How Time Magazine Sacrificed Its Standards to Promote Saturated Fat

How Time Magazine Sacrificed Its Standards to Promote Saturated Fat

By Plant Positive

June 28, 2014 

The editors of Time Magazine want you to eat butter. They said so on the cover of their June 23, 2014 issue. Why would they want you to eat butter? Butter is high in saturated fat so it raises our LDL-C[1], or “bad” cholesterol. The cholesterol in LDL particles is considered “bad” because it builds up the plaque in our arteries. Saturated fats also seem to promote inflammation[2]. Why would Time promote butter and other foods high in saturated fat? What was their argument to eat this way? 

The Time piece was written by Bryan Walsh and for the most part it was predictable rehash of the many myths and fallacies embraced by low-carbohydrate diet advocates for decades now. I’ve created a website and a YouTube channel to educate the public about the tricks of the low-carb promoters and this article offered nothing I haven’t seen already. What sets this article apart, however, was its prominence. Somehow the low-carb world’s distorted view of nutrition found its way into the pages of the nation’s leading news magazine. While this should be distressing to anyone who cares about public health, this failure of judgment by Time’s editors does create an opportunity to right a wrong. Perhaps now we can finally dispatch a particularly dishonest narrative pushed by the low-carbers, one they have circulated for years.

That narrative is an attack on the integrity of Ancel Keys. Keys was one of the most important contributors to the war against heart disease of the last century. Rather than celebrate his career, the low-carbers have ridiculed him relentlessly, especially since his passing in 2004. Walsh has joined this attack with his Time article. But despite all the critiques of Keys that have preceded his Time piece, Walsh doesn’t seem to understand what’s supposed to have been wrong with Keys’ work. As I’ve shown my viewers, Keys’ detractors often become confused about what papers of his they don’t like and what those papers were about. As you’ll see, Walsh seems to be confused as well. This confusion of his makes responding to him a little tricky but I’ll give it a try.

Would someone please explain to Bryan Walsh what cherry picking is?

“Keys' work became the foundation for a body of science implicating fat as a major risk factor for heart disease. The Seven Countries Study has been referenced close to 1 million times. But Keys' research had problems from the start. He cherry-picked his data.... Keys highlighted the Greek island of Crete… ‘It was highly flawed,’ says Dr. Peter Attia, the president and director of the Nutrition Science Initiative, an independent obesity-research center. ‘It was not on the level of epidemiology work today.’" – Bryan Walsh 

Keys is often accused of cherry picking. It’s a false charge but let’s not get into that just yet. The first problem with this quotation is that Walsh doesn’t seem to understand what data Keys is supposed to have cherry picked. Walsh is here clearly referring to Keys’ pioneering epidemiological study commonly called the Seven Countries Study[3], in which Keys collaborated with other researchers in a project spanning locales in seven different countries. The researchers followed a group of men in each of 16 communities over a period of years, taking note of their diets, cholesterol levels, blood pressure, weight, etc. with an eye toward seeing which of their traits correlated with coronary heart disease. This study was what we today call a “prospective cohort study.” Keys didn’t throw out the data from any of his cohorts. He published the results from all of them. Therefore, by definition, he could not have cherry picked data. Walsh’s charge makes no sense.

Let’s now pretend that Walsh understood and was able to express the common cherry picking claim against Keys. It’s likely he meant that Keys cherry picked in a 1953[4] paper which compared fat consumption with deaths from coronary disease, producing the scatter plot to the right. Four years later this paper was criticized by two other researchers who argued that Keys incorrectly excluded data from other countries to create that graph. You can see Keys compared total fat intake to coronary deaths in six countries. Data for at least 22 countries were available to him so why did he choose only these six?

Did Keys cherry pick in that earlier paper?

“Keys' unshakable confidence and his willingness to take down any researcher who disagreed with him was at least as important as his massive data sets. (When the biostatistician Jacob Yerushalmy published a 1957 paper questioning the causal relationship between fat and heart disease, Keys responded sharply in print, claiming that Yerushalmy's data was badly flawed.)” – Bryan Walsh

I’m not sure why but Walsh has left out the name of Jacob Yerushalmy’s co-author for that 1957 paper[5], Herman Hilleboe. He also excluded a rather interesting piece of information. Yerushalmy and Hilleboe found animal protein to correlate better with heart disease deaths than fat, better than any other factor in the diet, as you can see in this scan of their paper. But you’d never know that from Walsh’s article. He also left out the fact that two other researchers, Norman Joliffe and Morton Archer[6], scrutinized Yerushalmy and Hilleboe’s critique two years later and found them to have inexplicably ignored the crucial distinction between saturated fats, which raise cholesterol, and unsaturated fats, which don’t. See for yourself:

So what meaning did Joliffe and Archer find in their analysis of the same data? They said that “the intake of saturated types of fat was most important in accounting for the differences in coronary heart disease death rates.” Animal protein came in second place. 

Now ask yourself, if it was wrong for Yerushalmy and Hilleboe to have ignored the difference between saturated and unsaturated fat in 1957, how much worse is it for a journalist to ignore that difference in 2014?

Yerushalmy and Hilleboe weren’t the first to argue that the statistics from some nations made it hard to blame fats for coronary deaths. This argument was apparently first made by the National Dairy Council[7], who didn’t like the suggestion that the fats they marketed could be blamed for heart disease. They said that the lower death rates from heart disease in the Netherlands, for example, where dairy fats were consumed in greater quantity, argued against Keys’ scatter plot.

This, however, was an inappropriate comparison. It takes many years to develop heart disease. Most of us have to eat a lot of greasy foods over a long time to die from that habit. The conditions that would have enabled this dietary practice would have been highly unlikely in the Netherlands in those days. All that mortality data came from the 1950s, which happened to be preceded by World War II, when many populations suffered serious privation, including the Dutch. Walter Cronkite told America[8] that they lived “almost wholly on cabbages, turnips, and backyard vegetables” during the war. Cronkite didn’t mention finding an abundant supply of high-fat dairy products amid all that “poverty and want.”  The National Dairy Council should have known better. Other countries had unsuitable data as well. Mexico wasn’t able to certify the deaths of large segments of their population. These are but two examples. I’ve discussed others in my videos about Keys’ supposed cherry picking. As he explained in 1953 when he created the plot, he could only include those countries with "fully comparable" data. 

Recall from his quote that Walsh was trying to fault Keys for leaving out France and West Germany from that 1953 paper. But why should Keys have included them? France was known to have different practices in categorizing deaths from diseases of the heart, making their statistics unusable, as Ruth Puffer and Louis Verhoestraete noted here[9].

Keys ably defended himself against Yerushalmy and Hilleboe’s arguments in 1957[10]. If Walsh had bothered to visit a library while researching his article he could have learned why Keys ignored the data from West Germany. As Keys explained, the diets of the Germans had been affected by the war, and their population had been highly unstable during that period, making them a poor choice for inclusion in his graph. Keys wrote:

“I have mentioned West Germany where the diet changed little during the war years but where the fat intake was very low for several years after the war. A further complication is the tremendous migration into this country since the war. A population of 40 million has taken in about 11 million refugees and escapees from the East. The immigrants, as is always the case, are not a good sample in regard to age, vigor, and state of health of the population from which they migrated. And in the case of West Germany the majority of the immigrants left behind them a diet very different from that of their new land of settlement.” – Ancel Keys

In the same editorial, written to respond to the criticisms of Yerushalmy and Hilleboe, Keys also commented on the inconsistencies between countries with regard to their classifications of cause of death, as discussed above.

Keys also indicated that he understood he should have been comparing death rates with saturated fat intake, not total fat intake, back in 1953. He said, “Such epidemiologic suggestions as there are for an effect of animal protein are readily accounted for by the high correlation between animal protein and animal fat intakes in most human populations.”

So you see, Walsh was wrong about what Keys was supposed to have cherry picked, and the cherry picking charge is false anyway, and a more thorough investigation of these cherry picking claims actually argues against saturated fat consumption. Walsh seems to have had this story wrong in every way possible.

What about the Seven Countries Study?

Now let’s consider Walsh’s argument against the Seven Countries Study itself. He thinks a comparison between the cohorts in Corfu and Crete blows up the correlation Keys found between saturated fat consumption and coronary death. He wrote:

“Keys highlighted the Greek island of Crete, where almost no cheese or meat was eaten and people lived to an old age with clear arteries. But Keys visited Crete in the years following World War II, when the island was still recovering from German occupation and the diet was artificially lean. Even more confusing, Greeks on the neighboring isle of Corfu ate far less saturated fat than Cretans yet had much higher rates of heart disease.” – Bryan Walsh

The Seven Countries Study began in 1958*, well after World War II, so his first point about when Keys visited there is irrelevant. The study’s results were first published in 1970 but the study itself didn’t end then. Here’s a comparison[11] between its different cohorts showing saturated fat intake along the horizontal axis and coronary mortality at 25 years along the vertical axis. Corfu and Crete are highlighted. You can see that Walsh is excluding an awful lot of information when he limits his focus to these two places. Ignoring those other cohorts would be a form of cherry picking.

Why should Corfu and Crete have had such different outcomes? A better question might be, why assume that the only relevant difference between them was their saturated fat consumption? Saturated fat isn’t all that matters in the diet. The people in Corfu consumed much more alcohol than the Cretans[12]. High levels of alcohol consumption increase the risk of heart disease.

You can learn more about the Seven Countries Study here. You can also learn much more about Ancel Keys and the false charges against him at my website. I’ve been correcting the low-carb story about him since 2011.

What about the rest of his article?

There was a lot wrong with Walsh’s article, too much for me to properly address now (I’m not collecting a paycheck from Time or anyone else to write this). But I can give you a sense of what was wrong with the rest of his article. Walsh referred to another study. He wrote, “A 2010 meta-analysis – basically a study of other studies – concluded that there was no significant evidence that saturated fat is associated with an increased risk of cardiovascular disease.” I’ve addressed this meta-analysis at length already. It turns out when you look at the individual studies being studied in that meta-analysis, for the most part they make saturated fat look quite guilty of causing coronary deaths. Walsh related that meta-analysis to a more recent one when he wrote, “Those results were echoed by another meta-analysis published in March in the Annals of Internal Medicine that drew on nearly 80 studies involving more than half a million subjects.” I’ve written about this one as well. What sense would it make to include studies in a review of the effects of saturated fat in which every participant was taking cholesterol lowering medications? Remember, saturated fat increases the risk of heart disease by raising our cholesterol levels. But that’s exactly what the authors of that second meta-analysis did.

Walsh solicited most of the comments from experts in his article from fringe doctors who profit by promoting low-carbohydrate diets. For example, he quoted Eric Westman, Jeff Volek, and Stephen Phinney. All of them have received money from the Atkins Foundation, named for low-carber Robert Atkins, and they’re all authors of a recent book promoting Atkins.

To discover the influence of special interests in low-carb research, you sometimes have to do some sleuthing. Take the case of Jeff Volek, for example. He is working on a paper meant to “demonstrate that plasma saturated fat levels are a function of dietary carbohydrate intake rather than saturated fat intake, which would help neutralize the negative image of beef, dairy and eggs (all naturally low carbohydrate foods) by showing their intake per se is associated with favorable metabolic health effects.” This quote comes from a document from the beef industry[13] in which they give an accounting of their marketing efforts. They list their “subcontractor” on this promotional study, its outcome already anticipated, as the University of Connecticut, where Volek works.

But the beef industry isn’t the only purveyor of the fats that slowly kill us who is paying for Volek’s institution to produce research that is supposed to convince us otherwise. The egg industry is financing this study as well. This is the normal behavior of the animal food lobby.

Ronald Krauss is also quoted in the article. He’s one of the co-authors of that 2010 meta-analysis, and he’s also taken money from the Atkins Foundation and others in the animal food lobby. Krauss is Walsh’s reference for the now discredited claim that some LDL particles can cause heart disease while others can’t. But his judgment on that subject might be slightly influenced by the fact that he holds a patent, the value of which is riding on the acceptance of this notion.   

Walsh also quotes Peter Attia, a low-carb promoter looking for donations along with Gary Taubes so they can promote low carb diets through the “obesity-research center” mentioned above. You can see him here wearing a "Praise the Lard" t-shirt. I’ve made several videos about Attia and Taubes which reveal their obvious biases. David Ludwig, also named in the article, is working for them now.

But you didn’t need me to tell you all that for you to know that Walsh’s piece was almost entirely propaganda. In both his article and the accompanying video on the Time website, he only refers to “carbs” as a single entity, with nary a distinction to be made between the different types of carbs. Go ahead and try to find the phrase “whole grains” in either piece. You won’t be able to do it. This is a very basic omission. Everyone in nutrition knows there is a big difference between a sugary soda and a Russet potato. Why do you think Walsh failed to mention this?

How did this story get published in Time?

High cholesterol is a serious problem. Heart disease is our number one killer in America. A large fraction of our children now have high cholesterol. Why would Time want to make this problem worse?

Bill Maher, commenting on this edition of Time, answered this question by stating the obvious.

“They’re having such a hard time, and this is why they put out covers like this. Because they have to tell people, to try to sell a few goddamn copies, they have to tell people what they want to hear: Eat Butter!” – Bill Maher[14]

Time, Inc.’s profits have been suffering and they’ve been laying off staff. Apparently, they’ll even sacrifice their reputation for journalistic integrity for some short term positive cash flow. Time’s managing editor Nancy Gibbs should be the last person to let a story this biased and riddled with errors reach readers. She began her career at Time as a fact checker. Let’s hope my fact checking of this article helps her realize that America doesn’t need a Time magazine if its writers can’t produce better work than the typical low carb blog.

For more please find this related article I wrote for Dr. John McDougall’s newsletter.

* Date corrected 7/1/2014. 

---

[1] Nestel, P. J., A. Chronopulos, and M. Cehun. "Dairy fat in cheese raises LDL cholesterol less than that in butter in mildly hypercholesterolaemic subjects."European journal of clinical nutrition 59, no. 9 (2005): 1059-1063.

[2] van Dijk, Susan J., Edith JM Feskens, Marieke B. Bos, Dianne WM Hoelen, Rik Heijligenberg, Mechteld Grootte Bromhaar, Lisette CPGM de Groot, Jeanne HM de Vries, Michael Müller, and Lydia A. Afman. "A saturated fatty acid–rich diet induces an obesity-linked proinflammatory gene expression profile in adipose tissue of subjects at risk of metabolic syndrome." The American journal of clinical nutrition 90, no. 6 (2009): 1656-1664.

[3] Keys, Ancel. "Coronary heart disease in seven countries." Circulation 41, no. 1 (1970): 186-195.

[4] Keys, Ancel. “Atherosclerosis: a problem in newer public health.” J Mt Sinai Hosp N Y. 1953 Jul-Aug;20(2):118-39.

[5] Yerushalmy, Jacob, and Herman E. Hilleboe. "Fat in the diet and mortality from heart disease; a methodologic note." New York state journal of medicine 57, no. 14 (1957): 2343-2354.

[6] Jolliffe, Norman, and Morton Archer. "Statistical associations between international coronary heart disease death rates and certain environmental factors." Journal of chronic diseases 9, no. 6 (1959): 636-652.

[7] “National Food Supplies and Vital Statistics”. Dairy Council Digests. Vol. 28, No. 1. (September 1956).

[8] Cronkite, Walter. "Poverty and Want Rip Netherlands." The New York Times 29 Sept. 1944: 4. ProQuest Historical Newspapers.

[9] Puffer, Ruth R., and Louis J. Verhoestraete. "Mortality from cardiovascular diseases in various countries, with special reference to atherosclerotic heart disease: A preliminary analysis." Bulletin of the World Health Organization 19, no. 2 (1958): 315.

[10] Keys, Ancel. "Epidemiologic aspects of coronary artery disease." Journal of chronic diseases 6, no. 4 (1957): 552-559.

[11] Kromhout, Daan, Alessandro Menotti, Bennie Bloemberg, Christ Aravanis, Henry Blackburn, Ratko Buzina, Anastasios S. Dontas et al. "Dietary saturated and transfatty acids and cholesterol and 25-year mortality from coronary heart disease: the seven countries study." Preventive medicine 24, no. 3 (1995): 308-315.

[12] Kromhout, Daan, Ancel Keys, Christ Aravanis, Ratko Buzina, Flaminio Fidanza, Simona Giampaoli, Annemarie Jansen, Alessandro Menotti, Srecko Nedeljkovic, and Maija Pekkarinen. "Food consumption patterns in the 1960s in seven countries." The American journal of clinical nutrition 49, no. 5 (1989): 889-894.

[13] 2013 Evaluation of Beef Checkoff Programs, A report from the Joint Evaluation Advisory Committee. Cattlemen’s Beef Promotion and Research Board. Centennial, CO. 2013.

[14] Bill Maher. Real Time. Episode 322 (20 June 2014). HBO.

Recent Articles by Drs. Chowdhury and DiNicolantonio

March 23, 2014

I’ve been asked by viewers to comment on a couple recently published journal articles which have received undeserved attention from the media. These articles are a major meta-analysis examining associations between dietary and circulating fatty acids with coronary disease (Chowdhury, 2014) and yet another editorial proclaiming that we’ve been wrong all along about saturated fat (DiNicolantonio, 2014). If you’ve watched enough of my videos you should know by now what tactics are commonly utilized to keep us all ignorant and confused about cholesterol and heart disease. The present blog post will show you that these two articles are just more of the same. Because I’m so busy nowadays, I’m giving these two a very cursory treatment here just to give you a sense of what’s going on in them. Bear in mind that the first article is the product of a professional collaboration of many researchers who were paid for their efforts. I am but one person taking advantage of a brief chunk of free time. I’ll post corrections in my Errata if I see that that becomes necessary.

Let’s start with the Chowdhury meta-analysis. Dr. Chowdhury has admitted to a half dozen errors in his paper that he says do not affect his conclusions. This was partly in response to the comments of Walter Willett, Frank Sacks, and Meir Stampfer, who called his conclusions about MUFAs and PUFAs “seriously misleading.”

This paper is quite like the 2010 meta-analysis of Siri-Tarino, et al (Siri-Tarino, 2010), which I have previously discussed. Only a weak subset of the literature on heart disease is examined, excluding the most convincing evidence for Diet-Heart, yet an incautious and unsupportable conclusion is offered in its abstract, in this case proclaiming that “Current evidence does not clearly support cardiovascular guidelines that encourage … low consumption of total saturated fats.” This statement suggests to the naïve reader that the most important evidence in Diet-Heart has been considered and rejected in this paper, but that impression would be false. A few examples of what I consider strong evidence are presented together at the end of this video. These are mostly ignored by Chowdhury.

To understand why I consider Chowdhury and company’s evidence to be weak, have a look at some of the studies they thought were good enough to be included in their analysis (I’ve added the boldface, references found in the online supplement 1).

1.)    Referenced as EUROASPIRE. Relative risk: 1.00 for dietary SFA. (Erkkilä, 2003).

“The analyses were adjusted for sex, age, diagnostic category (CABG or PTCA compared with AMI or AMIS), education (< 12 compared with ≥ 12 y), serum cholesterol concentration, serum triacylglycerol concentration, body mass index, and diabetes, and models that included nutrient or food intakes were also adjusted for energy intake.”

"Virtually all the patients were taking cardiovascular drugs, and this could have confounded the observed associations." (quoting the authors of the paper)

2.)    Referenced as IIHD. Relative risk: 0.90 for dietary SFA. (Goldbourt, 1993).

“A curvilinear increase in fatal CHD risk with increasing total cholesterol was observed.”

3.)    Referenced as Caerphilly. Relative risk: 0.92 for dietary SFA. (Fehily, 1993).

 “An alternative explanation which has been suggested (Rose, 1985) is that, in populations where the majority have a high fat intake, factors other than fat become important in determining why some individuals develop IHD and others do not.”

4.)    Referenced as LURIC. Relative risk: 0.81 for circulating palmitic acid. (Pilz, 2007).

“In detail, we adjusted for age, sex, body mass index, systolic and diastolic blood pressure, hypertension, HOMA-IR, type 2 diabetes, triglycerides, low-density lipoprotein and high-density lipoprotein cholesterol, homocysteine, creatinine, smoking status (current and active smoker: yes/no), CAD, left bundle branch block, C-reactive protein, use of beta-blockers, ACE-inhibitors and statins, NT-pro-BNP, noradrenaline, and LV function.”

“Our study shows that elevated plasma FFAs are an independent risk factor for future SCD in patients referred to coronary angiography.” (SCD: sudden cardiac death).

Note: “Current ketogenic diets are all characterized by elevations of free fatty acids” (Veech, 2004).

5.)    Referenced as JELIS. Relative risk: 0.85 for circulating palmitic acid. (Yokoyama, 2007).

“Patients were randomly assigned to receive EPA with statin (EPA group) or statin alone (controls).”

In short, based on the few that I reviewed, many of the studies they selected have similar defects to those used in the Siri-Tarino paper, and in fact, it seems from quick inspection that they used some of the very same studies. The above are given equal weight to another study, one which observed a cohort in which real contrasts in the dietary habits might give us a better chance of learning something interesting.

Referenced as Oxford Vegetarian. Relative risk: 2.77 for dietary SFA (Mann, 1997).

“A gradient of risk is apparent with increasing intake of total animal fat, saturated fat, and dietary cholesterol as well as some of the major food sources of these nutrients.”

Given the considerable challenges inherent in Diet-Heart studies of free-living people in homogeneous populations, we should approach such a large meta-analysis with caution. Such an analysis can only be as good as the studies upon which it is based (Garg, 2008), so it is necessary to first assess them for their quality and winnow down the selection accordingly. It appears Dr. Chowdhury and colleagues were too permissive in their standards of inclusion to advance our understanding of Diet-Heart very much with this article. Additionally, it appears that one of the authors of this study, Dr. Dariush Mozaffarian, is misinformed about the effects of saturated fat upon lipoproteins. He told the Boston Globe that, “Saturated fat in the diet makes LDL particles bigger, but it doesn’t increase the number of LDL particles, which we now think is responsible for the increased heart risk.” Unfortunately, he is wrong about this (Zock, 1994). Please see my videos about foods that increase our production of atherogenic particles for further information. I wonder if his mistaken belief impaired his critical thinking on this issue.

Now let’s shift our attention to that opinion piece by Dr. DiNicolantonio. He begins by repeating that familiar old libel against Ancel Keys based on the highly flawed work of Yerushalmi and Hilleboe (1957). He says, “(Keys) excluded data from 16 countries that did not fit his hypothesis. Indeed, data were available at the time from 22 countries.” This assertion has been debunked by me in several videos, including this one and this one, and Keys’ arguments were later affirmed using the same data set in papers by Puffer and Verhoestraete (1958) and Joliffe and Archer (1959). The most innocent interpretation of this passage must be that Dr. DiNicolantonio has not bothered to research this matter properly. If he in fact knows the truth of this matter, that would be very troubling. The rest of his article is just another repackaging of the usual junk thought of the low-carb fringe. He asserts that “the belief that  … saturated fats increase total cholesterol” is a “flawed theory” without any reference, despite the fact that hundreds of controlled trials have shown that they do (Clarke, 1997). I could go on but I don’t think that’s necessary. Just search my site and watch my videos and you’ll see how misguided he is. 

Chowdhury, Rajiv, et al. "Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis."Annals of Internal Medicine 160.6 (2014): 398-406.

Clarke, Robert, et al. "Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies." Bmj 314.7074 (1997): 112.

DiNicolantonio, James J. "The cardiometabolic consequences of replacing saturated fats with carbohydrates or Ω-6 polyunsaturated fats: Do the dietary guidelines have it wrong?." Open Heart 1.1 (2014): e000032.

Erkkilä, Arja T., et al. "n− 3 fatty acids and 5-y risks of death and cardiovascular disease events in patients with coronary artery disease." The American journal of clinical nutrition 78.1 (2003): 65-71.

Fehily, A. M., et al. "Diet and incident ischaemic heart disease: the Caerphilly Study." British Journal of Nutrition 69.02 (1993): 303-314.

Garg, Amit X., Dan Hackam, and Marcello Tonelli. "Systematic review and meta-analysis: when one study is just not enough." Clinical Journal of the American Society of Nephrology 3.1 (2008): 253-260.

Goldbourt, Uri, Shlomit Yaari, and Jack H. Medalie. "Factors predictive of long-term coronary heart disease mortality among 10,059 male Israeli civil servants and municipal employees." Cardiology 82.2-3 (1993): 100-121.

Jolliffe, Norman, and Morton Archer. "Statistical associations between international coronary heart disease death rates and certain environmental factors." Journal of chronic diseases 9.6 (1959): 636-652.

Mann, Jim I., et al. "Dietary determinants of ischaemic heart disease in health conscious individuals." Heart 78.5 (1997): 450-455.

Pilz, Stefan, et al. "Elevated plasma free fatty acids predict sudden cardiac death: a 6.85-year follow-up of 3315 patients after coronary angiography."European heart journal 28.22 (2007): 2763-2769.

Puffer, Ruth R., and Louis J. Verhoestraete. "Mortality from cardiovascular diseases in various countries, with special reference to atherosclerotic heart disease: A preliminary analysis*." Bulletin of the World Health Organization19.2 (1958): 315.

Siri-Tarino, Patty W., et al. "Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease." The American journal of clinical nutrition 91.3 (2010): 535-546.

Veech, Richard L. "The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism." Prostaglandins, leukotrienes and essential fatty acids 70.3 (2004): 309-319.)

Yerushalmy, Jacob, and Herman E. Hilleboe. "Fat in the diet and mortality from heart disease; a methodologic note." New York State journal of medicine 57.14 (1957): 2343-2354.

Yokoyama, Mitsuhiro, et al. "Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis." The Lancet 369.9567 (2007): 1090-1098.

Zock, Peter L., J. H. De Vries, and Martijn B. Katan. "Impact of myristic acid versus palmitic acid on serum lipid and lipoprotein levels in healthy women and men." Arteriosclerosis, Thrombosis, and Vascular Biology 14.4 (1994): 567-575.

Watching Dr. Oz May Be Hazardous to Your Health

A friend contacted me this week to report that Mehmet Oz used his show to promote dangerous claims about cholesterol and heart disease. His guests were two long-time low-carb promoters, Johnny Bowden and Stephen Sinatra.

  

Both of them make a living by selling questionable supplements and deceptive publications. They have now co-authored a book called The Great Cholesterol Myth, an excerpt of which I include here so you can see the level of ignorance and dishonesty it contains. 

Typical of the low-carb promoters, they confuse the 1970 Seven Countries Study of Ancel Keys with his 1953 lecture and paper and completely mischaracterize both. Predictably, they blame heart disease on sugar and reimagine John Yudkin as a hero of diet-heart. Watch the three segments Dr. Oz handed over to these two and you’ll see he gave a full endorsement of their reckless, poorly researched, and biased claims, including the false assertion that large LDLs cannot contribute to atherosclerosis.

I am only one person but I’ve done a lot. I have provided all the evidence anyone needs to understand the truth about cholesterol. One can no longer claim that the science is too contradictory or confusing. Those with the most influence like Mehmet Oz need to educate themselves, accept reality, and stop harming people. To encourage him to face the science, I need you to become personally engaged. Please contact the producers of the Dr. Oz show at viewerfeedback@zoco.com. Let them know about my project. Direct them to the videos and blog posts that dispel the lies he has chosen to endorse. Insist that they give equal time to genuine experts in heart disease.

As long as there is money to be made by misleading the public about nutrition, there is much work for us to do.

Another Devastating Blow to the Cholesterol Deniers

A new study powerfully validates important points I repeatedly asserted in my cholesterol videos - heart disease risk is strongly mediated by lifetime cholesterol levels (rather than end-of-life levels) and LDL in particular is a key causal factor in heart disease. This elegant research by Dr Brian Ference of Wayne State University also further damages the claims of the few vocal cholesterol deniers that statins work through effects other than lipid lowering. How can a single study accomplish all this? It examined the effects of multiple cholesterol-lowering genotypes on heart disease risk.

Viewers of my videos will recall that genetic variations affecting LDL dramatically influence cardiac mortality, from homozygous hypercholesterolemia at one end of the spectrum (in one case causing a fatal heart attack in a fifteen year old) to hypobetalipoproteinemia on the other. These conditions are compelling evidence for the lipid hypothesis as they eliminate confusion which may arise from other methods of inquiry into the clinical significance of high cholesterol (off-target drug effects, the limitations of various animal models, confounding effects of various nutritional factors, patient comorbidities, LDL phenotype, etc.). With genetic research in humans, we can now bypass all that in favor of a clean look at the specific effects of LDL concentrations, pure and simple. We don't need to be distracted by failed $800 million drug trials that crackpots like Mark Sisson can use to confuse and endanger people.

Dr Ference's team studied nine single nucleotide polymorphisms which influence LDL levels. Paleo followers might appreciate Ference's clever use of a mechanistic principle that underlies evolution (Mendelian inheritance) to uncover the natural randomized trial being conducted all around us, allowing those SNP's to act as stand-ins for lipid-lowering therapies. As these SNP's are present from birth, this approach allowed for a comparison to be made between the effectiveness of statins administered later in life with low LDL levels maintained from childhood. The results are powerful: a threefold-greater benefit for natural early-life low LDL versus later statin-lowerd LDL. Ference stated, "the effect of each of the included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL, rather than through some other pleiotropic effect." This should cause us all to appreciate the potential for genetic variation to blur the effects of lifestyle factors like diet on disease. Because we are infinitely complicated homeostatic biochemical machines, there will always be a way for the cholesterol deniers to find superficial exceptions to the lipid hypothesis. With this study, you may once again be assured that the lipid hypothesis is rock solid.

Dr Ference is due credit not just for his ingeneous research, but for his responsible interpretation of his findings. He stated, "We are not suggesting that everyone take statins from childhood; rather, that lowering LDL through more attention to healthy diet and exercise from a young age could make a big difference to public health." His work strongly supports a prevention and public health strategy, and places LDL directly in the spotlight where it belongs. Dr Ference is not content with a general population with subclinical atherosclerosis. I couldn't agree more. I hope his work will bring clarity to this heretofore needlessly muddled issue.

A Quick Note on Cancer, Cholesterol, and Reverse Causation

If you have watched my video addressing the relationship between cholesterol and cancer, you know that I have attributed any observations of low cholesterol among cancer patients to reverse causation. In apparent contradiction of this view are the recently announced results of a study lead by Dr Paul Lavigne which calls into doubt the reverse causation hypothesis. I am not aware of any other study which has shown a relationship to exist between low LDL and cancer over such a long time span (18.7 years). In contrast, a 1987 study based on NHANES data documented a similar association extending only six years prior to cancer diagnosis. Therefore, this paper will surely reignite debate over the reverse causation hypothesis. As of this writing, this story has yet to be exploited by the cholesterol confusionists to promote dietary saturated fat. Nevertheless, I would like to offer a few words of caution to those who might misinterpet this news.

Here are a few considerations which should temper any overheated conclusions based on this announcement:

• These results were announced at a conference. They have yet to appear in a peer-reviewed journal.
• The LDL levels observed were "not that low," first assessed at 90-100 mg/dL and rising from there. Vegans have been observed to have LDL scores around 70 mg/dL.
• Low cholesterol levels have been associated with a decreased risk of aggressive prostate cancer. Exeriments in mice have supported this association.
• Other studies support the reverse causation hypothesis. This study from my video is the best of those, in my estimation.
• Of course, cholesterol-raising animal foods have been positively associated with cancer in some studies. I am not aware of any such studies associating high saturated fat consumption with a lower risk of cancer. Vegans and vegetarians appear to generally have lower rates of cancer than omnivores. (I will address the exception of colorectal cancer in the EPIC-Oxford study in a future post.)
• The study does not address the cause of the association they found. An unknown mechanism may exist which promotes cancer and incidentally lowers LDL. No responsible person proposes that cholesterol levels should be raised through diet to avoid cancer. The relationship between high LDL and increased heart disease incidence is well established.

The confusionist blogosphere is usually quick to make too much of anomalous and unexpected findings. You shouldn't fall into the same trap.