Exploring “The Great Cholesterol Myth”

Estimated reading time: 12 minutes

I have a strong interest in the prevention of heart disease. I believe healthy nutrition and lifestyle are the keys to our health and well-beingIn my early career as a cardiologist, working in the hospital setting, I was fascinated by the diagnosis and treatment of heart disease. Don’t misunderstand me, I still am. However, as the years have passed I have become more and more interested in disease prevention.

Exploring "The Great Cholesterol Myth"

Helping people stay healthy and avoid disease is very different from diagnosing and treating. Nonetheless, although prevention is important, it is not always easy to practice. It’s time-consuming, results are hard to measure and it deserves both patience and persistence. Therefore, it’s not surprising that doctors are often less interested in prevention than treating and curing. Let me quote Dr. Bernard Lown from his blog, The Lown Conversation: “Diligent prevention, unfortunately, plays second fiddle to heroic cures.”

I believe the most powerful tool to cut the burden of heart disease in our community is education. The remarkable Maya Angelou said: “When you know better you do better”. One of the most important roles for doctors and other medical professionals is educating people about healthy lifestyle, nutrition, exercise and other measures to prevent disease.

All things considered, education is a double-edged sword. Bad education is often worse than no education. A huge number of books and articles have been written on lifestyle, exercise, diet, and nutrition, and there is an overflow of information on the internet. Obviously, some of it is good and some of it is bad. In many cases, education and information is driven by a product line designed to enrich the bank account of the author. Obviously, such information may be misleading.

Much has been said and written about the role of cholesterol in heart disease. Elevated cholesterol is considered a risk factor for cardiovascular disease. Lowering cholesterol, low-density lipoprotein (LDL) cholesterol, in particular, is of key importance. Recently, however, the role of cholesterol in heart disease has been debated.

A few weeks ago a ran into a new book on the subject, called “The Great Cholesterol Myth written by nutritionist Jonny Bowden, PhD, and cardiologist Stephen Sinatra, MD. At first sight, I wasn’t interested in the book. There are so many similar books I thought: The Cholesterol Myths by Uffe Ravnskog, The Great Cholesterol Con by Malcolm Kendrick, The Great Cholesterol Con by Antonio Colpo and The Great Cholesterol Lie by Dwight Lundell. Sounds pretty boring. However, I decided to give Bowden’s and Sinatra’s book a chance.

Cholesterol and Heart Disease – Can We Ignore Contradictory Evidence?

The role of cholesterol in atherosclerosis and cardiovascular disease is often debated. In my opinion, the so-called lipid hypothesis is an oversimplification of a complex disorder. Sometimes we debate because we disagree on how to simplify complex mechanisms. Cholesterol is just one of many players in the atherosclerotic process. The main reason it has become such a popular player is that it is easy to measure, not because it plays the main role. However, medical debates are often quite interesting, and they may actually have some positives. They often provoke lively discussions, and they may stimulate scientific research. The downside is that if you have already chosen a side, you run the risk of neglecting, or not choosing to accept scientific results or arguments that don’t support your own opinion.

There are different ways for authors to present a hypothesis they believe is true. You can choose to present all available data, and then make an argument for the data you believe support your hypothesis. Such a balanced, informative approach is honest, and it gives the reader a chance to make up his own mind. However, it doesn’t necessarily catch the attention of the news media or make the headlines.

If you believe you’ve found the truth, you may prefer to select data that reinforce your own beliefs. We could call this the preacher’s approach. There is no reason to discuss any contradictory evidence. That’s just confusing.

In my opinion, the recent book by Bowden and Sinatra is a good example oft he preachers approach. Somehow the authors believe they’ve managed to unlock the hidden truth. In fact, you may admire how fearlessly they expose, what they call the misinformation fed by the scientific community. Let me quote the first sentence of the first chapter: “The two of us came together to write this book because we believe that you have been completely misled, misinformed, and in some cases directly lied to about cholesterol”. Interesting and provoking.

Conspiracy theories are likely to get media attention. I presume that’s a part of the procedure. Somehow, we like to read about how we have been cheated and mislead. Consequently, if you manage to convince people they’ve been cheated, they’re more likely to listen to your theories and arguments.

While reading “The Great Cholesterol Myth”, I had this strong urge that I had to play the devil’s advocate. It’s not necessarily because I dislike the book or disagree with everything the authors write. On the contrary, I think they have some great tips on healthy lifestyle and diet. It’s just because I believe people have the right to hear both sides of the story, and then make up their own mind. I’m not a book critique, so whether I liked the book or not is irrelevant. However, taking on the role of the devil’s advocate I want to bring forward some of my thoughts while reading the book.

“Cholesterol Does Not Cause Heart Disease” – The Main Arguments

In the first two chapters, the role of cholesterol in heart disease is discussed. The authors believe that cholesterol numbers are a poor predictor of heart disease. They point out that more than half of the people hospitalized with heart attacks have what they call “perfectly normal cholesterol levels”.  The importance of cholesterol for different bodily functions is underlined. The message is; because cholesterol is essential for life it can’t be bad. Let me quote the book: “Both of us became skeptical of the cholesterol theory at different points in our careers, traveling different pathways to arrive at the same conclusion: Cholesterol does not cause heart disease.

Exploring "The Great Cholesterol Myth"

The second chapter is called “Cholesterol is harmless“. In this chapter the people who write the special reports and guidelines, meant to help doctors make treatment decisions get a fierce amount of critique. A quote from the book: “When the National Cholesterol Education Program lowered the optimal cholesterol levels in 2004, eight of the nine people on the panel had financial ties to the pharmaceutical industry, most of them to the manufacturers of cholesterol-lowering drugs who would subsequently reap immediate benefits from these same recommendations”.

Atherosclerosis is the underlying cause of cardiovascular disease. It leads to the building of plaques within the walls of our arteries. These plaques are composed of several substances, among them is cholesterol.

Atherosclerosis typically affects the coronary arteries, the vessels supplying blood to the heart muscle. In medical school, I was taught that the exact cause of atherosclerosis was unknown. However, there were certain risk factors, which if present increased the likelihood of developing atherosclerosis and coronary artery disease. The main risk factors were family history of heart disease, smoking, high blood cholesterol, high blood pressure, diabetes, and obesity. None of these risk factors was considered to be the cause of heart disease. However, by modifying the risk factors, the likelihood of developing heart disease could be reduced.

I have never believed that cholesterol is the sole cause of heart disease. However, it is certainly involved, and it is quite clear that cardiovascular disease as we know it would not exist if cholesterol was not present. Is a tsunami caused by water? No, but it won’t happen without it. Is heart disease caused by cholesterol? No, but it won’t occur without it.

The fact that cholesterol is a very important biologic substance and essential to life, does not prove that high levels may not promote a disease process. There are many examples of this phenomenon. Iron, for example, has important biologic functions. However high levels of iron in the body can cause a disease called hemochromatosis. Although insulin is essential for our metabolism, research indicates that high levels are undesirable and may promote obesity. A certain level of blood glucose is essential for life. If we don’t get glucose through our diet, the body produces it. However, high blood levels of glucose are undesirable and associated with the disease we call diabetes. So, although cholesterol is an important biologic substance, high levels could certainly be associated with disease.

In animal models, atherosclerosis does not occur in the absence of greatly elevated blood cholesterol. Furthermore, heart attacks have been shown to be uncommon in humans with very low plasma levels of LDL cholesterol due to a sequence variation in the PCSK9 gene. In cell cultures, according to Nobel prize winners Brown and Goldstein, cellular needs for cholesterol can be met with an LDL cholesterol level of 25 mg/dl (0.65 mmol/L). Human newborns have an LDL cholesterol in the range of 40-50 mg/dl (1.1-1.3 mmol/L). Healthy adult levels are 3-4 times higher. The normal LDL cholesterol range is 50 to 70 mg/dl (1.3-1.5 mmol/L) for native hunter-gatherers, healthy human newborns, free-living primates, and other wild mammals, all of whom do not develop atherosclerosis. Randomized trial data suggest atherosclerosis progression and coronary heart disease events are minimized when LDL is lowered to <70 mg/dl (1.8 mmol/L). No major safety concerns have surfaced in studies that lowered LDL to the range of 50 to 70 mg/dl.

Familial hypercholesterolemia (FH) is a disorder characterized by high cholesterol levels, specifically levels of LDL-cholesterol. Many individuals with this disorder die prematurely of atherosclerotic cardiovascular disease. I have found no mention of this disorder in Bowden’s and Sinatra’s book. The most common problem in FH is the development of coronary artery disease at a much younger age than would be expected in the general population. So, try telling a thirty-year-old woman with FH, and an acute heart attack that cholesterol is harmless. Statin drugs have improved prognosis and quality of life in patients with FH.

It is important to emphasize, that it is lipoproteins that interact with the arterial wall and initiate the cascade of events that leads to atherosclerosis. Cholesterol is only one of many components of lipoproteins. LDL, the major carrier of cholesterol in the circulation, is the most atherogenic lipoprotein. High levels of LDL in the blood may lead to increased transport of this substance into the vessel wall. When inside the arterial wall, LDL can undergo a variety of modifications including oxidation, uptake by white blood cells called macrophages, formation of so-called foam cells and the initiation of inflammation. This cascade of events may ultimately result in an atherosclerotic plaque within the vessel wall.

Obviously, cholesterol is not the cause of all this, but it is always involved. So, could it be that atherosclerosis is more likely to occur if plasma concentration of LDL-cholesterol is high than if it is low? The answer is yes. A number of scientific studies indicate that this is definitively the case. However, this does not mean that cholesterol causes heart disease. That’s an oversimplification.

What Else Is Important?

The authors claim that inflammation is the true cause of heart disease. Let me quote the book: “So if cholesterol isn’t the cause of heart disease, what is? The primary cause of heart disease is inflammation”.

The authors point out that chronic inflammation is a significant component of virtually every single degenerative condition, including heart disease, Alzheimer’s, diabetes, obesity, arthritis, cancer, and many other diseases. They believe oxidation is an important contributor to inflammation and atherosclerosis.

Bowden and Sinatra consider the size of the atherogenic LDL particles to be important. Thus, the more of the large fluffy particles, the better. The more of the small dense particles, the higher your risk. They even suggest these parameters may be considered the “new good and bad” cholesterol, instead of the traditional HDL and LDL cholesterol.

Nature is complex and so are biological mechanisms that control bodily functions. A disease often occurs during specific conditions that involve many different biological pathways. Of course, environmental and genetic factors play a role as well. So, why should there be one simple cause of heart diseases such as chronic inflammation or cholesterol? Isn’t it more likely that lipoproteins, cholesterol, oxidation, inflammation and many other factors are all involved at the same time? So, again, we may disagree because our methods of simplifying complex mechanisms are different.

An association between LDL particle size and cardiovascular risk has been found in some studies. However, measurements reflecting the number of LDL particles appear to be a stronger predictor of risk than particle size in itself. LDL-P and apolipoprotein B reflect the number of LDL-particles. Interestingly, patients with FH usually have large LDL-particles, but their risk of heart disease is very high, and so is their LDL-particle number. It is likely that the association between small LDL and heart disease reflects an increased number of LDL particles in patients with small particles. Therefore, particle size in itself may be unimportant.

Bowden and Sinatra say the benefits of statin drugs have been widely exaggerated. Furthermore, they believe the side effects of these drugs to be much more common than previously thought. They point out that statin therapy may be associated with cancer and diabetes. Other common side effects may be memory problems, lack of energy and sexual dysfunction. They believe that much of the side effects of statin therapy may be traced to depletion of coenzyme Q-10. Dr. Sinatra only uses statin drugs for high-risk middle-aged men.

I share some of the author’s thoughts on statin therapy. I think side effects are underreported and doctors should be much more alert on the possible adverse effects on muscle, diabetes risk, energy, memory and cognitive function. However, most people tolerate statin therapy quite well.

Furthermore, I believe these drugs certainly reduce cardiovascular risk in patients with documented cardiovascular disease, and in many high-risk individuals without disease. However, in my opinion, statins are used too often in low-risk patients. We, doctors, should take the time to inform these low-risk individuals about possible alternatives to statin therapy, such as diet, exercise, and healthy lifestyle.

Interestingly, the chapter on statin therapy ends with a final cautionary note, let me quote: “Look, there’s not much doubt that statin therapy can significantly reduce the incidence of coronary morbidity and mortality for those who are at great risks of developing coronary artery disease“. Here I definitively agree with Dr. Bowden and Dr. Sinatra, but I have to wonder if they disagree with themselves.

What About the Supplements?

The seventh chapter of the book is called “Help your heart with these supplements”, and deals with different nutritional supplements.

There are a number of supplements the authors believe improve the health of our hearts. Among these are coenzyme Q10, which the authors call the spark of life, D-ribose, L-carnitine, magnesium, niacin, vitamin E, fish oils and Omega-3.

Interesting list, but somehow I could not help thinking that, if the authors owned companies that were selling these products on-line, it would seriously affect the credibility of the book and reduce its educative value.

However, keeping in mind they believe that the lipid hypothesis is kept alive by medical professionals getting paid by pharmaceutical companies, I will have to assume that Dr. Bowden and Dr. Sinatra have no conflict of interest.

57 thoughts on “Exploring “The Great Cholesterol Myth””

  1. This is a very balanced, accurate and authoritative review of the Bowden/Sinatra book and the whole cholesterol controversy. Well done Dr. Sigurdsson.

    • Walking round graves in Europe from 19th Century I wonder how all those people managed to live to be 88 working the whole time usually, without ever having a blood test in their lives!!! Years ago, a study was done linking stress to raised Cholesterol levels using Tax Accountants in March and early April. We have seen cholesterol bars lowered more and more ditto for bone density testing. I am now reading about how we are getting inflammation and fatigue due to not spending enough time in the sun sans sunscreen, and I do recall women gobbling down HRT meds etc. being told how good they were!!!
      Here is the best solution unless one has a genetic disease: Exercise daily, Eat healthily, not too much, mainly vegetables. Thanks for the interesting discussion. Ordinary elderly housewife, Lizzie.

    • It is a controversy, indeed. I have done extensive research and all I see is one contrary opinion after another. Same thing about statin drugs vs. red yeast rice. I cannot draw any conclusions at all.

  2. Great to read such a balanced view. You have addressed in some detail many of the controversial areas confounding the relationship between cholesterol and cardiovascular disease. I will be encouraging my friends to read this article.

  3. I am in the middle of the book so I appreciate your review. However I do not fault the authors for their spin. I found they repeatedly emphasized the value of statins for those cardiovascular patients who actually can benefit from them. But not for the vast majority of the population who are being put on these drugs “just because” we are aging and “may” have high cholesterol numbers (but without corresponding high Triglycerides). I agree there is a whole lot more to this “controversy”. But it is important that ordinary people not be put on drugs arbitrarily. Especially when the overwhelming evidence is that a change in diet and attention to proper nutrition can accomplish the same goal for free and with no side effects. That was their major point. As for their endorsement of certain supplements I suggest that you also read Dr. Sinatra’s book: “The Sinatra Plan: Metabolic Cardiology” for a more detailed explanation of why he advocates these four supplements for cardiovascular patients. I am not saying I agree or disagree with him – but it is his daily profession and it is based on his documented experience, however anecdotal it may prove to be.

  4. Dr. Bowden does indeed sell supplements on his website. Does this disqualify him from being an impartial voice? I don’t know, but writing the book with a Cardiologist was a good move on his part.

  5. It appears that both Dr Bowden an Dr Sinatra sell nutrition supplements on the internet, among them are those they promote in their book. They never mention this as a possible conflict of interest. One of the main message of their book is that people should not take statins, but should take the nutrition supplements they are selling.

    At the same time they consider it a problem that some of the doctors who write the clinical guidelines have financial ties with the pharmaceutical industry.

    In ethical terms, is there any real difference between these two, I can´t see it?

    • What about Dr. Siggurdson, isn’t he trying to sell you something? Yes he is selling something. He is selling his medical services. He’s His entire website is about cholesterol. What would happen, if he were wrong about cholesterol? I venture to guess his reputation and pride would be on the line. Perhaps Dr. Sinatra and Johnny Bowden saw the handwriting on the wall. I saw where cardiologists are abandoning LDL targets and just giving statins to everyone over a certain age. https://www.medscape.com/viewarticle/814152

  6. Actually statins are being pushed on everyone with a little high cholesterol (conveniently redefining normal to sell more of them), even here in Spain. I am not an MD, just a patient without any intention of taking them (CT=332mg/dl, HDL=110mg/dl, TG=79mg/dl; yes, I am quite low-carb high-dairy, hence these numbers). I’ll take my chances replicating effective clinical experience by myself.

    In respect to newborns’ and hunter-gatherers’ cholesterol I urge anyone to read Paul Jaminet’s take on the subject: https://perfecthealthdiet.com/2011/07/low-serum-cholesterol-in-newborn-babies/ and https://perfecthealthdiet.com/2011/07/serum-cholesterol-among-hunter-gatherers-conclusion/.

  7. Please. We live in a capitalist system. Although they may sell supplements (and it certainly would have been nice if they disclosed that fact) this is not a meaningful “conflict of interest”. First, anyone wishes to take these 4 particular supplements has a large and ever growing field of choice as to where to go to purchase them. These guys do not have any exclusive patents – and the high prices that usually go with them – to prevent competition and/or guarantee any income whatsoever from them. Need I point out how that is NOT generally the case for most approved FDA drugs (at least when they are first introduced)? Or is the current front page news about generic versions of various drugs – and the financial fears of their being introduced – just to be dismissed?

    Second, I hardly think they wrote this book as a marketing tool for their exclusive (or anyone’s) product line. Now, can we get back to focusing on the actual hard science and/or evidence they attempt to present?

  8. Thanks for very balanced view on this controversial topic. Your points on FH and iron, insulin & glucose are consistently dismissed by cholesterol denialists. I guess low-grade inflammation is bad, but the elevation of inflammation markers in infections is critical for human survival. So inflammation is equally two-edged sword as is cholesterol, if you wish. I can already see the books of 2020s: ‘all you were told about low-grade-inflammation is lie’.

    But the bigger question is how would your enthusiasm in prevention spread among cardiologists? Dariush Mozaffarian and yourself are doing wonderful work. Most cardiologists don’t care about nutrition. Where is their passion on improving the lives of people b all means? As JFK stated, ‘…not because they are easy, but because they are hard’

    • @Reijo. You are absolutely right about inflammation. It is a two edged sword. An imbalance between pro-inflammatory and anti-inlammatory factors is certainly present in many diseases, such as psoriasis, inflammatory arthritis, Crohn´s and ulcerative colitis. Anti-inflammatory drugs are usually helpful in these disorders. Studies also indicate, as you suggest that a mild immune system imbalance, or low grade inflammation may be present in atherosclerosis and diabetes. Anti-inflammatory drugs are being tested for coronary artery disease. One of the main concerns is whether the susceptibility to infections or cancer will be increased by suppressing the immune system.

      So, when it comes to food, we might certainly want to select food that reduces low grade chronic inflammation. At the same time we would like to select food that strengthens our immune system in order to protect us from infections and cancer. So, our main target should not always be to reduce inflammation, but rather to affect the imbalance between pro-inflammatory and anti-inflammatory mechanisms that characterize some disorders.

      Thanks for bringing up this important issue Reijo.

      • If you (overlysimplily) consider inflammation as the key component of healing, the inability of macrophages to clear the cholesterol residue from the intima/media region is the simple explanation. Failed healing is another way to put it.

        Intuitively, the small size of certain subspecies of LDL particles is a logical reason for for the association between LDL and CHD. It is easier to penetrate between the cells. Is there a reason to believe that all LDL particles of a given subclass and size are indeed identical? As a retired engineer, I am aware that not all ball bearings of a given alloy and size are identical especially when it comes to fracture and fatigue failure characteristics. Do we have any reason to believe that the biological quality of LDL particles is higher than the mechanical quality of ball bearings?

        It is still true that “a few bad apples spoils the barrel”, and maybe that has some application to LDL particles. Only some are bad, but this creates the negative association for the whole LDL barrel.

        Is it only small LDL particles that penetrate the artery wall, or do small HDL particles also do the same? Could small penetrating HDL particles be properly disposed of by macrophages and this would be consistent with the positive association between HDL and the incidence of CHD?.

      • Interesting thoughts. However, possibly the number of particles is more important than particle size. Individuals with familial hypercholesterolemia (FH) often have large particles but high risk of atherosclerosis. Maybe you´re right about the few bad apples”. There is still much we don´t know.

  9. An excellent article by the editor-in-chief of American Journal of Cardiology, William Clifford Roberts

    “It’s the cholesterol, stupid”

    “Presently, it is commonly stated that “atherosclerosis is an inflammatory disease.” Inflammatory cells, however, are infrequent in plaques of coronary arteries studied at necropsy or in endarterectomy specimens. When present, the few mononuclear cells—even giant cells—appear to be present due to a reaction to the deposits of lipid (pultaceous debris) present in the plaque.“ Inflammation” appears to be a surrogate for elevation of serum C-reactive protein or various cytokines (interleukins 1 and 6, tumor necrosis factor, etc), not for inflammatory cells in plaques. Thus, it is a definition situation, and the morphologic definition of inflammation is not applicable”

    –William Clifford Roberts, American Journal of Cardiology, editor in chief.

    Daniel Steinberg elaborating why the inflammation associated with atherosclerosis in just the downsteam provoked by elevated LDL cholesterol.

    Reijo wrote:

    “Thanks for very balanced view on this controversial topic”.

    I am waiting the day when opportunistic and fashionable relativist intellectuals come on the scene and declare that evolution theory is an over-simplification and debated by the experts,. .

  10. Dr. Steinberg’s first phrase: “The long-standing controversy over the validity of the lipid hypothesis of atherosclerosis has been settled.1–3”. Well, for me it has been settled, just it is the opposite conclusion. Just read Richard David Feinman’s take on the main evidence.

    Within second paragraph of Dr. Roberts piece (well, I have my ideas about stupidity, too): “The best study in my view supporting this thesis is the Seven Countries study [8–10].”. It is ridiculous this example of highly biased selection of countries due to a preconceived idea to be defended keeps being highly considered among some physicians. Even an English major can see it for what it’s worth. Moreover, anyone who sees beauty on JUPITER (not the planet, that is) is quite suspicious to me. I urge anyone to read Brian Scott Peskin or Dr. Lorgeril take on its shortcomings.

    I see NO reason to prescribe statins in primary prevention, except if you renegade of “first do no harm”, that is. Take a look at the second Figure of Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study (52087 healthy subjects followed during 10 years). Explain now to me why is a good idea to medicate a healthy subject (elevated cholesterol is not a disease, sorry) before any coronary event has taken place. Not to mention how anyone has arrived to think that statinizing healthy women is an act of intelligence.

    I am not delegating my health and disease prevention on anyone, thank you. I will happily ride the Spanish paradox while I can.

  11. Andre,

    If Richard Feinman was correct and there was controversy in the lipid theory it would follow that:

    a) Humans are the only mammalian specimen in the biosphere that is immune to dyslipidemia, elevation of LDL-cholesterol in particular.

    b) LD-lipoproteins make up the only substance in human body that do not cause harm in excess.

    To conclude that lipid theory is not valid equals an implicit statement against the darwinian foundation of our biomedical research paradigm. Moreover, it’s rather irrelevant what cholesterol denialists such as Feinman or de Lorgil thinks in their rather silly editorials. None of the people are experts in atherosclerosis/lipid research at the level of mechanism, unlike Steinberg and Roberts.

    Ancel Keys did not arbitrarily select countries to please his alleged agenda. In 1953 he held a speech in which he compared the the statistics collected by the F.A.O to the mortality statistics of WHO. He chose six countries out of the date of set of 22 because:

    Broadly speaking, death rates ascribed to specific causes are not very reliable under the best of circumstances. Certainly it would be difficult to insist that the values in Table 3 for “degenerative heart disease” in the different countries are stricktly comperable nor would it be reasonable to suggest that the values listed for all circulatory diseases are actually precise.”

    “The list in Table 2 includes the countries with good vital statistics which are reasonably compared in race, climate, culture, medical services and vital statistics. The omissions are Western Germany and Finland, because of major population shifts and other effects from the war, and Iceland, Luxemburg and some colonies and semi-independent states with very small populations. (…) So far it has been possible to get fully comparable dietary and vital statistics from 6 countries.”

    –Ancel Keys, 1953

    Pay attention that Keys left out both Finland and Ceylon (Sri-Lanka); two countries that were best targets for the diet-heart theory with the opposite examples. The 7CS (which included Finland and Netherlands; both of which were originally left out) had nothing to do with the data set of the FAO nor WHO, it was a prospective cohort study that began in 1958. It utilized chemical analysis, highly trained staff, standardization, etc. And yes the finding are rather destructive for the low-carb apostols. The Ancel Keys bashers online are equivalent to Cremlin revisionists who attempt to rewrite the history.

    Have you read the Norwegian HUNT -study? I have, yes the deniliasts manage to publish their articles in less prestiguous publications every now and then, just like the Intelligent Desing -folk do with their “irreducible complexity”-nonsense. Have you heard about the J-curve phenomenom? It’s widely known that the cholesterol levels of Western people starts to dramatically plummet after the age of 60. This happens usually with BMI and blood-pressure as well and it is co-founded with senile devitalization, and in the case of cholesterol metabolic changes in the intestine which lead to weakened cholesterol synthesis and absorption. If the follow-up is not long-enough and if these co-founders are not controlled for, spurious correlations may emerge. Did you know that there are people who “suffer” from hypobetalipoproteinemia. These are the opposite cases to FH. Some of these people live their life with just <15mg/dl (0,4mmol/) in their LDL-fraction. These people are immune to CHD and end up living 9-12 year longer than everyone else.

    I'd like to share with a study from Helsinki. Pay attention to the long follow-up, and the fact that the researchers did not just look at CHD but quality in life and total mortality. TC cholesterol is an excellent predictor of quality of life and mortality all the way to late mid-life after the relationship with cholesterol and mortality gets skewed due to co-founders.

    Effect of cholesterol on mortality and quality of life up to a 46-year follow-up

    “A strong and graded relation was found between the cholesterol level and total mortality, with the men with a cholesterol level ≤4 mmol/L (154 mg/dl) having the lowest mortality. In all, the men with the lowest cholesterol gained the most life years. However, no association was found with the cholesterol level in 2000 (when 16% were using statins) and subsequent mortality. The lowest (≤4 mmol/L) cholesterol value in midlife also predicted a higher score in the physical functioning scale of RAND-36 in old age. In conclusion, a low total cholesterol value in midlife predicts both better survival and better physical functioning in old age”.

    The finding from Helsinki matches nicely with a recent Mendelian randomization meta-analysis including +300 000 genotypes

    Background LDL-C is causally related to the risk of CHD. However, the association between long-term exposure to lower LDL-C beginning early in life and the risk of CHD has not been reliably quantified.

    Conclusions> Prolonged exposure to lower LDL-C beginning early in life is associated with a substantially greater reduction in the risk of CHD than the current practice of lowering LDL-C beginning later in life.

    Each 1mmol/l drop in LDL cholesterol since birth was associated with ~55% reduction in the risk of CHD. This happened with all the 9 SNPs studied, despite each of them lower LDL cholesterol with a differing mechanism. Diet and excersise should have similar impact in the risk of CHD as do genetic factors, although the benefits of LDL lowering depends of a) magnitude and b) timing.

    • And here it is 5 years later and evidence proves Ancel Keys cherry picked those countries because he was paid to come to a particular conclusion.

  12. Continues…

    “Explain now to me why is a good idea to medicate a healthy subject (elevated cholesterol is not a disease, sorry) before any coronary event has taken place. Not to mention how anyone has arrived to think that statinizing healthy women is an act of intelligence”.

    Andre, you are little behind your times. Here are the fresh mega meta-analysis from least year (2012). Elevated cholesterol is a pathway to disease, and no mammalian specimen should carry LDL-C above 2mmol/l (80mg/dl) and TC cholesterol above 3,88mmol/l (150mg/dl).

    Cholesterol Treatment Trialists’ (CTT) Collaborators. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet 2012;380:581–90.

    Statins reduce cardiovascular events and all-cause mortality in women: Meta-analysis

    Give statins to all over-50s: Even the healthy should take heart drug, says British expert

  13. Intriguing the Helsinki study.

    From the study commented on your link Statins reduce cardiovascular events and all-cause mortality in women: Meta-analysis, Meta-Analysis of Statin Effects in Women Versus Men:
    “Previous meta-analyses, most conducted before the publication of the JUPITER trial, have implied that some of the benefits of statins do not pertain to women in primary prevention and that all-cause mortality is not decreased in women.”

    Well, it doesn’t let me at ease the inclusion of the JUPITER trial, stopped just when mortality curves were converging. Moreover, take a look at page 1072 (page 5 of the pdf) in Statins for the Primary Prevention of Cardiovascular Events in Women With Elevated High-Sensitivity C-Reactive Protein or Dyslipidemia. Subtract “Nonfatal MI” from “Any MI” on men both in intervention and control. Yes, there is 7 fatal MI under Rosuvastatin and 2 fatal MI under placebo. Wouldn’t exactly the inverse result be expected for a medication designed to bring down cardiovascular problems?

    Statins have quite serious side effects, like diabetes, muscle damage and loss of memory. I don’t think the benefits are superior to the drawbacks.

    I’ll take a look at the 7 Countries Study though.

  14. Andrés,

    I am glad you find at least some of my material useful. The relationship of serum cholesterol to the risk of CHD and stroke is strong, independent, continuous and log-linear. This association starts from very low-levels, around 3mmol/l and it’s well-established in all high-quality prospective cohort studies that adjust for regression dilution bias. We can see this clearly even among populations that have very low levels of cholesterol compared to Western people. Lowering LDL with statin and non-statin therapy definitively lowers the risk of acute myocardial infarction, stroke, and premature cardiovascular death. The benefits have been demonstrated in older and younger patients, men and women, primary and secondary prevention, and irrespective of other modifiable and non-modifiable risk factors. The benefits of LDL lowering therapy are in direct proportion to the percent reduction in LDL, rather than the LDL at baseline. If would go against our mechanical understanding of HMG-CoA reductase inhibitors if they did not work in primary prevention nor in women. This is not the case.

    PrimitiveNutrition is out with a new 44-video serie about the grotesque falsification of science by certain segments of paleo/low-carb advocates. Videos 3-5 are about Ancel Keys, Yerusshalmy & Hilleboe and Yudkin.

    I took another look to the Norwegian Hunt-2 study. The authors even claim that statins are not used in primary prevention in Norway. This is very silly as everyone can verify these days easily online that Norway top the whole Europe when it comes to usege of statin use in primary prevention. De Lorgil has a track record of making exceptionally dubious comments based on half-truths that I don’t even know where to begin, thus I leave it at that 🙂

    I keep my own LDL-C at its current levels of 1.8mmol/l (TC cholesterol 3.2mmol/l) with diet and exercise alone. I follow-up, a prudent low-fat, high-carb, whole-food plant-based diet with loads of healthy starches, legumes, fruits and vegetables. There are great cardiologists out there who provide sound and responsible dietary advice

    “Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels. Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies” .

    –Nobel voittajat, Brown & Goldstein

    How LDL receptors influence cholesterol and atherosclerosis (Brown & Goldstein).

    ”If the LDL receptor hypothesis is correct, the human receptor system is designed to function in the presence of an exceedingly low LDL levels. The kind of diet necessary to maintain such levels would be markedly different from the customary diet in Western industrial countries (and much more stringent than moderate low-cholesterol diets of the kind recommended by the American Heart Association). It would call for total elimination of dairy products as well as eggs, and severely limited intake of meat and saturated fats” .

  15. Here’s an excellent interview with the chief inspector of SATURNUS-trial, Dr Nicholls. These drugs are nothing short of miracle and in terms of safety concerns, high-dose statins match with aspirin.

    Great, illustrative graph from the SATURNUS-trial, demonstrating the relationship of median % change in atheroma volume and LDL lowering. This ought to be viewed by every single cholesterol skeptic out there:


  16. Just a quick response. It will take me several days in order to have the time necessary to look at all your links.

    I suppose you are aware that LDL-C is a worse predictor of cardiovascular problems than LDL-P, just like Dr. Sigurdsson has commented. I like also the visual impact driven by Dr. Attia’s recollection of figures from cited sources on his blog. My point?: it seems having LDL-C < 60mg/dl may be not enough (LDL-C discordant with LDL-P, low the former high the latter) or even unnecessary (LDL-C high and LDL-P low, just look at third Dr. Attia's blog figure —I can't access the linked original source—). I think that when treating individuals and not populations the difference is highly important.

    Here in Spain we don't have LDL-P measuring available. Moreover, LDL-C is not measured but calculated from the Friedewald approximation. So, my personal bet is on CT/HDL as proxy of LDL-P, such as presented in this paper. I am almost at the CT/HDL < 3 level (actually, my CT/HDL was 3.02 last May).

  17. Andrés,

    if only did you watch the illustration from SATURNUS powerpoint slides I wired to you….:) The discordance with LDL-P and LDL-C is pretty much issue for only diabetic patients as cocluded by a large expert panel on advanced lipid testing (1). LDL-P is the LDL theory with a twist of metabolic syndrome. The LDL-P story was never made for Peter Attia to push his twisted relationship to food. I don’t have diabetes, LDL-C works very well with me. Friedewald works very well if your triglycerides are <200mg/dl. And no, there's no upside for having LDL cholesterol any more than 15mg/dl (0,4mmol/l), this why the praxis these days is to put people with metabolic syndrome on statins irrespective of their current LDL status.

    1) Davidson MH, Ballantyne CM, Jacobson TA, et al. Clinical utility of inflammatory markers and advanced lipoprotein testing: advice from an expert panel of lipid specialists. J Clin Lipidol. 2011;5(5):338-367.

  18. The Friedewald approximation seems to be quite good for triglycerides between 100 and 400mg/dl (from Dr. Eades’ blog, as this case study… yes, I know, just don’t shoot the messengers). My tryglicerides were 79mg/dl last year, as I said on my first comment. Not that a probable elevated LDL-C worries me, since I bet that my LDL-P would be discordant given my CT/HDL proxy. It seems that discordance due to diabetes is just in the opposite direction, that is, low LDL-C and high LDL-P. Perhaps I will look into possible ApoB direct measure around here, though.

    I have finished taking a look at the SATURN study report, that I located on the page of one of the cholesterol skeptics (Dr. Ravnskov even disputes the validity of angiography measures as a surrogate of actual atheroma). I am concerned mainly about Tables 1 and 4 of the paper. The population of the study is high risk (around 70% hypertensive, 30% smokers, higher than 50% overweight) and highly medicated (around 97% antiplatelet agent, 60% betablocker, 44% ACE inhibitor, 60% on statins last month before study). Why does it concerns me?

    First, I don’t feel myself represented. I am not hypertensive (120/70 most of the times, measured when I go and donate blood), I don’t smoke anymore (I quit 7 years ago; I am 44 years old) and I am not on any medication. I even can’t imagine why someone can still be smoking and at the same time being taking chronic medication.

    Second, even with this non-medicine-naïve population (at least 60% previously on statins), there was an unexplained drop of 193 patients (12%) after two weeks run-in at half-dose. Add an additional drop of around 13% as stated by Table 4 (Preference of patient + Loss to follow-up + Noncomplience + Other). Moreover, health drawbacks of high-dose statin treatment seems to be quite high: Creatinine > ULN (ULN = Upper Limit of the Normal range) plus New proteinuria plus Alanine aminotransferase > 3×ULN plus Aspartate aminotransferase > 3×ULN equals to around 8% negatively affected. I would like to see also incidence for values greater than ULN, by the way. Hence, I think that “well tolerated” is a highly subjective statement.

    With respect to the experts, I am concerned about the population-focused consensus giving rise to useless/damaging medication of a lot of individuals. It seems to me that more powerful techniques for screening are already available and not used. Apart from LDL-P, I think that HbA1c and coronary calcium score are two of those.

    With respect to HbA1c, just take a look at Table 1 or 2 of Relationship between HbA1c and mortality in a Japanese population and Table 2 or 3 of Glycated haemoglobin, diabetes, and mortality in men in Norfolk cohort of European Prospective Investigation of Cancer and Nutrition (EPIC-Norfolk). I don’t know what my HbA1c is, but I have bought a glucometer and I am quite confident that my postpandrial glycemia stays under 140mg/dl at 1 hour and under 120mg/dl at 2 hour post-meal.

    With respect to coronary calcium score take a look at Figure 2 of Progression of Coronary Artery Calcium and Risk of First Myocardial Infarction in Patients Receiving Cholesterol-Lowering Therapy (via other cholesterol skeptic). Relative risk of 17.9 (95% confidence interval of 4.3 to 74.2) of those with an annual increase greater than 15% with respect to those with an increase lower than 15%. Of course the population is a high risk one and on medication, so they don’t represent me either. Nevertheless so high relative risk seems to point to something. I will consider getting a coronary calcium score (two one year apart if the first is not zero) done in the future.

    I will try to look at the rest of your links (7 Countries Study and hypobetalipoproteinemia) next week. Nevertheless, at first sight hypobetalipoproteinemia doesn’t seem to be without risks: “Slight clinical signs of CNS abnormality were found in 4 of the 8 subjects with heterozygous familial hypobetalipoproteinemia” from A Clinical and Neurophysiological Investigation of a Danish Kindred with Heterozygous Familial Hypobetalipoproteinemia (I don’t have direct access to the full paper, though) or “Neurologic signs and symptoms of a spinocerebellar degeneration similar to those of Friedreich ataxia have been reported in several affected kindreds” from The Johns Hopkins Textbook of Dyslipidemia.

  19. Hey Andrés,

    everything that Ravnskov says is close to 100% nonsense. This is the man who started the nonsense about Keys. Again, I won’t even go there. Cholesterol denialism equals creationism and obviously a disassociation from Darwinian legacy of biomedicine. Good luck with that.

    Most, the majority of heterozygous hypobbetalipoproteinemia people do very well, and as said, they are immune to CHD and live 9-12 longer than others. Some of them indeed have problem; we need small amounts of LDL cholesterol for cell functions (around 0,3mmol/l), some of these folk have their LDL-C cholesterol around ~0mmol/l. Homegenous hypobetalipoproteinemia patients are a chapter of their own.


  20. Andrés,

    you appear to be a smart guy, just eat a diet based on healthy starches (brown rice, maize, oatmeal, ryebread, whole-wheat pasta, potatoes, etc) & vegetables and low in saturated fats and refined oils. I would not gamble on the fancy ratio’s the low carb online echo-chamber produces. Everything goes for them apart from the good o’le LDL. Healthy starches have never failed a population, from rural China and Guatemala to Central-Africa they’ve kept chronic disease at bay.

  21. Ok! I have taken a look at some results about mortality from coronary heart disease (I think that overall mortality is the only relevant measure, though) from Seven Countries Study, 25 yr Follow-up: The RRs for the highest compared with the lowest cholesterol quartile ranged from 1.5 to 2.3, except for Japan’s RR of 1.1. For a cholesterol level of around 5.45 mmol/L (210 mg/dL), CHD mortality rates varied from 4% to 5% in Japan and Mediterranean Southern Europe to about 15% in Northern Europe. However, the relative increase in CHD mortality due to a given cholesterol increase was similar in all cultures except Japan”. Well, even 2.3 (CHD mortality only) as relative risk is not high enough with respect to 2.46 (2.07 for overall mortality) found to the third (of 4) interval (positioned almost a the middle) for those with HbA1c between 5.5 and 6.9 in Table 2 from the EPIC-Norfolk paper.

    About overall mortality, from The Seven Countries Study: Addendum: “Long-term prediction. The study was one of the first to examine the relationship between baseline characteristics during health and subsequent longevity, variously defined as survival for twenty-five years or to age 75 or 85. In this instance, cigarette smoking was the main contributor, with a major contribution also from blood pressure, but very little from serum cholesterol and body mass index.” Since we all are going to die, I would prefer cardiac disease (two uncles, one heavy smoker and diabetic type II the other, and one grandmother, hypertensive; I’m not in a hurry, though) than cancer (mother, one grandfather and other grandmother).

    What I am concerned about is that the Seven Countries Study data don’t seem to be easily accessible, since it is not included in the meta-analysis about prospective cohort studies on saturated fat an cardiovascular disease pointed to by Dr. Sigurdsson in his post about saturated fat. I may be mistaken and haven’t recognized it.

    Finally, Dr. Lustig has exposed a not very balanced focus on saturated fat versus fructose consumption in the Seven Countries analysis (Page 11): His work, the Seven Countries: study (10), was one of the first multivariate linear regression analyses. A review of this document (P. 262) notes: “The fact that the incidence of coronary heart disease was significantly correlated with the average percentage of calories from sucrose in the diets is explained by the intercorrelation of sucrose with saturated fat. Partial correlation analysis demonstrates that with saturated fat constant there was no significant correlation between dietary sucrose and the incidence of coronary heart disease” (10). However, Keys neglected to perform the converse analysis demonstrating that the effect of saturated fat on cardiovascular disease (CVD) was independent of sucrose. In other words, sucrose and saturated fat co-migrated; it is impossible to tease out the relative contributions of sucrose vs. saturated fat on CVD from this study.

    I haven’t been able to find anything else about hypobetalipoproteinemia (already neurological risks in heterozygous ones).

    I still eat lots of vegetables, nuts and olive oil, but I also eat a lot of eggs, hard cheeses, seafood and butter. White rice or white potatoes in lower amounts daily too. And I don’t think a RR of 1.3 (CVD mortality only) is anything remotely near massive, 17.9 certainly is (myocardial infartation, fatal or not, though).

  22. The 7CS is powerfull, coronary heart disease mortality, a direct function of SFA’s & serum cholesterol. Now wonder the cholesterol confusionists hate the study and act like the Cremlin revisionist towards it. As stamler (2010) pointed out, it’s indeed very bizarre that 7CS was not included in the Siri-Tarino meta-analysis. After all, it is a prospective cohort study.

    The biological mechanisms which would link sucrose to CHD are not there: Cultures that have traditionally showed high sugar consumption Cuba, Costa Rica, Ecuador hace traditionally showed low levels of cardiovacular mortality. In animal models sucrose feeding open up the arteries of non-human primates. Sweden showed significantly higher sugar consumption in the 1960s than Finland did, yet its CHD rates were 1/2 of that of Finland as Ancel Keys pointed among other things. In human diabetics pure sucrose feeding (80% of calories from table sugar) improves the glucose tolerance, as measured by oral glucose test. I am not saying that sugar is innocent & harmless especially at the quantities it is now consumed. However, it’s very secondary next to saturated fat. Sugar is harmless only if it leads to weight-gain, saturated fats are always detrimental independent of weight status. The biological mechanism of how SFAs contribute to elevated cholesterol is well understood thanks to Brown & Goldstein.


    excellent video illustrating what kind of fraud Dr Robert Lustig is. BTW, am I the only who sees the irony with his sugar crusade and poor weight-management. “That’s what god did” says Lustig. Hilarious.

    25 Cholesterol Confusion 8 A Large and Fluffy Distraction

  23. First, the first 5 of 6 six paragraphs of your blog contain no relevant information — length of blog post does not equal intelligent analysis. Second, I suspect you didn’t actually read the entire book. The authors never suggest that cholesterol is ONLY good for you, no matter the levels. They instead explain why cholesterol should not be part of the heart attack prediction/prevention equation. Furthermore, the authors clearly explain that LDL does contribute to heart disease, as you suggest, if it is oxidized and glycated. The list goes on and on. If you want to challenge new medical ideas, go for it. Bowden and Sinatra are not know-it-all gods. Your “analysis” though is misleading, and most people who commented on your post said it was “well-balanced” without (apparently) having read the book.

  24. While I think your review shows some balance, too many seem to suggest you offer a better balance than do the book’s authors; I am not sure that is proven. The authors present both sides of the debate and simply put forth their analysis and argument against the mainstream thought process. What else would you expect a book like this to do?

    The authors point out many studies to support their view and I didn’t see one that you presented as a false report or analysis. So you simply seem to have a somewhat different opinion than do the authors. Why should we assume yours is right or better? I do not suggest that you are wrong nor that your approach may be better, just that you have given no factual rebuttal of the author’s position. You show some statistics, but you need to show how they have a greater validity than the author’s otherwise all you are both doing is showing how the field is still rather unresolved, which is part of their claim to start with.

    You also comment about the importance of cholesterol on atherosclerosis. The authors do not ignore this, their claim is that very high concentrations continually circulate throughout the vascular system without any ill-effects; they claim it is only cholesterol that has been damaged that actually forms the plaque. You did not address this contention at all.

    They claim and you mention “They point out that more than half of the people hospitalized with heart attacks have what they call “perfectly normal cholesterol levels”. ” Yet you do not dispute this? Why? Is this correct? If so then clearly cholesterol is not a strong marker for heart attacks.

    Their core position is that sugar, highly processed foodstuffs and environmental irritants that lead to inflammation are much greater risk factors than are serum cholesterol levels as a whole (specific cases could have different factors). Do you disagree with this? Their claim is based on the physiological effects of these factors on atherosclerosis. Do you disagree with their claimed mechanisms?

    Your discussion of FH is interesting, but the first thought that occurs to me is that it is a different mechanism than the that for the general public; therefore, it may not be unreasonable that cursory observations could show seemingly disparate results.

    • Michael. Thanks for your interest in my article. I do appreciate your comments and I find them completely valid. I don´t have a lock on the truth, no more than the authors of the book do. However, I don´t think there is enough scientific evidence to dismiss the lipid hypothesis completely as the authors seem to do. Furthermore, the inflammatory hypothesis remains to be proven and can not at this point in time be accepted as a scientifically proven concept. Atherosclerosis is a complicated disorder. Without doubt, lipoproteins and inflammation are both part of the mechanisms involved. It is quite possible that cholesterol in itself is just a surrogate marker. Time will tell.

      I certainly liked reading Bowden´s and Sinatra´s book. I think they present their opinion quite clearly and it is certainly a very well written and interesting book. However, I think they don´t present enough evidence to be able to make such strong end determined conclusions. They ignore the results of many scientific studies on the role of lipoproteins in atherosclerosis. At the at the same time they are guilty of using relatively soft data to draw their own conclusions. Take for example their remarks on the role of small and large LDL particles. I´m not saying that particle size doesn´t matter, but there isn´t evidence enough to conclude that it´s all that matters.

    • Michael,

      “You also comment about the importance of cholesterol on atherosclerosis. The authors do not ignore this, their claim is that very high concentrations continually circulate throughout the vascular system without any ill-effects; they claim it is only cholesterol that has been damaged that actually forms the plaque. You did not address this contention at all.”

      This is a false dilemma. Yes, when LDL-particles are retained in the arterial intima, they are more susceptible to e.g. oxidation. However, more particles –> bigger risk of that happening. Therefore, high concentrations of LDL are harmful, period.

      “They claim and you mention “They point out that more than half of the people hospitalized with heart attacks have what they call “perfectly normal cholesterol levels”. ” Yet you do not dispute this? Why? Is this correct? If so then clearly cholesterol is not a strong marker for heart attacks.”

      This is based on a study that measured blood lipids very shortly after MI. Now, Axel may correct me on this one, but I’ve understood that these kind of measurements do not provide solid results of what the levels were before the actual cardiac event. In addition, quite many of these patients still had LDL levels above what’s considered optimal for high risk patients plus low HDL. All in all, only 2% had both optimal LDL and HDL levels.

      “Their core position is that sugar, highly processed foodstuffs and environmental irritants that lead to inflammation are much greater risk factors than are serum cholesterol levels as a whole (specific cases could have different factors). Do you disagree with this? Their claim is based on the physiological effects of these factors on atherosclerosis. Do you disagree with their claimed mechanisms?”

      There’s no evidence that these are bigger risk factors, let alone that all of them are independent risk factors. E.g. sugar seems to “work” mostly because of its detrimental effect on blood lipids (and, indirectly, via increased risk of overweight).

      “Your discussion of FH is interesting, but the first thought that occurs to me is that it is a different mechanism than the that for the general public; therefore, it may not be unreasonable that cursory observations could show seemingly disparate results.”

      You are incorrect. People who suffer from FH are different from the rest of in one meaningful sense: they have mutations in the LDLR gene. This gene encodes the LDL receptor protein which normally removes excess LDL from the circulation within a couple of days. In FH patients, this time doubles which leads to problems. The actual pathophysiology of atherosclerosis is exactly the same.

      So Michael, to sum it up light-heartedly: Bowden and Sinatra are talking precisely what the first letter s of the last names stand for. 🙂

      • Mie. You took the words right out of my mouth. Couldn´t agree more. Thanks for responding.

  25. High cholesterol means your body is unhealthy and the cholesterol is used as a bandaid to try and repair the damage. As usual western medicine focuses on the symptom not the root cause. The root cause is internal unhealthiness. The answer? Bring the body back to a healthy state…the same answer for ANY issue you might have. I alledgedly have an incurable skin disorder in psoriasis, yet I have cleared over 50% in the past year focusing on nutrition, clearing toxins and other things I read about in study after study. I did a good job of connecting the dots. I will be clear from psoriasis soon, and it has to do with bringing the body back to a healthy state…prescription drugs have their place in short term and life threatening situations but aren’t needed for long term usage unless people have genetic disorders like epilepsy where it prevents seizures. In almost all cases there are natural things that are as good or more effective with no side effects…take Berberine and the diabetes drug Metformin for instance…Berberine performs just as well with no side effects other than good ones…

    If you take care of your body properly, you have little need for prescriptions anyway…

  26. I believe in the inflammation hypothesis and believe that insulin resistance is the root cause of obesity and heart disease. The explanations of cholesterols importance to fighting infection and it’s importance to the brain ring true to me. I have eliminated processed foods, most starches and eat a steady diet of eggs, organic non-cured meats, vegetables and a variety of fats from nuts, coconuts, avocado and butter and have never felt or looked better in my life. Allergies and colds are gone, muscle recovery is rapid and sleep is better as well as concentration. Dr. Sears ( Protein Power) and authors Bowden and Sinatra will soon be seen as illuminating the path towards optimum health is my prediction.

  27. Being just a normal, average American, I reacted to my recent result of a 236 overall cholesterol with alarm and quickly made plans to eliminate all animal products from my diet and lose tons of weight and try to get it down below 150 to “eliminate” heart disease risk. Anyways, then I came upon the Great Cholesterol Myth and was suspicious but decided I must research more as the people recommending ultra low blood cholesterol (i.e., Joel Fuhrman) are also making tons of money with books/selling stuff online. I very much appreciate this balanced, intelligent post and also the thoughtful comments!

    • Thanks Chaviva for bringing this up. That’s why it’s so often difficult for people to get useful information. So many health writers are trying to sell something or promote a product line designed to enrich their bank account.

  28. Hi,

    Nice review. At one point, you write ” Randomized trial data suggest [LINK] atherosclerosis progression and coronary heart disease events are minimized when LDL is lowered to <70 mg/dl (1.8 mmol/L). No major safety concerns have surfaced in studies that lowered LDL to the range of 50 to 70 mg/dl." However, the link is broken. Can you please provide the correct link (and fix the one in your blog entry)?


  29. The quote “No major safety concerns have surfaced in studies that lowered LDL to this range of
    50 to 70 mg/dl.” appears in the abstract (BUT NOT THE TEXT) of the paper…. “Optimal low-density lipoprotein is 50 to 70 mg/dl: lower is better and physiologically normal.” J Am Coll Cardiol. 2004 Jun 2;43(11):2142-6.


    Thanks to your previous writings, I am aware of this significant “cheap trick” used in medical literature.

    CHEAP TRICK # 12 — Insert strong claims in the abstract that are nowhere included in the text or references.

  30. MaterialGuy,

    the full text indeed discusses these safety issues in section “Is a target LDL…”. Including statin trials which such results and references these trials – where no major safety concerns have appeared.

  31. It is amazing that we find ourselves in this situation… It is obvious we can’t trust researchers and we can’t trust the media… Two of the most important watch dogs are now self absorbed, paid off, lap dogs.. very sad actually.

  32. You say “I have never believed that cholesterol is the sole cause of heart
    disease. However, it is certainly involved, and it is quite clear that
    cardiovascular disease as we know it would not exist if cholesterol was
    not present. Is a tsunami caused by water? No, but it won’t happen
    without it. Is heart disease caused by cholesterol? No, but it won’t
    occur without it.” Please reference the evidence to support your “it is quite clear that
    cardiovascular disease as we know it would not exist if cholesterol was
    not present”. Also re your use of a tsunami as an analogy is rather puerile – why not go one step further and say: cardiovascular disease is not caused by your arteries but it would not occur without them!!! Please do not treat your readers with the disdain of the average arrogant MD and reference your statements som please tell me why is it “QUITE CLEAR that
    cardiovascular disease as we know it would not exist if cholesterol was
    not present”?

  33. I got some curious notes about this:

    Several generations of my ancestors, including my grandparents, were born and raised in the country. A custom they all had (so my parents did it too until the end of 80’s) was raising pigs and then cutting and frying the skin (we call them “chicharrones”). All of that cooked fat -full of bad collesterol I guess- was then stored on big cans and used through the year for cooking; it was consumed, literally, every day by children and old people alike.

    The weirdest part: They ALL died very old (80+, 9X) for natural causes or smoking related habits (emphysema). Heart attacks and collesterol stuff were out of the equation all the time. So a question that I did myseft for decades has been how they survived for so long. We stopped consuming pork fat long ago but our grandparents did their entire life :-s.

  34. The opening line is “I have a strong interest the prevention of heart disease.” do you mean “in the prevention of heart disease” ?

  35. What a great review of the book. I work as an ER nurse and Stroke Response Nurse and have been reading about the effects of cholesterol for quite a while. At times I’m sick of what the status quo in the medical field pushes on patients in terms of statin therapy. I tend to take the inflammation is the culprit approach but I also agree that it’s not as simple as that. I think there are some lifestyle factors that could possibly turn on gene expression to exacerbate the cardiovascular risk with inflammation as a major component.

    That being said, is it easier to convince a patient to flip their lifestyle of inflammatory fats and refined carbohydrates to a healthier diet that cost more money or take a pill that Medicare will cover?

  36. I hypothesize that when scientists look into the differences in morbidity from heart disease comparing those who remain largely in fat burning metabolism, ketosis, versus those who remain largely in glucose burning metabolism, it will be found that the most effective foundational variable to prevent heart disease will be found to be…..diet. In control systems engineering when attempting to design controllers that deliver optimal “control effort” in driving a system to desirable states, you analyze and model the baseline systems to find these variables. You then calculate for those what is called the controllability and onservability of the variables. Diet will be found in human metabolism to be a highly observable and co trollable variable and therefore will become the focus for driving a human body tonnore optimal states of health related to heart disease.

  37. I was recently introduced to this debate by watching a documentary on the subject. The documentary’s posture was that the “cholesterol is bad for your health” position is a myth. However, after an hour and a half of “cholesterol study bashing”, I was left with several questions, such as “OK, then what causes atherosclerosis?” and “Can you describe in detail what are the mechanisms of heart disease”. I’ll be nice by saying that there was next to nothing in this documentary to answer such questions. Being an absolute cynic, I’m always willing to entertain that certain scientists may be – or may become – more interested in power and money than in establishing facts (the only difference is: I believe it’s the case with 99.99999% of humans – including myself – when they stop thinking about their “fellow humans”, which happens more or less quickly in “altruistic” endeavors, but that’s for another debate). Science is still the best way to establish facts, when conducted correctly. So to all the docs out there : “What causes atherosclerosis?”, “Is it the cholesterol in the foods that matters, or the one that is produced by our own bodies (metabolized)?”. Poor liver, maybe heart disease is simply its way of protesting against overwork and overtime without pay? At any rate, and concluding as a good cynic would, I think this debate (and others like this on the Internet) make me thankful that heart disease -and other forms of dying- exist.

  38. Are you 18-65 years old and taking atorvastatin (Lipitor or generic equivalent)?
    If so, Frontage Clinical Services is seeking volunteers to participate in a clinical study.

    Males or Females should be:
    18-65 years old
    Taking the same dose of atorvastatin (Lipitor or generic equivalent) for at least 4 weeks

    Study requires a screening visit of 1-2 days and then 1 visit each day for 15 days at our modern facility.
    Up to $3150.00 compensation for your time and travel.
    Ask us about our referral program!


  39. I think the author is still confused… or stubborn. If the “nature” of LDL cholesterol was to stick to coronary artery walls, wouldn’t you eventually get buildup in the arteries, no matter your LDL “number”??? Hint: YES.

    Or is the true “nature” of LDL to, among supporting other very necessary bodily functions, to HEAL inflamed artery walls? If arterial walls are INFLAMED… the LDL goes into healing mode and coats the inflamed areas like a band-aid. If inflammation continues, so does the “healing” process of LDL continuing to coat the arterial walls, eventually leading to clogged arteries! If no inflammation is present, it is very likely you will not have any clogging issues.

    I had a LDL count of nearly 190, and my small particle count was twice the high-end of the suggested “range”. Yet my cardiac CT scoring test came back a ZERO… no evidence of plaque buildup at all… even my cardiologist (a very good one) is confused as to the real cause of Atherosclerosis… he mumbled something about “good genetics”… BAH!! The reason that most cardio Docs are confused, is that they get their “research” information direct from BIG PHARMA, whose profits on statin drugs are off the charts… You can find many studies online that show that statins do NOT extend lifespans… for every patient they supposedly “save” from heart attacks… another patient dies early from the effects of statins or the effects of chemically reduced cholesterol levels (stroke, dementia, etc, etc).

    All that said, there IS some evidence that very LOW DOSE statin therapy can be of benefit… so do your research before just jumping into statin therapy! Pay particular attention to NIACIN therapy… which many think is as… or more… effective than statins, without the major risks (no time-release Niacin, please!)


Leave a Comment

This site uses Akismet to reduce spam. Learn how your comment data is processed.