November 19

The Statinator Paradox


Pity the poor lipophobes and statinators.  They’ve just taken another grievous wound to their favorite theory and haven’t even got sense enough to know it.  In fact, not only do they not have sense enough to realize they’ve taken the hit, they’re actually crowing about it.

The current issue of the Journal of the American Medical Association (JAMA) has an article titled Trends in High Levels of Low-Density Lipoprotein Cholesterol in the United States, 1999-2006 that puts another major dent in whatever validity remains of the lipid hypothesis of heart disease.

I’m going to start categorizing the types of findings published in this paper under the rubric of The Statinator Paradox.  I find it interesting that whenever scientists discover data that shows the opposite of what their hypotheses predict, they don’t conclude that their hypotheses might be wrong; instead they deem the contradiction a ‘paradox’ and bumble on ahead with their hypotheses intact.

The lipophobes hold the hypothesis dear that saturated fat causes heart disease.  When the data began to surface that the French eat tons more saturated fat than do Americans yet suffer only a fraction of the heart attacks, the French Paradox was born.  Nothing wrong with our hypothesis, it’s just those pesky French people who are somehow different.  It’s a By God paradox, that’s what it is.

Same thing happened with the Spanish.  Researchers looked at the food consumption data in Spain and discovered that Spaniards had been eating more meat, more cheese and more dairy while decreasing their consumption of sugar and other carbohydrate-rich foods over a 15-year period.  And, lo and behold, during this same period, stroke and heart disease rates fell.  Can’t be.  Saturated fat causes all these things.  But the data show…  Thus came the Spanish Paradox.

Statinators and lipophobes believe with all their little fat-free hearts that LDL-cholesterol is bad and is the driving factor behind heart disease.  So whenever I come upon data that gives the lie to this notion, I’m going to start calling it the Statinator Paradox.

This JAMA paper is a classic case of the Statinator Paradox.

Researchers using the NHANES data looked at the change in the prevalence of elevated LDL cholesterol and found that it fell substantially from 1999-2000 to 2005-2006.  In a period of about six years the prevalence of high LDL cholesterol dropped by a third, which is a lot of drop in a fairly short period of time.

And since everyone knows that high LDL cholesterol causes heart disease, it should go without saying that during this same time period there occurred a significant decrease in the prevalence of heart disease.  Right?  Uh, well, no, not really.  If anything, the prevalence of heart disease actually increased.  But not to a statistically significant degree.  So statistically there was no difference in the prevalence of heart disease during a time in which high LDL cholesterol levels were falling.  But if high LDL cholestrol causes heart disease…? It’s the ol’ Statinator Paradox writ large.

It was fun reading this paper because a basically fairly simple project was cloaked in all the regalia of academia and academic speak.

It starts out with a great opening sentence that is a paragon of academic weaselry:

High total blood cholesterol is recognized as a major contributing factor for the initiation and progression of atherosclerosis.

Recognized?  What does that mean?

I could substitute words in this sentence and come up with the following:

The policies of Barrack Obama are recognized as a major contributing factor in the initiation and progression of socialism in America.

What does that mean?  Depends upon whom you say it to.  If I were to shout this sentence at a Sarah Palin campaign event, I would be cheered loudly.  If I said it at a Nancy Pelosi event, I would be tarred and feathered.  Since the ‘truth’ of the sentence is a function of the bias of the person hearing it, it’s not a meaningful sentence.  As written, the sentence doesn’t mean squat, which makes it perfect for academic writing.

The authors, I’m sure, are believers in the lipid hypothesis but just can’t muster the gumption to write ‘high total blood cholesterol IS a major contributing factor…’  Instead they use the word ‘recognized,’ which makes the sentence meaningless and lets them off the hook should the lipid hypothesis ever blow up in their faces.

In setting up the study, the researchers went through a lot of rigmarole to allocate subjects to three different categories depending upon their degree of risk for developing heart disease.  In determining this risk, researchers used the Framingham risk equation, which relies to a great extent on cholesterol levels to allocate that risk.  Which is strange since the Framingham Study has never shown elevated cholesterol to be a risk factor for heart disease.

Once subjects were divvied into these three groups, the researchers measured LDL-cholesterol levels and calculated what percentage of subjects in each group had high LDL-cholesterol levels.  The threshold as to what was high varied as a function of the risk level of the group as a whole.  The bar for what was high was lowest in the high risk group and highest in the low-risk group.  In other words, if subjects had multiple risk factors, then an LDL-cholesterol level of anything over 100 mg/dl was considered ‘high,’ whereas in subjects in the lowest risk category, an LDL-cholesterol level over 160 was considered ‘high.’

Researchers calculated as a percentage the number of subjects who had high LDL-cholesterol in each risk group and did the calculations again six years later.

The weighted age-standardized prevalence of high LDL-C levels among all participants and among participants in each ATP III risk category decreased significantly during the study periods.

Which is what they were crowing about.  Our therapy dramatically decreased the number of people at risk for heart disease.

But as for heart disease itself:

No significant changes were observed in the prevalence of CHD or CHD equivalents from 1999-2000 to 2005-2006.

So what did our researchers conclude from the fact that there were one third fewer people with high LDL-cholesterol yet there was no decrease in heart disease?

They concluded the obvious.  There were still two thirds of people with LDL-cholesterol levels that were too high.  And, no doubt, these people were not on statins.

Don’t believe me?  Here it is in their own words.

However, our study found that almost two-thirds of participants who were at high risk for developing CHD within 10 years and who were eligible for lipid-lowering drugs were not receiving medication.

So, let me see if I’ve got this straight.  This study shows no evidence that lowering LDL-cholesterol levels decreases the prevalence of heart disease.  And what we conclude from this data is that we simply need to treat more people.  Brilliant!

As I was reading this paper online, I got a bing alerting me that I had an email from Medscape bringing me the latest in mainstream medical thought.  I opened the email and began scrolling through the various articles displayed when my eye fell on one titled “Lipids for Dummies.”

I clicked on it, and what opened was a video of a statinator of the deepest dye interviewing an alpha statinator about how to best deal with the risk of heart disease.

It was unbelievable.

Here in a short interview is everything that is wrong with mainstream medicine today.  We have two influential doctors at the pinnacle of their academic and clinical prowess – no doubt on the payrolls of multiple pharmaceutical companies – who are absolutely full of themselves blathering on about expensive treatments that have no true scientific grounding.  And their BS is being disseminated to practicing doctors everywhere. Instead of ‘Lipids for Dummies’ this interview should have been called Dummies for Statins.

Watch and just shake your head.


These guys aren’t really talking about reducing the risk for heart disease or early death; they’re discussing how to use extremely expensive medications that are not particularly benign to treat lab values.  As I’ve written countless times, statins can quickly and effectively treat lab values, but there is little evidence they treat much else.  So if you want to have lab values that are the envy of all your friends, statins are the way to go.  But if you want to really reduce your risk for all-cause mortality, you might want to think twice before you sign up for a drug that will cost you (or your insurance company) $150-$250 per month, make your muscles ache, diminish your memory and cognition, and potentially croak your liver.

If you wonder who underwrites these kinds of interviews, take a look at the actual Medscape link in which the video is embedded.  See if you, like Sherlock Holmes, can figure it out.

This link requires requires free registration.

(If I weren’t so pleased with a nice Sous Vide Supreme review we got today, this kind of nonsense would make me contemplate seppuku.)

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  1. OK, I give up. Mind you, in “Authors and Disclosures”, we learn that “Henry R. Black, MD, has disclosed that he has served as an advisor or consultant for Pfizer, Bristol-Myers Squibb, IntraCure, sanofi-aventis, Merck Sharp & Dohme, Forest Laboratories, Daiichi Sankyo, Boehringer Ingelheim, and CV Therapeutics.” Is there any stantinmeister he hasn’t worked for?

    The Two Stooges have some great lines. Like the study that implicated Zetia was “poorly designed” (which no doubt it was, but what statinism to write it off) and LDL is an “a very formidable predictor of atherosclerotic events” and that people need to get LDL below 35 (in mg/dl presumably, a level that increases mortality according to Kendrick).

    And if one goes up a level on the vid’s website, we see the following headline: “In Taking the Garbage Out, the More HDL the Better, but the Truck Should Function”. Those pesky garbage trucks again!

    So, the 8 percent solution, I should think, and then bore Dr Watson by scraping through a Paganini Caprice. (Perhaps I should be listening for the barking dog that wasn’t barking, a la The Hound of the Baskervilles!)

    6 Week Cure results so far: down 3kg waist down 6.5 cm to 101 cm. Need to do another cycle to get hip/waist below 1. But, hey, it’s weight that didn’t come off before!

  2. @Michael Richards

    If Sherlock could scrape through a Paganini Caprice, he was a pretty good fiddler. Back when I was actively working on my violin, the best I could ever scrape through was Kreisler’s Liebesfreud. And I’m talking ‘scrape through.’ Even trying one of the 24 Caprices was way, way beyond my even thinking about. Paganini is one of my musical heroes, but strangely, I don’t really enjoy his caprices other than the 24th. This video of Jascha Heifetz performing it shows why I didn’t ever give it a try. Amazing pizzicato and harmonics that were far, far beyond my modest abilities.

    Glad to hear the 6WC ‘scraped’ a little more weight off.

  3. doctors of symptomology….treat the symptoms, make the patient feel better, but the patient dies of a related death: “Well Mrs. Jones…the surgery was a success, but your husband died.”

    they are considering high ldl-c a symptom, and they must rid the patient of this symptom.
    getting the labs values within some arbitrary number.
    they talked of getting the ldl-c as low as possible….nothing is too low?
    then why does the body make something (ldl-c), sometimes a lot of it, that is needed to repair, or manufacture cell membranes, hormones, bile salts, myelin for your brain, etc?
    how about treating the inflammation first…that’s causing the elevated ldl-c
    would nearly 4.4 million years (fossil ardipithecus ramidus) of evolution permit humans to produce a detrimental blood chemical?
    they would have all died of CHD….yea, right…looks like we disproved that silly idea!

    what really amazed me was the comment that “we really only need ldl-c in the liver”….WHAT??
    you got to be kidding me….it’s amazing how money puts words in your mouth…
    dr john

  4. What a strange discussion!

    First, these guys hastily brushed off lifestyle changes, in favor of drugging America. Then, in pushing drugs, the challenge is to deal with … “poor marketing.”

    Good grief! These guys are shills for drug company marketing departments.

  5. Mike, could you clarify the sentence that begins “In other words…” To me it looks as if there’s something missing.

    Sorry about that. Thanks for the heads up. I wrote ‘than’ when I meant to write ‘then’ and then left out the bit about the LDL of 100. It’s fixed now.

  6. The Zero Paradox. What puzzles me is that Jimmy Moore (low carb blogger who eats mostly meat) and Dean Ornish (who eats mostly grains and vegetables) both scored zero out of a thousand on a heart scan, meaning that their arteries are awfully clean. Zero doesn’t necessarily mean that their diet is right, but it’s pretty interesting information. I try to think: what do they have in common: they both avoid sugar and white flour. Probably they have more in common, I’m not sure what, though. I does make me think, though, that neither meat nor whole grains are either the road to health or disease. What do you think about he Zero Paradox?

  7. @Peter Silverman

    Both say they had calcium scores of zero. Not that I’m doubting either one, but I’ve been in practice way too long to believe anything without seeing it myself. Plus, a calcium score isn’t the last word. People can have calcium scores of zero and still have heart disease (although the odds are low) and can have incredibly high calcium scores and not have heart disease. One of these days I’ll write a longer post delving into the nuances of calcium scoring and what it really means.

  8. Dr. Eades I can’t thank you enough. For the layman like myself, it is very hard to buck conventional wisdom…but you keep giving me the tools to acquire the information so that I can understand what I think I know. Thank you!

    Xmas present to myself is Sous vide machine…..I’m counting down the days.


  9. “I’m not so sure about what to do about triglycerides… we need to talk about that..”

    I wonder if the “lifestyle modification” of removing sugar and starch from the diet came up in that conversation? It more likely went along the lines of “gee, are there any promising new drugs that help a patient lower their tryglycerides?”

    what dunderheads!

  10. Hi Doc. Thanks a lot for that review.

    Not too long ago I came upon these article and this one from Science-Based medicine, a site that I like to read because they usually are quite on the mainstream side but with good critizism about it and it keeps me from loosing balance.

    But, If you go trough most of the comment, that are from MD I believe, it is astonishing to see how many believe that high LDL-C is a risk factor to CVD.

    Then my thought is this : Either they absolutly did not review all of the evidence, but talk like they did; or could it be that somehow high LDL-C contribute in some ppl to CVD and that’s why it’s hard to say it has nothing to do with CVD? Like, maybe if you have high LDL-C and you’re in a pro-oxidative environment, you have much chance of getting your LDL-C doing damage, and this high LDL-C could be a risk factor. I don’t know. I”m just trying to figure out how could so many people be blind to something that seems so obvious when talk about from people like you or Colpo or Ravnskov. And i’m not willing to belive that every doc. is dumd and trying to push pills as much as possible.

    On Science-Based Medicine, he quite talk like he knows about the literrature on the subject, but i’m not sure he does that much (he never refered to the primary studies that did not find any difference in mortality). He admit tho that the low-fat/low-cholesterol was promoted was too much, but his opinion is mostly based on statins that works trought decreasing LDL-C. He seems to based his opinion on a few recent paper that i’ve not look at because they repeat the same thing over and over (LDL-C is bad, statins lower LDL-C, statins lower CVD, then LDL-C is the bad guy). What a brillant sophism here.

    Anyway, i’d just like to have your thoughts on this. How can many people, with good critical thinking skills, can keep believing in the LDL-C hypothesis? Is it from the brain washing?

    Many thanks for your answer!

  11. Wait a minute: as I heard the video, the two participants clearly WERE saying that the lower your LDL-C the lower your risk for actual atherosclerosis. They were NOT just talking about the lab value itself. That is what they meant when they said that LDL-C is a “formidable predictor of atherosclerotic events.” Are they simply misrepresenting the data and science?

  12. @ Frank

    You’ve answered your own question. People skilled in critical thinking don’t believe in the lipid hypothesis, or if they do, they realize that it is an hypothesis and not a fact.

    @ Joel Marcus

    If at least half the people who have a heart attack have low or normal LDL-C (which is the case), how can LDL-C be a “formidable predictor”?

  13. Re Peter Silverman and the Zero Paradox, I’ve often wondered about that contradiction.

    My guess is that maybe fats are okay, OR carbs are okay, but the combination of fats AND carbs is a problem.

    Neither approach seems to be perfect. however. Ornish’s high-carb diet is a disaster for me, with my Type 2 diabetes. And Jimmy Moore has had spectacular weight regain on his low-carb diet. And according to Gary Taubes, some people can’t even just quit eating to lose weight, because Taubes claims that some people’s bodies will retain fat while burning protein.

  14. ” They’ve just taken another grievous wound to their favorite theory and haven’t even got sense enough to know it.”

    They DO have enough sense to know it… I can already hear the sucking sound as their research money dries up when they start singing the wrong tune.

  15. Keep the statin articles coming!

    A friend of mine went for a pre-op physical and found her liver and kidney enzymes elevated. A month of NOT taking statins found all her lab values vastly improved – except LDL, which went up. Not only that, the knee pain for which she was planning surgery also got much better. But because of that pesky LDL, she is back on a statin, this one supposed to be safer. Sigh.

    I keep sending her your posts.

  16. Thanks Doc. This was really fabulously written. Well-organized and more eloquent than ever. Speaking of Obama, it’s this kind of thing that makes the health care plan so terrifying. When statins are free for the citizen, and that money goes straight from taxpayer to pharmaceutical company, virtually every American will be taking Lipitor as if it were Vitamin C. I’m scared!

  17. saw a speech by one of the inventors of lipitor the other day. interestingly enough, he started his own company to work on developing a new drug that would raise HDL levels and leave LDL alone. but lipitor has made him a very rich man.

  18. So much for the language in scientific research reports… Just found this great Calvin and Hobbes strip:

    Calvin: “I realized that the purpose of writing is to inflate weak ideas, obscure poor reasoning, and inhibit clarity. With a little practice, writing can be an intimidating and impenetrable fog! Want to see my book report?”

    Hobbes: “The dynamics of interbeing and monological imperatives in Dick and Jane: A study in psychic transrelational gender modes.”

    Calvin: “Academia, here I come!”

  19. Good post. I think “The Statin Paradox” would be a great title for a NYTimes op-ed, or a book. “Statinator” is catchy but only if you’re already converted. Or better yet — “The Statin Myth,” a la Lierre Kieth. Maybe Gary Taubes can help get it out there. It’s important information. Interestingly, there are other pharmaceutical categories that are similarly counter-productive, which is not surprising given the same instutional biases hold for all classes of pharmaceuticals, and the same flawed FDA approval process.

  20. Thanks for another great post about statins. I have never taken them, and now after reading your blog for the last few months, I never will.

    p.s. My Sous Vide Supreme just shipped. I got the notification email this week. I can’t wait to get it. Big thanks for developing what looks like such a great product! I’ll post my results once I get started cooking with it.

  21. RE: Sous Vide review: Off topic, but it made me laugh when the reviewer said “I looked in vein for a true sous-vide chicken recipe.” I guess he could say that cooking is in his blood!

  22. @Peter Silverman

    I read your comment on the heart scan blog as well. I must caution you. As a physician who performs and interprets both CAC “heart scans” and coronary CTA which actually shows plaque that is not calcified, I can assure you that a zero calcium score absolutely does not prove you have no plaque. Just last week I scanned a patient with a score of only 8 (well below average for his age) who had an enormous burden of non-calcified plaque on CCTA and a 70% stenosis that was causing ischemia with exercise.

    Patients with acute coronary syndrome and zero calcium scores are well documented in the literature.

    The idea that a normal calcium score means zero plaque is total myth. Calcified plaques are in fact more likely to be stable and less likely to kill you acutely,

    If Ornish gets an intravascular ultrasound (IVUS) interpreted by a disinterested cardiologist skilled at their performance and that is negative, then I’ll believe he has no plaque.

    Two subjects with the same calcium score may have completely different plaque burdens, even if on a population basis they are both at relatively low risk.

  23. I should add, the highest calcium score I have seen is over 3000. I know the gentleman well. He was 80 years old at the time of the scan (he had it for screening, not at my facility). It is now 5 years later and he is still alive and well with no cardiac symptoms.

    CAC is an epiphenomenon to the main event of atherosclerosis, probably reflecting vit K status, among other things. It is not the main event.

  24. Here is the question to ask any MD. if lowering ldl reduces risk why has ezetimibe had such a rough time in clinical trails. Actually ezetimibe sort of a medically assured low fat diet should cause a reappraisal of the benefit of a low fat diet- no benefit. But as Santino said in the “Godfather” there is a lot of money in them white powders”

  25. Vince

    Do you have any clinical trial to cite? I’m trying to find something on pubmed but it’s always ezetimibe+statin that is being tested or some theorical paper on how ezetimibe is suppose to work is magic.

    I’m only aware of trials on niacin and clofibrate which are lowering cholesterol but not making any difference on CVD events.


  26. Michael Eades, I’m not entirely sure what you’re harping on about.

    This particular study was designed to study the trend in LDL-levels in a sample of the US population. It is not an outcomes study, i.e. not designed to see whether lowering LDL has resulted in lower cardiovascular mortality and morbidity.

    Any attempt to correlate this trend (based on a sample of roughly 7,000 participants) with national data on the incidence of cardiovascular conditions is wrought with fallacies. This is Epidemiology 101.

    By the way, wouldn’t it be fair that you have a financial conflict of interest here? Lest we forget, you make money off selling supplements and marketing them as an alternative to the current standard-of-care.

    Statins have been shown to decrease cardiovascular events and mortality both in prospective RCTs as well as large retrospective cohort studies. A meta-analysis published in the Lancet in 2005 noted that the incidence of cardiovascular events over a period of 5 years was reduced by about 20% for every mmol/L reduction in LDL-cholesterol. While this does not conclusively implicate LDL-C as having a causative role in CV events, at the very least LDL-C serves as a useful biomarker for statin efficacy. Given that statins have pleiotropic effects, it is possible that the benefits are mediated through different mechanisms than the reduction in LDL-C. But the bottom-line is that the lipid-lowering strategy through statin therapy does have an established benefit as demonstrated in the literature. Of course, the absolute risk reduction in all-cause mortality varies depending on a patient’s risk factors, and statins are not for everybody.

  27. NP, he is harping on about the oversimplified dogma about LDL = Satan that the guys in the video are enthusiastically and condescendingly preaching. He’s also pointing out the negative side of statins, and their ineffectual ability to lower total all-cause mortality, which is the real rub. This perspective needs to be highlighted, as it is often ignored in the wave of “statins to save humanity” propaganda that penetrates every news outlet the world over.

    You bring up good points, but the world is already getting that viewpoint. There is no balance. Eades and many other statin critics serve a valuable role – to keep us from getting totally swept away and blindsided by pharmaceutical company self-promoting information. It is not reliable, and it is packaged in half-truths.

  28. @ NP

    I agree that “statins have been shown to decrease cardiovascular evens and mortality both in prospective RCTs as well as large retrospective cohort studies” but these same RTCs haven’t shown statin use to decrease all-cause mortality, which, in my view, is the most important statistic. And retrospective cohort studies are observational studies and don’t mean diddly. Why spend a lot of money every month, have muscle aches and pains and risk losing your memory simply to trade one risk of dying for another? So if statins haven’t been shown to improve all-cause mortality, then pray tell, how does LDL-C serve “as a useful biomarker for statin efficacy”? I guess it means they’re lowering LDL-C, which no one doubts that they do, but to what purpose?

  29. @ Matt Stone and Dr. Eades:

    I appreciate you taking the time to respond.

    Statins do reduce all-cause mortality. A meta-analysis published in the BMJ by Brugts et al. (2009) showed that for primary prevention in patients with cardiovascular risk factors, all-cause mortality was reduced significantly by 12% (ARR: 0.6%) over an average follow-up period of four years. A meta-analysis published by Wilt et al. (2004) in the Archives of Internal Medicine showed that for secondary prevention, all-cause mortality was reduced by 16% (ARR: 1.8%). This translates to a number needed to treat of 167 for primary prevention, and 56 for secondary prevention to prevent one death from any cause, give or take.

    Whether or not it is worth treating 167 patients without established cardiovascular disease to prevent one death may be debatable (although in my opinion, it is). But I think this is an informed choice that the patient has to make, and any “balanced” discussion on widespread statin use must take this into account. Of course side effects are a concern with any intervention, and have to be considered in the risk-benefit evaluation. Myopathies and other muscle complaints occur in roughly 5% of patients taking statins, and are usually reversible. The 5% figure is usually what is reported in RCTs, but even taking underreporting into consideration, it is important to note that not everybody will experience these side effects while taking statins. Again, the decision to continue statins should be individualized to every patient depending on tolerance and their cardiovascular risk profile. As for memory loss, do you have any data that conclusively links statin use to this side effect and quantifies that risk?

    And I have to take you up on your suggestion that “observational studies…don’t mean diddly”. While I would agree that randomized, interventional studies are usually superior and more rigorous, conducting such studies is not always feasible nor ethical. Observational studies are typically biased, but that does not mean they are without value. For instance, they played an important role in establishing that smoking is linked to lung cancer risk. (The context of your statement is also ironic, given that you are using the results of an observational study to try and show that this somehow reinforces your “Statinator Paradox”. You still have not clarified how you have reached the conclusion that this paradox even exists.)

    The issue of LDL cholesterol is obviously not so simple, as it is just one of many risk factors associated with cardiovascular disease. But there is strong evidence that implicates high LDL cholesterol with elevated risk of CVD; to briefly summarize: (i) observations of elevated cardiovascular risk in patients with familial hypercholesterolemia, compared to the general populace (ii) well established reductions in cardiovascular mortality from statin and fenofibrate therapy (iii) data from large cohort studies like Framingham that establish high LDL-C as a risk factor for CV morbidity. I’d be more than willing to revise these assertions if the data shows otherwise.

  30. Fascinating stuff. But I’m amazed that no one has mentioned that the DENSITY of the LDL-a is the crucial measurement. Or that in virtually all routing testing, LDL isn’t measured, but is calculated. Or that the ratio of LDL to HDL and the ratio of LDL to total cholesterol is more meaningful that the LDL reading alone.

    I quit statins more than two years ago and was forced to find another internist as a result of that and other decisions I made as a result of heeding people like Dr. Eades and Dr. David Williams. I’ve never felt better or had better lab results, and at this point I’m making my own decisions about my health instead of relying on the ubiquitous disciples of mainstream medicine. And my SVS arrived last evening, so we’re as pleased as we can be…

  31. Dr. Eades.

    This reminds of me of something that happened recently. I went with my father to an oncologist to discuss radiation therapy for my father’s prostate cancer. When my father asked him if he had any numbers to show that radiatiion therapy would extend mortality, the doctor said that he couldn’t offer evidence of mortality increase through radiation, but he did guarantee that he could lower my Dad’s PSA through radiation. At that point I realized that the doctor’s goal was to lower PSA (not cancer) just as many want to lower cholesterol. That lowering these things might not be helpful is beside the point.

  32. James Le Fanu, MD ‘THE RISE AND Fall of Modern Medicine’. Pg 105-107.
    ‘In the 1990’s, the same argument was to be repeated, but this time with cholesterol, where again the benefits of treating those with high levels were extrapolated downwards. The notion of the lower the cholesterol, the better prevailed and millions started taking cholesterol-lowering drugs……..(this) has enormously expanded the scope of medicine from treating the sick to finding, in the majority who are well, “illnesses” they do not necessarily have, and treating them at enormous cost.”
    “High” cholesterol is correlated with heart attack and disease. It is ONLY a symptom and the ‘symptom’ is what is ‘treated’ with statins.
    The cause of heart disease and other ‘diseases of civilization’ is consumption of sugar, wheat and man-made, processed vegetable oils. Humans are not adapted to wheat. It’s primarily the proteins and phytates in wheat that are deleterious, more than the carbs, although carbs are NOT an essential nutrient in human nutrition. And the opioid addictive compounds in wheat are well, addictive. The adoption of agriculture 10,000 years ago allowed humans to reproduce at fantastic rates, but we are still not adapted to eating grains. With more people, the more chance for genius to arise. That’s why grains helped us advance. Consumption of grains pushes out more healthful saturated animal fat in the diet. Animal fat enhances the brain and immune system. The body and brains’s FATTY (100 trillion) cell membranes along with the FATTY neuronal axon’s ( there are 100 billion of them) coverings have a combined surface area of SIX football fields. The length of the FATTY covered axons is about 100,000 MILES (4 X around the earth at the equator).
    Brain and immune system: The two most complex and animal FAT dependent systems in the human body. One mechanism of degradation of a grain-based and low-fat diet is via insulin. Insulin (released when carbs are consumed) is the hunger hormone, the aging hormone, the fat storage hormone, and the artery-hardening hormone. The proteins in wheat also add to this tornado of negativity, as if over-secretion of insulin weren’t bad enough. And Lipitor just dissolves the brain and robs the immune system of its A #1 component—CHOLESTEROL. (Cholesterol isn’t technically a fat. It’s a high molecular weight alcohol that’s soluble in fat….and it is ONLY produced in animals). The brain is 50% cholesterol by weight and cholesterol is the precursor of ALL the NEUROTRANSMITTERS. We also need healthy gut flora to thrive (and cogitate well- believe it or not). They’re smaller (1000 trillion of them), but they turnover DAILY and we provide them with all their fatty food and supplies. So go ahead and take statins and eat low-fat. Mother nature will have the last laugh at you.

  33. Here’s a quote from the above comment:

    “High” cholesterol is correlated with heart attack and disease. It is ONLY a symptom and the ‘symptom’ is what is ‘treated’ with statins.

    I disagree with the first part of that statement, and so do lots of people. If high total cholesterol is correlated with heart attacks and coronary artery disease, why do about half of the people who suffer heart attacks have cholesterol within mainstream-prescribed limits? And why do people with cholesterol readings above the “limit” not all have heart attacks? It’s becoming more and more clear that inflammation in the arteries, sometimes exacerbated by stress, causes heart attacks, and that there’s no correlation to cholesterol, a substance that’s required for healthy living and which is crucial to the brain cells, among others. Blood viscosity is the important reading, and that’s not normally ordered by physicians when routine testing is done. It’s one of the advanced blood tests that are not done in most hospital labs, along with lp(a) and a couple of others. And diet, regardless of what’s consumed, has little or no effect on total cholesterol, which is regulated by the liver. Too little cholesterol can result in serious medical problems or even death, and can be a symptom of a stressed liver. Medications that slow the liver’s production of cholesterol also impair some of it’s more than 500 other functions.

    I learned this the hard way.

  34. @ NP

    With all due respect, the Statin meta-analyses you cite are worthless: I quote Malcolm Kendrick, MD:

    “By Malcolm Kendrick, MD

    For a few years now, studies have been concluding that statins not only protect against heart disease, they also protect against a whole host of other diseases, including — naturally — cancer.

    This was always rubbish. It is far more likely that statins promote cancer than protect against it. The only reason people taking statins seemed to have lower rates of cancer is due to the following:

    A: People with higher cholesterol levels have lower rates of cancer.
    B: People with higher cholesterol levels get put on statins.
    C: Ergo, people taking statins will automatically have lower rates of cancer.

    It is important to note that the apparent cancer-protecting effect of statins was found in a number of uncontrolled studies. Basically, people taking statins were found to have lower rates of cancer than people not on statins. And rather than the lower rate of cancer being put down — correctly — to the fact that the people on statins were already less likely to get cancer in the first place, the authors of these studies decided, “It was the statins wot done it….” Trigger a series of headlines hailing statins as “wonder drugs.””

  35. This is a very interesting website and I’m completely sure there is a whole lot about Cholesterol that doctors not only don’t tell you, but don’t look for and don’t even think about. I came to this conclusion from a rather different direction because I have gallstones and there’s nothing like a dose of extreme pain to encourage a bit of reading and careful study.

    What I discovered about gallstones is that a universal treatment for this disease exists, and the treatment is surgery to remove the gall bladder. Sadly, there is no evidence that the gall bladder was ever to blame for the stones, only minimal evidence that removing the gall bladder fixes anything, and the gall bladder is a useful part of the human body, and the entire medical industry has not the slightest interest in discovering what actually causes gallstones (nor do they care why the rate is increasing, because they have their answer and it makes them money).

    A few things are known — enough to sketch together a picture that drags in LDL-C and a whole lot of wilful ignorance too. Cholesterol and bile acids are closely linked. Some cholesterol is converted into bile in the human liver, and some humans seem to produce more than others (genetics? nutrition? stress?). The liver also recycles bile acids in a system something akin to a “conveyor belt” where bile runs into the digestive system (carrying cholesterol with it) partakes in the digestive process and gets picked up again in the small intestine round back to the liver. Bile acids travel into the blood to provide defence against bacteria and probably influence arterial plaques too.

    Sadly, although a lot of good clues are available, the follow up research to really understand this process is being completely ignored. Measurements of blood cholesterol are made every minute, but no one cares about bile acids! It’s an old saying, but you can learn a lot just by looking. We just have to bother to look.

  36. @ Jordi Posthumus

    Thank you for your response, but with all due respect, your comment has little to do with my post nor with the meta-analyses I reference. I never made the claim that statins have a protective effect when it comes to cancer, and the meta-analyses simply confirm that statins do not increase the risk of cancer. Mind you, if randomized controlled trials had shown a protective effect of statins in this regard, Kendrick’s criticism would not apply.

    There are a number of observational studies that have found no correlation between statins and the risk of cancer, just as there are studies which show a protective effect. No regulatory body worth its salt will approve statin use to protect individuals from cancer, and no competent health professional would recommend statins for this use. The media is a different story, however. In general, the quality of science reporting is poor, but I suppose it’s too much to ask journalists to provide an synopsis of other relevant publications when writing about a new study.

  37. Here is an interesting report from the – heartwire in my mail box this morning.
    JUPITER: Primary-prevention statin therapy in women cuts cardiovascular risk in half

    “Orlando, FL – Treating healthy women with low LDL cholesterol but elevated high-sensitivity C-reactive protein (hsCRP) levels with rosuvastatin (Crestor, AstraZeneca) cuts their risk of cardiovascular events in half, according to a new analysis of Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER).”

    The most interesting part of the report was this at the bottom of the page:” JUPITER was supported by AstraZeneca. Ridker reports having received research grant support from AstraZeneca, Merck, Abbott, Roche, and Sanofi-Aventis, and consulting or lecture fees from AstraZeneca, Novartis, Merck, Merck-Schering Plough, Sanofi-Aventis, ISIS, Dade-Behring, and Vascular Biogenics; he is listed as a coinventor on patents held by the Brigham and Women’s Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease, which have been licensed to several entities, including AstraZeneca”

  38. @ Pete Silverman

    Low-carbers, paleos, and plant-based eaters (vegan, mostly vegan, or whatever) are far healthier than the average person because they eat whole foods and avoid sugars and processed carbs. Their scores for any potentially negative aspect of health will likely be better than the averages, which are based on the average person eating an average diet.

    When people ask me what I think about diet, I just tell them to eat whole foods. It’s plain, simple advice that can make a huge difference. Maybe they’ll remember it and I don’t have to get technical because it makes sense anyway.

    Improving diet beyond that is a minefield of research that most people just won’t engage. Of course, if they want more direction, I can give them that. But I’d send them here, to a good vegan site I know of, and to a paleo-diet site. Which won’t give them anything conclusive, of course. But that’s sort of the point. Not examining and engaging different philosophies seems like lunacy to me. (Btw: I have this rule. I feel comfortable eating anything all three sites are okay with. And I won’t touch anything all three sites are against. And when I’m left unsure about something, I moderate until I get more info.)

  39. Dr. Eades,

    If you compare the numbers from 1999 to 2005 as shown in the Table 2 in the paper, it shows that there WAS a significant increase in:

    – coronary heart disease (from 2.8% to 3.7%)
    – strokes (from 2.0% to 2.9%)
    – diabetes (from 7.8% to 10.3%)

    I posted a video showing these numbers in the paper.

    I also included your comments in this video and posted it on YouTube so that more people will become educated about this.

    The link is shown below.

    Larry Hobbs

  40. Dave,

    Do you have a link to the vegan site that you were talking about in your post?
    I would like to check some out and see if they make sence.


  41. great Blog. Reading Tabes GCBC’s. Known as the diet delusion in Aus. Facinating. (I don’t think I’ve ever said that about anything…ever…appart from sarcastic effect.) Thanks for your great insights looking forward to reading more

  42. So, NHANES showed ‘bad’ LDL is going down in the U.S. and thus total cholesterol. Have a look here: in 150,000 white folk in Austria, being in the lowest 25% for cholesterol predicts early death, repeat early death. In WOMEN over age 50, that increased risk equalled the risk of [life long] smoking!!! Why would more people with low cholesterol be good if statistically that means earlier death?

    From here’s some perspective:

    A superb cartoon that NAILS it better than any scientist or MD It’s not how much cholesterol, it’s how clean that particle: has it got enough omega-3, enough CoQ10, vitamin E or carotene-like stuff [carotenoids] or too much tans fats and heat burnt cholesterol or heat damaged polyunsaturates?

  43. So does anybody have a substantive response to NP’s post?
    “Statins do reduce all-cause mortality. A meta-analysis published in the BMJ by Brugts et al. (2009) showed that for primary prevention in patients with cardiovascular risk factors, all-cause mortality was reduced significantly by 12% (ARR: 0.6%) over an average follow-up period of four years. A meta-analysis published by Wilt et al. (2004) in the Archives of Internal Medicine showed that for secondary prevention, all-cause mortality was reduced by 16% (ARR: 1.8%). This translates to a number needed to treat of 167 for primary prevention, and 56 for secondary prevention to prevent one death from any cause, give or take.”

  44. Yesterday I started having chest pains and ended up in the cardiac unit at the local hospital. I opened my tray this morning and low and behold a low fat/low salt “heart healthy” breakfast of six pieces of white toast, a big pile of potatoes, and about two tablespoons of egg beaters.
    Dr. Eades I would be interested to hear what you have to say about calcium scores in a more detailed fashion. My calcium score is 45 but I’m not sure exactly what that means. My HDL’s are 114, LDL’s are 67, triglycerides are 72, overall is 195. Blood pressure is 116/68 and pulse is 65 bpm. The cardiologist here says these are decent scores but I’m worried about the chest pains. I exercise regularly and although I do eat low carb, high protien, I also eat a ton of saturated fat. So with this pain I’m wondering more than ever which direction to move as far as diet. Supposedly a calcium score of 45 puts me in the 90th percentile of males 30-41 years old which sounds pretty ominous.

  45. I guess you mean LDL 114 and HDL 67. People would “die” to have those numbers as per conventional wisdom. How about 1 gram fish oil/day and use canola for omega-3 and make sure you get enough electrolytes, especifically magnesium, both antiarrhythmics.

    Has anyone ever checked your homocysteine level? Its only remedy a fairly high dose multivitamin pill. I have rarely seen heart problems when that number is near 7, near 11 is probably average and above 16 is a stroke / heart attack waiting to happen. That stuff is one genetic factor that OVER TIME causes artery damage but lowering it is no quick fix.

    Statins don’t lower calcification rate either and with your lipid numbers, few conventional doctors would put you on a statin [unless they’re afraid getting sued for not doing so].

    I’m not sure about vitamin D but that also could be a factor but that’s not nearly as clear as is homocysteine.

    One risk of being in a cardiac ward is that you may be surrounded by people making a carreer out of putting stents into arteries, something that all agree does not prevent the next heart attack or make you live longer — if this is done in a planned fashion.

    If the cardiogram was clear and troponin was zip, I’d take a cab out (for better food) but that is your decision after you’ve studied all the charts and discussed all the options. If there was troponin, I’d take it easy for at least a month; that is a sign of heart damage. Something else than heart? Best of luck, E.V., a non-MD

  46. A long long time ago, I think I asked you if there was anything approaching the truth at all to the animal-fat-is-bad-for-you meme that has taken hold of the world. I believe your response was none at all. (I may be mistaking you with somebody else.)

    I have recently been thinking about ways to convert others to my way of nutritional thinking that people will take seriously. In order for this to happen for most people, I think my views have to be stated in a way that doesn’t invoke any cognitive dissonance. So I think the following has to be true of my argument:

    1) it can’t suggest that the conventional wisdom is COMPLETELY wrong
    2) it can’t suggest that conventional wisdom researchers are COMPLETELY incompetent
    3) it can’t make reference to a self-interested cabal of researchers validating each others work, because that makes me sound like I’m suggesting a conspiracy which makes me the loony person
    4) it can’t suggest that the listener is a fool for continuing to believe the conventional wisdom

    I’m wondering if you’d agree with the following, in respect to the facts:

    Early measurements and studies on LDL cholesterol suggested to many researchers that increased LDL cholesterol was linked to heart disease, so they recommended behaviors such as avoiding avoiding animal fat consumption, which is known to increase LDL in many individuals. However, more precise, more recent studies measuring subtypes of LDL strongly suggest that small, dense LDL (typically increased by carbohydrate and most vegetable oil consumption) is a better marker of heart disease risk than total LDL. So earlier recommendations to reduce animal fat consumption and increase carbohydrate and vegetable oil consumption may have been a reasonable recommendations to make based on the earlier studies, but the newer studies suggest that those recommendations actually increase heart attack risk.

    1. Sounds good to me except for the vegetable oil part. I’m not sure that vegetable oils make LDL particles smaller; I think that comes primarily from carbohydrate and lack of fat.

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