The Great Polyunsaturated Swindle: New Research Reveals Previously Hidden Findings

Many of you by now know that in 1953, a bloke by the name of Ancel Keys published a paper linking higher dietary fat intake to increased CHD mortality.

That paper was given the rather unassuming title “Atherosclerosis: a problem in new public health”, and was published in a now-defunct journal called the Journal of Mount Sinai Hospital. That journal might be long gone, but Keys’ 1953 paper forever and dramatically changed the course of medicine and dietetics.

In this paper, Keys wrote at length about the potential role of cholesterol in atherosclerosis, but the most famous part is the section towards the end where he plotted total fat intake and CHD mortality for six countries (Australia, Canada, England/Wales, Italy, Japan, US) on a graph, and was able to show a positive, linear relationship between the two. It was this graph that eventually stole the show (a picture is worth a thousand words, right?), hence the paper has come to be more commonly known as the “Six Countries Study”.

The ridiculously inadequate nature of Keys' six-country comparison has been written about countless times. So too has the possibility Keys deliberately hand-picked the six countries to conform to his preconceived theory. Data was actually available for twenty-two countries at the time; Keys used just six and never explained why, apart from the throwaway line, “So far it has been possible to get fully comparable dietary and vital statistics data from 6 countries.”[1]

Exactly why data from the remaining countries was not “fully comparable”, Keys never explained. Furthermore, given their stark cultural differences, to claim that pre-1950 data from such disparate countries as the US, Italy and Japan was “fully comparable” seems like a bit (a lot) of a stretch.

In 1957, Yerushalmy and Hilleboe pointed out the numerous inadequacies of Keys’ 1953 analysis, and noted his lack of any meaningful explanation for omitting the other sixteen countries. They proceeded to gather the data for all twenty-two countries and, after accounting for the likely differences in diagnostic classification, were able to plot it on a graph with little fuss. And from this far more thorough analysis they found the association Keys claimed between fat and CHD was markedly weakened, so much so they had no hesitation in proclaiming it invalid[2]. Which does little to assuage suspicions Keys hand-picked his six countries in order to bolster his fledgling theory.

Before I go on, yes, I’m fully aware that a number of entities, including a clueless Australian Broadcasting Commission review panel and a couple of bloggers who should full well know better, insist Ancel Keys is just a poor misunderstood soul whose role in the diet-heart hypothesis has been greatly exaggerated.

Ancel Benjamin Keys. One gushing female blogger even described him as “handsome”. Forgive for me for disagreeing.

All I can say is these folks desperately need to read Chapter 5 from my book The Great Cholesterol Con. Those who have already done so will know Keys was indisputably a critical player in the birth and propagation of the reigning diet-heart hypothesis. The publication of his Six Countries Study was a pivotal development; it was promptly cited by others and opened the door for his jumbo-sized follow-up, the Seven Countries Study. Meanwhile dissenters like Yerushalmey and Hilleboe, and the UK’s Dr John Yudkin, who also discredited Key’s biased analysis, were largely ignored.

To this day, the 7C study continues to be cited in support of the diet-heart hypothesis, even though it’s riddled with data that flatly refutes said hypothesis.

There’s even a “Keys Equation”, still in use today, designed to estimate changes in blood cholesterol according to variations in the dietary percentage of saturated and polyunsaturated fats.

Again, this is explained in TGCC. Also appearing in Chapter 5 of that book is a quote from Keys’ friend Henry Blackburn, who recounts how Keys was roundly discredited at a 1954 WHO conference in Geneva when he proposed his diet-heart theory. When asked to provide what he considered to be the key piece of evidence for his new theory, Keys obliged – and was quickly rebuked. This was quite a shock for Keys, who reportedly had a domineering, bully-bluster personality and was used to getting his way.

As Blackburn recalled, “…he cited a piece of evidence and they were able to destroy it … he didn’t make his case. He cited a piece--destroyed. He got up from being knocked to the ground and went out saying, 'I’ll show those guys,' and designed the Seven Countries Study"[3]

Keys was reportedly "so stung by this event that he left the Geneva meeting intent on gathering the definitive evidence needed to establish or refute this Diet-Heart theory"[4].

As history shows, the angry, humiliated and driven Keys got his revenge, and then some. The world proceeded to become obsessed with cholesterol, with both serum and dietary cholesterol being blamed for causing heart disease.

Dietary fat was also blamed, but the anti-fat demonization focused primarily on saturated fats which, under controlled experimental conditions, showed the ability to raise blood cholesterol. Important to the rest of this sorry tale is that polyunsaturated fats high in linoleic acid had been shown in these same experiments to lower serum cholesterol. Monounsaturated fatty acids, which predominate in oils like olive and macadamia, had a neutral effect and hence were for a long time largely ignored in the Anglo-Western world.

While all this was going on, and the Anglo-Western world began developing a truly neurotic attitude towards perfectly healthy foods like butter and eggs, Ancel Keys left the US in the mid-70s, settled in Italy (where fat-phobia was virtually non-existent), started eating like a Mediterranean, and lived to be 100 years old.

Sly old bastard. If only I could leave crappy Australia behind, scoot off to Spain, and live to be 100 …

No more bogans. No more road-raging assholes who hate cyclists. Plenty of gorgeous olive-skinned women with names like Lola, Isabella and Lorena, instead of uncouth, drunken, tattoo-covered ferals called “Shazza” and “Raych”. No more iced-up fuckwits screaming at their imaginary friends/enemies in the middle of the street. And did I mention premium quality anise at 1/6th of the Australian price? Heck, the Spanish even have girl’s names in honour of this epic drink, like Aniceta and Anissa!

Spain: Beautiful one day, fucking awesome the next.

"Camarero! Otro vaso de anís, por favor."


“Alguna tarta de queso también!”

Double sigh.

Huh? What? Sorry … where was I?

Oh yeah, Ancel Keys and the bullshit anti-cholesterol, anti-fat theory.

anis-del-monoAnís del Mono: A damn sight tastier than any polyunsaturated oil. Much better for the soul too 🙂

The Rise of the Polyunsaturates

The next key development in this sordid story is a 1961 paper that appeared in the American Heart Association’s primary medical journal, Circulation[5]. Up to this point, even the AHA had been circumspect about the new diet-heart hypothesis, and a paper only a few years earlier in 1957 by its nutrition panel concluded there wasn’t enough evidence to say yay or nay[6]. The 1961 paper, however, gave it a yay, and suggested the world begin limiting saturated fat intake and replacing it with polyunsaturated fats high in the omega-6 fatty acid linoleic acid.

What is important to note here is the initial poly-mania was confined to oils rich in linoleic acid, which is an omega-6 polyunsaturated fatty acid. Initially and for decades after, polyunsaturated omega-3 fats, whether they were from plant sources like flaxseed or animal sources like fish, were largely ignored and certainly were not subject to the enthusiastic endorsement that linoleic acid enjoyed. It’s only been in the last two decades that omega-3 fats have come under any meaningful amount of research interest, and it’s only been in the last 15 years or so that health ‘authorities’ have begun publicly emphasizing their intake (mainly via fish, which is a problematic source for some due to its content of mercury, PCBs, etc. Yours truly gets his long-chain n-3s from fish oil which has had had these impurities removed).

I emphasize this, because we will see later how mainstream apologists like Walter Willett are trying to rewrite history and make it look as if authorities were recommending a balanced n-3:n-6 intake all along. They did nothing of the sort. To the contrary, their pro-linoleate antics contributed to a steady worsening of the dietary n-3:n-6 ration in countries like the US.

So what food items are high in linoleic acid? The ones that became darlings of the early lipid hypothesists were corn oil, sunflower oil and – what is now the most widely consumed source of linoleate in the USA and many other countries – soybean oil. Other linoleate-rich oils include peanut oil, safflower oil, and cottonseed oil.

Friggin' Ancel ... Again.

There had been no new evidence in the short time that lapsed between the 1957 and 1961 AHA papers to support this new stance. What had changed was the composition of the AHA's nutrition advisory committee. Only two of the five authors responsible for the cautious 1957 report returned to pen the 1961 guidelines; among the new arrivals were Ancel Keys and Jeremiah Stamler, another famous proponent of the lipid hypothesis. The remaining members of the committee were Irvine Page, Frederick Stare, Edgar Allen, and Francis Chamberlain.

Tell me again how Ancel Keys wasn’t really a key player in kicking off the anti-saturate sham?

In 1963, Jeremiah Stamler, along with Alan Blaketon, co-authored Your Heart Has Nine Lives, a self-help book advocating the “Prudent Diet”[7]. To the best of my knowledge, this book was the world’s first popular format anti-cholesterol, anti-saturate CHD prevention book. It encouraged readers to replace saturated fats from animal foods with polyunsaturated oils, and told readers to "de-emphasize" eggs, butter, full fat cheeses and untrimmed meats. The authors' support for polyunsaturated fats was not based in any way on sound evidence, but creative speculation that science would eventually, hopefully, validate.

According to the book's 'Acknowledgements' section, Stamler had received "significant research support" (that’s researcherspeak for “money”) from the Corn Products Institute of Nutrition and from the Wesson Fund for Medical Research (Wesson are a manufacturer of vegetable oils). Stamler also thanked the American Oil Company for its "invaluable cooperation" with his research activities.

Everyone knows that the biggest financial beneficiaries of the cholesterol sham nowadays are the drug companies; specifically, those that produce cholesterol-lowering drugs. But as history shows, the initial financial benefactors of the anti-cholesterol idiocy were manufacturers of seed and legume oils rich in linoleic acid.

Vested Commercial Interest, Meet Bogus Health Claim. Bogus Health Claim, Meet Vested Commercial Interest!

And we all know what happens when commercial interests seize upon the belief their product is healthy. They promote the living crap out of it. They pay “opinion makers” to promote it. They fund supportive research, which is then given to opinion makers, who then print fancy brochures, create stupid food pyramids, sell Heart Ticks and Checks, issue press releases to dopey journalists, and run print, radio and TV campaigns to brainwash the public.

Among the early pro-linoleate opinion makers was Frederick Stare who, in 1969 in his syndicated Los Angeles Times column, stated:

"To my knowledge, I've never heard of too much polyunsaturated fat for man…"[8]

Good one, Fred.

Then there were the promotional campaigns for Procter and Gamble's Puritan Oil featuring Framingham Study Director Dr.William Castelli and former AHA president Dr. Antonio Gotto, Jr. The latter's efforts included sending a letter promoting Puritan Oil printed on a DeBakey Heart Center letterhead to practicing physicians in 1988[9]. The DeBakey Heart Center at Baylor College of Medicine was named after famous cardiac surgeon Michael DeBakey; Gotto's use of the Center's stationery was rather ironic considering DeBakey himself had conducted a study in the early sixties showing little relationship between cholesterol and CHD in 1,700 patients.

Yep, the early and somewhat tentative anti-saturate, pro-linoleate recommendations soon transformed into unbridled demonization of saturates, and recklessly enthusiastic endorsement of polyunsaturates.

Unbelievably, all this idiocy kicked off before the relevant randomized clinical trials (RCTs) were completed. And when those RCTs were completed, and consistently returned results showing that replacement of saturated fats with linoleate-rich polyunsaturated oils was a dismal failure in reducing CHD deaths or overall mortality, guess what health authorities did?

They ignored them and kept promoting polyunsaturated oils.

Fucking brilliant.

Data emerged showing these oils increased tumour incidence and growth in rats, compared to beef tallow, coconut oil, and MCTs. In fact, the latter two, comprised almost entirely of saturates, caused the least tumour growth of all!

But that didn’t stop our irrational guardians of health. Oh no. They still kept awarding Heart Checks (AHA) and Heart Ticks (Australian National Heart Foundation) to linoleate-rich oils, and kept slandering saturates as “artery-clogging” killers.

Mind you, these outfits – utterly undeserving of their 'authority' status – weren’t completely oblivious to their monumental, linoleate-soaked screw-up. When increasing evidence began to mount that these oils did not prevent heart disease, and may in fact be causing cancer, they quietly altered their dietary guidelines to recommend no more than ten percent of calories be consumed as polyunsaturated fats.

The ten percent limit on polyunsaturated fats nominated by the AHA may still be too high; rodent studies have shown these oils can induce tumour development at relatively low thresholds, and lipid researchers stipulate that no more than 4.5 percent of calories should come from polyunsaturates[11,12].

Furthermore, the reasons for the guideline changes were never explained to the public. As a result, millions of people continue to consume polyunsaturated vegetable oils in complete ignorance of their potentially dangerous properties.

Again, keep this stealthy behaviour of our (unelected and largely unaccountable) health authorities in mind when we discuss the revisionist antics of modern-day apologists a little later.

Meet Some Researchers Who Don’t Have their Heads Stuck Up their Butts


The name of the gentleman in the picture above is Christopher E. Ramsden. I’ll leave it to the ladies to determine whether or not he’s handsome (I’m still creeped out by that Ancel Keys picture), but what I can tell you is Ramsden and his team are doing some vitally important research that is rattling the cages of some of the more constipated, set-in-their-ways stalwarts of the old anti-saturate guard. As you can see at this link, Ramsden has a pretty impressive and extensive CV, but his current focus is researching the effect of altering dietary intake of n-3 and n-6 fatty acids on inflammation and pain relief.

In 2013, Ramsden and his colleagues published a paper in the British Medical Journal that contained a re-analysis of the old Sydney Diet Heart Study[12].  I have already written about this study and the Ramsden re-analysis here, but in short the SDHS was an Australian RCT published back in 1978, in which men aged 30-59 with pre-existing CHD were randomly assigned 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.

The intervention failed. The overall death rate was only 11.8% in the control group, compared to 17.6% in the intervention group[13].

The first and only Australian clinical trial of the polyunsaturate paradigm found it was a total flop.

The original published paper only reported the overall death rate. While undoubtedly the most important mortality figure of all, it’s extremely puzzling that the researchers chose not to present any data on CHD outcomes, given that linoleate-rich oils were being loudly hailed as “heart healthy”.

The SDHS authors also concluded that diet, along with cholesterol level, showed no significant relationship with mortality.

When Ramsden et al dug up the old magnetic 9 track tape containing the original SDHS data and re-analyzed it, they found some interesting data. As per the original report, Ramsden et al 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.

The figures for cardiovascular disease mortality – ignored by the original researchers - were almost identical (17.2% vs 11.0%, RR 1.70).

For coronary heart disease, the mortality data were 16.3% vs 10.1%, RR 1.74.

This was despite the fact that, as expected, serum total cholesterol decreased more in the LA intervention group than in the control group (−13.3% v −5.5%).

Now, remember how the original research group claimed that dietary changes were unrelated to mortality outcomes?

Ramsden and his team took a look at the dietary records also, and came to an entirely different conclusion. 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.

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.

These findings raise some important questions:

-Why was the SDHS incompletely reported back in 1978?

-Why were the CHD outcomes ignored and omitted from the paper?

-Why did the researchers claim diet had no relationship with mortality outcomes, when a subsequent analysis clearly showed a relationship between increased LA intake and increased CVD and overall mortality?

Were these key facts kept hidden because they constituted a major – and embarrassing - contradiction to the reigning linoleic-centric diet-heart hypothesis that was being vigorously promoted to an unsuspecting public?

The 2013 paper by Ramsden et al also included a meta-analysis of other trials involving manipulation of the dietary saturate:polyunsaturated ratio. 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) among the intervention groups.

From Sydney to Minnesota

Ramsden et al recently caused quite a stir with another re-analysis of an old RCT. This time it was the Minnesota Coronary Experiment (a.k.a the Minnesota Coronary Survey) which, like the SDHS, was poorly and incompletely reported.

In the original MCE report, it was claimed that over an average patient follow-up of 384 days, cholesterol levels fell to a greater degree in the treatment group than in the control group (175 mg/dl versus 203 mg/dl, respectively), but there was no difference in CHD incidence, CHD deaths, or total mortality[14].

As you’ve probably guessed, this wasn’t the full story.

The MCE (which ran from 1968-73) was a double-blind RCT designed to test whether replacement of saturated fat with linoleate-rich oil reduced CHD and death by lowering serum cholesterol. The participants were 9,423 patients (aged 20-97) of one nursing home and six state mental hospitals in Minnesota.

The MCE was funded by the US Public Health Service and National Heart Institute (i.e. taxpayers), with Ivan Frantz as principal investigator and none other than hunky handsome Ancel Keys as co-principal investigator.

The intervention was a cholesterol-lowering diet that replaced saturated fat with linoleic acid (from corn oil and corn oil polyunsaturated margarine). The control diet was high in saturated fat from animal fats, common margarines, and shortenings.

Needless to say, conducting a double-blind RCT with almost 10,000 participants was a huge endeavour. In addition to all the other work involved in organizing and running a regular dietary RCT, the double-blind conditions additionally necessitated the use of specially formulated foods. Such a project would have required lots of manpower (or personpower for you PC types), lots of time, and lots of money.

Lots, I tell you.

Despite this, key data analyses pre-specified by the original MCE investigators were never published.

The effects of serum cholesterol-lowering in the prespecified subgroups?

The association between longitudinal changes in serum cholesterol and risk of death?

The effects of the intervention on any autopsy endpoints?

Inexplicably, the authors never saw fit to publish the answers to these - their own - questions.

Yep, nothing to see here folks, now move along!

Which is where Ramsden and his team come in. They recovered raw MCE data, including previously unpublished records of serum cholesterol and autopsy reports, and an extensive collection of study documents, including a 1981 master’s thesis by University of Minnesota student Steven K Broste. The Broste thesis, which includes detailed survival analyses for the full randomized cohort and for the prespecified age and sex subgroups, had never previously been cited or considered part of the scientific evidence base (you can access it right here).

Before I relay Ramsden et al’s findings, it is important to note that the MCE had some important limitations. I’m not sure who came up with the bright idea to conduct a dietary RCT involving mental hospital patients (Ancel, was that you?); by their very nature, these institutions feature unstable patients whose hospitalization can range from days to years. The data from someone who is housed for a month then disappears from the study is hardly going to be of any use in ascertaining the effect of diet on a chronic disease like CHD.

As a result, out of a cohort of 9,423 patients, there were only 2,355 randomized participants who remained in the study for a year or longer. In this greatly reduced cohort, the intervention and control groups were well balanced at baseline. The age ranged from 20 to 97, with a mean age of 52. Slightly more than half were female, and 25% were 65 or older. Average BMI was 24.5 and average serum cholesterol concentration was 208 mg/dL. Mean follow-up for participants in this cohort was 2.9 years.

And the results?

As predicted, participants in the intervention group significantly lowered serum cholesterol compared with the control group. But this did them a fat lot of good (no pun intended).

Ramsden et al were able to confirm a lack of mortality benefit in the intervention group, and information from the Broste thesis indicated a higher rate of death in intervention subjects over 65. In the absence of the raw data, however, Ramsden et al could not determine the statistical significance of this finding.

MCE participants with greater reduction in serum cholesterol, however, had a higher risk of death. In this case, the association was robust, and was also seen in the control group. Among both groups combined, a 30 mg/dL decrease in serum cholesterol was associated with 22% higher risk of death from any cause.

Yeah, go polyunsaturates. Woo-fucking-hoo.

The higher risk of death associated with decreased serum cholesterol seemed to be driven by the subgroup aged ≥65. To explore the possibility that frailty (which is associated with both low cholesterol and death) could confound these results, they ran a sensitivity analysis adjusting for two known markers of frailty (changes in body weight and changes in systolic blood pressure). These adjustments did not materially change the results, which remained significant in both groups.

Autopsy results were available for 149 of the MCE patients. The original MCE researchers hypothesized that participants in the intervention group would have fewer myocardial infarcts confirmed by autopsy and less advanced atherosclerosis. In reality, 41% of autopsies in the intervention group showed at least one myocardial infarct, compared to only 22% in the control group. Also, participants in the intervention group did not have less coronary atherosclerosis or aortic atherosclerosis. Ramsden et al note these findings should be interpreted with caution because of partial recovery of autopsy files.

Meta-Analysis, Round 2

As they did after their SDHS re-analysis in 2013, Ramsden et al included a meta-analysis including the MCE data with that of other trials that provided vegetable oils rich in LA in place of saturated fat and not confounded by other interventions.

Again, there was no evidence of benefit on mortality from CHD (hazard ratio 1.13) or all-cause mortality (HR 1.07).

 vegetable-oils-supermarket-shelves-540WRow upon row of useless linoleic-rich crap that does absolutely nothing to reduce the risk of heart disease.

The bottom line is what anyone who read TGCC way back in 2006 has already known for a decade:

Replacing saturated fats with so-called “heart-healthy” polyunsaturated fats does indeed produce reductions in serum cholesterol, but does SFA to reduce cardiovascular or overall mortality[15].

The reason?

Because cholesterol has SFA to do with the causation of heart disease.

Of course, the motley assortment of ‘experts’ and ‘authorities’ who comprise our terribly inept health orthodoxy aren’t having any of this. Oh no. In their minds, cholesterol causes heart disease, always has, always will, end of story.

Cop this pearler from Professor Jeremy Pearson, Associate Medical Director at the British Heart Foundation:

"This is an interesting study which shows that decreasing your intake of saturated fat can have a positive impact in helping lower cholesterol. However more research and longer studies are needed to assess whether or not eating less saturated fat can reduce your risk of cardiovascular death."


RCTs going as far back as the 1960s have repeatedly and consistently shown that eating less saturated fat does nothing to reduce heart disease – and this joker thinks more studies are needed?

Is he going to pay for them out of his own pocket? Because its high time taxpayer funds went to something far more useful than stubbornly flogging a dead horse.

Then there was the BMJ Rapid Response of Walter Willett, from Harvard University. I’m sure you’ve all heard of Willett - he's a media darling frequently quoted in articles about nutrition. In 2007, he was ranked the world's second most widely-cited author in clinical medicine (if you’re wondering who beat him to the top spot, that was fellow Harvard epidemiologist and professor Meir Stampfer[14]).

You can read Willett’s response to the publication of the Ramsden et al MCE re-analysis here:

Willett’s arrogance is truly astounding. Here’s a guy who, along with Stampfer, presides over the world’s most prolific disseminator of epidemiological hogwash, the Department of Nutrition at the Harvard School of Public Health. Year after year, Willett and his colleagues relentlessly dredge the data obtained from their epidemiological bonanzas: The Nurses’ Health Studies, Health Professionals Follow-Up Study, and the Physicians’ Health Studies.

And from these massive data goldmines, they publish papers with the same old absurd conclusions that are eagerly embraced by the media and then relayed to a public sadly ignorant of just how nutrition science works.

These epidemiological escapades are hopelessly riddled with confounding variables, and have no business being cited as proof of anything. They can only detect statistical associations of unknown veracity. That’s it.

Years ago, budding young scientists used to be taught one of the most fundamental rules of good science:

“Association does not equal causation”.

Nowadays, based on a highly misguided and selective interpretation of the Bradford-Hill criteria, they are taught that with the right software package and clever statistical manipulation, they can go ahead and “infer causality” from such woefully deficient data.

Hence we have papers emanating from Harvard and other bastions of bollockery issuing such absurd pronouncements as “red and processed meats are associated with increased cancer incidence”, even though this association is easily explained by glaring discrepancies in the baseline characteristics of the participants. Thanks to the inordinate amount of red meat propaganda that Westerners have been subjected to, those with overall healthier lifestyle habits tend to eat less red and processed meats. As a result, people who eat less of these meats also smoke less, exercise more, and have lower bodyweights.

Little bloody wonder they get less cancer.

Of course, epidemiologists, deluded sods that they are, earnestly believe they can wave a statistical wand known as “multivariate analysis” that can magically "adjust" for these confounders. There are in fact a multitude of multivariate analyses, and like the numerous Gods people believe in, they can’t all be bonafide.

Personally, I think they’re all hogwash.

That the multivariate analysis charade is a farce can be evinced by the fact that among the Japanese, red and processed meat intake bears no relationship to cancer, nor heart disease or any other studied health outcome.


Because, to their credit, the Japanese have never bought into this anti-red meat malarkey that we Westerners have. As a result, Japanese folks with good overall lifestyle habits eat similar amounts of red and processed meats as those with poorer overall lifestyle habits.

Further debunking the multivariate adjustment sham is the inconvenient habit RCTs have of completely destroying the findings of epidemiological studies.

For example, we are repeatedly told that epidemiological studies show a lower risk of colorectal cancer and heart disease among whole-grain eaters. But when this thesis was tested in RCTs, which offer a level of control and quality no gargantuan epidemiological orgy could ever match, it was repeatedly and decisively rebuked.

As I explain in Whole Grains Empty Promises, RCTs examining the effect on increased whole grain and cereal fibre intake on colorectal polyp and cancer incidence found worse outcomes in the intervention groups.

And the one RCT that looked at the effect of increased cereal fibre intake in CHD patients (the DART trial) found a slight albeit statistically insignificant increase in CHD mortality in the fibre group.

It’s the same with the saturate versus polyunsaturate issue. Epidemiological studies repeatedly show a lower risk of heart disease ‘associated’ with increasing linoleic acid intake. But again, far superior RCTs show that linoleic-rich oils do absolutely nothing to decrease the risk of CHD; in some instances, they in fact show an increased risk.

Despite the utter uselessness, irrelevance and outright redundancy of the mountain of epidemiological pap he oversees, Willett nonetheless has the temerity to label the truly interesting and useful work of Ramsden et al as useless and “irrelevant” … !

I’ve never written a BMJ Rapid Response before, but after reading Willett’s derisory and revisionist reply, I had to respond. You can read my reply here:

A read through the remainder of the Rapid Responses is also insightful, or disheartening, depending on your disposition.

Instead of acknowledging the obvious – namely, that the anti-saturate theory is a load of repeatedly disproved nonsense - some of the respondents perform all manner of mental gymnastics in an attempt to explain away the results.

And then there are the folks who point out the numerous flaws in the MCE, as if these were somehow Ramsden et al’s fault. Never mind that Ramsden and his team clearly explained all these flaws in their paper, and never mind that examination of every other linoleate vs saturate trial, irrespective of quality, fails to support the anti-saturate theory.

Instead of trying to shoot the messenger, what these respondents should be asking is how such a hopelessly flawed trial ever came to fruition in the first place? And, having been given approval, why were the results incompletely reported and the bulk of the data hidden away? It is taxpayers who footed the bill for this carry on, yet they never got to see the final, complete results.

Are these respondents not bothered by such shady behaviour?

Elsewhere, a number of commentators have joined Willett in attempting to rewrite history, pretending that health authorities and the clueless guidelines they issue never really recommended high intakes of linoleic acid.

A sterling example is this blog post by Marion Nestle, who is quick to point out conflicts of interest in safe, politically correct targets like the sugar and meat industries, but not so quick to recognize the endless absurdities inherent in mainstream dogmas such as the anti-saturate and pro-whole-grain shams.

It seems Nestle didn't even read the Ramsden et al paper that she's writing about, so instead she defers to others who apparently have. Among these are David Katz, who writes that this study "tested something that nobody expert in nutrition is recommending: an extremely high dose of omega-6, linoleic acid … we already got the memo that this is a dubious proposition."

Katz also takes issue with Ramsden et al's (perfectly correct) observation that “A key component of dietary guidelines has long been to replace saturated fat with oils rich in linoleic acid…”

According to Katz, this isn't true, never happened, no sirree.

As a number of readers have commented underneath Nestle's article, Katz is wrong. Not only were authorities recommending liberal use of these oils for decades, some of them are clearly still at it. Here's the utterly clueless AHA's current advice on how to pick 'healthy fats':


Apart from monounsaturate-rich olive oil - which, in its extra virgin form is truly healthy and has proven itself in two large RCTs (Lyon and PREDIMED) - and n-3-rich canola, all the above oils are linoleate-rich junk. Several decades of controlled experimentation has repeatedly shown they have no business whatsoever being labelled as 'healthy'; they are far more likely to shorten lives than to extend them. But as we've seen, valid science does little to stop outfits like the AHA from continuing to spout their unscientific dogma.

You can read the rest of the AHA's appalling dietary fat advice here.


-The AHA has long recommended a total dietary fat intake of 30% of calories, and;

-5 of 7 of its recommended oils are exceedingly high in linoleate.

-It recommends consumers to avoid saturates and, again, only one of its recommended oils is high in monounsaturates.

So tell me again how no-one is still recommending high linoleate intakes?

The great irony to Willett's denial is that the official title of his Harvard chair is “Fredrick John Stare Professor of Epidemiology and Nutrition”.

Yes indeed – Willett's Harvard professorship is named after the same Frederick Stare who helped author that pivotal 1961 paper which effectively served as the official green light for the anti-saturate sham; the same Frederick Stare who in a 1969 Los Angeles Times column, stated:

"To my knowledge, I've never heard of too much polyunsaturated fat for man…"


We live in a world where bullshit reigns supreme. In hunter-gatherer and agricultural times, you had to produce real, tangible goods of actual benefit (food, clothing, shelter) in order to survive. Nowadays, people can sit at desks all day, fire up their software packages, and concoct intangible wankery of no real use or value – and get rewarded very handsomely for it, both socially and financially.

The anti-saturate, anti-cholesterol theory is one such manifestation of this sad state of affairs. There are just too many people who profit from this theory, or who have become so irretrievably enmeshed in its ideology that they simply do not possess the requisite cognitive characteristics necessary to impartially reassess it.

As a result, we’ll be stuck with this anti-saturate idiocy for a long time to come.

In the meantime, let’s hope folks like Christopher Ramsden ignore pompous naysayers like Walter Willett and keep chipping away at the pseudoscientific facade of modern health ‘wisdom’.


Anthony Colpo is an independent researcher, physical conditioning specialist, and author of the groundbreaking books The Fat Loss Bible, The Great Cholesterol Con and Whole Grains, Empty Promises.

For more information on Anthony's books, click here.



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  12. Ramsden CE, et al. 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. BMJ, 2013; 346: e8707.
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