I just love it when I state a plain fact that has ample support in the published scientific literature, then get called a liar, lunatic and heartless profiteer (as if there’s untold riches to be made from telling people unpalatable truths…yeah, I wish).
Actually, I don’t love the above at all. The bit that I do relish is when, inevitably, someone with the ability to think for themselves reviews the relevant research then publishes a paper in a major journal confirming what I’ve been saying all along.
If you’ve read The Great Cholesterol Con, you’ll be in no doubt as to my opinion of the polyunsaturated fat thesis of CHD prevention: It is not just wrong, but dangerous.
This is the belief, still clung to by stubborn epidemiologists and ‘Heart Associations/Foundations’, that cutting saturated fat from the diet and replacing it with polyunsaturated vegetable fats will prevent heart disease. To see how this dangerous myth ever gained traction, let’s take a quick trip back in time.
A Brief History of the Polyunsaturated Vegetable Oil Sham
Nowadays, the biggest beneficiaries of the nonsensical cholesterol hypothesis of heart disease are unquestionably the drug companies, whose motley assortment of statin drugs – atorvastatin, lovastatin, pravastatin, simvastatin, rosuvastatin, pitavastatin – rewards them with tens of billions of dollars each year.
What many folks don’t know, however, is that the original industry beneficiaries of the cholesterol hypothesis were not drug companies, but vegetable oil and margarine manufacturers.
Most of you, at least those of you especially bright folks that constitute my regular readership ;), already know the story of Ancel Keys. He’s the researcher from Minnesota who abandoned clinical trial research in the 1950s to become one of the dodgiest and most destructive epidemiologists the world has ever known. Out of 22 countries for which relevant data was available at the time, the shameless sod handpicked data for only 6 – the 6 that just happened to support his fledgling thesis that fat intake was related to heart disease mortality – and published it in a journal whose peer review standards were evidently lower than a snake’s belly.
He didn’t stop there, though. The countries in his cherry-picked sample with the highest total fat intake also had the highest saturate intake and had the highest mean cholesterol levels. Emerging research was also showing that by replacing saturated fats with polyunsaturated fats, human beings could lower their serum cholesterol levels.
Using the kind of simplistic and patently stupid reasoning that has been instrumental in transforming the cholesterol hypothesis into a central pillar of modern medicine, Keys and his mates on the AHA nutrition advisory panel made the following assumptions:
1) Countries with higher mean saturated fat intakes and higher mean cholesterol levels have higher rates of heart disease, so therefore saturated fat and cholesterol cause heart disease!
2). Polyunsaturated vegetable oils, high in the omega-6 fatty acid linoleic acid, lower cholesterol. Therefore, they will prevent heart disease, too!
3). Everyone should cut their saturated fat intake and increase their polyunsaturated fat intake!
The problem with assumption #1, as we already know, is that it was derived from a fraudulent cherry-picked analysis. The further problem with assumptions 2 and 3, is that they were arrived at before being tested in a controlled clinical trial setting. Of course, that didn’t bother the vegetable oil manufacturers who stood to gain handsomely if their products came to be viewed as an effective method for preventing deadly heart disease. The vegetable oil manufacturers sponsored early studies and gave money to key researchers of the era, who then enthusiastically recommended omega-6-rich oils like corn and sunflower in medical journals and newspaper columns. The first ever popular-format CHD prevention book, Your Heart Has Nine Lives, featured a dietary section that read like an advertorial for vegetable fats.
The Great Linoleic Stuff-Up
The vegetable oil hypothesis eventually did get tested in clinical trials – and it was a resounding failure. In most studies, it completely failed to lower CHD mortality. In others, polyunsaturate-rich diets actually raised CHD mortality.
But these studies were roundly ignored by the ‘prestigious’ Heart Associations and Foundations. Not only did they fear looking foolish if they admitted the polyunsaturates they’d enthusiastically endorsed were at best useless and quite possibly harmful, they were also collecting tidy sums of money by selling “Heart Checks” and “Heart Healthy Ticks” to the manufacturers of these products.
But then evidence began to accumulate showing that not only were linoleate-rich oils and spreads useless for CHD prevention, they were also carcinogenic. Study after study showed when rodents were placed on linoleate-rich diets, they invariably developed more tumours and had a higher death rate than rodents placed on diets rich in saturates (for these furry little critters, the safest fats of all appeared to be the almost entirely saturated coconut oil and its refined derivative MCT oil).
Now, I’ll be the first to stress research findings in other species, including those with tails and abundant fur, do not always translate to humans. However, epidemiological findings began to stack up showing high linoleic acid intakes were associated with higher cancer rates in humans, too. More importantly, clinical trial evidence surfaced showing the same thing. In the Los Angeles Veterans Study, the group assigned to a polyunsaturated-rich diet experienced a lower rate of CHD – but it wasn’t due to their alleged atherosclerosis-preventing diet. If anything, they had slightly more atherosclerosis in their aortas, as revealed by autopsies performed on deceased study participants from each group.
The polyunsaturate-group experienced a lower rate of CHD simply because they were much less likely to be heavy smokers (cigarette smoking can induce heart attacks via arterial spasm, increased blood clotting and increased likelihood of plaque rupture). Despite this substantial advantage to the intervention group, they still suffered a significantly higher rate of cancer. By the time the study wound up, overall death rates were similar in both groups.
Health authorities began quietly watering down their polyunsaturated fat recommendations, although the Heart organizations were still happy to take money from oil manufacturers (even as recently as last year, I was stunned – and disgusted – during a trip to the supermarket to see a brand of refined linoleate-rich oil proudly sporting the Australian National Heart Foundation Tick of Approval).
One big problem with these omega-6-rich vegetable fats, as many folks now know, is that they aggravate the already distorted ratio between omega-3 and omega-6 fatty acids found in modern diets. Our diet is relatively sparse in n-3-rich foods such as fatty fish, brains, walnuts, pumpkin seeds, etc, and using n-6-rich oils in cooking and salads and eating packaged foods containing n-6 oils aggravates the situation by further throwing the n-3:n-6 ratio out of whack.
The importance of adequate n-3 intakes is supported by the fact that, while n-6-rich oils have proved a dud, n-3-rich fish oil supplements and diets in which fish intake was increased have indeed shown the ability to significantly lower heart disease and overall mortality.
OK, but why am I mentioning all this now? How does all this tie in with the vindication scenario I described at the start of the article?
The Sydney Diet Heart Study
The Sydney Diet Heart Study (SDHS) was first conceived in 1964, not long after the vegetable oil bollocks kicked off in the United States. Australia, for some reason, loves to follow crap American trends and the vegetable oil sham was no exception. So researchers from the University of Sydney, noting that despite all the hooplah the linoleate hypothesis had not yet been tested in clinical trials, decided to conduct a trial of their own.
They recruited 458 men aged 30-59 with pre-existing CHD, then randomly assigned them to either their usual diet or one in which saturated fat intake was decreased and polyunsaturated fat intake increased. To achieve this, intervention participants were provided with liquid safflower oil and safflower oil polyunsaturated margarine. It should be mentioned that, by the end of the study, the diet of the control group had also increased in polyunsaturate content thanks to prevailing propaganda, but to a lesser extent than the intervention group.
The control group should have ignored the propaganda: Their overall death rate was only 11.8%, compared to 17.6% in the intervention group.
The first and only Australian clinical trial of the polyunsaturate paradigm found it was a total flop.
But Wait, There’s More
In the original SDHS report, which can be accessed here, the authors concluded that diet, along with cholesterol level, showed no significant relationship with mortality. Rather, those who entered the study overweight, with hyperuricemia, or with more severe coronary disease were more likely to die during the trial. Those who maintained higher levels of physical activity were more likely to survive.
The original SDHS paper was published in 1978. A week ago, the British Medical Journal published a new paper, co-authored by one of the original SDHS researchers and several American researchers. The researchers noted:
“Advice to substitute vegetable oils rich in polyunsaturated fatty acids (PUFAs) for animal fats rich in saturated fatty acids (SFAs) has been a cornerstone of worldwide dietary guidelines for the past half century.”
“However, there is currently no clinical trial evidence indicating that replacing SFAs with n-6 LA, without a concurrent increase in n-3 PUFAs, lowers the risk of cardiovascular disease or death.”
The researchers then dug up the old magnetic 9 track tape containing the original SDHS data, reanalyzed it, and included it in a meta-analysis with data from other saturate vs polyunsaturate trials.
The original published paper only reported the overall death rate, which obviously is the most important mortality data of all. Hey, no use avoiding premature CHD only to get struck down by premature cancer instead. But of course, when the intervention being tested is supposed to be heart healthy, it’s still nice to know what if any effect it had on cardiovascular morbidity and mortality.
As per the original report, the researchers of the new BMJ report noted the intervention group had higher rates of all-cause death than the controls (17.6% vs 11.8%), giving a relative risk ratio of 1.62 at a probability of 0.05.
The figures for cardiovascular disease mortality were almost identical (17.2% vs 11.0%, RR 1.70, P=0.04).
For coronary heart disease, the mortality data were 16.3% vs 10.1%, RR 1.74, P=0.04.
This was despite the fact that serum total cholesterol decreased more in the LA intervention group than in the control group (−13.3% v −5.5%; P<0.001).
Now, remember how the original research group concluded that diet changes were unrelated to mortality outcomes? The new research group took a second look at the dietary records also, and came up with an entirely different conclusion. For the dietary re-analysis, only participants with baseline dietary measurements were included (n=429, 63 deaths). To further hone in on which of the prescribed nutrient changes could have produced the increased mortality observed in the intervention group, they repeated the same analysis limiting the sample to the intervention group only (n=207, 35 deaths).
Using this criteria they found that, among intervention patients (in whom the PUFA increase was pretty much all n-6 LA from safflower oil), an increase of 5% of calories from n-6 LA predicted 35% and 29% higher risk of cardiovascular death and all cause mortality, respectively (adjusted for age, dietary cholesterol, body mass index at baseline, smoking, alcohol use, and marital status).
Increases in the LA:SFA ratio in the intervention group were also significantly associated with higher cardiovascular death and all cause mortality; however, the reduction in SFA was not significantly related to any mortality outcome.
Among controls (in whom polyunsaturate source was not restricted to safflower oil and hence PUFA changes may not have been specific to n-6 LA), changes in PUFA and SFA consumption were not significantly related to risk of death.
Among the control and intervention groups combined, an increase of 5% of calories from unspecified PUFA predicted about 30% higher risk of cardiovascular death and all cause mortality.
A reduction in SFA and increase in the PUFA:SFA ratio were also associated with increased risks of all cause and cardiovascular mortality.
“Among patients in this intervention group, the increase in n-6 LA was associated with higher all cause and cardiovascular mortality, providing supporting evidence that LA itself was a key component mediating the unfavorable effects.”
In other words, the SDHS re-analysis strongly suggests that in patients with pre-existing coronary disease, safflower oil is more than just useless – it is potentially deadly.
The researchers concluded: “These findings could have important implications for worldwide dietary advice to substitute n-6 LA, or PUFAs in general, for SFA.”
Translated into plain English:
—To all health authorities, stop recommending this junk instead of saturated fats as a means of reducing CHD, because it doesn’t work!
–To all you Heart Associations/Foundations that masquerade as charities but are in fact incorporated entities raking in tens and even hundreds of millions of dollars annually and whose upper level staff enjoy salaries that would make many CEOs of for-profit companies green with envy…stop taking money from vegetable oil manufacturers so they can use your shambolic “Heart Ticks/Checks” to trick people into believing this junk is healthy, when it is in fact anything but.
By the way, astute readers may be wondering about the role of trans fatty acids in all this. Unfortunately, little was known about trans fats and their detrimental effects in the SDHS era, so their intake was not recorded.
When the researchers included the updated SDHS data with two other secondary prevention trials (Rose et al, Minnesota Coronary Survey) specifically examining n-6 LA, they found a marked increase in coronary heart disease mortality (1.84, P=0.02) among the intervention groups.
In contrast, analysis of four randomized controlled trials that increased n-3 PUFAs alongside n-6 LA showed reduced cardiovascular mortality (0.79, P=0.04).
This fat source is 100% natural, comes from a cow, and is the product of relatively little processing. It has never, I repeat never, been shown in actual clinical trials to cause heart disease or any other other health ailment. Health authorities nonetheless want you to avoid it, and instead eat highly refined vegetable fats that have been shown in clinical trials to raise the risk of heart disease and cancer. Bloody geniuses.
Oils Ain’t Oils
When I write articles like this, I have to remember that while many of my readers are very intelligent individuals, some appear to have the perception and reasoning capabilities of a bath plug. I’ve previously written articles on the danger of excessive n-6 PUFAs, then had people criticize me for recommending fish oil which is high in n-3 PUFAs. Their brilliant reasoning being, of course, that n-3s are polyunsaturated also, and therefore they must also be harmful.
Yeah, I know.
For the benefit of these folks, let’s point out a few quick facts:
–n-6 and n-3 fatty acids are not the same thing. No, really! I guess that’s why researchers gave them different names. Who would’ve thought?
–Not being the same entities, they often exert markedly different effects inside the human body.
–Both n-6 and n-3 fatty acids are harmful when consumed in excess. Which is why you should not only ignore health ‘authorities’ who tell you to eat sunflower/safflower/corn/soya oil instead of saturates, but also all those Wallys who tell you to throw down twenty fish oil capsules a day in the hope of achieving some totally unproven health or body composition benefit.
Just because n-3s have been shown in clinical trials to reduce cardiovascular and overall mortality, that doesn’t mean one should apply standard Western thinking (“If some is good, a truckload must be better!!”) and down a half-bottle of fish oil daily. It’s well-documented in the literature that the Inuit eskimos, famed for their very high intake of n-3s and low CHD, suffered a disproportionately high incidence of bleeding disorders. I’ve received plenty of anecdotal reports of people who acted upon the advice of so-called diet and strength ‘gurus’ who recommend supplementation with large amounts of fish oil, then suffered nose bleeds and runny, fishy smelling expulsions from you-know-where.
That’s just not cool.
So long as you use a high quality source of long chain n-3 such as fish oil, the research so far indicates it doesn’t take a whole lot to get the job done for CHD prevention. In the huge Italian GISSI study, a mere 900 mg of EPA/DHA (the amount found in 3 typical 1000mg fish oil capsules) was enough to significantly improve survival outcomes, and that was in folks with pre-existing CHD. There is simply no valid scientific justification for the use of fish oil megadoses in healthy human beings.
Another thing I want to stress is that not all vegetable oils are high in omega-6 fatty acids. Olive oil, macadamia oil, avocado oil are examples of oils high in n-9 monounsaturated fatty acids and – so long as you use a high quality, pure, minimally processed product – are healthful and tasty additions to one’s diet. Sesame oil makes for an interesting case study; although relatively high in n-6 it seems to return only positive results in research and has shown the ability to enhance, rather than antagonize, n-3 absorption.
I can’t stress the aforementioned qualifying statement about quality strongly enough: A lot of olive oil emanating from Southern Europe is surreptitiously filtered down with cheaper and inferior oils such as soy, for the sole purpose of increasing profit margins. And the problem of poor quality oil manufacture extends far beyond the Mediterranean. Last year, a major South Australian olive oil company – Big Olive, whose products can be found in supermarkets nationwide – was exposed as a purveyor of shockingly inferior oils. When lab tested, many were found to be “lamp grade” and unsuitable for human consumption (it behooves me to point out that since the Today Tonight expose, the company has changed hands, and I cannot comment on the current quality of their products).
Needless to say, you need to be real choosy about the plant oils you consume. Our family is in the lucky position of having Greek and Italian friends who make their own olive oils; we know where the olives come from and how they are processed, and know for a fact the oil is top notch. On occasions when these oils run out, I buy only certified organic, extra virgin, cold-pressed products.
Hey Anthony, How Do I Know Which Oils Are High in Omega-6 Linoleic Acid?
Good question. Here’s a list of the worst offenders in terms of n-6 LA content (g of LA/100g of oil), as derived from the USDA Nutrient Database:
Here’s a sample of oils low in n-6:
Butter oil 2.3
Anthony Colpo is an independent researcher, physical conditioning specialist, and author of The Fat Loss Bible and The Great Cholesterol Con. For more information, visit TheFatLossBible.net or TheGreatCholesterolCon.com
Copyright © Anthony Colpo.
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