On February 5th, the British Medical Journal published the subject of today’s post: Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. (1)
To those of you unfamiliar with the Sydney Diet Heart Study (SDHS), it was a randomized controlled trial that was conducted in Australia between 1966 and 1973. It sought to determine whether substituting polyunsaturated fatty acids (PUFAs), specifically safflower oil, for saturated and monounsaturated fat and cholesterol in the diet of men who suffered from coronary heart disease would extend their lives.
The results of this trial were unexpected to those unfamiliar with the Rose Corn Oil study that I wrote about here. When published in 1978, the Sydney Diet Heart Study reported an increase in all-cause mortality in the intervention group consuming omega-6 vegetable oil in contrast to the control group that was given no dietary advice.
Like the Rose study, these results were met with deafening silence lest it derail the anti-saturated-fat-and-cholesterol gravy train that was gaining momentum in the English-speaking world. Ignore the awkward is how Uffe Ravnskov would put it.
Curiously enough, deaths from cardiovascular disease and heart attacks were never reported in the original publication of the results. The purpose of this most-recent paper was to correct this omission by including the missing data.
However, before I report these findings, let me briefly describe how the original study was structured.
Eligible participants were men aged between 30 and 59 who had experienced a coronary event, i.e. a heart attack, acute coronary insufficiency or angina. These men were divided into two groups. 221 were randomized to the treatment or intervention group, and 237 were placed in the control group.
Members of both groups who were active smokers were advised to quit. Likewise, all overweight participants were encouraged to lose weight.
The intervention group was instructed to increase their polyunsaturated fat intake to about 15% of calories. They were also instructed to drastically reduce their dietary intake of saturated fat and cholesterol.
The intervention group was provided liquid safflower oil and safflower margarine. Safflower oil was used because it is the richest source of omega-6 polyunsaturated oil on the market.
The safflower oil and margarine were to be substituted wherever possible for animal fats, commonly available margarine, butter, shortening, salad dressing, baked goods and all other products and recipes containing or utilizing fat. As in the Rose Corn Oil trial, these men were also instructed to take omega-6 oil as a supplement.
Apart from being instructed to stop smoking or losing excess weight, the control group was given no dietary advice to follow. It was assumed they would continue eating their “artery-clogging” saturated-fat and cholesterol diet.
However, it was subsequently learned that some members in the control group took it upon themselves to substitute polyunsaturated margarine for butter. Some of these men obviously found out what the other group was being instructed to eat and decided to follow in their footsteps hoping to benefit from their “heart-friendly” diet.
Nevertheless, there is no indication these subjects reached comparable levels of PUFA intake. That said, given the results of this study, some of these men unwittingly hastened their encounter with that great defibrillator in the sky by mimicking their cohorts.
Just as in the Rose Corn Oil study, participants who increased their consumption of omega-6 vegetable oil saw greater drops in total cholesterol (-13.3% vs. -5.5%). There were no significant differences seen between groups in triglycerides, blood pressure or BMI.
This drop in total cholesterol also mimics what was seen in the 1966 Veterans Administration study. (2) However, the Veterans Administration study recorded increases in BMI with higher omega-6 oil intake.
The group substituting omega-6 oil for saturated and monounsaturated fat experienced an increased risk of all-cause mortality, 17.6% vs. 11.8%. However, for the first time ever, this recent paper reported that an increase of 5% in omega-6 oil intake resulted in a 35% increased risk of death from cardiovascular disease in the intervention group.
When combining the results from both the intervention and control groups, a 5% increase in unspecified PUFA intake predicted a 30% increase in both cardiovascular death and all-cause mortality:
These three charts graph differences in all-cause mortality, incidence of cardiovascular disease and coronary heart disease. The polyunsaturated omega-6 oil group is represented by the green line, the control group by the red. Higher is most definitely not better!
These results occurred despite the fact that restricting or eliminating the consumption of commercial margarine and shortening likely meant a total reduction in trans fat intake by the men in the intervention group in contrast to their colleagues in the control group!
As these authors note:
“Increasing dietary n-6 LA [omega-6 linoleic acid] in place of SFA [saturated fatty acids] lowers serum total cholesterol, primarily by reducing low density lipoprotein with little or no effect on high density lipoprotein. The traditional diet-heart hypothesis predicts that these favorable, diet induced changes in blood lipids will diminish deposition of cholesterol in the arterial wall, slow progression of atherosclerosis, reduce clinical cardiovascular risk, and eventually improve survival. As expected, increasing n-6 LA from safflower oil in the SDHS significantly reduced total cholesterol; however, these reductions were not associated with mortality outcomes… Moreover, the increased risk of death in the intervention group presented fairly rapidly and persisted throughout the trial. These observations, combined with recent progress in the field of fatty acid metabolism, point to a mechanism of cardiovascular disease pathogenesis independent of our traditional understanding of cholesterol lowering.” (Emphasis mine)
Now one mechanism the authors point to to explain these results is the fact that polyunsaturates are the most abundant fatty acids found in oxidized low-density lipoprotein (LDL) cholesterol. Oxidized LDL is a characteristic feature of heart disease. As I wrote here, polyunsaturated fats are delicate by nature and prone to oxidation when subjected to heat and light.
They point to smoking and excess alcohol intake as habits predisposing to oxidized LDL. And indeed, these habits do increase the odds of developing cardiovascular disease.
However, my faithful readers know that another huge and under recognized source of oxidation emanates from inflammation provoked by the translocation of gut pathogens to systemic circulation and the lipid peroxidation that occurs in the liver as a result of PUFA intake.
Now, let’s turn to the number-one reason these oils are sold to the
public as health food: their demonstrated ability to lower total cholesterol. This study, along with the Rose Corn Oil and Veterans Administration study witnessed this same effect.
While most “health” organizations and nutritionists consider this a wonderful “benefit”, it obviously isn’t. I explained why in part five of my heart disease series:
“…inflammation in the liver lowers total cholesterol. The more severe the inflammation, the lower your cholesterol goes, including LDL cholesterol. With its negative effects on tight junctions in the small intestine and oxidation in the liver, you now know why the polyunsaturated omega-6 oil group had the outcomes they did and why focusing only on high cholesterol is a potentially deadly mistake…”
“…So the solution to this puzzle comes down to this: chronic, low-level translocation of gut pathogens caused by disturbed gut flora and increased intestinal permeability raises both LDL and triglyceride levels but lowers HDL levels. Acute endotoxemia, however, lowers not only HDL levels, but LDL and total cholesterol levels. Neither is ideal but if you ask me, I’d rather have the former than the latter because at least I would still have a functioning immune system.” (Emphasis mine)
In the discussion section of this paper the authors write:
“In this cohort, substituting dietary n-6 LA in place of SFA increased the risks of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of LA intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute n-6 LA, or PUFAs in general, for SFA.”
Yes, these findings “could have important implications” for dietary advice. However, I seriously doubt much will come from this paper other than a blurb here or there in the press, and even those have been relatively scarce over the past few days.
Why do I believe this?
According to Hoovers.com:
“The US edible oils manufacturing industry includes about 200 companies with combined annual revenue of about $55 billion. Major companies include Archer Daniels Midland, Bunge, Cargill Foods, and CHS. The industry is highly concentrated: the eight largest companies account for about 80 percent of industry revenue.”
That is some serious money don’t you think?
How much of that money is spent, oh, I don’t know, endowing university nutrition and dietetic programs in the United States and elsewhere? Or advertising in nutrition and dietetic journals? On funding “research” favorable to their products?
How much is spent on print and television advertising? How hesitant do you believe the editor of a media outlet would be in publicizing what I just covered in this post? Do you think receiving angry telephone calls from the head of their advertising department might just stay their hand?
And what role do you think the United States government plays in promoting the sale and export of these oils?
And what of the reputation and funding of the American Heart Association? An organization that along with the edible oils industry has done more to demonize saturated fat than any other? Would a fall in their donations be welcomed by the well-heeled upper echelons of this “non-profit”?
So regardless of the sound scientific intentions that motivated the authors of this paper to revisit data from this study, I wouldn’t hold my breath waiting for nutritional advice to be swayed by these conclusions.
It has been almost 48 years since results from the Rose Corn Oil trial were first published in the literature. And it has been 34 years since the original Sydney Diet Heart Study went public.
Nevertheless, the “health” establishment and their lackeys in the media continue to trumpet confounder-prone epidemiological studies that are inherently incapable of proving anything in order to keep the anti-saturated-fat and lower-total-cholesterol-is-always-good-for-you dogmas alive and well. The tragic toll this takes on public health apparently causes these people little loss of sleep.
Ignoring the awkward indeed.
The only hope is change from the grass-roots. Do your part to tell your friends and family about these studies.
Not all of them will be receptive to the message. Overcoming decades of nutritional brainwashing and slick marketing will be just too much for some people to handle. But trust that you will get through to some. You may very well help prevent an untimely death.