Catalyst_apocalypseIt looks like the statinators are sharpening their knives.
Apparently the Catalyst shows from a month or so ago have had an effect and it was one the statinators, who felt they didn’t get equal time, did not like. And I’m sure their life support system, Big Pharma, didn’t enjoy it either.
A few hours ago, a popular Australian online news source published an article claiming that the Catalyst show could end up causing 3000 heart attacks. How did they arrive at this specific number?

The Heart Foundation has made the estimate after a survey it conducted found a third of those taking cholesterol lowering statin medications stopped them or reduced them in the wake of the Catalyst program on ABC.
When extrapolated to the entire population of 2.1 million Australians who take statins the survey found 55,000 people completely stopped taking their pills after the program.

We don’t know the number of subjects the Heart Foundation of Australia (HFA) sampled to arrive at their countrywide estimates, but they extrapolate them not only to estimate the number of people who stopped their statins, but also to the 130,000 who changed their medications by stopping then restarting or reducing their dosage and to the 120,000 people who discussed their statin with their doctor. One presumes a few of those went off the pills as well.
Dr. Norman Swan, the Australian Broadcasting Corporation’s  own medical expert, has publicly announced that “people will die” as the result of the Catalyst show.
The NHF survey estimates that 2-3,000 people will have heart attacks over the next five years if all the patients who discontinued their statins as a result of the show continue to stay off the drugs.
Since each heart attack costs the Australian nationalized health service somewhere in the range of $6,000-$12,000, the total cost could end up being around $33 million. A pretty big chunk, indeed, to be extracting from the publicly financed health system. If it proves out that way.
I did a little calculating on my own and came up with some other interesting figures. Using their figures of just the 55,000 people they estimate will completely quit their statins (we’ll ignore the other couple of hundred thousand, some of whom may have quit the drug and others of whom may have decreased their dosage), we can calculate the savings to the Australian nationalized health system.
Statins are pretty expensive drugs that can, depending upon the kind and dosage taken, cost upwards of $100 per month. But let’s assume the Australian health system can buy at a deep discount and get their statins for a mere $10 per month and calculate the savings from 55,000 people quiting the drugs.
55,000 X 12 months X 5 years X $10 per month = $33 million.
So, it’s a wash at those prices as far as the Australian health system outlay goes.
But according to what I’ve read, Lipitor (atorvastatin), even though it is off patent, still costs Australia’s health service $51.24 per month. Let’s rerun our calculations using that number.
55,000 X 12 months X 5 years X $51.24 = $169,092,000.
So, if the Australian health service were looking at this strictly from a cost savings basis, it would see a savings of $136 million if 55,000 people quit their medicine and 3000 of them have heart attacks.
And that doesn’t include the new cases of diabetes, which the NHF conveniently forgets. The true figure isn’t in yet, but it looks like somewhere in the range of 2 percent of patients who go on Lipitor are going to develop diabetes. (In the US, the lawsuits are already flying. Google: Lipitor lawsuit diabetes, and you’ll see what I mean.)
Let’s look at the stats on that.
55,000 patients who stopped statins X 2 percent who would develop diabetes = 1,100 cases of diabetes the Australian health service won’t have to pay to treat. Assuming the lifetime cost of dealing with diabetes is $8,000 per year (that’s about what it is in the US), that would mean the health service would be saving another $8.8 million per year.
But wait. These people are going to live longer than a year.
Let’s assume they live another 15 years. Not an unreasonable assumption. Then the total cost would be $8.8 million times 15 years or another $132 million, about four times the cost of the number of heart attacks the NHF estimated would occur should 55,000 people decide to quit their statins. We don’t even want to think about the numbers should these people live 20 or 30 more years.
So, if these 55,000 people stay on their statins, the Australian health service is going to be out $301 million ($169 million for the statins plus $132 million for diabetes care).
If the 55,000 people go off the statin as per the NHF estimate, then they estimate 2,000 − 3,000 will have heart attacks in the next five years. Which they say will cost the taxpayers $33 million. But where to they get their numbers?
Is their 2,000 to 3,000 number accurate?
Let’s dig a little deeper.
The NHF estimates that 55,000 people quit their statins. They also figure that one in four of these people had already had a heart attack, which means that 13,750 of the people who quit had had a heart attack and 41,250 had not had a heart attack.
Let’s look first at those who hadn’t had a heart attack.
According to the published data on treatment with statins, 1.6 percent of these 41,250 people will have a heart attack who otherwise wouldn’t had they taken the statin. That calculates to 660 people.
Of the other 13,750 who had previously suffered a heart attack, the data show that 2.6 percent or 358 people would have another heart attack who otherwise would not have had one, had they not quit their statins.
So, according to the data, if 55,000 people really did quit their statins, over the next five years 1,018 of them will have heart attacks who would not have had one had they continued their statins.
What this means is that the Australian health service is paying $169 million dollars to prevent 1,018 heart attacks. Which calculates to $166,011 for each heart attack prevented. Do you think that is a rational preventative health policy? I don’t.
Especially in view of the fact that approximately 10 percent of the 55,000 people will suffer some adverse effects of the statins and two percent of them will develop diabetes.
Forget the other adverse effects, the short term memory loss, the muscle aches and weakness, the liver damage, the rhabdomyolysis, the kidney failure, and all the rest. Just the two percent who get diabetes will end up costing (as per our calculations above) $132 million more. So if you factor that in, the health service is paying almost $300,000 per each heart attack prevented.
But wait, you may be asking. What about the 2,000-3,000 heart attacks the NHF predicted if 55,000 people go off their statins? That’s a lot more than the 1,018 we just calculated. Where did the NHF get its numbers?
Well, Big Pharma doesn’t like to admit it, but people have heart attacks all the time even while taking statins. Taking a statin is no guarantee you won’t have a heart attack, although many people erroneously think it is.
The 2,000-3,000 number includes the number who will have heart attacks despite being on statins, which is kind of disingenuous way to present the statistics.
So why are all these people so hot to discredit this TV show, which simply told people there was another perspective to the statin story? And maybe to discuss it with their doctor.
Remember that number we calculated? The one that showed how much the Australia health service would save if those 55,000 people quit taking their statins? The $169 million?
The Australian health service will save that much. But there is another side to the equation. If the Australian health service saves $169 million, that means someone else doesn’t receive $169 million. Figure out who that is, and you’ll see the rationale for all the consternation.
Cherchez l’argent.
If you’re new to this blog and are wondering what all the fuss is about, here is the link to my post on the Catalyst show on statins.  You can watch the entire show on this link.
And here is the link to part one of the two part Catalyst series on diet and drugs.  The first show is on the notion that maybe cholesterol isn’t really the risk most people think it is.


  1. Great post. I like “cherchez l’argent”. Round my way, the locals pronounce “cherchez la femme” as “cherchez la famma” in a way that could easily be heard as “pharma”.
    ex-rosuvastatin user (2006-2011)

    1. Once you’re in your 70s, numerous studies have shown that anti-hypertensive drugs do more harm than good, even if your blood pressure as high as 220/120 IS THIS TRUE ////>//?//

  2. I know this is nothing to do with this current thread but I wanted to get this to you Dr Eades. I thought, regarding diet you might be interested in this recent study published at “Site Distribution at the Edge of the Palaeolithic World: A Nutritional Niche Approach” which shows that even extremely early, 100,000 to 500,000 years ago, our ancestors had a very healthy diet !

      1. It’s an interesting paper. What I don’t think is mentioned is that a 100,000 years ago was during the last Ice Age. Most of the areas of settlement then are now underwater. So, any conclusions are limited.

  3. Let’s talk about the cost of statins in the USA.
    Walmart has Lovastatin and Pravastatin for $4/month or $10/3 months so 1 year would cost as little as $40/year.
    Now – I do not have prescription drug coverage so I pay out of pocket. I currently take 10mg Atorvastatin/day
    If you go to you will see that Atorvastatin 10mgs is available from Walmart for $19.10/3 months which comes to $74.40/year.
    I’ll be 60 in July – assume I live a long time – say I make it to 95 – assume tthe prices stay the same
    $76.40/year for 35 years = $2,674.

    1. Typo – my bad – Atorvastatin is $19.90/3 months
      So – 1 year = $79.60 and 35 years = $2,786 – a difference of $112.00

      1. I do not consider statins to be poison. I went on a low carb paleo type diet and my lipid panel went to a point I didn’t like – high LDL-C, high LDL-P and high TC. In addition I have a few genetic polymorphisms which lead to high cholesterol (not FH as I’m Apo 3/3. I have the polymorphisms on C825T (Chromosome 12) and on H72Y (Chromosome 16) so I decided , after extensive research, to take a statin drug. I take 200mgs of CoQ-10/day and have not experienced any side effects so far. I have not gone on a low fat diet as I still eat grass fed ground beef (raw), raw goat milk, full fat yogurt and kefir and 1 raw egg yolk per day. I also eat nuts, seeds, fruit, veggies, etc. The major change I made was giving up coconut milk, oils (olive/coconut) and reducing the eggs.
        In 10/12 my lipids were
        TC – 274
        LDL-C (calculated) – 199
        HDL – 69
        Trigs – 31
        ApoB – 104
        LDL-P – 1430
        Small LDL-P – 132
        In 10/13 (after being on 10mg Atotvastatin/day for 3 months)
        TC – 126
        LDL – 71
        ApoB – 64
        HDL – 48
        TG – 36
        non-HDL 79
        Vitamin D3 – 46

        1. “I do not consider statins to be poison. I went on a low carb paleo type diet and my lipid panel went to a point I didn’t like…”
          But Nature is poisoning you with your lipid panels? Gonna outsmart Nature?

            All individuals differ when it comes to the balance between cholesterol production and absorption. Some people synthesize cholesterol more than they absorb, while others absorb more than they synthesize.
            Not so much outsmarting as working with what you’re given.
            Despite their proven efficacy, studies estimate that 25—50% of patients with CVD stop taking their statin medications as directed. Many do so because of statin induced myopathy—the onset of muscle aches, spasms, and pain associated with statin therapy. This condition can be extremely unpleasant and, for some, completely debilitating.
            An association has been established between statin induced myopathy and variations in the SLCO1B1 gene.
            The SLCO1B1 gene encodes for the organic anion transporting polypeptide 1B1 (OATP1B1), an influx transporter produced in the liver that mediates the hepatic uptake and metabolism of statins.
            Inherited variations in the SLCO1B1 gene known as SNPs (single nucleotide polymorphisms) affect the function of this transporter.1 The presence of this variant, especially in homozygotes, results in significantly decreased ability to take up statins, less effectiveness of the statin in lowering LDL-C, higher blood levels after dosing, and an increased risk of myopathy. Studies show that people who have particular inherited variations on the SLCO1B1 gene are four- to 10-times more likely to suffer myopathy as a side effect.
            Also – I assume you know not to eat grapefruit while on statins?

        2. I don’t think we know the answer as to whether a statin has benefit in this sort of case or the cholesterol is abnormal (low carb real food diet). You made the decision with your eyes wide open, which is more than most (almost all?)

          1. Studies have shown negligible benefit for primary prevention. These studies show average effect for a large number of individuals. Since there is biochemical individuality, probably equal numbers of people were harmed as helped.
            The question is are you an individual who would be harmed or helped by the drug? It’s a gamble.

        3. Hi Charles,
          One of the things I see pretty often is physician and sometimes patient fixation on lipid numbers. I noticed that it appears that your statin decreased your HDL significantly. If you look at the plot of HDL over the range of LDL plotted with CHD risk you went from a nearly completely protected, across the board range of LDL verses CHD risk. That is to say that with an HDL of near 80 on the graph the incidence of CHD is quite small regardless of what your LDL is even if it’s very high. Yours was almost 70 and that is/was excellent.
          A Harvard study came out a few years ago that demonstrated the TG/HDL ratio to be a far better indicator for future CHD risk. With ratios in either case under unity you seem to be very well protected. The TG/HDL ratio is more of an indicator or carbohydrate sensitivity which you seem to have licked with your dietary approach.
          In my book I discuss these differences. In my lab recommendations I no longer even recommend a LipoScience study. Rather simply check the Triple Marker which is an HDL, hsCRP and an oxLDL. I think the oxLDL will be the final word on whether you are doing the correct thing and as you know your oxidation status has nothing to do with your lipid numbers per se. Rather it has to do with the amount of inflammation you are generating through lifestyle choices:exercise, proper foods, drugs, excitotoxins, municipal water, etc. I should know I am or was a cardiac patient who has regressed his atherosclerosis over time. (long story)
          I would be much more concerned that your TC is far too low and that you are now at risk for increased all-cause mortality. Once you drop TC below about 140 you start climbing up the left side of the U shaped cholesterol curve where mortality increases for all sorts of unique and different reasons like increases in accidents, homicides, hemorrhagic stroke, cancer, etc. The better spot for TC is about 200.
          If you wish to fixate on numbers you were better off with the higher HDL because HDL is a better indicator than LDL for risk. Furthermore it’s really oxidative stress and inflammation that is at the root of endothelial activation (damage). Therefore make sure you are safe in that direction. I’ll bet you have an hsCRP and I’ll bet it’s probably pretty good to excellent. I say that because I think your diet rocks! Get an oxLDL test and see if indeed you are at a low state of oxidative stress. In the end it’s your oxLDL (it’s at least one real risk factor as opposed to LDL which is harmless) that matters your LDL number doesn’t since it has weak predictive power if at all. Check out my statin blogs at
          Please let me know when you get an oxLDL I think it will help sort things out.

          1. @Chris
            It is generally believed that fully oxidized LDL does not exist in the circulation; blood is rich in antioxidants. In addition, such highly oxidized particles would be rapidly cleared in the liver via scavenger receptors.[49] In contrast, circulating minimally oxidized LDL, in which oxidative modification has not been sufficient to cause changes recognized by scavenger receptors, was demonstrated.[50] Therefore, all assays for ox-LDL presumably detect minimally oxidized LDL. This ox-LDL is only a minor fraction of LDL ranging from 0.001% in healthy controls[51] to approximately 5% in patients with acute coronary events.[44] Since LDL is the substrate for oxidation, concentrations of ox-LDL correlate with LDL concentrations and, in turn, with the cholesterol within LDL. In addition, concentrations of ox-LDL depend on the sensitivity of LDL particles to oxidation; small dense LDLs contain smaller amounts of antioxidants and are, therefore, more prone to oxidation.[52] Figure 4 demonstrates that various mechanisms lead to the oxidation of LDL, indicating that various interventions will be needed to block it efficiently.
            So – it doesn’t look that important or am I wrong?

            Some studies demonstrated that statin treatment reduced concentrations of circulating ox-LDL.[90-94] As yet, it is unclear whether this reduction is independent of cholesterol lowering or reduction of metabolic syndrome components as insulin resistance and whether this antioxidant effect is different for different statins. To our knowledge, there are no large studies of the effect of the PPAR agonists on the oxidation of LDL in relation to their capacity to decrease the severity of metabolic syndrome components.
            Choi S H, Chae A, Miller E et al.: Relationship between biomarkers of oxidized low-density lipoprotein, statin therapy, quantitative coronary angiography, and atheroma: volume observations from the REVERSAL (Reversal of Atherosclerosis with Aggressive Lipid Lowering) study. J. Am. Coll. Cardiol. 52(1),24–32 (2008).
            Ky B, Burke A, Tsimikas S et al.: The influence of pravastatin and atorvastatin on markers of oxidative stress in hypercholesterolemic humans. J. Am. Coll. Cardiol. 51(17),1653–1662 (2008).
            Paniagua JA, Lopez-Miranda J, Perez-Martinez P et al.: Oxidized-LDL levels are changed during short-term serum glucose variations and lowered with statin treatment in early Type 2 diabetes: a study of endothelial function and microalbuminuria. Diabet. Med. 22(12),1647–1656 (2005).
            Shin MJ, Chung N, Lee JH et al.: Effects of simvastatin on plasma antioxidant status and vitamins in hypercholesterolemic patients. Int. J. Cardiol. 118(2),173–177 (2007).
            Tavridou A, Efthimiadis A, Efthimiadis I, Paschalidou H: Antioxidant effects of simvastatin in primary and secondary prevention of coronary heart disease. Eur. J. Clin. Pharmacol. 62(6),485–489 (2006).

          3. Hello,
            This may or may not be important but the article you referred me to is almost 5 years old now. The oxLDL assay that I learned about I think has only been around for about a year or so. I might be wrong. Do a search for the Triple Marker test and you can check if you wish.
            In the blog directly below your response I see you mentioned statins preferentially lowering oxLDL. I reference a study that shows just the opposite in my book.
            Barry Sears in his blog also refers to a study that shows the direct linear, positive correlation between serum oxLDL and CHD risk. So it appears that oxLDL can and does exist in some measurable amount and is of massive clinical importance. Another reason to take CoQ10. No such correlation for native LDL and CHD risk as we all know.
            I do not know if you are wrong or right on this. I don’t know if anyone knows the exact time/place that LDL oxidizes. If you refer to any of the standard latest editions of Cecil’s or Harrison’s neither specifies whether LDL first becomes oxidized then inserts into and under the endothelium only to become further oxidized (completely) or if it needs to become acted on once under the endothelial surface. I believe they skirt the issue because the do not know for sure.
            Regardless LDL is only one of many players in atherosclerosis. In my book I emphasize that it is naive and dangerous to think that whatever you do with or to your LDL completely protects you from heart disease. One must do everything right to prevent this disease. Unfortunately we Americans have many habits that injure our endothelium and some we can’t help like infectious causes. But it’s endothelial injury that is absolutely the key. That’s what I stress.
            I can only speak from my own personal experience after 16 years which I can show very clearly that I am correct. If not (with my initial horrid lipid profile at the time of the heart attack) I would not be around to discuss it. Or be much, much sicker which is not much proof for writing a book on curing your heart disease!
            I just finished scheduling my next three blogs all on Sunday mornings at 9. The last one 2 Sundays from tomorrow goes into some of my labs and my heart scan results.
            That’s of course another thing you could check is a scan. That can be used then to see if what you are doing is helping or hurting you by following your CAC score.
            But don’t fool yourself the ultimate proof is in the clinical outcomes and only major lifestyle changes have ever been shown to truly reverse or prevent heart disease regardless of what the scientists squabble over. That my friend is what my entire 1,000 pages covers.

          4. Charles, you said: “”It is generally believed that fully oxidized LDL does not exist in the circulation; blood is rich in antioxidants. In addition, such highly oxidized particles would be rapidly cleared in the liver via scavenger receptors.[49] ———Figure 4 demonstrates that various mechanisms lead to the oxidation of LDL, indicating that various interventions will be needed to block it efficiently.””——“So – it doesn’t look that important or am I wrong?”
            Yes, you are wrong, oxidized LDL is a very important factor in increasing CHD risk as indicated in the article “The Discovery of LOX-1 (lectin-like oxized LDL receptor). its Ligands and Significance”. 2011, Japan
            “LOX-1 is an endothelial receptor for oxidized low-density lipoprotein (oxLDL), a key molecule in the pathogenesis of atherosclerosis.The basal expression of LOX-1 is low but highly induced under the influence of pro-inflammatory and pro-oxidative stimuli in vascular endothelial cells, smooth muscle cells, macrophages, platelets and cardiomyocytes. Multiple lines of in vitro and in vivo studies have provided compelling evidence that LOX-1 promotes endothelial dysfunction and atherogenesis induced by oxLDL. The roles of LOX-1 in the development of atherosclerosis, however, are not simple as it had been considered. Evidence has been accumulating that LOX-1 recognizes not only oxLDL but other atherogenic lipoproteins, platelets, leukocytes and CRP. As results, LOX-1 not only mediates endothelial dysfunction but contributes to atherosclerotic plaque formation, thrombogenesis, leukocyte infiltration and myocardial infarction, which determine mortality and morbidity from atherosclerosis.”
            While LOX-1 rapidly removes oxidized LDL from circulation, it is not “rapidly cleared by the liver” as stated in your post, but is removed from circulation by the LOX-1 receptors located in caveoli in the vascular endothelium where it emits free radicals thereby causing endothelial dysfunction until such time as the ox-LDL is removed from the endothelium by HDL cholesterol and delivered to the liver for recycling. Obviously the average length of time the ox-LDL spends in the endothelium wreaking havoc depends on the number of actively occupied LOX-1 receptors (ie the level of inflammation) and the amount of circulating HDL available to remove the ox-LDL from the endothelium.
            There are many mechanisms that lead to oxidation of LDL and to increased expression of LOX-1, including excessive intake of linolic acid (n-6 LA), elevated blood glucose levels, high CRP, inflammatory markers such as IL-6, icam-1, rho ROCK, TG and smoking. While studies about the correlation between all of the aforementioned ligands and LOX-1 expression are available, all except the latter factor (smoking) are increased by excessive intake of n-6 LA. Accordingly, the following discussion of LOX-1 ligands is limited to n-6 LA. .
            Linoleic acid: Omega-6 LA appears to be the most pro-inflammatory and atherogenic fatty acid and causes endothelial cell activation and dysfunction that leads to atherosclerosis. It appears that increased intake of LA reduces circulating levels of LDL cholesterol by the action of LOX-1 receptors located in the vascular endothelium in removing oxized LDL from circulation, thereby causing vascular endothelial dysfunction. Because of the ability of LA to reduce LDL cholesterol, government dietary guidelines have advocated substitution of vegetable oil for saturated fat. A Harvard professor famously publicly drank a glass of corn oil to demonstrate his faith in its healing properties of n-6 polyunsaturated fatty acids. It has been estimated that during the past century intake of LA has increased from 2% to 7% of calories. An epidemiological study found a strong correlation between the increased intake of foods high in LA and the increased obesity that has occurred during the past century.
            The study “Linoleic acid increases lectin-like oxidized LDL receptor-1 (LOX-1) expression in human aortic endothelial cells.” outlines some of the mechanisms by which LA increases expression of LOX-1 as follows:
            “Results from in vitro studies suggest that selected fatty acids, and especially linoleic acid (LA) can elicit endothelial dysfunction (ED). Lectin-like oxidized LDL receptor-1 (LOX-1) is the major endothelial receptor for oxidized LDL (oxLDL), and uptake of oxLDL through LOX-1 induces ED. To evaluate whether LA may contribute to the upregulation of endothelial LOX-1, we studied the effect of LA on LOX-1 expression in cultured human aortic endothelial cells (HAECs). Treatment of HAECs with LA increased, in a time- and dose-dependent manner, endothelial LOX-1 protein expression. Pretreatment of HAECs with antioxidants and inhibitors of NADPH oxidase, protein kinase C (PKC), and nuclear factor-kappaB (NF-kappaB) inhibited the stimulatory effect of LA on LOX-1 protein expression. Furthermore, in LA-treated HAECs, increased expression of classic PKC isoforms was observed. LA also led to a significant increase in LOX-1 gene expression and enhanced the binding of nuclear proteins extracted from HAECs to the NF-kappaB regulatory element of the LOX-1 gene promoter. Finally, LA enhanced, through LOX-1, oxLDL uptake by endothelial cells. Overall, these results demonstrate that LA enhances endothelial LOX-1 expression through oxidative stress-sensitive and PKC-dependent pathways. This effect seems to be exerted at the transcriptional level and to involve the activation of NF-kappaB. Upregulation of LOX-1 by LA may contribute to ED”
            Excessive intake of LA increases LOX-1 expression and increases CHD risk by many mechanisms which I won’t get into. Suffice it to say that excessive LA intake increases expression of LOX-1 receptors induced by ox-LDL and thereby greatly increases CHD risk.

          5. Thanks very much for this on LOX-1. I have long been wondering what was the mechanism behind the bad effects of n-6 PUFA.

        4. The most predictive figure for heart disease is triglycerides divided by HDL. In your case, that number actually got worse after you started taking statins.

            Effects of Diet and Exercise on Qualitative and Quantitative Measures of LDL and Its Susceptibility to Oxidation
            Considerable controversy has been caused by the tendency for very-low-fat diets to reduce serum HDL levels. In the United States and other western countries there is an inverse relationship between the risk for atherosclerosis and HDL-cholesterol levels.1 In countries traditionally consuming low-fat, high-complex-carbohydrate diets, this correlation is not found.36 37 In such countries, HDL-cholesterol levels tend to be below the minimal safety standards set by the National Cholesterol Education Program, yet coronary artery disease (CAD) is rare. Research by Brinton et al38 39 suggests that reduction in HDL-cholesterol due to a reduction of fat in the diet is due primarily to a modification in apo A-1 production by the liver and intestines, while differences in HDL between individuals on diets high in fat content appear to be due to an elevated clearance of apo A-1 and HDL particles associated with a reduced ratio of lipoprotein lipase to hepatic lipase.39

  4. I congratulate you on doing the figures. I always reckoned that people are far better off avoiding drugs. Is the medical profession where ‘the drug culture’ begins?

    LDL-C — How Low Should You Go?
    William Virgil Brown, MD
    Professor of Medicine, Emory University School of Medicine, Atlanta, Georgia; Chief of Medicine, Atlanta VA Medical Center, Emory University Hospital, Atlanta, Georgia
    Disclosure: William Virgil Brown, MD, has disclosed that he has received grants for clinical research from AstraZeneca, Kos Pharmaceuticals, Takeda, Eli Lilly, and Abbott. Dr. Brown has also disclosed that he has received grants for educational activities from, and served as an advisor or consultant to, Abbott, AstraZeneca, Pfizer, AtheroGenics, Bayer, Takeda, Eli Lilly, Reliant, Merck, Schering-Plough, sanofi-aventis, Kos Pharmaceuticals, and GlaxoSmithKline
    “Finally, from a totally theoretical argument, the concentrations of LDL in fluid bathing human and other primate cells in culture have been found to completely saturate LDL receptors at approximately 2.5 mg/dL.[43] Even allowing for the relative reduction of LDL in extracellular fluid (estimated from lymph concentrations) to 10% of that in plasma, values well below 50 mg/dL should still indicate that the LDL receptors on extrahepatic cells are saturated and performing maximally under physiologic conditions. Again, this suggests that there should be no intrinsic harm in producing blood plasma concentrations under 50 mg/dL.”
    Nobel lecture, 9 December, 1985
    Department of Molecular Genetics,
    University of Texas Health Science
    Center, Southwestern Medical School, 5323 Harry Hines Blvd. Dallas, Texas,
    When LDL-cholesterol levels are below 100 mg/dl (equivalent to a total plasma cholesterol level of 170 mg/dl), heart attacks are rare. When LDL-cholesterol levels are above 200 mg/dl (equivalent to a total plasma cholesterol level of -280 mg/dl),heart attacks are frequent. Controversy arises over the middle ground, i.e.,individuals with plasma LDL-cholesterol levels between 100 and 200 mg/dl (total plasma cholesterol of 170 to 280mg/dl). This is the, range in which the vast bulk of heart attacks occur. Somewhere within this range there is a threshold value of cholesterol at which heart attacks begin to become more frequent. In this middle ground how much of the heart attack burden is attributable to plasma cholesterol? There is no definitive answer. In addition to cholesterol, heart attacks in this group are aggravated by smoking, hypertension, stress, diabetes mellitus, and poorly understood genetic factors. However, it seems reasonable to propose that plasma cholesterol does have something to do with heart attacks in these subjects, and that the incidence of heart attacks would be reduced if plasma cholesterol could be lowered .
    The LDL receptor studies lend experimental support to the epidemiologists’ suggestion that the levels of plasma cholesterol usually seen’ in Western industrialized societies are inappropriately high (9). This support derives from knowledge of the affinity of the LDL receptor for LDL. The receptor binds LDL optimally when the lipoprotein is present at a cholesterol concentration of 2.5 mg/dl (28). In view of the 10 to 1 gradient between concentrations of LDL in plasma and interstitial fluid, a level of LDL-cholesterol in plasma of 25 mg/dl would be sufficient to nourish body cells with cholesterol (118). This is roughly one-fifth of the level usually seen in Western societies (Fig. 16 and ref.119). 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 (Fig. 16 and ref. 120). 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 (9,119). Second, the LDL level in newborn humans is approximately 30 mg/dl (121), well within the range that seems to be appropriate for receptor binding (Fig. 16). 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 (116)
    Once LDL receptors become saturated, the removal rate of LDL is proportional to the number of receptors. Whenever the number of receptors is reduced, plasma LDL levels must rise. Experiments in animals indicate that the consumption of a high fat diet decreases the number of LDL receptors in the liver (123, 124). We believe that this mechanism operates through feedback suppression as described above. That is, when excess dietary cholesterol accumulates in the liver, the liver responds by decreasing the production of LDL receptors (Fig. 13C). The entry of dietary cholesterol into the liver is mediated by a receptor, termed the chylomicron remnant receptor, whose activity is genetically distinct from the LDL receptor (125). The chylomicron remnant receptor is unaffected by cholesterol accumulation (126), and it causes cholesterol to accumulate to high levels in liver when the diet contains excess fat. The combination of saturation and suppression of hepatic LDL receptors contributes in a major way to the buildup of LDL in plasma when a diet rich in saturated fats and cholesterol is ingested. Insofar as such a diet also may increase production of LDL in the face of a fixed or declining removal capacity, the LDL level would rise even higher If the LDL receptor does limit the removal of LDL from plasma, then maneuvers that increase LDL receptor activity might be effective in individuals who have high plasma LDL-cholesterol levels, but who do not have defective LDL receptor genes. Such therapy seems feasible with the development of HMG CoA reductase inhibitors. However, it is still too early to tell whether such therapy would decrease the incidence of myocardial infarctions in individuals with moderately elevated plasma LDL-cholesterol levels in the range of 100 to 200 mg/dl. There is much circumstantial evidence to expect such improvement (127), but unequivocal data are simply not there. Hopefully, with the availability of powerful receptor-stimulating drugs, the hypothesis should be susceptible to testing in the near future. In considering the role of diet and drugs in treatment of high cholesterol levels, physicians and public health authorities must bear in mind the genetic variability between individuals. This variability exists at three levels: 1) The degree of increase in plasma cholesterol upon ingestion of a high cholesterol diet is variable. Not all people develop hypercholesterolemia. Some people, such as the Pima Indians, maintain low plasma cholesterol levels despite ingestion of a high fat diet (10). 2) Even when the plasma cholesterol level becomes elevated, the propensity for atherosclerosis varies. For example, a substantial proportion of FH heterozygotes (10 to 20%) escape myocardial infarction until the 8th or 9th decade despite pronounced hypercholesterolemia from birth (14). 3) Genetic susceptibility to contributory risk factors is variable. Some people can withstand hypertension and cigarette smoking for decades without developing atherosclerotic complications; others are highly sensitive.

    1. Hello Doctor,
      Perfect example of missing the forest through the trees. It’s like saying flow dynamics improve as we drop hematocrit (to a point as in the heart room on CPB). So let’s say we know better than Nature and bleed everyone down a liter. After all you simply don’t need all those red cells even if natural selection had a say in it over several million years.
      Regardless of my bad analogy I suffered a massive heart attack 16 years ago. At the time I let myself go. I got fat, ate fast food, worked as much as I could, took everyone’s call. My HDL at that time was 23, LDL very high, TC about 275 if I remember correctly, TG about 300.The normal trajectory for me with state of the art cardiology care, as you fully know if you are honest, would have been further escalation of atherosclerosis. In time another MI (even while on a statin as you know) and another intervention followed by yet another “event” perhaps this time a stroke because my lifestyle would have kept me hypertensive. Eventually perhaps developing heart failure from my 20 years of statin use or dementia or some other frightening possibility and that’s it-then I die. Story of the American cardiac patient but not me. I was too smart and stubborn.
      The MI left me with severe angina. At the time I was offered a one vessel bypass to “cure” my chest pain. Having a fellowship in cardiothoracic anesthesia under my belt I was repulsed (and terrified) by the whole idea. I knew the real risks involved. As a consequence I decided that there had to be a better way to cure my angina first and then cure my heart disease. To do that I had to go outside the Box.
      My cardiologist calls me the poster boy for the AHA. The only thing he doesn’t mention is that I NEVER TOOK A STATIN or any other drug considered essential in modern cardiac care. I did it all with a change in diet, exercise, supplements, minerals and vitamins. My goal was to decrease not my LDL but my inflammation and high oxidative state. Lowering my LDL, while ignoring my inflammation and the dozens of ways that increase it, would have been suicide. My whole story is in an upcoming book I hope to have published soon. See
      Hey and guess what? I no longer have any angina and never had another event. That’s 16 years so far. I am a normotensive, lean and mean gym rat now (always was in my distant past before the MI). I run hills, do intervals and I’m happily back using the heavy bag (ten years of martial arts). Furthermore, all of my labs prove I’m doing the correct thing. Plus even more importantly I feel alive and strong not like a feeble, sickly, statinized caricature of myself simply hanging on with erectile dysfunction, anxiety and no vitality. We call that being in a state of wellness. This is something that most of you guys have no clue about I’m sorry to say.
      I made the decision to avoid the misguided AHA type diets as too inflammatory, much too high in carbohydrate. While lowering my cholesterol with a toxic drug, interrupting several key metabolic pathways including decreasing CoQ10, all sex and stress hormones, vit D as well as the overall decrease in what is perhaps the most important molecule in all of human biochemistry-cholesterol, did not seem very smart intuitively. Plus statins hurt so much that I simply said to hell with them. I felt like I was poisoned because I was.
      Now I know I’ll never convince you of anything meaningful as far as how I was able to do this because you’ll probably chalk it up to getting lucky. But riddle me this: if statins are so vital in the management of heart disease how come I’m still alive and have a heart scan with a CAC score of only 42 and an hsCRP that is nearly unmeasurable it’s so low. If I were naive and cavalier and your statins were the real life savers, I really should be dead don’t you think? We can’t both be right.
      Outside of the fact that I think there is overwhelming laboratory evidence that statins are metabolic poisons and that nobody should take them, I feel they place patients into a confident state of ignorance where they feel totally protected from a cardiac event and do nothing toward addressing the true cause of atherosclerosis which is free radical induced oxidative stress and glucotoxicity or inflammation to keep it to one word. This helps explain why statins have never been shown to be helpful in primary prevention and why so many patient continue to infarct with therapeutic LDL levels. I’m just glad I’m not one of them and no thanks to the Doc in the Box who can only offer a pill and doesn’t understand the meaning of wellness.

      1. Hey Chris,
        Congrats on saving your life, your brain, and your body! However, I’m … not quite sure … which “doc” you’re addressing in your greeting. Clearly not Dr Mike, who started this all with his decades-long-and-strong anti-statin stance…. Not Dr Rasmussen, who provides good info in response to Charles. Not Charles who doesn’t identify as a doctor (and has seemingly several old studies to back up his arguments: Charles? are you just not interested in keeping up to date, or are you in fact a doc who has stood on his (old?) med school ‘education’ and not gone beyond it?).
        So, Chris, just whom are you accusing of missing forests?

        1. @Elenor
          If you’re referring to me – no I’m not a doctor – just an informed consumer who has probably read more research on stations – both pro and con – than most, if not all of the people here.
          Unlike the cholesterol deniers – including Dr Eades (who I’m surprised to earn is a climate denier as well – very ant-science I must say) – I read both sides of the argument and do not cherry pick the studies to prove or disprove my point. I look at the preponderance of the evidence and base my decisions on that.

          1. @Jack
            I’ve haven’t been reading too much vegan propaganda – IMHO. I still eat raw meat, full fat raw goat milk, goat milk yogurt./kefir, eggs, etc.
            So – I’m hardly a vegan now and will never become one.
            It’s just that I have a CAC score of 48 (progression from 30 in 12/07) and I’m doing everything to stop and regress this plaque.
            Statins do help

          2. Hey Charles–
            Progression of CAC scores don’t always mean increase in risk. In fact, sometimes it’s just the opposite. According to a recent paper in JAMA, risk is much more a function of area than of calcium. The Agatston score is a combination of the area and the calcium density with much more emphasis put on the density. Often patients on low-carb diets – the only ones I follow, so I can’t speak to other diets – will reduce the area of their plaque, which concentrates the calcium and actually increases their CAC a bit. By using the equations in this paper, you can more accurately determine your real risk based on your CAC score as long as you were provided your area and calcium density along with your score. Here is the appropriate paragraph:

            Thus, to calculate the individual area scores, the volume scores in cubic millimeters were divided by the appropriate slice thickness, 2.5 mm or 3 mm, resulting in the area score in square millimeters. The Agatston score was then divided by the area score and the quotient was the average CAC density score for each participant. The formula was: Agatston score/area score = density score.

            Density scores ranged from 1 to 4, with those in the higher ranges representing much lower risk.
            Hope this helps.

          3. I’m saying check your density to see what’s happening. Find out if your calcium scoring used a 2.5mm or a 3.0mm slice (most use a 3.0mm slice). Once you know whether it’s 2.5 or 3, divide that number into the area score (should be listed on your CAC score printout). Once you divide the slice size into the area, divide the number so obtained into your calcium score. The closer the resultant number is to 4, the lower your risk.
            Since the Agatston scoring equation (which calculates the calcium score) gives enormous emphasis to calcium density, your actual amount of plaque can decrease giving you a higher score because of the relative increase in density. In other words, you could go on a good diet and reduce your plaque area by one unit while increasing your calcium density by 0.7 units. Since the preponderance of your calcium score is derived from the calcium density, your calcium score would go up while your actual plaque volume went down. It’s the soft plaque that’s prone to rupture, so the more dense your plaque is, the lower your risk.

          4. Charles,
            The phrases “cholesterol denier”, “preponderance of evidence” and the ad hominem attack on Dr. Eades come directly from the vegan playbook. As you know, I have been exposed to those discussions. Whether you have adopted a vegan diet or not, the telltale influence on you is quite clear.
            The vegans are motivated by ideology. The health claims they make are a disingenuous tactic for their cultural marxist agenda to force their ideology on the rest of us.
            It is not possible to evaluate the science presented without an understanding of the politics involved. And the language I point out is politically motivated.

          5. @jacklabear
            “The phrases “cholesterol denier”, “preponderance of evidence” and the ad hominem attack on Dr. Eades come directly from the vegan playbook.”
            That is so wrong. For me a cholesterol denier is someone who will not admit the possibility that high LDL-P, high small LDL-P, high non HDL-C contribute to CVD is a denier.
            True or False
            “In animal models, atherosclerosis will not occur in the absence of greatly elevated levels of plasma cholesterol. High levels of plasma cholesterol also appear to be an important contributor to atherosclerosis in humans, although the threshold level that must be exceeded to produce clinically relevant disease appears much lower than that in animal models, possibly because lesion formation occurs over many decades.
            Atherosclerotic clinical events are uncommon among people with lifelong very low plasma cholesterol levels.”

          6. Are you sure you provided the correct numbers?
            If you divide the volume (21) by 3 you get 7. Dividing 7 into your CAC of 48 gives almost 7, which is the highest density I’ve ever seen. Most aren’t over 4. Double check you numbers for me. Is the volume of 21 the total volume? And are the slices 3mm or 2.5mm. Even 2.5mm would give you a density of almost 6.

      2. Dr. Rasmussen, I’m a big fan of Dr. Eades, & am really looking forward to Your upcoming book. I really appreciate the time you have taken to help not only Charles, but the rest of us that have been following this thread & trying to learn/ make the best decisions about statin use. My husband (55) recd. a type 2 diabetes diag. late July, + classic “bad lipid”…profile w/ scary low HDL, Pattern B LDL, high triglycerides… I’m family “researcher”, so he has mostly been following a keto paleo diet, has lost over 40 lbs, (~ 40 to go), & most of his #’s have improved quite dramatically. I anguished over when he should ditch the statin (no heart attacks, but had tia’s ~ 10yrs ago). In Nov. he ditched them w/out telling me for a few weeks. Anyway, he is no longer type 2, & his LDL is now fluffy pattern A. Yay!!! His HDL is still too low though. (37). He rides an indoor bike, Mountain bikes weather permitting (Winter not helping at all! I’m trying to get him to start weight lifting & some HIIT to raise his HDL. We eat plenty of healthy saturated fats, Grass fed meats when possible, Kerrygold butter & cheeses, eggs, w. caught salmon & coconut oil. What do you think we need to focus on the most to raise his HDL?
        I appreciate any insight you have, & thank you for sharing your story of turning your own health around!

    2. Charles, I suggest you read “How Statin Drugs Really Lower Cholesterol: and kill you one cell at a time” to get a better understanding of how stains really work:
      Statins do not lower serum cholesterol by “inhibiting endogenous cholesterol synthesis” as is widely believed. Statins lower cholesterol by disabling existing reductase, and enzyme in cells that makes mevalonate,the source of “cell foods” (isoprenoids), including cholesterol, that are vital to cell function. Cells respond to statin deactivation of their source of nutrients by producing more reductase, and hence more cholesterol, to meet cellular nutritional needs. Simultaneously, cells increase the number of LDL receptors to provide cells a second source of nutrients. The increased LDL receptors move cholesterol from the bloodstream to cells thereby lowering serum cholesterol while stuffing cells with more cholesterol than they can metabolize. When scientists looked inside statin-treated cells they found crystals of excess cholesterol.
      The FDA initially approved statin trials for patients with defective LDL receptors (FH) who have high serum cholesterol. Statins caused a 50% increase in serum LDL cholesterol in patients with 100% defective LDL receptors because the increased cholesterol synthesized by the liver could not be removed from the bloodstream by defective receptors. In patients with 50% defective receptors the increased number of LDL receptors triggered by the statin blockade of mevalonate lowered serum cholesterol. This was the first clue that statins lower serum cholesterol by increasing the number of LDL receptors.
      The statin blockade of mevalonate deprives cells of isoprenoids vital to normal cell functions, including isopentenyl adenine that is required for DNA replication, CoQ10 which is needed for cellular energy production and regeneration of anti-oxidants, and GGPP that is essential for prevention of neuro-degeneration and contractile dysfunction of skeletal muscles. Statins thereby cause many injuries including cognitive dysfunction, blindness, diabetes, muscle wasting, kidney failure, liver failure, heart failure and cancer.
      The Japanese scientist Akira Endo, who won a Nobel prize for his work on statins, was known to occasionally tell the truth when a lie would have served him better. When Endo was asked why he did not take statins for his high cholesterol, he responded with a Japanese proverb: “The indigo dyer wears white trousers.” Endo knows that indigo and statins are both toxic.

      1. I should warn readers that while the authors provide thorough and entertaining documentation of the scientific data used in developing statin drugs, they erroneously state that increased intake of n-6 linoleic acid (n-6 LA), the main component of most vegetable oils, reduces risk of coronary heart disease because it reduces serum cholesterol. While excessive intake of LA may indeed reduce serum cholesterol, it increases risk of coronary heart disease by many mechanisms:
        (1) Excessive intake of LA increases oxidized LA metabolites (OXLAMS) which increases oxidation of LDL cholesterol and causes an increase in endothelial “lectin-like oxidized LDL receptors” (LOX-1) which reduces oxidized (and total) LDL in the bloodstream by moving it to the endothelium where it causes dysfunction and increases risk of CHD. An increase in OXLAMS has been associated with increased atherosclerosis.
        (2) Increased n-6 LA intake results in a decrease in tissue omega-3 ALA, DHA and EPA and abrogates the anti-obesity functions of n-3 fatty acids.(N-3 fatty acids reduce obesity by increasing lipid oxidation in liver and small intestine and decreasing liver de novo lipogenesis (conversion of carbohydrates to lipids)). The resulting increase in obesity, insulin resistanceand leads to diabetes and increased CHD risk.
        (3) N-6 LA is the precursor to n-6 arachidonic acid which is the backbone of n-6 eicosenoids, signalling molecules that regulate many physiological functions. Increased n-6 LA intake results is decreased tissue n-3 fatty acids and results in an excessive n-6 eicosenoids and alters many physiologic functions. To date ten types of eicosenoids have been identified each with many subtypes. Two eicosenoids known to contribute to obesity and increased CHD risk are prostacyclins and endocannabinoids.
        Prostacyclins: In rodents and humans, long-chain fatty acids act at the preadipocyte stage and trigger the formation of adipocytes. Fatty acids as well as eicosanoïds arising in from the metabolism of linoleic acid (LA) play a role as precursor of the eicosenoid prostacyclin, and the adipogenic effect of prostacyclin takes place only at the preadipocyte stage. Pups from mice fed a diet high in LA are 40% heavier one week after weaning than those from mothers fed an n-6 LA and n-3 ALA diet or standard diet The LA-induced enhancement of fat mass is abolished in mice bred to have no prostacyclin receptors demonstrating the critical role of the prostacyclin receptor in excessive adipose tissue development. The effect of LA diet is confined to the gestation/lactation period. Importantly, the weight difference between mice fed LA and LA/LNA diet is maintained at the adult age. Adipocytes once formed exhibit little or no turnover in the body. Therefore the high increase in LA with slight or no change in LNA observed in breast milk and formula milk over the decades may be responsible, at least in part, of the dramatic increase in the prevalence of childhood overweight and obesity
        Endocannabinoids are eicosenoids that activate the same receptors (CB1 and CB2) that are activated by marijuana. Excessive LA intake elevates endocannabinoids which induces obesity by impairing thyroid function causing reduced energy expenditure and increased converstion of carbohydrates to lipids which are preferentially directed to belly fat. Elevated endocannabinoids also also offset the appetite reducing ability of leptin thereby increasing appetite. Like excess marijuana, excess LA intake causes reduced energy expenditure and increased appetite that leads to obesity.
        It has been estimated that during the past century n-6 LA intake has increased from 2% to 7% of calories. An ecological study that examined the correlation increased intake of 273 different food commodities between 1909 and 1999 and the increase in obesity during that time found that only increased intake of foods high in LA (soybean oil, poultry and shortening) were strongly associated with increased obesity. Faulty government dietary guidelines that advocate substituting vegetable fats for animal fats have greatly contributed to increased LA intake.
        It has been found that cholesterol lowering statins increase serum n-6 AA which may partly explain the increased incidence of diabetes associated with statin use.
        In spite of unfortuante erroneous comment about LA, aforementioned book is of value due to the excellent information on statin toxicity which is not available elsewhere

      2. I recently came across a 2012 review by Dr.Uffe Ravnskov of “How Statin Drugs Really Lower Cholesterol and Kill You One Cell At A Time” t
        Dr. Ravnskov was one of the first scientists to criticize the use of cholesterol lowering statins. When the lipid hypothesis came to be promoted strongly in Sweden Ravnskov felt there was an incongruity between the Diet-Heart Idea and scientific literature. He reexamined data from past scientific studies, and came to the conclusion that the scientific foundations of the Diet-Heart Idea were scientifically flawed, with what he characterized as all the “inaccuracies, misinterpretations, exaggerations and misleading quotations in this research area.”[20] His book Kolesterolmyten (“The Cholesterol Myths”) was subsequently published in Sweden in 1991.
        With the popularization of the internet in the late 1990s, Ravnskov saw the opportunity to publicize his conclusion and, in 1997, published selected sections of The Cholesterol Myths on the world wide web. Ravnskov’s website soon became ranked as one of the top ten most popular websites about cholesterol. As a result of this worldwide interest, his book was translated into English and published in the United States as The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol cause Heart Disease in September 2000 by a publishing house established by the head of the Weston A. Price Foundation, Sally Fallon. It was later published in Germany in 2002 under the title Mythos Cholesterin. Die zehn größten Irrtümer (“Cholesterol Myth: The Ten Biggest Errors”).
        “How Statin Drugs Really Lower Cholesterol and Kill You One Cell At A Time” was reviewed by Dr. Uffe Ravnskov from his headquarters in Stockholm, Sweden. Ravnskov said he learned more about the background of the creation Statin Drugs than he knew before. “Scary reading indeed.” Dr. Ravnskov said he didn’t know about Marvin Siperstein and he will start reading Dr. Siperstein’s papers.
        Ravnskov said he was depressed when he learned about Brown and Goldstein´s fraudulent behavior and suggested the Yosephs send a copy of their book to Peter Englund, the secretary of the Nobel Prize committee. “Now I understand why I never got an answer from these guys – I sent them a long kind, letter some years ago to tell them about the many clinical and epidemiological observations that contradicted their hypothesis. Naively I thought that they, being biochemists, didn´t know about them.”
        Dr. Ravnsknow made a few “minor” criticisms of some of the opinions given in the book and asked the author for references on a half dozen statements given. Dr. Ravnskov promised to mention “How Statin Drugs Really Lower Cholesterol” in his next newsletter and also to members of THINCS (The International Network of Cholesterol Skeptics).

  6. Clearly your voice makes a huge difference to pharma, since one of their oft paid public speakers (self described), Gregory Pokrywka MD FACP FNLA NCMP, made an appearance on your blog to launch an attack on your scientific acumen and position on their use.
    It’s a measure of your success.
    So grateful for your consistently accurate, direct and fair assessment of the statin industry and the threat to public health that it poses.

  7. As Malcomb Kendrick said in one of his pieces, “Thank God, he didn’t die of a heart attack!” When the statinators are waxing poetic about the benefits of statins, they never mention the increase in cancers in statin users….

      Areas Covered in This Review
      In this paper, we review evidence on the association between statin use and cancer risk. Specifically, we report on clinical trials and observational studies that measured all cancer or site-specific cancers of the breast, colorectal, lung, prostate, and reproductive organs associated with statin use.
      Take Home Message
      Few strong or consistent associations between statins and cancer incidence overall or for any of the sites reviewed were detected. Data is lacking for any effects of statins on cancer prognosis and secondary prevention; with the exception of consistent evidence that statins are associated with reduced risk of advanced/aggressive prostate cancer. Statins appear safe in relation to cancer risk but any chemopreventive effect in humans remains to be established and should not be recommended outside the context of clinical trials. It is encouraging that numerous trials are on-going. The prospect of reducing the incidence and burden of some of the most prevalent cancers with a safe, affordable, and tolerable medication that already reduces the risk of the leading cause of death, cardiovascular disease, warrants further exploration in clinical trials and observational studies of prognosis and survival.

      1. Charles, The “study” you quote, which was done by the Group Health Research Institute, 1730 Minor Ave, Suite 1600, Seattle, WA 98101, is nonsense. It is evident that it is more stuff bought and paid for by the statin industry.
        Statins are often erroneously called “reductase inhibitors” when in fact they stimulate increased production of reductase which mimics the condition of out-of-control cell cycles in cancer cells that disrupts the mevalonate pathway . Work by Marvin Siperstein found that statins disrupted the mevalonate pathway thereby inducing cancer. Chapter 9 of the aforementioned book “How Statin Drugs Really Lower Cholesterol and Kill You One Cell at a Time” describes the connection between statins and cancer in great detail.

      Background— Although most randomized trials and meta-analyses suggest a slight or no increase in the risk of cancer in statin users, results from observational studies have been conflicting, and some have even suggested a large protective effect of statins on certain cancers. Long-term statin users tend to be healthier, less frail, and more adherent to therapy than nonusers, however. This could explain such apparent “protective” effects.
      Conclusions— These data from a large population of typical older patients who began using statins indicate that it is unlikely that statins confer a clinically important decrease or increase in the risk of colorectal, lung, or breast cancer over the durations studied.

      1. “Long-term statin users tend to be healthier, less frail, and more adherent to therapy than nonusers…”
        Please go to YouTube and watch Tom Naughton’s “Science for Smart People” talk. (Yes, you may indeed already know the *stats* training he provides — please pay attention to the *examples* he uses to explicate the statistical concepts — specifically the Harvard Nurses’ Study.
        In this study, it was determined that the ‘nurses taking estrogen replacement had fewer heart attacks.’ (Observational, so no causation… despite the follow-on massive surge in estrogen scrips being written. {eye roll})
        When clinical studies were done (and Tom describes one), it turned out that the nurses taking estrogen had HIGHER numbers of heart attacks (and strokes) — but their generally more careful health-life styles (less smoking, more exercise and healthy food, etc.) led to more health DESPITE the estrogen replacement!!
        I’m sure you’re not suggesting that somehow the *statins* caused “healthier, less frail, and more adherent”?
        (Are you?)

        1. “Long-term statin users tend to be healthier, less frail, and more adherent to therapy than nonusers…”
          A perfect example of the adherer effect, an effect usually overlooked in studies of any kind of drug.

  8. If 3000 have heart attacks, but another 30,000 *don’t* develop various side effects from statins (or are protected from neurological degeneration by their higher cholesterol) … where’s the net loss??

  9. @Dr Eades
    If people follow your advice and discontinue statins – what will you say if any of them die of a heart attack??

    1. How am I to know that they wouldn’t have died of a heart attack anyway? All I’m doing is stating what the published data on statins show, which most non-medical people (and, sadly, most medical people) don’t know. They can then speak to their own physicians regarding their true risk.

    2. Charles..instead of rabidly cut and posting and asking bizarre rhetorical questions..why not try following the actual story and read what Dr Eades is actually writing.
      If you see any maths or claims that are incorrect..then state it..but so far..this is just hand waving.
      Your obviously out of your depth…. 🙂

    3. What is the likely outcome of discontinuing cholesterol lowering statins?
      The following study by Dr. Peter Langsjoen describes the improvement in health of 50 patients who had suffered adverse side effects from taking statins and who subsequently discontinued statin drugs and took coenzyme Q10 to help recover from the adverse effects of statins: None of them had any heart trouble during the three year followup.
      “Fifty consecutive new cardiology clinic patients who were on statin drug therapy (for an average of 28 months) on their initial visit were evaluated for possible adverse statin effects (myalgia, fatigue, dyspnea, memory loss, and peripheral neuropathy). All patients discontinued statin therapy due to side effects and began supplemental CoQ(10) at an average of 240 mg/day upon initial visit. Patients have been followed for an average of 22 months with 84% of the patients followed now for more than 12 months. The prevalence of patient symptoms on initial visit and on most recent follow-up demonstrated a decrease in fatigue from 84% to 16%, myalgia from 64% to 6%, dyspnea from 58% to 12%, memory loss from 8% to 4% and peripheral neuropathy from 10% to 2%. There were two deaths from lung cancer and one death from aortic stenosis with no strokes or myocardial infarctions. Measurements of heart function either improved or remained stable in the majority of patients. We conclude that statin-related side effects, including statin cardiomyopathy, are far more common than previously published and are reversible with the combination of statin discontinuation and supplemental CoQ(10). We saw no adverse consequences from statin discontinuation.
      PMID: 16873939
      Note that the patients suffering such side effects were most likely older than the average patient and had lower CoQ10 before starting statins. otherwise they would not have suffered such severe side effects from the statins.
      Dr. Langsjoen has one of the few labs in the country, in Tyler Texas, that can accurately determine serum CoQ10 levels. Many years ago Dr. Langsjoen provided me with invaluable assistance regarding my aortic valve problems. At the time Dr. Langsjoen told me that he would not hesitate to prescribe statins to a patient if he thought they would benefit, but went on to say he has yet to meet such a patient.

        1. Free access to to study is not provided so the only information on the study readily available is the abstract which is given in its entirety above. I would think that lipids would have been routinely measured along with more important measures (for old folks) such as ejection fraction.
          I made an unsuccessful effort to see if I could find the entire study on the net. (many times I have found full studies that do not indicate free access on pubmed.) I did find out that the study has been cited by 75 other studies which is a lot of citations.

          1. The full study is available as a pdf download
            Lipids were NOT measured
            A prospective analysis of 328 consecutive new cardiology clinic patients over a two-year period of time between January 2002 and December 2003 identified a subset of 50 patients who were actively taking statin drug therapy at the time of their initial visit. Patients were excluded if they were being seen as a one-time consultation and therefore would not be available for follow-up. Patients who had previously been on statin drug therapy but had stopped the drug prior to their initial visit were also excluded. Furthermore, we excluded patients taking red yeast rice extract even though this over-thecounter product has HMG-CoA reductase inhibitor activity. All patients were evaluated for five possible
            categories of statin adverse effects: myalgia with or without muscle weakness, fatigue, dyspnea, memory loss and peripheral neuropathy. Realizing that all of these symptoms can have many possible causes, we excluded those symptoms with clear non-statin drug etiologies. For example, peripheral neuropathy was excluded as a possible statin adverse effect in all patients with diabetes mellitus or vitamin B12 deficiency. Further, memory loss was excluded in all patients with the diagnosis of Alzheimer’s, Parkinson’s or previous stroke. Myalgia, fatigue and dyspnea were much more difficult to sort out and most of these were included as possible statin adverse effects, but all symptoms had to be chief complaints on initial visit. Echocardiography was performed on initial visit, and on follow-up visits as clinically indicated. All echocardiograms were performed by the same technician on a Toshiba Power Vision with standard measurements of chamber dimensions and left ventricular function. Diastolic function was measured by pulsed wave Doppler of the mitral valve inflow at the leaflet tips from the apical four chamber view. Mitral valve inflow slope (EF slope in m/sec2), and E/A ratio were recorded as indices of diastolic function. All 50 patients presented with one or more statin-related adverse effects as their chief complaint and therefore their statin drug therapywas discontinued upon initial visit and all patients simultaneously began supplemental coenzyme Q10 at an average dose of 240 mg per day. Because of the well documented coenzyme Q10 depleting effect of statin drug therapy, we chose to supplement all of these symptomatic patients with coenzyme Q10 in order to maximize their recovery [4,5]. Patients were then carefully followed in the clinic for an average of 22.4 months (range of 2 to 41 months) with 84% followed now
            for more than 12 months, and 51% followed now for more than 24 months. The average number of follow-up visits per patient was six visits (range of 1 to 13 visits). Eight patients who have not been seen for over 12 months are considered to be now lost to follow-up. Twenty-eight out of the 50 patients had both initial and follow-up echocardiograms for analysis.

          2. @Charles,
            Thanks for posting the methods portion of the study.
            I am sure that lipids were recorded but they were just not deemed pertinent to the study. I have read all of Dr. Langsjoen’s studies on Q10 and have talked to him a number about some of the studies. I know that he routinely measures the coenzyme Q10 levels of his patients in order to adjust the Q10 dosage to maintain a minimum serum level. Cholesterol level is included in the primary Q10 test results.
            As far as I know, the measurement of coenzyme Q10 has not yet been automated so it must be done by a tedious 17 step process developed by the Japanese. Dr. Langsjoen’s lab is one of only a few in the country that can accurately measure Q10.
            In 2006 I realized that I was going to have to get my stenotic tri-cuspid aortic valve replaced. Most aortic valves are bicuspid, but about 1% of men have a tricuspid valve which works ok for many decades but begins starts to crap out when you get into your 60s and 70s. Tricuspid valves are largely genetic and account for about half of aortic valve replacements.
            I began researching Q10 after my wife was badgered into taking statins by her doctor. She took them for three days and then quit as they made her very ill.
            From my studies on Q10 I learned that my heart had to work harder because of the stenotic valve which resulted in increased utilization of Q10 which caused Q10 depletion. I started taking 300 mcg Q10 to try to delay the need for valve replacement. I called up Dr. Langsjoen to get his advice and he suggested I boost Q10 intake to 450. After several weeks on the higher dose I had blood drawn at a local hospital and the sample shipped to Langsjoen’s lab in Texas. The test showed my Q10 level to be 4.5 mcg/ml and cholesterol 5.4mM (208 mg/dl) which Dr L. said was great. The ratio of Q10 to cholesterol, oxidized Q10 and vitamin E were also included in the primary results and many other secondary results were given. The results of an echocardiogram showed significant improvement in heart function after taking the high Q10 dose.
            On the high dose of Q10 my HDL was 110 and my TG was 30. I told Dr. Langsjoen that I thought the high HDL was due to the high dose of Q10but he disagreed.
            in 2007 I got a pig valve to replace the stenotic aortic valve. Thereafter continued taking 150 mcg of Q10. My HDL dropped to about 90. I had the VAP cholesterol test done a couple of years ago which showed a non-atherogenic llipid profile even though my LDL was 136.
            I see no need to get cholesterol levels measured again and I understand why Dr. Langsjoen did not include lipid levels in the report.
            The Q10 you are taking and your relatively young age should protect you against the worst side effects of statins. Since you are taking statins you should consider getting your Q10 level testing to make sure the dosage you are taking is adequate.

    4. Most people taking statins are fooling themselves. They are marketed to lowering cholesterol, but what they really do is SHUT IT OFF, doing real damage to your body. Statins are really good at lowering inflammation – however at what cost? Whatever has been causing your body’s inflammation will not be helped much by artificially lowering it (and being a slave to side affects for life).

  10. very interesting and well done post. My total cholesterol always runs about 230 with an HDL of about 75. My coronary calcium score was 0. I haven’t been pressured to take statins in the past but I suspect that is about to change with the advent of Obamacare (or whatever replacement emerges over the next several years). Your post, however, is a reminder of the big pharma dollars which now drive the medical establishment.
    For me the consequence, I believe, is to stay out of the system. With the new system, becoming a non-compliant patient (refusing to take statins) may result in insurance becoming even more unaffordable. You still need insurance for the big expenses (accidents…).
    So, put the statinators in charge of my health care – no thanks, I don’t think I’ll play.

    1. My husband and I have chosen to stay out of the system at this point in time. When we were “in” the system, the doctors pushed for more appointments, tests and yes, drugs. even though both of us are very healthy individuals. Should we get sick and need a doctor, there are a lot of urgent care facilities around to receive treatment; if one of us was hospitalized, we would be under the care of a hospitalist anyway and not our regular doctor (if we had one).
      Our current system stinks. Guidelines have become required care. Should you decline anything your doctor decrees as necessary, you most likely will be dumped from the practice…
      Wish I had hope for improvement!

  11. Excellent article. The estimate of 2000-3000 heart attacks may based on assumption that many of these 55000 will take again statins after coordinated pressure from media/doctors/big farma/”health” organizations 😉

  12. You need to determine the net lives lost in Australia by adding in the lives saved by allowing the Australian Medical Service to spend that $169 million in other areas or in other prevention programs where lives could actually be saved. The net might actually result in thousands of lives saved by some people discontinuing statins.

  13. Thank you for this:
    “The 2,000-3,000 number includes the number who will have heart attacks despite being on statins, which is kind of disingenuous way to present the statistics.”
    The way the statinators talk (thanks for coining that term, too!) you’d think that statins absolutely prevent anyone who takes them from ever having a heart attack. Not so! A person who has a heart attack on statins couldn’t care less that the statins supposedly decreased his risk of having that heart attack!

  14. Doc you are beautiful! What a way to blast away the statinators with their own pure, indisputable numbers.
    I only wish your article be available in Australia.

  15. I was delighted to find your posts on the Catalyst show (the October 31 post and the current post) on the subject of cholesterol lowering statins. I am going to forward both posts to my cardiologist.
    I have been seeing my cardiologist periodically since I had to get a pacemaker in 2004 (and subsequently a pig valve in 2007) due to a calcified stenotic tricuspid aortic valve.
    During my first visit to the cardiologist when it was mentioned that my cholesterol was somewhat high I made it clear to the doctor that I considered cholesterol lowering statins to be a hoax of sorts similar to the HRT scam that had victimized many women, including my wife, for decades. At the time only a year or two had passed since it was revealed that synthetic progesterone increased CHD and cancer risks rather than decreasing those risks as had been claimed for decades.
    My wife suffered from the adverse effects of HRT for about 15 years. Many other drugs were prescribed to offset the adverse side effects of HRT. When my wife became aware of the fallacy of the propaganda about the “benefits” of HRT around the year 2000, at age 63, she tried to quit the hormones cold turkey but had a bad reaction after fifteen years on the stuff. She then asked a half dozen doctors to prescribe her natural progesterone but they all refused, telling her that if she went off the synthetic hormones she would soon (1) have a heart attack and die or (2) break her hip and die or (3) get breast cancer and die. We then went to a compounding pharmacy and got the name of a doctor who prescribes natural hormones which she took for a while before quitting entirely. Within a couple of years the word got out on the dangers of synthetic hormones and the HRT empire collapsed.
    Around the year 2000 I began reading articles about statins by authors such as Peter Langsjoen, Uffe Ravnskov, Dwayne Graveline and Mary Enig on the THINCS website (The International Network of Cholesterol Skeptics.) so when I first met my cardiologist in 2004 I told him that it was only a matter of time before the word got out on true effects of statins and the whole statin industry collapsed!! Your articles make it clear that the collapse is near!.
    Thank you for your excellent articles!

  16. As a side note, I saw a commercial for a statin this weekend — I think Lipitor but am not sure — where a man has a bobble-head fashioned in his image. When he pushes on its head to make it bob, a disclaimer appears at the bottom of the screen that says the item is not for sale. This implies to me that people have been requesting the item. So, I wonder how long it will be before big pharma will be merchandising for the general public.

  17. Someone brought up Obamacare… I’m wondering if in its future, people who have ‘high cholesterol’ might be *required* to be on statins as a condition of continuing their insurance, because after all we shouldn’t have to insure against “risky behavior”.

    1. I suspect you will not be denied insurance, instead your rates will increase to compensate for your risky behavior i.e. refusal to take the appropriate medications

  18. Today in the UK the main news story is ‘researchers discover eating an apple a day is as effective as taking statins’
    I followed the link to read the original paper (thank you Dr Eades for teaching me that I should always do this!)
    At first I thought ‘bad science’ but when I got to the footnotes I thought more ‘tongue in cheek’. What I think they are actually reporting is that taking nothing in particular for your vascular problems is more effective than taking statins. Am I correct in this?
    The press misreporting again, anyway…

    1. You have interpreted the study correctly. It is kind of tongue in cheek, but makes the point that almost any therapy is equivalent to statin therapy because for most people statin therapy is pretty much worthless.

  19. My wife got a very ominous phone call from my doctor’s office a couple of years ago because they said my cholesterol levels were too high. She could not even remember to tell me what the exact numbers were because she was so upset. They pretty much told her that I needed to get on a statin right away or I was going to be a goner soon for sure. In a panic she flew right down to the pharmacy and picked up the drug and brought it to my work almost in tears begging me to take it right away. Needless to say I was furious that my doctor or his staff had panicked my wife so. When I called to find out what the count was I asked some of the nurses at the hospital where I work if the number I had been given was truly high and needing to elicit such alarm. The nurses told me that the number I was given over the phone was actually equal to the number considered normal a few years back and that the number considered normal had been cut in half during a wave of possibly displaced cholesterol phobia. They told me that it was anybody’s guess as to whether the new number is accurate or not. This got me even more frustrated. But nothing could have prepared me for the side effects of the drug that started occurring the following night. That is when I found out the stating drugs cause psychiatric side effects in some people. I had horrible nightmares and heard sounds in the hallway of our house that weren’t there. It was a terrifying experience. The doctor switched me to another statin and the same thing kept occurring with increased severity and frequency. Of course I discontinued the drug within a week. After two years my numbers continue to be about the same, as well as all the other numbers from my regular physical exams that are still all very good. I am not a perfect specimen but at age 45 I am naturally careful and mindful of my health. I remembered some of the cautions about drugs that you mention in your books. This was a valuable and terrifying lesson learned first hand. Thanks for reading.

    1. Thanks for posting. I’m sure it was a terrifying experience.
      Take a look at my post today to see what your real risk might have been. Probably not all that much to get worked up over.

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