;). I thought I might go ahead and bring out the research I have available on the topic. The best collection of information, that I know of, on the mistaken link between saturated fat intake and CHD–happens to be from a short presentation that I believe was from a student (TA?) in my UNC-CH nutrition program. I showed up a little late that day to find they were finally giving a bit of my view and was basically dumbfounded as to how the information snuck into our classroom. Looking at the powerpoint, I’m happy to say I hit the highpoints already in my previous article, fats.
To skip to the finale–there were multiple tables at the end of the presentation listing study after study (approximately 60) of dietary intervention trials showing no link between saturated fat intake and CHD mortality outcomes (some participants in each study with preexisting CHD diagnosis, and others not). Again, I honestly don’t know where these tables come from, it seems to be a photocopy of a published article though–you know, back when we did that. However, for the truly skeptical reader, I’ve got the author name and date of each of the individual studies in the tables, as well as their follow-up period, number of participants CHD/not and age/gender information.
It is an obvious oversight that this paper did not report on any incidence differences. Statin drugs, which lower serum cholesterol, have been shown to decrease CHD incidence (not mortality). This merely says that if we artificially lower serum cholesterol, the mechanisms of heart vessel repair which go awry in CHD are less likely occur. This fact seems minor, almost off-topic, given the information below–specifically the shaky foundation of the lipid hypothesis, the attempted connection of actual fat intake to CHD, and the astounding words of the original researchers. paraphrasing and direct quotation of the presentation follows
Ancel Keys first proposed that saturated fat and cholesterol was responsible for CHD, he “tested” his theory by comparing fat intake and coronary mortality in various countries, selected only 6 of 22 countries with available food intake data, found a correlation with this limited data. Other researchers analyzed all 22 countries and found no such link (fat in the diet and mortality from heart diesase. a methodological note. New York State Journal of Medicine, 1957).
John Yudkin (1957) examined the data from 15 countries and found strongest association with CHD was carbohydrate consumption and TV/radio ownership.
The famous framingham study is another such foundational study, one which I’ve often heard is the proof of the fat/CHD link. It observed 5,000 residence of Framingham, MA over 16 yrs. Conclusion: for people under 50, CHD is “stringkly related to the serum total cholesterol levels” (11% higher in those with HD). Note: 95% of CHD deaths occur in those over 55. Important facts in the study: 1) for people over 55, those whose total cholestrol levels had decreased during the study experienced an increase in both total mortality and CVD mortality. 2) For every1mg/dl per yr drop in cholestrol, 14% increase in CVD death and 11% increase in overall mortality.
More striking is the quotes from William Kannel, the framingham study director, in the Lancet 1982: “serum cholesterol is not a strong risk factor for CHD, in the sense that blood pressure is a strong risk factor for stroke or cigarette smoking is a risk factor for lung cancer”, “in framingham, Mass, the more saturated fat one ate, the more cholestrol one ate, the more calories one ate, the lower the person’s serum cholesterol…we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least, and were the most physically active.
Frederick Stare (former AHA member, in JAMA in 1989): “The cholesterol factor is of minor importance as a risk factor in cardiovascular disease. Of far more importance are smoking, hypertension, obesity, diabetes, insufficient physical activity, and stress,” and that the National Cholesterol Education Program was “most unfortunate, because it gives undue emphasis to a minor risk factor in cardiovascular disease and thus false hopes to millions”
The presentation moves on to the biochemical science. PUFAs (polyunsaturates) are the most susceptible to free radical damage due to the multiple double bonds — especially when heated (and almost all vegetable oils are heated during processing). Heated vegetables oilds increase free radical damage in animals in humans (cited 8 studies: annals of nutrition and metabolism, 2001; lipids, 1999; food and chemical toxicology, 1991; lipids, 1999; atherosclerosis, 2002).
Linoelic (om6) consumption (in 4-week intervention trials) is found to be prooxidative and vasoconstrictive compared to a diet high in saturated fat diet (prostaglandins, leukotrienes, and essential fatty acids, 1998). LDL carrying PUFAs oxidize more readily (am. journal clinical nutrition, 1991). Theory: PUFAs may lower LDL and cholesterol, but increases LDL oxidization.
In US, om6 found mostly in soy, corn, sunflower, safflower, cottonseed and peanut oils; ratio of consumption of om6:3 used to be 1:1 or 3:1, now it is 15:1. Diet high in om6 reduces conversion of ALA to EPA/DHA. Om3-> prostaglandins -> artery dilator, inhibits clotting; Om6->thromboxanes->inflammation, blood clots, arterial constriction. Ateromas are 50% pufa, 30% mufa (Monos), 20% saturated, when compared to normal arterial tissue, advanced plaque in the aorta contains a higher proportion of om6 (lipids and oxidized lipids in human ateroma and normal aorta. biochimica et Biophsica Acta, 1993).
Fat type and MI: Double-blind, randomized control trial (lancet, 2003) found the higher the linoleic acid (om6) content of the atheromas, the greater the likelihood that the fibrous cap ruptures (thin, inflamed fragile cap); the higher the EPA, DHA content, the thicker the fibrous cap, the less likely the plaque will rupture). Association of n-3 polunsaturated fatty acids with stability of aterosclerotic plaques: a randomized contorl trial. Lancet, 2003).
Given 75g glucose: incrased thrombin (blood clotting enzyme), increased blood pressure, catecholamines, and heart rate, increase free radical activity (glycation stimulates formation of AGEs), decreased vitamin C and E (antioxidants). Harvard nurse health study of 75,000 women found women with the highest dietary glycemic load = 2x CHD risk (2000).
To repeat, the presentation concludes with multiple tables of dietary intervention studies which speak for themselves: dietary intervention which decreases saturated fat intake very rarely produces any reductions in CHD mortality. When lowering saturated fat seems to have a therapeutic effect, often the dietary intervention improves the diet in other ways than only replacing saturated fats with PUFAs. These are not small studies, they involve many thousands of people representing a variety of demographics.
Discussion: So–what the hell? With this kind of information, what gives? I think it best just to provide some possibilities, with the honesty that I’m not sure what’s going on/went on.
One theory is to simply say, “Oops!” we screwed up, we thought it was true, it seemed like a good idea, maybe we were blinded by enthusiasm to cure CHD and weren’t quite objective enough. To go ahead and go to the opposite pendulum swing, there is some theory that unhealthy encouragement of this type is part of a Rockafeller conspiracy to make money and control overpopulation by getting people to be unhealthy. Another common theory is that sales of cheap oils/margarines and soon later, statin drugs, relied heavily on the theory, financial concerns overtook good judgement for those in power and the AHA and others might have made a lot of money in making the low-fat recommendation. With the monetary concerns comes is the expelling of all those who oppose the theory and a massive public-health campaign to “educate”/advertise the importance of reducing fat, and especially saturated fat intake, to the public.
So what do I think? Probably a bit from column A, a bit from B, those columns being mistaken good intentions, uncritical evaluation evidence and more greed-driven intentions yielding excess promotion of what was bad science to begin with. Whether it be oversight or greed, as part of the American people, my family and I have been harmed by this misinformation. It is disheartening to know that the same thing happens quite often, research is turned into infomercials aimed at convincing doctors and ‘consumers’ alike rather than conduction of proper science. That, however, is the topic of another, to-be-written post: eager readers can jump the gun and read the well-researched book “Overdo$ed America” by a truly caring, honest and brilliant M.D. John Abramson.
A sort of late addition, but I thought I’d add what I’d like to see in research. 1) Dietary intervention trials which compare, for example, intake of ‘regular milk’, versus unpasteurized unhomogenized pasture-raised varieties. 2) Something to explain how low saturated/cholesterol can yield CHD morbidity but not mortality.
To wrap up: don’t be afraid to consume health-giving coconut, palm oil, or animals fats. Support your local farmer and buy some fresh dairy or humanely raised meat. Support yourself and your community, listen to your gut and question.