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    Cholesterol Myths by Uffe Ravnskov MD PhD: Myth 7: The Statins — Gift to Mankind (Part 1)

    Posted by .(JavaScript must be enabled to view this email address)
    Wednesday, November 12, 2014 10:14 am Email this article

    “It’s easier to fool people than to convince them they have been fooled.”
    —Mark Twain

    In the late 1980s, the pharmaceutical companies introduced a new type of cholesterol-lowering drug called the “statins.” These drugs inhibit the body’s production of many important substances, one of which is cholesterol.

    Sold as Zocor®, Mevacor®, Pravachol®, Lipitor® and Lescol® these new drugs have received wide acclaim because of their supposed lack of serious side effects and, in particular, because of the substantial cholesterol they can achieve. Whereas the earlier drugs could lower cholesterol by 15-20 percent at most, the statins can lower it by 30-40 percent or more. As of January 2000, the results from the large controlled, randomized and double-blind studies, including more than 30,000 test individual, and numerous angiographic trials have been published. More data will come.

    Most doctors believe that the outcome of these trials is a victory for the cholesterol hypothesis. However, a closer look reveals that the cholesterol lowering effects are unimportant and actually rather a drawback. Furthermore, the benefits are trivial and if present, only apply to certain patient groups. In addition, by process of statistical manipulation, ingenious criteria for selecting the test individuals, and generous limits to what are considered as normal laboratory results, the directors of the trials and the drug companies have succeeded in belittling the side effects and thus presenting the statins as harmless.

    4S—The Scandinavian Simvastatin Survival Study

    In 1994 the results from a large Scandinavian, multi-center trial using simvastatin (Zocor®) were published.[179] These results were noteworthy, indeed. For the first time a trial had succeeded in lowering the risk of both fatal and nonfatal coronary heart disease, and even total mortality. The results were heralded in the British Medical Journal: “Lower patients’ cholesterol now! There is no longer any doubt about the benefit and safety of treating hypercholesterolemia in patients who have had a myocardial infarction.”

    The results of the 4S trial were published in The Lancet on November 19 and presented on the same day at a press conference arranged by the producer of simvastatin and sponsor of the trial, Merck Sharp & Dohme. Present at the conference were the discoverers of the deficient LDL-receptor in people with familial hypercholesterolemia, Nobel Prize winners Joseph Goldstein and Michael Brown who, according to a Merck representative, proclaimed: “This is Christmas Eve!”

    Their excitement is understandable; they must have had many sleepless nights thinking about the many disappointing results from the previous cholesterol-lowering trials. In the vigorous marketing campaign that followed, 4S was heralded as the milestone trial and simvastatin as the missing link.

    The study was performed in cooperation with 94 Scandinavian medical departments and directed by Dr. Terje Pedersen from the cardiology section at Aker Hospital, Norway. The steering committee and monitoring staff also included employees from Merck, and all data from the trial were processed without outside supervision at Merck’s laboratories in the US.

    Altogether 4444 men and women with a previous heart attack were treated, half with simvastatin, half with a placebo. After 5.4 years, 8.5 percent had died from a heart attack in the control group, compared with 5 percent in the treatment group. (Table 8A.) This improvement included men only; the number of women who died from a heart attack was equal in both groups, or to be more correct, a little more women died in the statin group.

    But there were other benefits. The number of nonfatal heart attacks was lowered even more, from 22.6 percent in the control group to 15.9 percent in the simvastatin group, a gain of 6.7 percent. Furthermore, the number of strokes was reduced significantly, from 4.3 percent to 2.7 percent.

    Curiously, in the following, even larger HPS trial[180] the results were only half as good as in 4S although it was the same drug and the same dose that was tested on the same type of participants, and although cholesterol was lowered just as much.

    However, it is the figures from the 4S trial that are used in the marketing of Zocor, and they are expressed as percentages, not as percentage points. More about that in the following.

    CARE, the Cholesterol and Recurrent Events Trial

    A similar study, the CARE trial, conducted by Dr. Franck Sacks and his co-workers from seven American, Canadian and British university hospitals, used pravastatin (Pravachol®) to lower cholesterol, again in patients with a previous heart attack.[181] After five years, 5.7 percent had died from heart disease in the control group, compared to only 4.6 percent in the treatment group. Considering the large number of participants, this result doesn’t seem particularly impressive and, indeed, it was not statistically significant either. In fact, the reduction in heart disease deaths was offset by more deaths from other causes.

    There were other benefits, however. As in the 4S trial, the number of strokes was smaller in the treatment group, and there were also fewer nonfatal heart attacks.

    WOSCOPS, the West of Scotland Coronary Prevention Study

    The two statin trials mentioned above studied the effect on patients who already had heart disease. Is it possible as well to prevent heart disease in healthy individuals whose only “disease” is high cholesterol? This was the question asked by Professor James Shepherd and his team from the University of Glasgow, Scotland.[182] To that end they assigned more than 6,000 middle-aged men with average cholesterol levels to receive either pravastatin (Pravachol®) or a placebo drug in a new trial, called WOSCOPS, the West of Scotland Coronary Prevention Study. Although the effect of that trial was trivial and as well could have been due to chance, no one expressed any reservations about cholesterol lowering in healthy people. If your cholesterol is high it doesn’t matter how healthy you are. Lower your cholesterol!

    AFCAPS/TexCAPS, the Air Force/Texan Coronary Atherosclerosis Prevention Study

    Is it possible to prevent heart attacks in healthy individuals with normal cholesterol? If so, it would mean that all of us would benefit from taking a statin drug, starting at middle age and continuing for the rest of our lives. The economical ramifications are breathtaking, both for the stockholders of the drug companies and, in a less pleasant way, for the directors of health care systems all over the world, which would pay the bill.

    A new statin trial called the Air Force/Texas Coronary Atherosclerosis Prevention Study, or AFCAPS/TexCAPS was organized to answer this question. It was directed by the former president of the American Heart Association Professor Antonio Gotto from Cornell University, New York, and his co-workers from various institutions and hospitals in Texas. Three of the co-workers were employees at Merck & Co., the company whose drug lovastatin (Mevacor®) was tested in this trial. More than 5,000 healthy men and almost 1,000 healthy women with no signs or symptoms of cardiovascular disease were assigned to treatment, as usual half with the drug, half with a placebo.[183]

    After five years 2.4 percent had died in the treatment group, but only 2.3 percent in the control group. But as the trial directors proclaimed, the primary target in this trial was not to lower mortality, but to reduce the number of fatal and nonfatal heart attacks, and by classifying angina as a non-fatal event, the trial was indeed a success on that point.

    LIPID, the Long-term Intervention with Pravastatin in Ischemic Disease study

    Another pravastatin trial named LIPID included patients with previous heart disease with all ranges of cholesterol levels. This is a logical approach because the statins were found to prevent cardiovascular disease whether the cholesterol is high or low, therefore there was no reason to look at people’s cholesterol at all.

    This trial was conducted by Drs. Andrew Tonkin and John Simes at the University of Sydney, Australia, along with a team of 63 other researchers. Three of the co-workers came from the drug company Bristol-Myers Squibb, the sponsor of the trial.[184]

    After six years 14 percent had died in the control group, but only 11 percent in the treatment group. There was also a small effect as regards heart mortality, but these effects were seen in men only. And as mentioned, the benefit was gained, whether their initial cholesterol was high or low, a finding the researchers noted with much satisfaction. Obviously they didn’t realize that this finding was a serious challenge to the very idea about dangerous cholesterol.

    How do you explain that cholesterol lowering is beneficial in people with normal cholesterol if normal cholesterol is not a risk factor? By changing the definition of normal, of course. Today the authorities believe that all of us have too much cholesterol in our blood and, if there are other risk factors present, that this cholesterol should be forced to its knees, even if it is already low.

    Summing up

    First, the statins were almost as effective for women as they were for men. Indeed in the CARE trial the effect was most pronounced for the female sex, although almost all studies have shown that high cholesterol is not a risk factor for women.

    Second, in several of the trials, the effect was independent of age, although almost all studies have found that high cholesterol is not a risk factor in old people.[185]

    Third, patients who had suffered a heart attack were protected even though most studies have shown that high cholesterol is a weak risk factor, if any at all, for those who have already had a heart attack.[186]

    Fourth, the number of strokes was reduced after statin treatment, although all studies have shown that high cholesterol is a weak risk factor for stroke, if any at all.

    Most important, there was no association between the degree of cholesterol lowering and the outcome, the benefit was independent on the degree of cholesterol lowering. Atherosclerosis is allegedly caused by high cholesterol in the blood; the higher cholesterol is, the greater is the risk, and the more we lower cholesterol, it is said, the more benefit will we achieve. The most important proof of such a hypothesis is therefore an association between the degree of cholesterol lowering in the blood and the outcome of the lowering. Such an association is called exposure-response. (A similar term is dose-response, which means that there is an association between the dose of an added factor to a medium, in this case the dose of the drug given to a patient, and the effect of that dose, in this case the outcome of the disease.)

    Presence of exposure-response between degree of cholesterol-lowering and outcome doesn’t prove causality, because the concentration of cholesterol may be secondary to the real cause, but absence of exposure-response definitely disproves it. Curiously, only a few of the clinical trial reports included a calculation of exposure-response.

    From the CARE trial the lack of exposure-response was documented in a separate paper, and the authors’ words left no doubt: “…in a multivariate analysis that included LDL concentration during follow-up, the change of LDL from baseline, expressed either as a percentage or absolute change in concentration, was not found to be significantly related to coronary events.”[187] Put in plain words, benefit was seen whether cholesterol went down very much or only a little.

    Many words were used to clarify this unexpected finding. The most likely explanation, that LDL has nothing to do with cardiovascular disease, wasn’t mentioned, of course.

    The directors of the WOSCOPS trial came to the same conclusion: “… there was no obvious correlation between percent LDL reduction and event rate.” Their conclusion was that the statins must have other beneficial effects.[188]

    It is easy to calculate exposure-response once all the trial data have been recorded and tabulated. I leave it to the reader to speculate why it hasn’t been done in the many clinical trials that followed. But in conflict with these results, many authors claim that the trials did show exposure-response. Their argument is based on an association between the mean degree of cholesterol lowering and the outcome in each trial. But presence of exposure-response demands that individual values are used in the calculation.

    How come the statins are effective for individuals for whom cholesterol s not a risk factor? And how come he effect of the statins does not depend on how much they lower blood cholesterol? If the cholesterol level for these people is not a risk factor for heart disease, how could a lowering of that cholesterol improve their chance of avoiding a heart attack? If the level of our cholesterol is so important, as we have been told for many years, why doesn’t it matter whether we lower it by large or small amounts?

    It is obvious that the statins have other, more beneficial effects than cholesterol reduction, and this was also the conclusion of the WOSCOPS trial directors. Statins lower the risk of individuals for whom cholesterol is not a risk factor and their effect does not depend on how much they lower blood cholesterol.

    When the results from the 4S trial were presented to Swedish doctors, one of the findings was the lack of exposure-response, both for total and LDL-cholesterol. I was present at two of the meetings and pointed out this striking deviation from the cholesterol hypothesis. On both occasions, it was obvious that the speaker had not recognized the implications of this phenomenon. It was not mentioned either in the first report published in The Lancet in 1994. Therefore I sent a manuscript to The Lancet presenting the above arguments and several more. The paper was rejected by the editor Robin Fox with the following words:

    Dear Dr. Ravnskov

    I was not surprised to hear from you about the 4S study. The article gave rise to some useful correspondence, and it is clear that the argument about cholesterol and heart disease is not yet over. We need more data, and I know that the 4S group are already investigating some of the points that you raise. Let us see, for example, whether the benefit is related to initial cholesterol concentration. I am not persuaded that publication of your hypothesis would be helpful to readers at this stage.

    Yours sincerely

    Robin Fox

    The correspondence mentioned in Dr. Fox’s letter indeed produced results. Four years later a new 4S report was published, and in that paper the authors claimed the presence of exposure-response. However, the finding concerned only the first year of the trial.[189] In a letter in Läkartidningen, the Journal of the Swedish Medical Association, I asked one of the authors, Professor Anders G. Olsson, to explain why they had published the exposure-response calculations for the first year, but not for the whole trial, in which, according to the presentations at the meetings in Sweden, there was no exposure-response. Olsson answered with the following words: “Anyone obsessed by a particular idea is able to draw cocksure conclusions from selected subgroup analyses.”

    I still wonder to whom Olsson referred.

    There is strong evidence for alternative, so-called pleiotropic effects of the statins, which I pointed out in my rejected manuscript and also in a subsequent letter to The Lancet,[190] and the following year other researchers also published similar ideas.[191]

    The statins inhibit the body’s production of a substance called mevalonate, which is an early precursor to cholesterol, but also to many other substances with biological importance. The way the statins interfere in mevalonate metabolism is therefore complex and difficult to predict, like guessing what will happen if a hammer is thrown into a complicated machine. It is possible to draw a few conclusions, however.

    Reduced amounts of mevalonate may explain why statin treatment has anti-inflammatory effects,[192] makes smooth muscle cells less active[193] and platelets less inclined to produce thromboxane.[194] One of the first steps in the process of atherosclerosis is the growth and migration of smooth muscle cells inside the artery walls, and thromboxane is a substance that is necessary for blood clotting. By blocking the function of smooth muscle cells and platelets, statin treatment may provide benefit for cardiovascular disease by at least two mechanisms, both of which are independent of cholesterol levels.

    The protective effects of simvastatin were demonstrated in heart transplantation studies in rats.[195] Normally, the function of transplanted hearts gradually deteriorates because the coronary vessels are narrowed by an increased growth of smooth muscle cells in the vascular walls. This condition is called graft vessel disease, a condition with many similarities to early atherosclerosis. However, rats that received simvastatin had considerably less graft vessel disease than control rats that did not receive simvastatin, and this was not due to cholesterol reduction because simvastatin does not lower cholesterol in rats. In fact, LDL-cholesterol was highest in the rats receiving simvastatin.

    In another experiment a flexible collar was placed around an artery in rabbits.[196] After two weeks the arteries with collars became narrow, but less so if the rabbits had received simvastatin. Again, the effect had no relation to the rabbits’s cholesterol levels.

    Thus, the statins in some way protect against cardiovascular disease, but their effect is not due to cholesterol reduction. The proponents of the cholesterol hypothesis have simply had incredible luck in finding a substance that prevents cardiovascular disease and at the same time lowers cholesterol. The question is, however, whether the benefits would have been even better if the statins didn’t lower cholesterol.

    But why bother about mechanisms? Isn’t it wonderful that the statins work? Shouldn’t we all take statins?

    The costs

    To answer that question it is necessary to look at the figures from the trials. Take a look at the figures for “number of heart disease deaths, relative risk reduction,” in Table 7A. You will find that coronary mortality in these trials was lowered between 19 percent and 41 percent, most in the 4S trial and least in the CARE trial. These are the so-called relative risk figures that are used by the trial directors and by the drug companies in their ads. But let us also look at the absolute figures, the “absolute risk reduction,” on the next line. Here you will find that death from a heart attack was prevented in only a small percentage of the treated individuals. This figure was highest in the trials that included patients with heart disease, whereas it was a trivial 0.12 percent in the AFCAPS/TexCAPS trial, which included healthy individuals with normal cholesterol.


    Table 7A. Summary of the outcome of the first six statin trials.

    Type of participantsHealthy people with high cholesterolPatients wit heart disease and high cholesterolHealthy people with high cholesterol
    Total number of death
    Drug/control group; numbers?182/256106/135
    Relative risk reduction; percent+150-29-21
    Absolute risk reduction;percent+0.3-3.3-0.9
    Statistical significance?***NS
    Number of heart death
    Drug/control group; numbers?111/18938/52
    Relative risk reduction; percent?-41-27
    Absolute risk reduction; percent?-3.5-0.42
    Statistical significance?***NS
    Type of participantsPatients with heart disease and normal cholesterolHealthy people with normal cholesterolPatients with heart disease and all levels of cholesterol
    Total number of death   
    Drug/control group; numbers180/19680/77498/633
    Relative risk reduction; percent-8+3.9-21
    Absolute risk reduction; percent-0.77+0.09-3
    Statistical significanceNSNS***
    Number of heart death
    Drug/control group; numbers180/19680/77498/633
    Relative risk reduction; percent-8+3.9-21
    Absolute risk reduction; percent-0.77+0.09-3
    Statistical significanceNSNS***
    Number of heart death
    Drug/control group; numbers96/11911/15287/373
    Relative risk reduction; percent-19-27-23
    Absolute risk reduction; percent-1.1-0.12-1.9
    Statistical significanceNSNS***
    Table 7C. Results from the first six statin trials.
    NS: Not statistically significant.    * p<0.05 ** P<0.01 *** p<0.001

    Put another way, the chance of not dying from a heart attack over four to six years for a patient with heart disease and high cholesterol is about 92 percent without treatment, and increases to 93 or 94 percent if he takes a statin tablet every day.

    For healthy individuals, the figures are even less impressive. In the WOSCOPS trial, for instance, the chance for a healthy man with high cholesterol of not dying from a heart attack during the five years of the study was 98.4 percent without treatment and 98.8 with treatment. In the AFCAPS/TexCAPS trial, the chance of surviving was 99.55 percent without treatment and 99.67 with treatment. Most likely, no effect was seen at all because such small differences may just as well be caused by chance.

    Let us compare these figures with another kind of treatment, for instance, treatment of urinary tract infections. Nine out of ten women with a urinary tract infection will recover immediately if treated with an appropriate antibiotic for a few days, at the cost of a few dollars. But in the 4S trial, for instance, they treated 28 patients for five years to prevent one fatal heart attack; in the other secondary prevention trials, they treated at least twice as many to achieve the same result. So, while one of the patients benefited from the treatment, the others took the drug in vain because they would have survived anyway.

    The costs for the drug alone amounts to about $150,000 per saved life, but that was in 1994, the year for the publication of the first statin trial; to-day it is much cheaper. In the trials, all expenses are paid by the drug companies, but in real life, the patient or society must pay, not only for the costs of the drug but also for the doctors’ fees, laboratory analyses and loss of income during the doctor visits. And to prevent one fatal heart attack in healthy people, if it is possible at all, 235 individuals with high cholesterol and 826 individuals with normal cholesterol have to consume a statin drug for four to five years.

    Of course, there may be other gains. Not only did statin treatment prevent coronary death, it also prevented more than twice as many nonfatal heart attacks. We should also subtract the costs for hospital care and other treatments for the patients whose heart attacks we prevent, not to mention the grief and pain associated with the loss of wives or husbands or close friends. In the most optimistic calculations, the costs to save one year of life in patients with heart disease have been estimated to be about $10,000; much more for healthy individuals.

    This may not sound unreasonable. Isn’t a human life worth $10,000 or more?

    The implication of such reasoning is that in order to add a few more years of life for a few people, more than half of mankind should take statin drugs every day from an early age to the end of life. It is easy to calculate that the costs for such treatment would consume most of any government’s health budget. And if this kind of money is spent to prolong the life of a few healthy individuals with statin treatment, what will remain for the care of those who really need it? Shouldn’t health care be given primarily to the sick and the crippled?

    But what is even worse, those who recommend statin treatment for healthy people ignore the fact that the treatment may produce disease instead of preventing it.

    The side effects

    Drugs that interfere with normal bodily functions usually have unexpected and unintended effects and so is the case with the statins. According to the drug producers and the trial directors, adverse effects from statin treatment are rare and mild, as indeed they should be, because they are aimed at life-long treatment for millions and millions of patients and healthy people. And the drug companies are of course eager to tell us that they are harmless considering the huge income they have already generated. According to Marcia Angell, former editor-in-chief of The New England Journal of Medicine, the combined profit for the ten drug companies on the magazine Fortune’s list of the world’s 500 most profitable companies was higher than the profit of all the other 490 put together.[197] And the statins are by far the most prescribed drugs today. In 2002, for instance, the income to Pfizer for atorvastatin was $9 billion in the US alone. Evidently, as Dr. Angell says, the drug companies’ aim is “to load the dice to make sure their drugs look good.” And they are clever enough to do so.

    Myopathy and rhabdomyolysis

    Statins block an enzyme called hydroxymethylglutaryl coenzyme A reductase, an enzyme that is necessary to produce mevalonate, and mevalonate is the building block not only for cholesterol, but also for a substance called coenzyme Q10, or simply Q10. This substance is located to the mitochondria of our cells, and the mitochondria is the cell’s power plant. No energy is produced without this vital molecule and its importance is particularly great where energy is needed the most, in the muscle cells. And muscle complaints are also the most frequently reported side effect from statin treatment.

    Authors of the statin trial reports claim that muscle complaints, or myopathy, occur in less than 1 percent of patients, but this is with all certainty an underestimation. Other authors, independent of the drug companies, have found much higher frequencies. Thus, a research group lead by Helmut Sinzinger at the University of Vienna found that muscular side effects are seen in about 25% in patients who do regular exercise. They also studied this problem in 22 professional athletes with familial hypercholesterolemia who were treated with various statins. Sixteen, or three out of four, discontinued the treatment because of muscle side effects.[198] Competitive athletes may be more sensitive to muscle pain and muscle weakness than the rest of us, but even mild symptoms may have a deleterious effect on elderly people who already have muscular weakness. And considering that the best, the cheapest and the least risky way to prevent heart disease is regular exercise, muscular problems may directly counteract any possible benefit achieved by statin treatment.

    Now compare these figures with those given in table 6A. Whereas at least 20 percent suffered from muscular problems, only a few percent gained benefit from statin treatment.

    When muscles are damaged, the concentration of an enzyme called creatine kinase, or CK, becomes elevated in the blood. Elevated CK is thus an early sign of muscle damage, both of the skeletal muscles and the heart. We are told that elevated CK is seen in less than one percent of patients treated with statins as well. But trial directors insist on a CK elevation ten times higher than the normal upper limit and taken at two successive determinations before they call it elevated.

    Similarly, liver damage, another side effect, is only reported if the liver enzymes in the blood are more than three times higher than the normal upper limit, and again, only if it has been reported twice.

    I have never heard or read about anyone questioning this practice. No one seems to be asking what happens to the liver after ten or twenty years of statin treatment in those whose liver enzymes are only 2.5 times higher. And what happens to the muscles of those whose CK is only nine times higher?

    The habit of diagnosing muscle damage only if CK is elevated, whether just a little or quite a lot, is also questionable, because microscopic examinations of muscle tissue from statin-treated patients have shown signs of damage in patients with a normal CK.[199] And even patients on statin treatment, but without muscular symptoms, may be damaged. In a study of muscle tissue using electron microscopy, the structural integrity of skeletal muscle fibres was compromised in 10 of 14 statin-treated patients without any subjective complaints, but in only one of eight control individuals.[200]

    In rare cases, myopathy progresses to the destruction of muscle tissue, a condition called rhabdomyolysis. Large amounts of a muscle protein called myoglobin are liberated into the blood, and too much myoglobin in the blood clogs the kidneys leading to renal failure. A few years after the introduction of Bayer’s statin drug Baycol, fifty patients receiving Baycol were reported to have died from renal failure, and Bayer was therefore forced to withdraw the drug from the market. According to a more recent report from Bayer, more than 100 patients had died from kidney failure. The number of patients who needed dialysis or a kidney transplant as a result of Baycol treatment is unknown. This number must be much higher because to-day treatment of end-stage renal failure is highly effective, in particular in young and middle-age people.

    Rhabdomyolysis is seen after treatment with other statins also, but less frequently. In a recent review of statin side effects the authors found 4.4 cases of rhabdomyolysis per 100 000 patient years after pravastatin, simvastatin and atorvastatin treatment. But there is obviously something wrong with such figures. In the TNT trial (see later), where statin doses up to eight times higher than normal were used, five non-fatal cases of rhabdomyolysis were reported, four of them during the treatment period. However, the authors claimed, that these cases had nothing to do with the treatment because they were not dose-dependent.

    But if the four cases observed in the TNT trial were not due to treatment, and if the figure for rhabdomyolysis mentioned above is true, it means that rhabdomyolysis should be twice as common in untreated people as in those treated with statins. This is obviously not true. Rhabdomyolysis is rarely seen spontaneously; it always occurs secondarily to something else, for instance severe muscle injuries as a result of arterial occlusion or deep venous thrombosis in the legs, or to exposure to toxic chemicals or drugs. The odds are that arterial thrombosis may have been the cause in one of the cases. But even so it is highly unlikely that none of the cases were associated with statin treatment. Obviously, trial directors try to cover up the truth about statin side effects. And this is only part of the evidence.

    Heart failure

    The heart is also a muscle and therefore should be affected by a decrease in Q10. As early as 1990, the biochemist Karl Folkers, who first described the molecular structure of Q10, reported that lovastatin lowered the concentration of Q10. What he also found was that the function of the heart went downhill whereas Q10 treatment was able to improve it.[201] Several recent trials have confirmed the beneficial effect of Q10 treatment in patients with heart failure.[202]

    Heart failure is not reported as a side effect of statin treatment according to the trial reports, probably because patients with heart failure are routinely excluded from statin trials, but also because heart failure may be seen as the result of the primary disease rather than an adverse effect. This is most likely what the practicing doctor will think as well, because heart failure is not mentioned as a potential side effect on the drug labels.

    Brain problems

    Apart from the adrenal glands, the highest cholesterol concentration is present in the brain. The brain cells themselves produce practically all of this cholesterol because in the brain, little or no LDL-cholesterol is taken up from the blood. The rate of cholesterol synthesis is extremely high in the central nervous system of the fetus and the newborn, probably explaining the severe malformations and dysfunctions of the brain seen in children with Smith-Lemli-Opitz syndrome, an inborn error of cholesterol metabolism that leads to extremely low cholesterol values. Cholesterol is used as a component in the membranes of the brain cells and the nerve fibres and is also vital for proper function of the synapses, the connections between the nerve cells. It is therefore not too farfetched to assume that low cholesterol levels may adversely affect brain function in normal people. Indeed, we have much evidence to support this idea.

    In several of the trials a larger number of the treated individuals died from violence or suicide. In none of them was the difference statistically significant, but all studies pointed in the same direction. Most diet-heart proponents belittle this problem. It must be coincidental, they say. It is out of the question to conclude that lowering cholesterol makes people more likely to die from violence or suicide.

    Matthew Muldoon and his team from the University of Pittsburgh, Pennsylvania, were the first to point out this phenomenon.[203] Their conclusion was that if all the trial results were added up in a meta-analysis, the increased number who died from violence and suicide was, in fact, statistically significant. Fewer died from a heart attack, but more from violent and sudden deaths. The authors also stressed that low blood cholesterol levels are seen more often in criminals, in people with diagnoses of violent or aggressive-conduct disorders, in homicidal offenders with histories of violence and suicide attempts related to alcohol, and in people with poorly internalized social norms and low self-control.

    In a comment on the paper, David Horrobin, the editor of Medical Hypotheses, wrote that the most serious consequence of cholesterol-lowering measures is invisible. If low cholesterol levels cause violence and depression, then intervention to reduce cholesterol on a large scale could lead to a general shift to more violent patterns of behavior. Most of this increased violence would not result in death but in more aggression at work and in the family, more child abuse, more wife-beating and generally more unhappiness. Such events are not recorded in the trials—no one asks about them—and they are therefore never detected.[204]

    In other words, we are told about the number surviving a heart attack, but not about the number surviving violence or suicide attempts.

    The conclusions of Muldoon and co-workers were strengthened by a large investigation in Sweden by Dr. Gunnar Lindberg and his team. They measured cholesterol in more than 50,000 men and women and kept track of them for 20 years. During the first six years, five times more had committed suicide among those with low cholesterol compared with those whose cholesterol was high.[205]

    The increased risk of suicide disappeared with time. The authors therefore concluded that the increased risk may be associated with a concentration of cholesterol below a subject’s habitual value, which means that the risk of suicide is greater if low cholesterol is induced by diet or drugs.

    Several others have confirmed the association between low cholesterol and depression, suicide and suicidal attempts.[206] Not unexpectedly, relapse in cocaine addiction is also seen more often in people with low cholesterol,[207] and cholesterol levels in monkeys, dogs, and human beings with a violent behavior patterns fall most often in the lower end of the scale.[208]

    Beatrice Golomb, a professor of medicine at the University of California in San Diego, has devoted much of her research on the side effects of statins and she is today the most knowledgeable researcher in this area. In a meticulous analysis of all studies published since 1965 that looked at the association between low or lowered cholesterol levels and violence, she concluded that the association is causal, and that the risk of creating violent behavior should be taken into consideration before doctors advise their patients cholesterol lowering measures.[209] Together with her co-workers she reported about patients with severe irritability and short temper on statin treatment. All of them recovered after discontinuation. A strong argument for a causal role of the statin treatment is that re-challenge with the drug in four of the patients led to reappearance of their anti-social behavior.[210]

    There is no medical term for irritability and shortness of temper, so therefore the statin trials do not record these changes in behavior. As far as the trial directors are concerned, these effects are not on their radar screen. But they are in full view of the family members and friends who must cope with the personality changes in the patient taking statins, as well as hugely present with the patients themselves, whose golden years may suddenly become overcast with a bleak and grumpy outlook on world… all for the presumed benefit of adding a few months of life to the human carcass.

    Progressive dementia in two patients on atorvastatin was described by Dr. Deborah King at the University of Mississippi. After discontinuation of the drug a dramatic improvement was observed in both patients.[211]

    Leslie Wagstaff, and his team at Duke University searched the FDA’s MedWatch surveillance system for reports of statin-associated memory loss and found 60 cases. The symptoms varied between short-term memory loss, and total amnesia. Usually the symptoms appeared after several months of treatment and disappeared after its withdrawal.[212]

    The influence of cholesterol on memory was studied in hundreds of women by Professor V. W. Henderson and his team at the University of Arkansas. They found that LDL-cholesterol, but no other lipids, was strongly associated with the memory score, just as was the case in Professor Muldoon’s study. Women with high cholesterol scored better than women with medium cholesterol, and women with medium cholesterol scored better than women with low cholesterol. They also compared the score with changes in LDL-cholesterol levels over several years and found that women whose cholesterol increased had a better score than women whose cholesterol went down.[213]

    Memory loss, or amnesia is a common and entertaining theme in the movies. In real life it is very rare, at least before the statins were introduced. One of the victims of this scary condition was Dr. Duane Graveline, astronaut, aerospace medical researcher, flight surgeon and family doctor. In his book Lipitor, Thief of Memory, Graveline described how he himself became a victim of temporary but total memory loss.

    Six weeks after his annual astronaut physical, where he had been prescribed Lipitor because of high cholesterol, he was found by his wife aimlessly walking around close to their home. He didn’t recognize her and refused to go into their house, and it took her much time and persuasion before he, utterly reluctantly, got into their car so they could go to their family doctor. He was finally examined by a neurologist who, after a thorough examination couldn’t find anything wrong except for the amnesia. No recommendations were given and shortly after the examination he felt completely normal. Eventually, however, Graveline began suspecting that the cause of the amnesia might have been his treatment with Lipitor and he therefore stopped taking it.

    At the next physical Dr. Graveline was again prescribed Lipitor. Neither the NASA doctors, nor any of the many doctors or pharmacists whom he had consulted, had ever heard about this side effect, so he followed their advice. Six weeks later he experienced a second episode of amnesia that lasted for twelve hours. This time he couldn’t recall anything that had happened after high school. His years on college, his training at medical school, his time as a USAF flight surgeon, his marriage and his four children, his selection by NASA as a scientist astronaut, his twenty years as a family doctor, his busy retirement and his eight books, all of it had disappeared, and also all that he had learned. Afterwards he realized that he would not even have been able to treat a common cold.

    Again, everyone denied any possibility of a Lipitor association. But this time Dr. Graveline himself was convinced that the drug was the villain. He wrote a letter about his experience that was published in the nationally syndicated column, The People’s Pharmacy.

    Graveline was referred to a statin drug study at UCSD College of Medicine, where the principal investigator, Dr. Beatrice Golomb told him that she knew of several similar cases, and after publication of his letter, hundreds of distraught patients and relatives and even a few doctors contacted him. They told about a full array of cognitive side effects, from amnesia and severe memory loss to confusion and disorientation, and all of them were associated with statin treatment.

    Similar stories are still reported to and filed by the Federal Drug Administration. However, to date the agency has taken no action—not even issued a warning. “The subject is still being reviewed,” was their most recent response according to Dr. Graveline, if they bothered to reply at all.

    Anyone who has been prescribed a statin drug is urged to read his book and its follow-up, Statin Drugs Side Effects and The Misguided War on Cholesterol, or at least go to his website, where he summarizes what he has learned from thousands of victims who have contacted him after the publication of his first book. Here are his words about amnesia:

    “For every reported case of transient global amnesia there are hundreds of case reports of impaired memory, disorientation and confusion among an older group of patients that rarely, if ever, get mentioned. All too frequently, this group is willing to accept old age, ‘senior moments’ or incipient senility as the cause, particularly when their physicians are also ignorant about this side effect.”

    Meanwhile, pilots taking statins still fly planes, truck drivers taking statins still drive trucks and parents and grandparents taking statins still drive their children and grandchildren in cars. Is anyone safe with such a large proportion of the population on statins?

    Peripheral polyneuropathy

    If low cholesterol is bad for the brain, it is reasonable to assume that it is bad for the peripheral nerves also. A reasonable guess and, unfortunately, it seems to be true. Damage to the peripheral nerves is called polyneuropathy. This is a most disturbing and painful condition that starts in the feet and legs and may spread to other parts of the body. Pain, burning, tingling and even total loss of sensation are common symptoms. Polyneuropathy may lead to muscular weakness and difficulty walking as well.

    In Denmark all residents have a civil registration number that is used in discharge prescription registries, so that it is possible to find all residents with a particular disorder and find out which drugs they have been taking. In one of Denmark’s counties with a population of 465,000, Dr. David Gaist and his team at Odense University Hospital asked all patients who had polyneuropathy of unknown cause to see how many were on statin treatment compared with the general population in the county. They calculated that the risk for definite polyneuropathy was 16 times higher for statin users than for non-users, and even higher for those who had used statins for more than two years.[214]

    The authors stressed that the frequency of polyneuropathy was very small, but they also pointed out that it increased over time. The question is, of course, how many statin-treated individuals may have polyneuropathy after 20 or 30 years of treatment? Nobody knows. The problem is particularly serious for patients with diabetes, because even without statin treatment diabetics run a much greater risk to develop polyneuropathy than other people. Polyneuropathy in statin users has been seen by other researchers as well. For example, Elias Ragi, consultant clinical neurophysiologist at Royal Devon and Exeter Hospital, Exeter, reported about 16 patients with statin-induced polyneuropathy in just one year, and many of them had severe symptoms.[215]


    There are many reports about erectile dysfunction after statin treatment. To get an impression of its frequency, Dr. Anthony Wierbicki and his team at St. Thomas Hospital, London asked 82 patients who were gong to start on statin therapy about their sexual functions. Six months later 20% of the patients had become more or less impotent.[216]

    Again, drug labels provide no mention of this embarrassing side effect, and from my clinical experience I know that few men would dream of bringing it up with their doctors.

    It is also worth mentioning that Dr Wierbicki’s study was sponsored by Pfizer. However, nothing is mentioned about this potential side effect on the official Lipitor site. And why should they? Just take a Viagra pill, another bestseller from Pfizer.

    Worse than thalidomide

    On the drug labels pregnant women are warned against statin treatment. But how many read the fine print? Furthermore, about half of all pregnancies are unplanned, and any adverse effects on the fetus occur already within the first two months.

    To learn more about these effects, Drs. Robin Edison and Maximilian Muenke at the National Institutes of Health reviewed 178 cases of statin exposure reported to the FDA. After having excluded those with spontaneous and voluntary abortions they ended up with 52 cases considered valuable. Almost half of them had serious malformations of the brain or the limbs.[217]

    But that is not all. At the Oncogenetic Laboratory of the Tel Aviv University, Dr. Tartakover-Matalon and his team studied living placental tissue retrieved from normal pregnancies that had been terminated legally. They found that if they added small doses of simvastatin to the culture medium, several vital functions of the placental cells were inhibited. They concluded that these toxic effects might have caused the higher abortion rate and malformations seen in previous studies of animals given statins during pregnancy.[218]

    There is reason to believe that the many cases of spontaneous abortions reported by Drs. Edison and Muenke also were caused by the statins.


    Statins produce cancer. This was the conclusion of University of California researchers Thomas Newman and Stephen Hulley after having analysed all studies of what happened when laboratory animals were treated with statins.[219]

    They asked themselves why these drugs had been approved by the Food and Drug Administration at all. The answer was that the doses used in the animal experiments were much higher than those recommended for clinical use. But as Newman and Hulley commented, it is more relevant to compare blood levels of the drug. Their review showed that the blood levels that caused cancer in rodents were close to those seen in patients on statin drugs.

    Because the latent period between exposure to a carcinogen and the incidence of clinical cancer in humans may be 10 to 20 years or more, the absence of any controlled trials of this duration means that we do not know whether statin treatment will lead to an increased rate of cancer in coming decades. Thus, millions of healthy people are being treated with medications the ultimate effects of which are not yet known. Newman and Hulley therefore recommended that the statins should be used only for patients at very high risk for coronary disease, not for people with life expectancies of more than ten years. Healthy people with high cholesterol as their only risk factor belong to the latter category. Yet these are the very people targeted for cholesterol-lowering drugs in the current trend toward mass medication. There is good reason to exercise caution in the use of the statin drugs because there is already much evidence that statin treatment may lead to cancer in humans as well.[220]

    If statin treatment is cancer-provoking, cancer is likely to show up first in people with the highest risk of cancer, for instance in old people. There are also great differences between the incubation period for different cancers. Those that appear the earliest are, of course, those that are easy to detect. The results from the statin trials are therefore disquieting.

    In the first two simvastatin trials, 4S and HPS, more patients in the treatment group got non-melanoma skin cancer. However, although these figures appeared in the tables, the authors did not mention this alarming finding in the discussion or in the summary of the reports. The reason may be that the difference was not significant in each trial. However, if the numbers from both trials are added together, the difference becomes statistically significant, meaning that it is highly unlikely that the result was due to chance.

    Non-melanoma skin cancer is considered unimportant because it is easy to treat; nobody dies from non-melanoma skin cancer today. However, a cancer is a cancer. If statin treatment or low cholesterol are able to create various types of cancer as in the animal experiments, the first type we should expect to see is, of course, skin cancer, simply because it is easily detected and at an early stage. Besides, there is evidence that non-melanoma skin cancer may be a harbinger of more vicious types of cancers later on.[221] But by unknown reasons the trial directors of all studies published after HPS haven’t bothered to report the number of skin cancers.

    No significant increase of cancer was seen in a ten-year follow-up of the participants in the 4S trial and the authors therefore concluded that ten years of statin treatment does not induce cancer.

    Neither does ten years smoking.

    Another easily detectable malignancy is breast cancer. In the CARE study, breast cancer was more common among those who took the drug than in the control group. In the treatment group 12 women got breast cancer during the trial, whereas there was only one case in the control group, a difference that is highly statistically significant.

    The authors of the CARE report were eager to explain away the increased frequency of breast cancer. “These findings could be an anomaly,” they wrote. It is possible that they are right because the expected number of breast cancer cases in the control group, calculated from the frequency normally seen in the population, should have been five cases. Nevertheless, thirteen is more than twice as many as five.

    Breast cancer has not been reported in any of the more recent trials, but after the publication of the CARE trial, all patients with cancer, including those who have underwent cancer treatment, have been excluded from the trials. This is a most curious decision because supporters of statin treatment claim that statins are able to prevent cancer.

    In the package insert for Pravachol, you can read about the risk of various less dangerous side effects, although none of these was reported significantly more often in the treatment group. But nothing is mentioned about the possible risk of breast cancer, the only side effect that was seen significantly more often.

    And there is more evidence that statin treatment may cause cancer. Let us take a look at PROSPER, a large trial involving elderly people.[222] This trial was directed by Professor James Shepherd, the director of the WOSCOPS trial. In PROSPER, men and women aged 70-82 were included only. All of them had either vascular disease or had a raised risk of such disease. At follow-up, 4.2 percent had died from a heart attack in the control group, but only 3.3 percent in the treatment group. This small benefit was neutralized by a higher risk of dying from cancer. Indeed, there were 28 fewer deaths from heart disease in the pravastatin group, but 24 more deaths from cancer. If we include non-fatal cancer in the calculation, the cancer difference between the two groups became statistically significant; 199 in the control group and 245 in the pravastatin group. Furthermore the difference between the two groups increased year for year.

    To put this finding in context, as they wrote, they counted the number of new cancers in all pravastatin trials together and found that there was no significant increase of cancer. However, in this calculation they did not include the number of skin cancers.

    What they also forgot to mention was that in the previous trials the participants were 20-25 year younger than in their own trial. Cancer is primarily a disease of old age and cancer is a frequent finding at post-mortem of old people who have died from something else. Cancer in the elderly is often dormant or it grows so slowly that it never becomes a problem during their lifetime—unless of course the growth is stimulated by something like statin treatment.

    If cancer appears within a mere three or four years in the elderly, isn’t it likely that cancer will become a problem in young people, those who have been told to take a statin drug every day the rest of their life?

    There is another way to determine whether statin treatment is able to produce cancer. At five hospitals in Tokyo a group of Japanese researchers studied whether cancer patients had been treated with statins more often than other people. To that end they selected patients with various forms of lymphoid cancers and control individuals of the same age and sex without cancer admitted to other departments at the same hospitals during the same period. A total of 13.3 percent of the cancer patients, but only 7.3 percent of the control individuals were or had been on statin treatment.[223] Again, just as with skin and breast cancer, lymphoid cancer is easily detectable, at least compared with cancers in the internal organs. Had the Japanese researchers chosen patients with pancreatic cancers for instance they might not have found any difference, because this cancer type may go undetected for many years.

    Effect and side effect

    As you can see from Table 6C, the gain in the number of fatal heart attacks in the CARE trial was 1.1 percent whereas the loss in numbers of breast cancers was 4.2 percent. Calculated in the way trial directors usually do, as relative rather than absolute risk, the difference was even more striking, with 12 percent fewer heart attacks but 1500 percent more breast cancers. However, you will never see side effects calculated in this way—only positive effects. (Unfortunately, the authors did not give the number of fatal heart attacks for each sex. The figures in the table relate to both sexes.)

    How to minimize side effects

    Patients chosen for the statin trials do not look like the typical patient sitting in the doctor’s waiting room. To be included they must satisfy a long list of criteria. As an example I shall tell about how the participants were selected for the TNT trial, but the principles used in that trial are similar to those of the others.[224]

    At the start, the researchers screened 18,469 patients with evident coronary heart disease. Of these, 15,464 were deemed eligible. We are not told why the other 3,005 patients were not eligible, but from the many previous trials we know that patients with all kinds of pre-existent conditions or frailty are disqualified. As mentioned above, cancer is one of the exclusion criteria, but any serious condition, such as kidney and liver disease, heart failure, uncontrolled diabetes, hormonal dysfunction, and gastrointestinal disorders belong to that category—including, of course, any patient who has previously shown intolerance to statin therapy.

    After that the 15,464 potential participants were given a small dose of atorvastatin, the drug to be tested. This procedure led to the exclusion of a further 5,462 patients. According to the authors, most of them were excluded because they did not meet the randomization criteria, a most curious argument as these criteria were already defined from the beginning. Why weren’t they excluded in the first round? Others were excluded because they experienced adverse effects from atorvastatin, or they died, or had a vascular event during the test, or they showed lack of compliance.

    Thus, from the original group of 18,469 patients only 10,001 patients, or 54 percent were included in the trial. It is obvious that the participants in the trial represented a selection of unusually strong and healthy patients. Taken together with the unwillingness to record obvious signs of organ dysfunction as side effects, the figures for statin side effects are obviously completely unreliable.

    Another note of caution

    To test a drug on many thousands of patients is extremely costly and laborious. The only groups willing to spend several hundred million dollars for such trials are the drug companies because the potential profit is gigantic. Consequently, all statin trials are sponsored by the company whose drug is tested in the trial. Not only do the companies pay for the necessary meetings, workshops, conferences, authors’ and speakers’ fees and travel expenses for the many hundreds of participating doctors and researchers in each trial, they also prepare the trial, take part in the selection of patients and control individuals, design and produce the protocols, participate in monitoring of the results, analyze blood cholesterol and are responsible for the complicated statistical calculations. The companies may even hire professional writers to prepare the reports. Can we be totally confident that their vested interests have no influence at all on the outcome of these trials? Can the wolf play the role of shepherd?

    And are the results really blinded as we are told? In most of the trials the lipid analyses are performed at the drug company laboratories, and these results are not released to the doctors and patients throughout the whole trial. But what about the lipid analyses that were performed at the individual clinics and departments—were they blinded also? When the first favorable results from the trial are announced in the press, for example, how do you think the participants would react? Wouldn’t they want to know whether they were taking the new wonder drug or whether they were taking an ineffective placebo? An easy way to find out is to take a cholesterol test. Almost certainly, all of them knew their cholesterol level at the beginning of the trial. A new cholesterol test would in most cases have told them to which group they belonged, and even if their trial doctor hadn’t analyzed their cholesterol, it would have been easy to have it done somewhere else.

    So it is not unreasonable to assume that a substantial proportion of the patients and their doctors knew to which group the participant belonged and such information might have unintentionally influenced the results.

    But let us assume that the doctors and the patients were not influenced at all. What about the trial directors? By now you are familiar with the tendency of the previous directors to exaggerate the trivial effects of their treatment and minimize the side effects. In fact, many of these reports do not appear to have been written by scientists in search of the truth and nothing but the truth.

    Consider also that positive results are much more financially rewarding for researchers than negative ones. Researchers, who come up with positive results, in particular positive results from drug trials, are more often invited as speakers to meetings and congresses and more often chosen for further lucrative research projects.

    Should we, therefore, be confident that statin research results have been presented in a nonpartisan manner? And why haven’t we heard about the outcome of the first statin trial, the EXCEL study?

    ——— Here are links to the other chapters in the book.

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