According to the current dietary guidelines we shall exchange saturated fatty acids with polyunsaturated fatty acids to avoid cardiovascular disease. But what is the difference between saturated and polyunsaturated fatty acids you may ask.
The main part of a fatty acid is composed of a core of carbon atoms to which hydrogen atoms are attached. When the number of hydrogen atoms is optimal, as in saturated fatty acids, their electrons form stable pairs with those of the carbon atoms. Saturated fatty acids are saturated with hydrogen atoms.
Unsaturated fatty acids are missing hydrogen atoms. Monounsaturated fatty acids are missing two atoms; polyunsaturated fatty acids (named PUFAs in the following) are missing four or more. Therefore, instead of sharing one pair of electrons with each other, some of the carbon atoms are sharing two pairs of electrons with their neighbour carbon forming a so-called double bound. Lack of hydrogen atoms makes the fatty acids unstable; they go easily rancid. The more double bonds they have, the more unstable they are.
Two of the PUFAs, linoleic acid and alfa-linolenic acid are essential, meaning that we cannot produce them ourselves, but require small amounts in our food. The first one is an omega-6 PUFA, the second one is an omega-3. (The name omega refers to the placement of the double bound).
Seafood is rich in omega-3 PUFA and oils from corn, sunflower and soybeans are rich in omega-6 PUFA:. To be very short (the PUFA biochemistry is complicated) omega-6 PUFA stimulates inflammation and omega-3 lowers it. Inflammation is a useful process, for instance if we become infected, but not if it goes too far. This explains why eating much omega-6 is associated with various human diseases, for instance asthma, arthritis, vascular disease, thrombosis, immune-inflammatory processes, and tumour proliferation. Now to the scary issue of this letter.
Thirty-five years ago a dietary experiment was performed in Sydney, Australia. About half of 458 male patients with heart disease were given a diet low in saturated fat and cholesterol and with a high content of linoleic acid. The others ate as usual.
Five years later 17.2 per cent in the diet group had died from a cardiovascular disease, but only 11 per cent in the control group. As only total mortality was reported in the original report (17.6 versus 11.6 per cent), the results were published recently once again in British Medical Journal, because the authors wanted to warn against eating too much omega-6 polyunsaturated fat.
For that purpose they included an analysis of the combined result from four similar trials, where saturated fat was exchanged with omega-6 PUFA, and in all of them mortality was highest in the treatment group. They also analysed four trials, where the diet was composed of both omega-3 and omega-6 PUFA, and in these trials mortality was a little lower in the treatment groups.
At a closed consensus meeting in 2010 in Copenhagen invited scientists (no, I was not invited; researchers with a controversial view are never invited to consensus conferences in this field) concluded that “the evidence from epidemiologic, clinical, and mechanistic studies is consistent in finding that the risk of CHD is reduced when SFAs are replaced with polyunsaturated fatty acids.” You can read more about that in a paper authored by seventeen international experts.
As I have shown in my books, in my papers and in my newsletters, there is no such evidence whatsoever. Read also what was written by authors of one of the sections in the recent WHO/FAO report (p 191):
The available evidence from cohort and randomised controlled trials is unsatisfactory and unreliable to make judgement about and substantiate the effects of dietary fat on risk of CHD.
However, in spite of the result of their review, they found no reason to change the current advice.
Most PUFAs in our food to-day are of the omega-6 types. Nothing is mentioned in the guidelines or in the mentioned paper about which type of PUFAs we shall eat, meaning that if you ask people to eat more PUFA, they automatically end up with eating much more omega-6 than omega-3 PUFAs, and those who produce sunflower, corn and soybean oils clap their hands, of course, as do researchers that are sponsored by the industry.
Already in 1991 Scott Grundy, one of the main actors in the cholesterol campaign, warned against eating too much omega-6 PUFA. According to Grundy there was no epidemiological support for this advice; it suppressed the immune system; it lowered the “good” HDL, it promoted LDL oxidation, and it increased the risk of gallstones. Of special concern was that linoleic acid might promote carcinogenesis in humans, as it does in laboratory animals. Since then many studies have confirmed his warnings. Associations have been found between omega 6 PUFA and prostate, pancreas, colon and in particular breast cancer. One of he first and longest dietary trials, where saturated fat was exchanged with PUFA also resulted in cancer. Fewer died from a heart attack but more died from cancer. (That fewer died from a heart attack could at least partly be explained by the fact that there were many more smokers in the control group).
After the introduction of the dietary guidelines for Americans in 1977 our intake of saturated fat has decreased and our intake of carbohydrates has increased. A few years later an obesity and diabetes epidemic started, and it has continued up to today in many countries. Are we going to see a cancer epidemic as well? The question is relevant because cancer may also be an effect of statin treatment
A few weeks ago I was invited to a conference in Oslo by The Norwegian Heart and Lung Patient Organization. I took up this problem at the end of my talk, which is available on Youtube