The Great Cholesterol Consensus, Pt. 1

consensus“Historically, the claim of consensus has been the first refuge of scoundrels; it is a way to avoid debate by claiming that the matter is already settled. Whenever you hear the consensus of scientists agrees on something or other, reach for your wallet, because you’re being had.” – Michael Crichton

Introduction

Today’s undoubtedly controversial article will be but one of many articles dismantling the myth surrounding cholesterol, saturated fat and cardiovascular health. Indeed, it’s not uncommon, even from so-called medical and health professionals, to hear something along the lines of;

“Cholesterol and saturated fat are bad because they increase blood cholesterol levels; therefore we must try to limit both in our diets such that we lower our blood cholesterol levels and prevent heart disease.”

Bad fats AHAStraight from the American Heart Association website

Indeed, the anti-saturated fat, anti-cholesterol fear-mongering propaganda campaign – or as it’s commonly known in medical and research circles as the ‘lipid hypothesis’ or ‘diet-heart theory’ – is the scientific consensus that saturated fat and cholesterol promote cardiovascular disease (CVD) through elevated levels of blood lipids. What’s worse is that this flawed dogma has dominated medical and nutritional orthodoxy for decades, affecting the lives of millions of people worldwide. Despite not having one shred of convincing evidence showing either of these nutrients as causative of CVD, major health organizations around the globe still promote diets lower in saturated fat and cholesterol to help reduce purportedly deadly levels of blood cholesterol. This has undoubtedly caused many people to take potentially harmful prescription medication and completely transform their diets into an unpalatable one that has no cardiovascular benefit whatsoever. In reality, some of the recommended changes (like consuming so-called ‘heart-healthy’ polyunsaturated fats) have actually been shown to increase ones risk of CVD, as well as, all-cause mortality and even some cancers!

Today we will be looking through a historical lens whilst unraveling the myth at hand. In doing so we will examine some of the fundamental research that pushed the idea that saturated fats and cholesterol promote CVD. In subsequent articles we will delve further into the research that both (apparently) supports the diet-heart theory, as well as, outright contradicts its. By the end of this series (however long it is), I hope you will see what complete and utter nonsense it is to fear arbitrary blood levels of cholesterol, and more importantly, some of your favorite fatty foods that have never been proven to cause CVD. In addition, I hope to shed some light on the actual causes of CVD as well as outline some recommendations that will assuredly do more for preventing CVD than our currently flawed dietary ways.

So without further ado, let us examine the foundation for which the greatest scam in the history of medicine was built upon!

From Russia with lipids [1]

Our story begins over 100 years ago in the, then, Russian Empire. Here in 1908, Alexander Ignatovski of the Russian Imperial Military Medical Academy first demonstrated that diet-induced atherosclerosis could be produced in rabbits fed full-fat milk, meat and egg yolks. The following year, Starokadomsky and Ssobolew verified Ignatovski’s results using a similar feeding protocol. While Ignatovsky and others thought that it might be animal proteins that clogged the arteries of the rabbits, it wasn’t until 1913 when NW Wesselkin and, subsequently, Anitschkow et al. demonstrated that it was indeed cholesterol, and not protein, that was the primary driver behind the aortic lesions and cardiovascular buildup in the rabbits.

It was from these among many, many other animal studies that pushed the idea that dietary fat and cholesterol cause CVD – an idea that apparently never let go. Of importance, however, is that these studies are hardly evidence of cholesterol’s artery clogging capabilities in humans. For one, rabbits are herbivorous animals and are not well-adapted to metabolize large amounts of animal protein, fat or cholesterol (and believe me, these animals were eating an insane amount of each). It’s no wonder that, when force-fed a completely alien diet comprised of animal sources, the rabbits developed atherosclerosis, cirrhotic livers, and kidney disease. Indeed, subsequent trials to induce experimental atherosclerosis were effective in other herbivorous animals – such as chickens and guinea pigs – but failed completely in carnivorous animals –like cats and dogs – that are well-adapted to consume animal protein, fat and cholesterol. It is only until the dog’s thyroids are experimentally removed and/or suppressed with drugs that scientists see any effects from diet on serum cholesterol and CVD.

It is also worth noting that cholesterol feeding in rabbits and other experimental animals has a profound effect on serum cholesterol levels and producing CVD. Unlike early animal experiments, however, more recent human feeding trials have consistently shown cholesterol elevations to be trivial with respect to dietary cholesterol intake [2]. While these early animal studies offered a potential model for human CVD, they were far from supportive of cholesterol’s causative role in human disease progression, despite what many proponents of the diet-heart theory initially believed.

The diet-heart theory

Before we continue, it would behoove me to expand on what the ‘diet-heart theory’ or ‘lipid hypothesis’ is (I’ll be using them interchangeably throughout the article). After all, it is this very hypothesis that health professionals base their (blatantly unfounded and politically biased) medical and nutritional guidance off of.

As alluded to earlier, the diet-heart hypothesis proposes that cardiovascular disease – that is, the buildup of cholesterol in the arterial walls – is due simply to high levels of cholesterol in the blood. Moreover, the relationship between cholesterol and cardiovascular disease has been (falsely) deemed linear, meaning that the higher one’s blood cholesterol levels the more sclerotic one will become. Don’t believe me?

The American Heart Association states online that;

“When too much LDL (bad) cholesterol circulates in the blood, it can slowly build up in the inner walls of the arteries [;]”

While the Centers for Disease Control and Prevention states that;

“Low-density lipoproteins (LDL) cholesterol make up the majority of the body’s cholesterol. LDL is known as “bad” cholesterol because having high levels can lead to a buildup in the arteries and result in heart disease [;]”

And lastly, the National Heart, Lung and Blood Institute states that;

“When there is too much cholesterol…in your blood, it builds up in the walls of your arteries.”

It is from this insanely simplistic and faulty reasoning that these same organizations promote the unnecessary lowering of cholesterol – usually with the mindless prescription of toxic statins as well as flawed nutritional guidance – because, if high cholesterol is bad, than lower is obviously better. Unfortunately, this outdated and politically driven claim has no roots in sound science whatsoever.

Early autopsy studies

If we are to take the lipid hypothesis at face value, one should expect to see greater plaque buildup in the arteries of people whose serum cholesterol is higher than those whose is lower. One of the first autopsy studies to examine this relationship was conducted in 1936 by pathologist Kurt Landé and biochemist Warren Sperry of the Department of Forensic Medicine at NYU [3]. Landé and Sperry meticulously analyzed the fatty buildup in the aortas of subject’s who had just violently died and compared that to the patient’s post-mortem measurements of serum cholesterol. As you can see below, they found absolutely no relationship between serum cholesterol and fatty deposition in the arteries. This flies right in the face of the lipid hypothesis!

Lande Sperry 1936For years, however, this research was discounted by early diet-heart proponents based on the claim that serum cholesterol measurements taken post-mortem weren’t reliable.

The next autopsy study wasn’t conducted until 1956 in London, Canada [4]. Here, Paterson and co. took blood samples – starting in 1953 – of 800 hospitalized war veterans periodically over the course of each patient’s lifespan. Upon death, the patient was autopsied and the degree of atherosclerosis was evaluated in the aorta and compared to ante mortem blood concentrations of cholesterol. Like Landé and Sperry, Paterson et al. found no relationship between blood levels of cholesterol and the degree of fatty deposition in the arteries of the 136 patients for which they had autopsy and blood measurements for. Again, however, these results were largely ignored by diet-heart theorists.

It wasn’t until the early 1960’s that another autopsy study, conducted by KS Mathur in Agra, India, lent some much needed credence to the aforementioned Landé and Sperry paper [5]. Here, over 500 subjects were autopsied and their blood levels of cholesterol were compared to the degree of atherosclerotic buildup. This time, however, samples were taken both before and after death in a subgroup of 20 patients to see whether or not ante and post mortem blood lipid samples remained similar. The researchers noted two important findings; 1) serum cholesterol levels remain relatively unchanged after death as long as the sample is taken within 16 hours post-mortem, and; 2) there was no relationship between serum cholesterol and atherosclerotic buildup in the 200 patients whose serum cholesterol levels were taken within 16 hours post mortem. This was important as these findings verified Landé and Sperry’s highly criticized study 30 years earlier.

If higher cholesterol truly is – as we are brainwashed to believe – indicative of worsening atherosclerosis, there should be a strikingly and convincingly obvious relationship between blood lipid levels and arterial fatty deposition. The strongest correlation, however, between serum cholesterol and atherosclerosis that any of the autopsy studies could provide was a paltry r value of 0.36 [6-10]. To put this into perspective, an r value is a statistical method used to determine the strength of the relationship between two values – like that of serum cholesterol and arterial fat deposition. A perfect association would be 1. Much to the chagrin of lipid hypothesists, a weak r value of 0.36 is, at best, nothing more than wishful thinking. The more probable possibility – and something that we will talk about more in the next installment – is that any association seen between cholesterol and atherosclerosis is secondary in nature.

Enter Ancel Keys’ Six Countries “Study”

As reality would have it, the current cholesterol theory of heart disease was founded upon highly irrelevant animal feeding experiments as well as some of the worst “research” ever conducted. And yes, I’m talking about the “research” of one, Ancel Keys from The University of Minnesota. Keys is probably one of the most well-known and often cited researchers when it comes to our current understanding of diet and cardiovascular health. And while his diet-heart “research” is complete and utter bat crap, I feel some obligation to at least mention that he made great advancements in what we known about human physiology during his famous Minnesota Starvation Study during the Second World War [11]. While his earlier career and prestige are not in dispute, I do take umbrage with the carelessness that scientists and researchers, to this day, still cite his rubbish of coronary heart disease “studies” – the first of which was his hugely biased Six Countries “Study” [12].

Quite simply, this “study” examined six hand-picked countries and their intake of fat and compared that to the number of deaths from coronary heart disease. Keys noticed a perfectly positive curvilinear association between fat intake, as a percentage of calories, and coronary deaths (shown below, EDIT: must click on graph to see it, for some reason the image doesn’t show properly within the text).

Keys Six Countries GraphWhile Keys was initially somewhat conservative in his concluding remarks, stating that, “dietary fat somehow is associated with cardiac disease mortality at least in middle age,” ZA Leitner, in a subsequent publication in Medical World, interpreted Keys’ findings slightly more emphatically [13]:

“There appears to be a strong if not convincing correlation between the amount of fat in the diet and the death rate from degenerative heart disease.”

Perhaps this gave Keys a sense of confidence over his prior remarks, because in a follow-up publication using the same data, one could read from Keys that [14];

“[T]here is a remarkable relationship between the death rate from degenerative heart disease and the proportion of fat calories in the […] diet.”

Leitner’s and Keys’ enthusiasm, however, was not unanimous. Researchers skeptical of Keys’ “study” pointed out that relevant data was available for 22 countries at the time and that Keys did nothing more than cherry-pick his data set to include the countries which supported his preconceived hypothesis of diet and heart disease. Indeed, when data from all 22 countries are incorporated into the analysis, the perfect relationship between fat and heart disease disappears [15]. Anyone who even considers themselves a student of science should be appalled at Keys’ blatant disregard for the scientific method. Indeed, at a subsequent World Health Organization convention held in Geneva, Switzerland in 1954, Keys’ “study” was met with considerable criticism leaving him completely embarrassed and humiliated. Long-time research assistant from The University of Minnesota, Henry Blackburn, recounts the occasion [16];

Ancel fell into a trap, he made a mistake; he cited a piece of evidence and they were able to destroy it. Instead of citing ‘well, this theory’s based on a body of evidence that we’ve seen here and here from the clinic, from the laboratory, and from comparing populations’, he didn’t make his case. He cited a piece–destroyed.”

It was from this public humiliation that Keys’ more widely known Seven Countries Study was born (hell, if six countries weren’t good enough surely seven will do the trick!).

The infamous Seven Countries Study

Unfortunately, Keys’ subsequent “study” in the late 1950’s was nothing more than a fancier extension of his first piece of epidemiological garbage. As before, another hand-selected set of seven countries were analyzed and, again, another positive association was seen between countries with the highest intakes of saturated fat/cholesterol and rates of coronary, as well as, all-cause mortality [17]. However, when the “study” is analyzed more closely, one starts to notice that comparisons within countries – as opposed to between countries – start to dismantle Keys’ initial claims about diet and heart disease. It is funny how science doesn’t give a damn about one’s preconceived dietary biases.

Within-country contradictions

Take for instance the reported similar intakes of saturated fat in the Finnish populations of Turku and North Kerelia. Despite comparable intakes diets, heart disease was three times higher in North Kerelia than in Turku.

In Greece, despite the residents of Crete and Corfu having near identical levels of serum cholesterol (202mg/dl and 198mg/dl, respectively), heart disease was five times higher in Crete than in Corfu.

Lastly, Crevalcore and Montegiorgio – two cities in Italy – had identical levels of serum cholesterol despite Crevalcore having almost two and half times greater heart disease mortality rates!

Nevertheless, despite these discordant findings, Keys’ went on to conclude that lower cholesterol and saturated fat intakes reduce the risk for heart disease. Perhaps he also overlooked that, while the Japanese (a population we will cover more in subsequent articles) had the lowest levels of cholesterol in the entire study it was actually the residents of Crete, Greece who, despite having considerably higher cholesterol levels, exhibited the lowest overall rates of heart disease and all-cause mortality! Only in American can biased research get you a cover spot on Time magazine and have your false conclusions become dietary dogma for the next 60+ years!

Keys TimeThe Anti-Coronary Club

Riding in the wake of the early animal feeding experiments and the poorly conducted paper-excise that was Ancel Keys’ Six Countries Study was one of the first U.S. trials to be published on diet and heart disease – The Anti-Coronary Club Program (ACC) [18]. This study took place around the same time that Keys’ was conducting his follow-up Seven Countries Study and was meant to test whether or not lowering one’s cholesterol via dietary means would be associated with a decreased incidence of heart disease. Before we continue, though, I just want to point out the humor with which diet-heart theorists conduct themselves in the scientific literature.

In a 1980 publication of The American Journal of Clinical Nutrition some of the original members of the ACC study tried to justify their reasoning for their experimental dietary intervention – albeit 14 years late and a dollar short [19]. Indeed, the original paper makes no mention of the previous research suggesting potential dietary strategies for the prevention of heart disease – quite simply because there was none! Nevertheless the authors, over a decade later, state that:

“At that time, sufficient epidemiological evidence […] implicating serum cholesterol in the development of coronary heart disease (CHD) was already available to warrant a public health approach to the prevention of CHD by means of dietary intervention.”

However, in 1957 when the ACC study was just taking flight, a review paper in Circulation, examining the literature to-date, concluded the following [20]:

“Thus, the evidence at present does not convey any specific implications for drastic dietary changes, specifically in the quantity or type of fat in the diet of the general population, on the premise that such changes will definitely lessen the incidence of coronary or cerebral artery disease.”

It’s funny how people only see what they want to see when trying to push their dietary agenda.

Still, in the ACC study, researchers assigned one group of men with no prior history of heart disease to replace their saturated fat intake from whole milk, eggs, butter and beef with polyunsaturated fats from vegetable oil, margarine, and fish (the ‘Prudent Diet’ group). The control group, on the other hand, went on consuming their normal diet, rich in eggs, whole milk, butter and beef. After four years, the Prudent Dieters successfully managed to lower their cholesterol levels from about 260mg/dl to an average of 225mg/dl while the control group shamefully maintained their cholesterol around 250-255mg/dl. Throughout the paper the authors heralded the prudent diet’s ability to drive down cholesterol levels as well as reduce non-fatal heart disease events. However, one must read the paper carefully, because amidst all the praise and commendation, ones sees clearly that eight subjects in the experimental group – that’s right, those consuming ample amounts of “heart-healthy”  PUFAs (which lower LDL and raise HDL) and hammering down their cholesterol levels by an average of 30mg/dl – died of coronary heart disease (CHD). The control group on the other hand, tallied not one death from CHD. So while the control group had a slightly higher incidence of heart disease events, the prudent diet actually caused more deaths from heart disease than control diet rich in “artery clogging” saturated fat and cholesterol. Perhaps it was the vegetable oil talking when the authors touted a huge success of the dietary intervention.

Concluding remarks

The facts presented above aren’t just a recount of a few isolated cases. No, the blatant disregard for contradictory research and the misquoting or playing down findings is rife within the diet-heart literature over the past 60+ years. To quote Professor George Mann of Vanderbilt University, the diet-heart hypothesis it is quite possibly, “[t]he greatest scam in the history of medicine.” As we continue analyzing the literature it will become more and more obvious how those who are fully invested in the lipid hypothesis only hear what they want to hear, see what they want to see, and disclose what they want to disclose.    

Next time we will talk about cholesterol and its role in the human body as well as take a look at more of the often cited epidemiological evidence and see why the very studies used to support the lipid hypothesis do no such thing and, in most cases, outright contradict it!

References

1.         Kritchevsky D: Dietary protein, cholesterol and atherosclerosis: a review of the early history. J Nutr 1995, 125:589S-593S.

2.         McNamara DJ: The impact of egg limitations on coronary heart disease risk: do the numbers add up? J Am Coll Nutr 2000, 19:540S-548S.

3.         Landé K, Sperry, W.: Arch Pathol 1936, 22:301-312.

4.         Armstrong EC, Cornish BR, Paterson JC: The serum lipids in human atherosclerosis; an interim report. Circulation 1956, 13:224-234.

5.         Mathur KS, Patney NL, Kumar V, Sharma RD: Serum cholesterol and atherosclerosis in man. Circulation 1961, 23:847-852.

6.         Feinleib M, Kannel WB, Tedeschi CG, Landau TK, Garrison RJ: The relation of antemortem characteristics to cardiovascular findings at necropsy–The Framingham Study. Atherosclerosis 1979, 34:145-157.

7.         Solberg LA, Strong JP, Holme I, Helgeland A, Hjermann I, Leren P, Mogensen SB: Stenoses in the coronary arteries. Relation to atherosclerotic lesions, coronary heart disease, and risk factors. The Oslo Study. Lab Invest 1985, 53:648-655.

8.         Mendez J, Tejada C: Relationship between serum lipids and aortic atherosclerotic lesions in sudden accidental deaths in Guatemala City. Am J Clin Nutr 1967, 20:1113-1117.

9.         Rhoads GG, Blackwelder WC, Stemmermann GN, Hayashi T, Kagan A: Coronary risk factors and autopsy findings in Japanese-American men. Lab Invest 1978, 38:304-311.

10.       Okumiya N, Tanaka K, Ueda K, Omae T: Coronary atherosclerosis and antecedent risk factors: pathologic and epidemiologic study in Hisayama, Japan. Am J Cardiol 1985, 56:62-66.

11.       Keys A, Brozek, J., Henschel, A., Mickelson, O., Taylor, H.L.: The Biology of Human Starvation I-II. Minneapolis, MN.: University of Minnesota Press; 1950.

12.       Keys A: Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp N Y 1953, 20:118-139.

13.       Leitner ZA: Diet and coronary disease. Med World 1954, 81:249-254.

14.       Keys A, Anderson, JT. : Symposium on Atherosclerosis, National Academy of Sciences, National Research Council. 1955, 338.

15.       Yerushalmy J, Hilleboe HE: Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med 1957, 57:2343-2354.

16.       Health revolutionary: The life and work of Ancel Keys. School of Public Health, University of Minnesota: University of Minnesota; 2002.

17.       Keys A: Coronary heart disease in seven countries. Circulation 1970, 41:1-211.

18.       Christakis G, Rinzler SH, Archer M, Kraus A: Effect of the Anti-Coronary Club program on coronary heart disease. Risk-factor status. JAMA 1966, 198:597-604.

19.       Singman HS, Berman SN, Cowell C, Maslansky E, Archer M: The Anti-Coronary Club: 1957 to 1972. Am J Clin Nutr 1980, 33:1183-1191.

20.       Page IH, Stare FJ, Corcoran AC, Pollack H, Wilkinson CF, Jr.: Atherosclerosis and the fat content of the diet. Circulation 1957, 16:163-178.

Advertisements
This entry was posted in Reviews. Bookmark the permalink.

15 Responses to The Great Cholesterol Consensus, Pt. 1

  1. Jo says:

    Awesome article! Love your approach

  2. natalyas says:

    Very interesting article! Looking forward to the next installment!

  3. Pingback: Stuff You Should Check Out: July Edition | DeanSomerset.com

  4. Greg says:

    This was great! Can’t wait to see the rest of the series.

  5. Art says:

    Another reader eagerly awaiting Part 2! Good stuff.

  6. WreckshopRob says:

    Thank God someone is awake out there. i pretty much take everything I hear on Dr. Oz and similar TV shows, see on Magazines and hear Doctors say and I do the EXACT Opposite. Guess What… but all measures I’m healthy as a freakin Clydesdale. Blood work, fancy antioxidant scanning machines, physical appearance and overall health. It all comes down to using your BRAIN and thinking about how the human body was designed. You were meant to be outside, working hard and eating plants, animals, fruits and nuts of all sorts. Dogma: “a point of view or tenet put forth as authoritative without adequate grounds “

  7. wreckshoprob says:

    Dogma: “a point of view or tenet put forth as authoritative without adequate grounds.” I pretty much do exactly the OPPOSITE of whatever the mainstream media and pharmaceutical driven medical model tells me is health. Guess what, I’m health as a Clydesdale. Blood work, fancy antioxidant scans, my appearance, my overall health and well being – all perfect. Just use your brain and understand how the human body was designed.

  8. Julie Royster says:

    I am delighted to find your blog. The new recommendation that a third of Americans should take statins came out yesterday, and I am eager to see the next part of your series. I am incredulous at this recommendation!

  9. Kevin says:

    http://advances.nutrition.org/content/4/3/294.abstract

    Not sure if you caught this one but figured it might be useful as you write the series

  10. Dylan- fantastic. Not to mention the original AHA recommendations completely disregarded the role of sugar. Didn’t even talk about it, then very quietly 2 years ago, decide that 7 and 9 tsp of added sugar should be a component of their recommendations.

  11. Pingback: The Great Cholesterol Consensus: a long overdue Pt. 2 | Calories in Context

  12. Pingback: Die Fehlentwicklung der modernen Ernährung anhand von elf Grafiken | Aesirsports

  13. Pingback: 8 Nutrition & Exercise Myths That Won't Die | MyoBrain by Greg Farris

  14. mcberko says:

    Terrible article – grossly misrepresents diet-heart history and outright distorts the scientific literature.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s