Statin denialism (current version) is a RationalWiki article created by Darryl L. Smith, as User:John66 (Contributions) continuing a campaign against skepticism of mainstream concepts, ironic for a site supposedly dedicated to critical thinking. This was a continuation of the editing of Skeptic from Britain.
This article confuses skepticism of the role of cholesterol in heart disease, and skepticism of the efficacy of statins. It treats what may still be a majority view (though not necessarily in the journals) as if it is unchallengeable gospel, written on stone tablets, with anyone who challenges it being a dangerous heretic, a “pseudoscientist.” Let’s go over this in detail.
Statin denialism (also known as cholesterol denialism) is a form of pseudoscientific denialism that asserts that cholesterol does not cause cardiovascular disease and/or that statin usage does not reduce the likelihood of cardiovascular disease.
The advantage of creating an entity called “denialism” is that one may then lump together all claims or ideas of alleged “denialists” as if the same. From the RW denialism article:
Denialism is the refusal to accept well-established theory, law, fact or evidence.[note 1] “Denialist” is pejorative.
Indeed. Note 1 is from a blog devoted to denialism. It gives the definition:
“Denialism is the employment of rhetorical tactics to give the appearance of argument or legitimate debate, when in actuality there is none. These false arguments are used when one has few or no facts to support one’s viewpoint against a scientific consensus or against overwhelming evidence to the contrary. They are effective in distracting from actual useful debate using emotionally appealing, but ultimately empty and illogical assertions.”
So, how can we distinguish skepticism from denialism? What is a “scientific consensus“? How do we know that an argument is “false”? If it is false because contrary to some kind of consensus, the definition becomes circular. What if one makes true arguments against an apparent consensus. Is this denialism? (Apparently not, by the definition). I’ve linked the RW article, which has:
Scientific consensus is what most scientists in a particular field of study agree is true on a given question, when disagreement on the question is limited and insignificant.
That’s a decent practical definition, though it has an ontological problem. My training in science led me to understand that science develops models, and it is possible that none of the models are “true,” but they are more or less useful. If we find a model so useful that we use it without questioning its validity or precision, we may call that “truth,” but it is not absolute. Science is always open to amendment, even, on rare occasions, revolutionary amendment. Another problem is the definition of “limited” and “insignificant.” That can be subjective.
There is also two more problems: the “field of study” is defined how? Science becomes increasingly specialized, and, as an obvious example, few “scientists” are intimately familiar with the methods and findings of parapsychology, but parapsychology is condemned by some wiki editors because “most scientists” allegedly consider it “pseudoscience.” Parapsychology is defined as the scientific study of the paranormal, so when did “scientific study” become “pseudoscience”? What question were those scientists answering? I would suggest that it was not about parapsychology, but, as interpreted, about “belief in non-material phenomena, as “extra-sensory perception.” “Paranormal” really means “not normal, not having a known scientific explanation.”
So the author makes two assertions that are allegedly denialist rather than skeptical.
. . .cholesterol does not cause cardiovascular disease . . .
Cholesterol in the diet or cholesterol levels in the blood or cholesterol in arterial plaque? Let’s look at each.
It was proposed decades ago that cholesterol in the diet caused heart disease. That view has been totally demolished, it is now a general consensus that dietary cholesterol is harmless. Eggs are now considered a healthy food, by many or most.
Cholesterol in the blood is called a “risk factor,” something measurable that is associated with some result, presumably an undesirable one. That does not equal “cause.” “Cholesterol skeptics” question the role of cholesterol, which is a natural substance. I just finished reading all of Dr. Kendrick’s sixty blog posts on the issue, as listed on this page.
I was previously familiar with the work of Gary Taubes, a science journalist and very careful and thorough investigator. Bottom line, there exist common opinions among scientists in the fields of nutrition and cardiology and the problem is that common opinion has not necessarily been formed through a rigorous scientific process. The RW author is considering the “lipid hypothesis” (Wikipedia article) as if it were an established scientific fact. From that article:
The lipid hypothesis (also known as the cholesterol hypothesis) is a medical theory postulating a link between blood cholesterol levels and occurrence of heart disease. A summary from 1976 described it as: “measures used to lower the plasma lipids in patients with hyperlipidemia will lead to reductions in new events of coronary heart disease”. Or, more concisely, “decreasing blood cholesterol… significantly reduces coronary heart disease”.
An accumulation of evidence has led to the acceptance of the lipid hypothesis by most of the medical community; however, a minority of fringe researchers contends that the evidence does not support it, and that mechanisms independent of blood cholesterol levels are responsible.
According to Note 2, what “ended the controversy” was the discovery of statins and the showing that lowering cholesterol levels with statins (and other means) lowered “coronary heart disease events.” What is not mentioned in this paper is that, generally, the rate of deaths from all causes was not reduced. Generally, a cholesterol skeptic like Dr. Kendrick will acknowledge that lower cholesterol for some people may lower cardiac death rates, but he also looks at a great deal of evidence that has largely been neglected. The lowering of rate is small, often exaggerated in how it is presented. From my reading of Kendrick and my understanding of the field (which is very personal: I have a diagnosis of cardio-vascular disease) cholesterol is not a causal factor. Correlation is not causation, and there is ample evidence that he advances. He is making a scientific argument, not a “denialist” one, and it is, at this point, in some circles — not in others — a minority view. This situation, where Bad Science took over in the last quarter of the 20th century, is what Taubes has written about, continuing his long-time theme of noticing and documenting how social and political phenomena have dominated some field. Continuing from Wikipedia:
An accumulation of evidence has led to the acceptance of the lipid hypothesis by most of the medical community; however, a minority of fringe researchers contends that the evidence does not support it, and that mechanisms independent of blood cholesterol levels are responsible.
Note 3 is the same series of articles from 2006 as Note 2. A thorough review of this topic would require studying that and other papers. The source, however, does not appear to establish the claimed fact about “most of the medical community.” I have doctors and talk to them, and they are not nearly as confident in the lipid hypothesis as would seem. But those are my doctors and don’t disprove the point.
This is clear to me: the lipid hypothesis does not have the level of evidence behind it that would establish reasonable skepticism as ‘denialist.” Further, evidence-based critique of even well-established theory is not denialist or pseudoscientific, particularly if it is testable. The lipid hypothesis is testable, and the lowering of heart disease incidence associated with lowered cholesterol (what kind of cholesterol? This has been a moving target for many years) is not a proof of the lipid hypothesis, it would be supporting evidence. Kendrick notes that statins have other effects, and those other effects, when caused in other ways, also reduce cardiac events; further, Kendrick shows, from many studies, that cholesterol levels themselves are a poor predictor of cardiac events, and, further, that, at least in some populations, lowering cholesterol levels increases death rates from other causes.
The Wikipedia article, for the claim of “fringe,” cites Rafniskov and Taubes, which only establishes that there are critics of the lipid hypothesis, not that they are “fringe.”
The article has a section on the infamous Seven Countries Study by Ancel Keys, which, with some other studies,
. . . led to the acceptance of the lipid hypothesis as orthodoxy by much of the medical community;
By the end of the 1980s, there were widespread academic statements that the lipid hypothesis was proven beyond reasonable doubt, or, as one article stated, “universally recognized as a law.”
A 2017 consensus statement from the European Atherosclerosis Society concluded that “consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.”
There is no doubt that the lipid hypothesis is “orthodoxy” by this point. What Taubes pointed out in a series of articles and then a major book was that this orthodoxy was never established through clear scientific process, but was adopted and promoted politically and emotionally.
It did become practically universal. When in something like 1980 my doctor noted that I had high cholesterol and that I should go on a low fat diet, this had become standard of practice. The ultimate result of that advice: long-term weight gain (this is utterly unsurprising to anyone who knows much about low-fat diets) and possibly prostate cancer. (What I do know is that what became a strict LCHF diet upon that diagnoses led to lack of growth of the cancer, which, again, is somewhat expected.) I trusted that doctor, and he was just following what had become consensus *without science.*
I would agree that cholesterol skepticism is a minority position at this point, but I am not aware of an actual study that shows this. From what I can see, the lipid hypothesis is in serious trouble, but something as well-established in practice guidelines is quite resistant to change. A doctor who recommends contrary to standard of practice can lose his or her license. Scientists who publish contrary research can lose grants and suffer widespread attack. Now, the “2017 Consensus Statement.” All this means is that those on a particular panel agreed with the statement, this does not establish their conclusions as a broad scientific consensus. Pseudoskeptical editors commonly rely on accidents of language like that, it is how they insert bias that is allegedly based on “reliable source.” It’s about context and framing and creating impressions.
The abstract of that Statement:
To appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD).
METHODS AND RESULTS:
We assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects.
Consistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.
I am not expert in this field,. but I can immediately recognize the non sequitur. Correlation is not causation. They show that many studies “demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C.”
Great, if it does that. A review would not be complete without a thorough consideration of contrary evidence. I don’t know if they do that. However, what they show is an “association.” That is, a correlation. This does not establish causation; further, the strength of the association is of high interest. A very strong association, such that if X exists, Y invariably follows, or something approaching that, could show a causal effect, though if there is no known mechanism. Kendrick observes that lipid levels do not show that strong association. When I found that I had high cholesterol, I asked my mother, who was in her nineties, about her cholesterol levels. “Oh, very high,” she said. She died from congestive heart failure, clearly associated with lack of exercise when she stopped walking. Not from CVD. I may have HFC (high familiar cholesterol), which can actually be cardio-protective (or at least not a high risk of death, except as we all have that risk, period), which is a black swan for the “consensus” hypothesis, and it still is a hypothesis, and they state it that way.
They go on. “[the evidences] consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects.”
They are stating a hypothesis to be tested. Notice the hedge, the “provided that.” The problem is twofold: there is, if Kendrick has not been lying to us, plenty of contrary evidence that they seem to be ignoring, but it’s fine to advance a hypothesis in the presence of contrary evidence. One goes ahead and tests it. And then, there are “competing deleterious off-target effects.” The body’s lipid system is complex and monkeying with it can have unexpected effects. Statins do have side-effects and the drugs are often not well-tolerated. So the question becomes the magnitude of the benefit. In any case, statins do work to lower lipid levels, but that they do so does not show that they reduce risk of ASCVD. Further, a reduction in ASCVD risk that is not accompanied by a reduction in risk of death from all causes has simply traded one problem for another. And if there are side effects and expense involved?
To repeat the definition from the RW article.
Statin denialism (also known as cholesterol denialism) is a form of pseudoscientific denialism that asserts that cholesterol does not cause cardiovascular disease and/or that statin usage does not reduce the likelihood of cardiovascular disease.
Above I consider the first half, and then there is the second half.
. . . Statin usage does not reduce the likelihood of cardiovascular disease . . .
I’m a writer and I look at what is written. The above is supposedly the claim of “denialists.” I’m only familiar with Kendrick at this point, and that is not a fair statement of Kendrick’s position. As one interested in the scientific method, reduction of “likelihood” is a reduction of an opinion. What can be tested is two-fold, reduction of “risk factors,” or reduction of incidence. Reduction of risk factors is circular, and reduction of incidence is measurable. Kendrick acknowledges that statins, in at least some studies, reduced the incidence of CVD. But it did not reduce the incidence of death from all causes. Further, the “consensus study” was about reduction of incidence for ASCVD. I am diagnosed with ASCVD, already. What I want to know is about the risk of dying from it. That is, I have a cardiac blockage, which only shows up in a nuclear stress test. (What fun! Radioactive pee for a day!)
Everyone agrees on one recommendation: an exercise program. My cardiologist put me in an intensive one, in the local hospital. This is well understood to reduce risk of death from all causes. He also recommended statins. He knows I’m not taking them, but he also knows that compared to exercise, this is a minor treatment. He also recommended an angiogram and possible stent. Again, he knows that this does not reduce (in my situation) risk of death, and it’s a very, very expensive procedure with substantial rates of serious complications.
The claim (from Kendrick) is not that statins don’t reduce the “likelihood of CVD” but that this reduction is minor, must be, from the overall death rate evidence, accompanied by harm, and thus statins are not accomplishing what patients want, or are they merely looking for “better numbers” on that blood test?
Calling reasonable, evidence-based skepticism of common opinion “pseudoscientific denialism,” is, well, pseudoskepticism. (Wikipedia article). Susan Blackmore is quoted:
There are some members of the skeptics’ groups who clearly believe they know the right answer prior to inquiry. They appear not to be interested in weighing alternatives, investigating strange claims, or trying out psychic experiences or altered states for themselves (heaven forbid!), but only in promoting their own particular belief structure and cohesion.
This means you, Darryl Smith.
Proponents claim that statins should be avoided and are evil because they are sold by Big Pharma and cause adverse side effects. It is promoted by LCHF conspiracy theorists and has a presence on social media platforms such as Twitter.
Once gain, by critiquing a group, one can then make claims about the group, if even one member of the group makes some statement. The idea that some physical thing is “evil” would be a religious concept, certainly not a scientific one. Drugs in general are sold by “Big Pharma,” in more ways than one, and the system of drug research has been heavily influenced by commercial motives. That’s hardly even controversial. Notice how two reasons for avoiding statins are collapsed, with “sold by Big Pharma” being stated first, and then a real reason (adverse side effects) is tacked onto it. But with any drug, I consider both intended effect and possible side effects and this influences my choices. As do many people my age, I experience reflux when I lie down in bed, so I take ranitidine in the evening. I could take omeprazole, which may be more effective, but it apparently increases the risk of serious side-effects if taken regularly, including CVD.
That a drug was developed by a pharmaceutical company is irrelevant to the issue of taking it or not. That is a social and political issue, not a medical one. Cost can be an issue. As Kendrick points out, stress creates risk of CVD, and if I run out of money, that can create stress. When my insurance won’t pay for a drug, I won’t take it unless the benefit is clear.
As presented, this is a straw man argument, and does not apply to Kendrick, for sure, but also not to the other physicians and scientists and journalists questioning the lipid hypothesis and the effectiveness of statins.
Statin denialism is not taken seriously by the medical community. It has been described by a medical expert as an “internet-driven cult with deadly consequences.”
If it has deadly consequences, surely it should be taken seriously! Again, what is Smith describing? There is an incredible variety of positions expressed on the internet, including flat earth theories, moon-landing conspiracy theories, etc . By lumping together serious authors and scientists with cultists, Smith accomplishes his defamatory, pseudoskeptical purpose, and, yes, possibly pleases his paymaster.
(Smith has claimed to be paid and his brother Oliver confirmed that, in email to me. However, he would not be receiving support from Big Pharma, nor from “vegan activists.” It would be from “skeptical organizations” that believe they are promoting “critical thinking.” Too bad their belief is pseudoscientific, it ignores ample evidence that what they are promoting is character assassination and confusion — and, if they are supporting Smith, active deception, impersonation, and the rest.
Note 1 is a reference to this article by Nissen. Appalling, I found it. It starts out by pointing out that “Although precisely gauging the relative contributions of various public health measures to the decline in cardiovascular morbidity and mortality is impossible, most critical observers consider the introduction of statins in 1987 to be one of the keys to this success.”
Correlation is not causation. In this case, though, if the lipid hypothesis is useful, there would be a mechanism. But Kendrick proposes another mechanism, which is the anti-clotting behavior of statins. Further, there is a problem that Nissen glosses over, though it is staring him in his face. Compliance with statin prescriptions is poor. People stop taking them. If that is a major effect, then statins would be unlikely to be the cause of the lowered CVD rate. If it not a major effect, then the point of his whole editorial is bunk. He then writes:
Indeed, some patients do have statin-related adverse effects, as we documented recently in a prospective randomized trial, but intolerance in many patients undoubtedly represents the nocebo effect (7).
One of the points made by Kendrick, very well, in his blog series is that whenever evidence appears to contradict the lipid hypothesis, or any other fixed idea, some explanation is invented. The story here is that people are so affected by the nonsense on the internet that they are afraid to take their statins like good little children.
To the extent that this is true (it may be true to some extent), this would show that physicians have failed to respect the intelligence of their patients, to guide them to developing their understanding of their conditions and treatments. Dr. Nissen would prefer that patients blindly respect the standard of practice. Which I know for a fact can be deadly *even if it would be good practice for some.*
I expect honest advice from my physicians, and my cardiologist might disagree with me on this or that, but he fully respects my responsibility to become informed about my condition and the treatment options. I had a urologist at one point who denied what I mentioned to him, claiming it was preposterous. He told me a number of things that I checked out. He was wrong, it wasn’t even close. (I was asking about variation in PSA tests, he said, “Oh, it’s very accurate!” He was completely wrong, and if one reads the literature, it’s obvious. So he, recognized professional, was ignorant.) I pity any patient of that guy. I found a far better urologist, who still recommended the standard of practice (doctors must do this, but I’ve learned how to make it safe for them to be honest). It is essential to become informed. In the end, what my urologist said to me, after following me through two biopsies and an MRI, “whatever you are doing, keep it up.” Had I followed the standard of practice, I would be missing parts of my anatomy, with no benefit and very likely serious complications.
Statin or cholesterol deniers claim that saturated fat has wrongly been demonized by medical scientists and is healthy for dieting in very high quantities.
This is lumping together the lipid hypothesis with the consumption of fat. Some cultures consume a very high percentage of their calories as fat. Fat was indeed “demonized,” to the extent that when people attempt to reduce carbohydrate consumption, they will often attempt to avoid fat, which makes their food plan unsustainable. There are really only two alternatives, broadly speaking, to carb consumption: fats and proteins, and increasing protein more than modestly can be truly hazardous. The problem with the Keys study mentioned is that when one looks at all countries, instead of a cherry-picked set, there are places where very high fat consumption is associated with low rates of CVD. We have moved very far from instinctive eating patterns. Fat is highly palatable; when I visited Morocco, we were given a package, easily a pound of sheep fat, which had been aged, a delicacy to be delivered to the son of the family in American. But our guide told us that we would not be able to get this through customs, so we gave it to him. He ate the entire package on the spot. Fat is prized everywhere, except where people have been afflicted by the “consensus” of the 1980s.
Is fat healthy for eating in “very high quantities.” I don’t know who is saying that, and Smith does not provide sources. However, this is well-known about fat and is often the reason given by the mainstream for the success of the Atkins diet: fat satiates. One will naturally limit how much fat one eats. Especially saturated fats (which have been the most “demonized.”) Fat consumption in studies that have looked at that has not been correlated with increased CVD. But many think “it should be, better be safe, Atkins (for example) has never been proven to be safe.” But low-fat diets, never proven to be safe, were cheerfully recommended.
I highly recommend Taubes, all of his books, starting with Bad Science (which was about cold fusion!). I haven’t read his latest books, though, just Good Calories, Bad Calories. He is a science journalist, and does thorough work, heavily documented.
In any case, the Nissen article was hosted on this site: The skeptical cardiologist. I’m pretty sure that Darryl did not read that blog, because his head would have exploded. Yes, this cardiologist is skeptical, and even (maybe) in some ways pseudoskeptical, but that’s a more complex issue. He apparently considers statins useful, but that’s not all.
- there is no evidence that full fat dairy increases your risk of heart or vascular disease.
- Sugar as toxin: avoiding added sugar, fructose, and stealth sugar.
- Eggs and heart disease. He tells the story of the recommendations against eggs that uselessly damaged the diet of millions. How did it come to pass that non-science came to be widely accepted as “scientific”? Any genuine skeptic would be seriously interested in this. This is the story that Taubes took on, not as a believer in low carb diets as some imply, but as a science journalist.
- Should all men over sixty take a statin drug? His answer is “No,” but he is careful and thoughtful. Talking about one patient’s possibilities, and considering standard recommendations, he has, “If we were to tighten up on his diet by, say reducing red meat, eggs and high fat dairy, all we would accomplish would be to lower his LDL and HDL cholesterol levels and make his life and meals less satisfying. The lower total cholesterol and LDL cholesterol would not lower his risk of ASCVD. ” This is aligned (though not the same) as Kendrick. (Lower stress and more satisfaction in life is cardio-protective. Is this fellow a “cholesterol denialist”?
- What Diet is best? He recommends the Mediterranean Diet, which is fairly common. It is not low-fat. And he states: Fat Doesn’t Make You Fat or Cause Heart Disease. The evidence that fat in general is bad for heart health is nonexistent. The fat/ heart health relationship is very complex. National guidelines were issued before there was evidence to support reducing fat in the diet. Now recommendations are to reduce saturated fat (the kind mostly found in animal fat and dairy fat ) however there are good saturated fats and bad saturated and even this recommendation is not well supported by scientific data.
So how is it that guidelines were issued before evidence was available? This is the story that Taubes tells, in great and documented detail. Basically, an uncontrolled experiment was run on our population, they believed that it would be, at worst, harmless. After all, aren’t we getting too fat, and shouldn’t we therefore reduce our fat intake? Scientists were warning the politicians that there wasn’t enough evidence, but Keys was a very effective lobbyist. And once the guidelines were in place and enough people believed the nonsense, it became extremely difficult to publish anything contrary, journals would be inundated with protests that they were publishing unproven speculations that could kill millions of people.
Meanwhile, it’s quite possible that millions of people died prematurely because of that lack of critical thinking. Tim Farley has a blog, What’s the Harm?, showing “the stories of over 670,000 people who have been injured or killed as a result of someone not thinking critically.” The harm from the premature adoption of guidelines that attempted to shift the dietary habits of millions of people may have cost many more losses than that. Farley focuses on non-mainstream ideas, and his approach is anecdotal, and does not balance possible benefits. For example, someone is reported as using homeopathy and dying. Someone else might have followed the same advice — and let’s grant that homeopathy does not work according to homeopathic theory — and lived, and because they didn’t use mainstream medical intervention, they avoided a fatal side-effect, which can happen. My view of homeopathy is that it is almost pure placebo effect. The placebo effect works. I consider the remedies as symbols, a language. (I discussed this with Andrew Weil years ago, before he became famous. It would explain why homeopathy is clinically effective, but utterly fails double-blind testing.)
There is a certain darkness and contempt found far too commonly among some kinds of “skeptics.” Susan Blackmore wrote more about that…..
They say that high cholesterol is good for health and there is no link between cholesterol levels and the risk of heart disease and other cardiovascular diseases.
“No link” would probably be an overstatement, but there is statistical evidence for high cholesterol being protective in some conditions. Note 2 links to a Guardian article, Butter nonsense: the rise of the cholesterol deniers. What that article shows is that (1) there is vigorous scientific debate, (2) there are vigorous attempts to suppress dissent from what has become dogma, instead of encouragement to actually find broad consensus, (3) some cholesterol skeptics (the writer calls them “deniers” which is not a neutral position and she uses many rhetorical devices to promote her apparent point of view) blame poor research on “big pharma.” What I have seen, in research articles, is presentation of fact in ways that push particular conclusions favoring the product they were researching. As an example, a drug might “reduce risk by 20%, which sounds like a lot. However, reducing the rate of some harmful outcome by 0.2% doesn’t sound like so much. If the original risk was 0.5% and it was reduced to 0.4%, guess which form of reporting is used? There was a journal article on this practice recently….
To the point here, is criticism of the lipid hypothesis and statin appropriateness “pseudoscientific” if it is based on published science and clear analysis? The Guardian article is practically hysterical about this topic. It leads with:
Butter is back. Saturated fat is good for you. Cholesterol is not the cause of heart disease. Claims along these lines keep finding their way into newspapers and mainstream websites – even though they contradict decades of medical advice. There is a battle going on for our hearts and minds.
Consider “the skeptical cardiologist.” To me, he seems mainstream. He is claiming that fat is not a problem. Kendrick has skewered the idea that cholesterol is “the cause of heart disease.” The “consensus statement” is quoted in this Guardian article, but from the abstract, at least, it does not establish what it purports to establish, a causal relationship, it only shows an association. Kendrick points out, very effectively, that as a cause, cholesterol makes no sense at all, from the actual mechanisms of atherosclerosis. The Guardian author, Sara Bosely, goes on:
According to a small group of dissident scientists, whose work usually first appears in minor medical journals,
Right there, bias. This is an attempt to dismiss immediately. It’s circular. First of all, some of the work does appear in major journals, but, then, this is a group challenging the mainstream. As can be seen in what she reports, there is vigorous opposition, to the extent that if a journal publishes the work, it can be and probably will be attacked. That takes courage, then, and the effect is that many editors will simply reject work that challenges common thinking. It’s very human, and deadly to the progress of science. If work is controversial and edgy, present it as such. But criticizing work because it appears in a minor journal is pseudoskeptical. My opinion is that the thinking of this author (which is not particularly uncommon) is dangerous to humanity. She continues:
by far the greatest threat to our hearts and vascular systems comes from sugar, while saturated fat has been wrongly demonised. And because cholesterol levels don’t matter, they argue, we don’t need the statins that millions have been prescribed to lower them. A high-fat diet is the secret to a healthy life, they say. Enjoy your butter and other animal fats. Cheese is great. Meat is back on the menu.
Notice how similar the alleged claims of the dissidents are to the skeptical cardiologist. These views are actually common! There are differences of opinion about statins, but it’s pretty clear that there are alternatives to taking statins that may have larger protective effects than the drugs. Do cholesterol levels matter? How much? Over a dozen years ago, I started paying attention to all this. What I found was that cholesterol levels were a terrible measure of risk, only weakly associated. But they were cheap tests. I began having C-reactive protein measured as a better risk monitor. I also got a cardiac cat scan, a calcium score, probably much better. But expensive and I had to pay for it out of pocket, insurance would not cover it. But it actually measures calcification. I now suspect that calcification may not be all that great as a measure of true risk either. Kendrick has calcification as being the mechanism the body uses to protect us against rupture of the atherosclerotic lesions, which, if they rupture in a major way, suddenly, can cause full blockage and ischemia. He goes into substantial detail in how these lesions develop. It is likely, from his description, that cholesterol plays no role, and his explanation is plausible. However, what that means to me is that it’s worthy of test.
But Kendrick does not claim that cholesterol is not associated with risk; the issue is causality. What treats high cholesterol may have other effects that do affect causation, and that’s exactly what Kendrick proposes.
My cardiologist is happy that I have an exercise program, because he knows that this is far more important than whether I take statins or not. He knows it is far more important than whether I eat a high-fat diet or not.
And we don’t need hysterical newspaper articles that support burning dissident scientists at the stake, professionally, i.e., by rejecting their papers and denying them funding, and firing journalists who dare to report on dissident views. Sara Bosely is obviously biased, reporting from a debunking perspective. She seems completely unaware of the irony in this (my emphasis):
Maryanne Demasi, a journalist in Australia whose TV programmes questioning statins were pulled from the ABC network because of concerns over impartiality, wrote in January – again in the British Journal of Sports Medicine – of a “crisis of confidence” in the public because “the raw data on the efficacy and safety of statins are being kept secret and have not been subjected to scrutiny by other scientists … Doctors and patients are being misled.”
So a journalist is rejected because of alleged bias, what about Bosely? I have a problem with her story being presented as fact. There are certainly facts in it, but there is a presentation that is designed to emphasize a particular point of view. Notice how what Demasi wrote in a scientific journal is prefaced with apparent evidence of bias about her work as a journalist — which might be based on actual bias or on a prejudice against her conclusions. The Wikipedia article on Demasi. Quite a woman! Journalist (with scientific training, like Taubes, even more so, perhap — she has a doctorate in medical research), reports story where she could have expertise, is attacked by those who don’t like what she reports. Do we support journalism?
This view is contradicted by scientific evidence and has been described as bad science and dangerous.
Yes, it has, but it is also supported by scientific evidence. What is truly dangerous is our ignorance, and ignorance is not dispelled by fervent attachment to beliefs based on shallow conclusions from
Bad Science, even if those beliefs were widely accepted for a time. That has all, in the last fifteen years or so, come seriously unravelled. But some will cling to their beliefs until they die. Science advances one funeral at a time (paraphrase of Max Planck). So it is ironic that the Guardian article closes with:
One thing is for sure – the dissidents are not going to shut up shop. “My belief about the cholesterol sceptics is that they are a bit like religious fundamentalists,” said Neely. “They are not open to argument. Whatever argument you present, they will find another argument because this basically defines who they are.” He cites a cardiologist in the 1980s, Prof Michael Oliver, who was a sceptic of the cholesterol hypothesis that more LDL increased the risk of heart attacks and strokes. Oliver did a U-turn as more evidence accumulated, saying: “When the facts change, I change my mind.” But, says Neely, “unfortunately the cholesterol sceptics we know currently don’t do that”.
This is typical of pseudoskeptics: the attached thinking, the stubborn beliefs are those of other people, never the people with “correct beliefs.” Reading Kendrick, I see someone quite willing to change his opinions, and explaining why. Taubes went through a whole process of revising his views surprising himself as he learned more about the history of the lipid hypothesis. Religious fundamentalism rejects challenged to existing belief. What’s the existing belief? Religious fanatics will attempt to sanction heretics. Yes, heretics can be stubborn. We have seen evidence for the cholesterol hypothesis. It’s blatantly weak, which doesn’t make it wrong. But that it was widely accepted, as it was, doesn’t make it right. The jury has yet to return a definitive verdict.
What Taubes recommends and is working for is more research. That’s the same as I am with low-energy nuclear reactions. That’s the same as has been recommended by expert panels, both with regard to cold fusion and with regard to nutrition. If we already know the Truth™, we don’t need more research, we just need to fund delivery of services or products. We don’t know the Truth, except a little, here and there, and we know it through the scientific method and personal reflection (both), not through a vote. Ever. When it’s found, Truth may be sung by masses as in a chorus, or it may be a lone voice, crying in the wilderness. Are we listening? Pseudoskeptics are not listening and only care about what is popular (or, alternatively, they decry the popular, certain that they know better. Hence Fad Diet™ is practically a synonym for quackery. To the arrogant, if it is popular, it must be stupid.
Arrogance is stupider than stupidity.
Professor of Medicine and Epidemiology Rory Collins has compared statin denialism to flat earthism, he has noted “the claims that blood LDL cholesterol levels are not causally related to cardiovascular disease (which is really in the same realm as claiming that smoking does not cause cancer) are factually false.”
Because he says so. It is not in the same realm, that is completely obvious, so no matter who he is or how much he has stuffed in his shirt, he’s an idiot. I can verify the curvature of the earth personally, it’s easy, actually (especially with modern tools like a cell phone). However, the causes of cardiovascular disease are complex (and when someone points out the problems with the lipid hypothesis, that is a common response, that causes are complex.” What we can do is to examine the evidence, and, because there are plausible reasons to suspect some of the older research, to look at the most recent research especially.
However, I’m not sure that Rory Collins actually said that. This is from the Guardian article, and it’s not in quotes. Looking at what she links to, Collins was involved in some of the studies in the 198o that began the statin craze. He’s defending his own work by attacking skeptics. What I see is that there are studies under way. There is actually a vast amount of work to sort through to develop any kind of informed opinion on this subject.
Meanwhile, I have only so many years to live, and choices to make. I know how to make choices, how to take responsibility. There is no guarantee of making the “right choice,” and, in fact, over-concern about it may suppress intelligence. Reading Dr. Kendrick, I made one immediate change. I started taking Vitamin D, he presents very good evidence that this could be protective. Much of what he recommends I already do. I will discuss all this with my cardiologist, and I will continue to read, including reading contrary views.
I am responsible for my life.
According to cardiologist Steve Nissen, “We have abundant scientific evidence demonstrating that treatment of high risk primary prevention patients substantially reduces the risk of cardiovascular morbidity.” Whilst acknowledging that statins, like other drugs, have adverse effects, “the benefits are so well documented that every effort should be made to encourage use of these drugs in appropriate patients.”
There is a serious quantitative issue here, and I’m afraid that the medical profession has badly blown it with a series of errors based on Bad Science. I no longer trust pronouncements like that. “We have abundant evidence” is like Senator McCarthy, “I have evidence …” Great. How can the reality here be assessed? By shouting down dissent? That is what seems to be the idea in much of this “expert opinion.” The reference is to the Nissen “Internet cult” editorial, which was clearly p0lemic, agenda-driven. I will be looking for reviews of all these sources.
The leading advocates of statin denialism are associated with the The International Network of Cholesterol Skeptics (THINCS).
We need to be very clear about this: nobody advocates “statin denialism.” That leading skeptics of the lipid hypothesis are organized is not surprising at all.
They have been accused of “cherry-pick[ing] the scientific literature to find studies that support their theses, ignore the flaws in those studies, and ignore the vast body of literature that contradicts them.” Statin denialists are known to exaggerate the side effects of statins and utilize scaremongering tactics.
What I find reading Kendrick is that when evidence appears that appears to negate the lipid hypothesis, and it still is a hypothesis in spite of substantial acceptance for a substantial time, it is ignored.
I’m far more familiar with cold fusion literature. It is commonly claimed that there is a vast body of literature “contradicting” the reality of “cold fusion.” What I find is that once becomes familiar with the field, there is a vast body of consistent literature, for what supposedly contradicted “cold fusion” actually confirmed what is known about it. For example, it does not produce substantial ionizing radiation, nor neutrons. That was considered “negative,” since, supposedly “fusion” would produce such radiation. Yet “cold fusion” is not actually a defined reaction, so its characteristics cannot be predicted from theory. Many early attempts to replicate failed to find anything. Later study did Bayesian analysis of those early studies and showed that, from what became known later, none of them would have been expected to show the effect, they had not set up the necessary conditions. So the early work is not in contradiction to the later, only to premature conclusions.
Again, if someone exaggerates, shame on them. What are the side-effects of statins, how common are they? Will a cardiologist warn a patient? If they do, will this then cause a perception of the side-effects from the “nocebo effect”? One of the major problems with statins is that they have been oversold. Statins, at best, reduce risk. From what I’ve seen, they do not reduce risk of death, only of a cardiac event. Is that true? But suppose they reduce risk, the issue would then be how much, at what cost and at what risk of side effects. There are actually many possible interventions. Which ones are the most important, have the greatest effect?
For CVD, the risk reduction intervention that is almost universally accepted as having a large effect is an exercise program. How does this compare to statins?
How do any of these interventions compare? A baby aspirin a day. Niacin (enough to get the flush). A high-fat, low carb diet, eaten with gusto (and with relatively low quantities of food, compared to what I used to eat). Metaprolol, a beta blocker, I take on my cardiologists’ recommendation, and I wonder about it. So far, I’ve seen no research on the critical question: does metaprolol suppress the formation of collateral circulation, otherwise encouraged by exercise. (It keeps my heart rate lower than it would otherwise be from the exercise. If I forget to take it, my heart rate still doesn’t go up to a worrisome level).
I always want to know possible side effects. If I get one, I will consult a doctor. I have taken drugs with major side effects possible. I have seen none of them. I take ibuprofen occasionally, “chiropractor in a bottle,” my doctor used to say. I worry about the possible impact on CVD, it could raise the risk. So I only take it occasionally, large doses, but often only one-shot.
I would not stop taking a prescribed drug without consulting my physician. It’s my decision, not his, but I consider it crucial to discuss these things. So what is Nissen’s worry? Well, it would have to be people who have poor communication with their doctor. Another way to state this is that a cardiologist, say, has not established rapport with the patient. Instead, perhaps, he believes his role is to be a patient manager, and the job of the patient is to be compliant. This attitude is not uncommon. It’s a tragedy, because the prognosis for general health is poor if these are the conditions.
In 2017, Aseem Malhotra and colleagues published an article which disputed the link between blood cholesterol levels and occurrence of heart disease.
What I’ve seen is that there is evidence for this view. (that is, specifically for a causal link. There can be links that are not causal.) So what is an appropriate response? If Malhotra is correct, surely this would be extremely important to (1) take seriously, (2) look for consistency of the claim with what is known and “what is known” is not hypothesis or theory, but the actual evidence from studies, and (3) design new studies that would clarify the issues, allowing deeper and more complete understanding to arise. Instead, it appears, the response is to circle the wagons.
The article was written by Demasi, Lustig, and Malhotra. Demasi is the Australian scientist/journalist who was panned in the Guardian article (as she is on Wikipedia, to a degree). Malhotra also has a Wikipedia article. Looking at it, it is under pseudoskeptical attack (which included Skeptic from Britain, the Wikipedia incarnation of Darryl Smith).
The authors also suggested that “stopping statins may paradoxically save more lives”. The article was criticized by the medical community. Cardiologist Tim Chico commented that “high cholesterol has been proven beyond all doubt to contribute to coronary artery disease and heart attack […] to say the cholesterol hypothesis is dead is simply incorrect.”
Reading the article by Demasi, Lustig and Malhotra, it’s devastating to the cholesterol hypothesis. It is obviously not dead, because there are people wearing it, moving around, making noises. However, let me put it this way, If Chico were my cardiologist, and he said that, I’d fire him. “Beyond all doubt” is very strong language, practically hysteric, and I don’t want someone hysterical as my doctor.
What is the reality? What is the actual causal association between cholesterol and heart attack? This is what Kendrick has written about for several years. Is high cholesterol a cause or an association? Or is it neither? What does this article actually say, and what evidence is asserted? Does Chico actually consider the evidence, or is he rejecting the conclusions ab initio, since they contradict what he obviously firmly believes?
Chico’s quotation is from a page from the Science Media Centre, which, lucky guess, is British (and with a noble purpose, it appears to me). The page is “expert reaction to new report on statins and the cholesterol hypothesis.”
The claim that the cholesterol hypothesis is dead is probably an overstatement, if “dead” means that hardly anyone believes it or uses the model any more. However, that claim is not actually in Demasi et al. It’s a headline, and headlines are not uncommonly written by editors, not original authors. It varies, so I don’t know what happened. The title is:
The cholesterol and calorie hypotheses are both dead — it is time to focus on the real culprit: insulin resistance
Detailed study of this issue is beyond the scope of this review. Rather, my interest is largely in the counterclaim, that skepticism about the cholesterol hypothesis is being characterized as “pseudoscientific denialism,” by blatant pseudoskeptics who are not concerned about real science, but about whether or not something is “mainstream,” and if it is not clearly mainstream, and if some strongly criticize it, they characterize it as dangerous, pseudoscientific, denialist, the latter being a term often used with corporate astroturfing and the like, as with tobacco industry denialism around the harm of smoking, or global warming denialism based on political or economic interests. The cholesterol skeptics generally have no conflict of interest, though may market vitamins, etc. (Which in my view should properly lead to some level of suspicion about an author’s motives). As well, some may sell books, but so do many experts. That is not, in itself, a disqualification. The work should properly be judged on its own.
And there are various kinds of conflicts of interest. One of the critics of the Demasi article was a major researcher involved in one of the major studies that claimed to show the effectiveness of statins back in the 1980s, he’s not exactly independent when he claims that there is absolute proof.
The Demasi article actually has more than one theme. One is about the cholesterol hypothesis and the other is about diet, and it is quite possible, from what I have seen, that the dietary recommendations coming out of the Keys trial and other work like that have cost millions of premature deaths, and anyone involved in that could be expected to fight exposure of what happened, tooth and claw.
In the 19th century, Semmelweiss found, by careful study, that doctors were causing peurperal fever by doing autopsies on people who had died from certain infections and then examining women in labor. He was scathingly rejected and the practice continued long after reasonable excuse. To be sure, Semmelweiss himself developed what may have been senile dementia of some kind and unskillfully promoted his work, but he had made some basic and very clear discoveries and it is very clear why it was rejected.
It was rejected because if he was right, doctors were killing thousands of women by their practices. It was unthinkable. One of Semmelweiss’ colleagues actually committed suicide when he realized that he was responsible for the death of his niece, I think it was.
So that the dietary recommendations of the 1980s and on could have resulted in millions of premature deaths — unthinkable! But it must be thinkable, or, if this is reality, it will not go away because we claim it is preposterous. Is there a conspiracy? There was no conspiracy, as such, to suppress Semmelweiss, but there were many individual actions that had a similar effect. Sometimes, “believers” in cold fusion think that there is a conspiracy to suppress it. I’ve been accused of being in the employ of the evil Industrial Heat in a plot to suppress the technology of Andrea Rossi, in order to rescue their foolish investments in solar power.
I don’t believe that cardiologists and various organizations are suppressing “cholesterol reality” in order to benefit statin manufacturers. Not consciously, anyway. Rather, they believe the “information cascade” that arose in the 1970s and 1980s, that exaggerated the harm of fat in the diet (or even invented it, since it does not appear that natural dietary fat is actually harmful), and that also exaggerated the benefits of statins and overstated the case for the cholesterol hypothesis (and those two are very much connected.)
Statin denialists are known to spread misinformation. James Stein a Professor of Cardiovascular Research has stated that “many lives have been lost or impaired because of statin non-compliance.”
Those are two unconnected statements, and no actual “misinformation” has been shown. If there is misinformation, say, on the Kendrick blog, I’d very much like to know. But pseudoskeptics, “debunkers,” will claim misinformation without actually pointing to specifics. What Stein is claiming is not shown by any study, it’s speculation. Is speculation presented as if demonstrated fact “misinformation.” Is it true, and how would we know. That statement is actually pseudoscientific, for several reasons:
- It is not possible to determine if someone died “because of statin noncompliance.” There is no death certificate stating “cause of death: failed to take their statin prescription.” Some people take statins and die, and people stop taking statins and don’t die, at least not right away.
- There are no reliable statistics, then, on this, no way of falsifying the claim. It’s pseudoscientific hysteria aimed at shutting up skeptics, and it’s ironic that RationalWiki would support this crap. The controversial issue is one of whether stains reduce risk of death or not; the claims that they reduce risk of heart incidents commonly fail to mention that they do not reduce death rates. I.e., you might get fewer heart attacks, say, but not fewer deaths from all causes. So it is possible, indeed, that someone stops taking statins and it saves their life, but, again, we would not know. We do know that if one is experiencing certain side effects from statins and stops taking the drug, the side effects stop. And that is exactly what will be prescribed if those effects show up (and this is often presented as an argument for taking statins). Yet if someone is going to die if they stop taking their statins, as Stein appears to assume, a physician would surely advise them to simply tolerate the side effect.
How could stopping a statin save your life? Well, consider this mechanism. If you are taking the drug, a possible side effect is myalgia, muscle pain. If you are experiencing myalgia, you might reduce exercise, and reducing exercise can definitely increase the risk of CVD. So if you stop the statin and exercise more as a result, and a fatal heart attack avoided, a life has been saved. So it’s all a question of balance, and black and white thinking is not conducive to finding balance.
List of notable statin denialists
Source 4 is the Skeptical Inquirer, which is far from a reliable source. It is the equivalent of yellow journalism. Harriet Hall, the author of “Statin Denialism,” starts off on Leonard Coldwell. Who the hell is Larry Coldwell? She provides a link in her end notes to his video, and she claims that “not a word of what he says is true, and much of it is hilariously funny.” I didn’t wait for the “funny part,” but even though “not a word is true” may be hyperbole, the first sentences were quite sufficient to establish for me that this guy is far, far from sane. So, lead with a complete idiot, and then see if some of it rubs off on saner targets? Because this is Skeptical Inquirer, that is more or less what I expect.
I was surprised to see half of her article go on and on with walls of text repeating Coldwell’s nonsense. Finally, she leads into something else.
Leonard Coldwell is far from the only one spreading “alternative facts” about statins. Joseph Mercola8 says “Cholesterol is NOT the cause of heart disease.” And “if you take statins, you MUST take CoQ10.” He claims that statins impair numerous biological functions, including all your sex hormones. He says ninety-nine out of 100 people do not need statins. He says that statins are teratogenic, that they cause birth defects if taken during pregnancy. The evidence says otherwise.9
Mercola’s conclusion about cholesterol is nowhere near as preposterous as Coldwell’s rant. Further, statins do impair some functions (and some of the possible beneficial effects result from that). Is there a problem with recommending CoQ10? I don’t know. It unclear how many people actually “need” statins. Statins, at best, reduce risk. Pregnant women taking statins? They must have some extraordinary risk factors. (I would be very hesitant to recommend statins to a pregnant woman!) What does she cite as evidence? This paper. Her reading of it is naively optimistic. The evidence does not “say” otherwise, and that’s a common pseudoskeptical trick, claim that the evidence says something when really it is the author saying it. Evidence never says anything, the “saying” comes as interpretation of evidence, and this case shows it. She is effectively claiming proof of non-teratogenic effects of statins, whereas the review says something different. What is actually in the abstract:
In this systematic review of both human and animal studies on the teratogenic effects of statins during pregnancy, we found that most of the available data in fact suggests that statins are unlikely to be teratogenic.
In humans, the observed congenital anomalies were isolated and no consistent pattern has emerged to suggest that a common mechanism could underlie these observations. Animal studies show conflicting results, but in the reports in which an excess of congenital anomalies was reported in the statin-treated rodents, excessive doses were used compared with the regimens we commonly prescribe to human subjects.
This is far from a clear conclusion that statins are safe in pregnancy. One would need to balance this evidence (which does indicate some possible risk) with benefit.
Mercola, from my perspective, is overconfident. But he does come up with reports and ideas that are worth investigating. For example, if one chooses to take statins, how about CoQ10? I don’t know, but I know that it’s not uncommon to see it recommended. Statins have side effects, certainly sometimes, and understanding them and understanding how to reduce them could be important. I recommend to everyone that if they have a condition or are taking a medication, research it. Don’t believe anything! Which does not mean think it is all lies. But there is plenty of misleading or useless information out there, understand that, so simply be aware of what is being stated, and especially factual statements (such as what was actually done in studies), the conclusions are not necessarily as significant as fact.
Our RatWiki pseudoskeptic treats “accepted conclusions” as if they were “fact.” But this guy lies routinely, and most especially about his identity.
The next target is Mike Adams. Mike who? Well, apparently the editor of Natural News and possibly a marketer of natural products. Not a scientist. I did not find the headlines she cites (and she only linked to one article, a rather dumb one on salt that mentions glass in the same idiotic way as Coldwell, apparently that story gets around. The articles she writes about were not written by him, a distinction she doesn’t seem to notice. Are Statins Right for You? is certainly not rabidly anti-statin.
What is it that the “Skeptical Inquirer” is promoting? That one should uncritically accept whatever one’s doctor recommends. That one should believe in whatever the orthodox authorities declare? Whatever happened to genuine skepticism? Anyway, she goes on, finally getting to some meat. Or bones. Or gristle, because she just names targets.
And then there is the International Network of Cholesterol Skeptics (THINCS), a group that disputes the role of cholesterol in cardiovascular disease. They are led by Uffe Ravnskov, author of The Cholesterol Myths, and Malcolm Kendrick, author of The Great Cholesterol Con. They cherry-pick the scientific literature to find studies that support their theses, ignore the flaws in those studies, and ignore the vast body of literature that contradicts them. In The Skeptic’s Dictionary, Bob Carroll explains how they use distortions and deceptive techniques in their arguments.11
What I found with the “skeptical faction” on Wikipedia was source cherry-picking, and the active exclusion of sources of equal or better quality (by Wikipedia standards). I have not yet read Ravnskov, nor Kendrick’s books, I have a thin book budget. However, I have read all of Kendricks blogs in the last two years about the causes of heart disease, and he’s quite convincing. Is he cherry-picking data? What I ask at this point is whether or not Harriet Hall is cherry-picking sources, first of all to find sources she can use to discredit what is more neutrally called statin skepticism, and then to find sources to support the “mainstream position.” That is what some forms of skepticism has become: a defense of orthodoxy, not what it imagines, a defense of the scientific method. Rather, it’s what Feynman called “cargo cult science,” which pretends to be science but is actually a belief in developed interpretations instead of a living inquiry into the nature of reality.
Hall turns to the evidence for statins. She comes to this remarkable statement:
Statins may not work only by lowering cholesterol. Statins also have anti-inflammatory effects that probably contribute to the reduction in cardiovascular events.
I just read that, or the like of it, on Kendrick’s blog. Kendrick examines in great detail and with high patience the etiology of heart disease and that atherosclerosis is an inflammatory process has become a rather widespread idea. I have made a point to have my C-reactive protein levels measured, because that is a marker for inflammation, which is much more clearly associated with atherosclerosis than cholesterol. So statins lower cholesterol, yes, that does not appear to be controversial. That they also had beneficial effects with atherosclerosis (at least allegedly) was then taken as if proof of the cholesterol hypothesis. However, Kendrick is quite certain that the cholesterol hypothesis, as to causaility, is bosh, and his arguments are plasuble, and they do not deny the existing research. Rather, they explain it,and this is a piece of it. If the critical factor is inflammation, and it is clearly a part of the process, then statins might have a beneficial effect and the cholesterol-lowering effect is actually a side-effect.
Cold fusion is a whole lot simpler. How did I end up with this mess?
She went on:
But the authors of the Lancet article felt there was sufficient evidence from various sources to establish a causal relationship between cholesterol and atherosclerosis. They noted that lower concentrations of cholesterol have been associated with higher death rates, particularly in the elderly (something the statin denialists love to point out), but they say those associations can be shown not to be causal.
That Lancet article is obviously aware that there are open questions. Some feel the evidence is sufficient, some not, and when there is disagreement among experts who are seeking to examine an issue with care and caution, it’s a clue that more research is probably necessary. Kendrick is looking for clear causation, and the cholesterol hypothesis doesn’t provide it, it is far too simplistic. And those who are claiming that it is already proven are merely sitting on what was believed for what has been for some of them their entire career. And this is why Taubes got involved: he had been working with cold fusion, where there were unwarranted conclusions from research, inadequately confirmed (and actually difficult to confirm), and then he turned to nutrition, first on the issue of salt and, no, no nonsense about glass in salt cutting veins. Simply that the harm of salt was being vastly overstated without adequate scientific evidence, and then he found the same on the issue of fat in the diet, which then leads to cholesterol, though that is not his main focus.
Bad Science. And Bad Science being promoted by “Skeptics.”
I have not studied Hall’s article in detail as to the statin benefit arguments. She ends with
statins, while they are not a panacea for everyone, have been clearly shown to do more good than harm for patients at risk.
That is getting quite close to “a panacea for everyone.” The alleged statin denialist, Malcolm Kendrick — specifically named by her– however, does not deny that statins may benefit some patients.
“good” and “harm” are relative terms, and they require an understanding of balance. Recent recommendations for statins effectively suggest that everyone beyond a certain age take them. I’m 74, and when my doctor, about 15 years ago, told me that “every cardiologist in town will say you should be on statins,” as he sent me to a cardiologist, I did enough research to make a choice, and it was not to take statins. Instead, I had my cholesterol test fractionated (not common then), I had CRP measured, and I got two major tests: a cardiac cat scan to measure calcification, and a stress test. The overall results were, low risk. Then, fast forward about 13 years and I was about to fly to my son’s wedding and I had some tightness in my chest. I was not about to miss that plane, so I flew, but I saw my doctor as soon as I came back, it was a few days. He found nothing wrong, but sent me for another stress test. They found a minor abnormality under stress and scheduled me immediately for a nuclear stress test. The diagnosis: significant cardiac blockage, enough to cause oxygen deprivation in a section of the heart.
The cardiologist then recommended an angiogram and possible stent. And statins, of course. I’m still considering both of them, about two years later. He also wanted to put me into cardiac rehab, but there were some delays. I had flown a long fight to my son, and I was about 72, and do they tell you about how dangerous that can be? Well, I found out. After I had the nuclear stress test and was about to sign up for cardiac rehab, I woke up in the middle of the night with severe pain in my side. I thought of calling an ambulance, but I drove myself to the emergency room, and after some fuss they finally did an MRI of the lung and found multiple pulmonary emboli. Apparently sitting in the plane caused a clot to form in my leg, and eventually it broke free and travelled to the lungs. This is the only time in my life when I have been hospitalized. You know I’m crazy because I say the food was fantastic! So I was on a powerful anticoagulant at first, I had to inject myself with it, every day, and then I was on coumadin (rat poison!) for six months. It took some work, but my cardiologist convinced the insurance company that even though I had not had a heart attack, cardiac rehab would be beneficial, and then I started up an exercise program at my local senior center.
And everyone agrees on this: exercise is the number one treatment for heart disease, if you can do it. And here is why, and doctors don’t talk much about this, and I’m not sure why. If there is blockage of a cardiac artery, collateral circulation will develop, that is, additional blood vessels form. From the Harvard Medical School:
When cholesterol-clogged plaque narrows an artery …
Wait a cotton-picking moment! “Cholesterol-clogged plaque.” That is standard cant. But plaque is a complex structure and I highly recommend Kendrick’s blog for a very detailed exploration of this. People have the idea that cholesterol blocks arteries like garbage in pipes. No, plaque forms through a process, and as Kendrick lays it out, it starts with damage to an artery, possibly from mechanical stress, and he points out that this arises only at certain locations, where such stress would be greatest. Something damages the endothelium, the cells that line the artery and make it leak-tight, and as a result, tissue factor is released, which is a powerful clotting agent, so blood clots immediately to seal the artery to prevent leakage. That clot does its job, then what? Apparently some of this has only recently been understood. Endothelial progenitor cells, circulating stem cells that can become endothelium, will grow over the clot, and some of these same stem cells can become macrophages that will “eat” the blood clot and return it to the body through the lymphatic system. That takes time, and if damage is happening more rapidly than repair, plaque, the buildup of the wreckage from the blood clotting, can grow, from layers of buildup. The blood cells that form the clot contain cholesterol, so the interior of the plaque contains cholesterol. But cholesterol does not cause plaque formation. Cholesterol cannot penetrate the endothelial lining of the artery. I don’t understand calcification yet, because the plaque can calcify, which I suspect is more resistant to repair. But “cholesterol-clogged” set me off, because that image is part of what encouraged the whole “cholesterol story” that, at this point, I do think is a myth. My sense is that we don’t have enough data to fully understand heart disease. But back to what I was quoting:
that feeds the heart, the body responds by trying to bulk up tiny blood vessels in the heart. As these so-called collateral vessels grow more muscular and interconnected, they begin to reroute some of the blood flow around the blockage. Scientists have been trying for years to nudge collateral blood vessels to develop and prosper, but without great success. However, you can do it at home without anything more high-tech than a comfortable pair of shoes, reports the Harvard Heart Letter in its January 2008 issue.
Growing new collateral blood vessels can ease chest pain (angina), limit heart attack damage, improve survival, and perhaps even offer extra time for emergency therapy in the case of a heart attack. And exercise can boost these blood vessels.
Exercise dramatically increases blood flow through the coronary arteries. The inner lining of the arteries responds to this “stress” much as it does to the stress of atherosclerosis, by stimulating collateral blood vessels to elongate, widen, and form new connections.
Institute for Natural Healing [another Darryl article]
There are those who pretend that statin denialism is similar to vaccine denialism. There is quite a difference. There are social and political issues with vaccine denialism; on the one hand, vaccination against communicable diseases is not simply a personal choice, the choices we make affect others. I think reasonable people will agree that we should be very careful about requirements that anyone undertake some medical procedure because it has been centrally decided that this is necessary to protect the public. That is, if this is going to happen, the research should be the highest quality, isolated from commercial interest, etc. I made the choice with vaccination that my children should be vaccinated. I also had a friend who contracted polio and eventually died from it after his child was vaccinated with Sabin oral vaccine, and he had never been vaccinated. Very rare, but . . . it happened. There can be risks from anything, especially anything new. Life is about balancing benefit and risk. Whatever we do, there will be risks. And if we don’t do anything, that is even riskier. A solution to this is to accept risk: we are all going to die. In my training, they said, “Survival is a game you are going to lose.” And the point is not to be a “loser” but to play different games!
I will format the references later….
Nissen SE. (2017). “Statin Denial: An Internet-Driven Cult With Deadly Consequences”. Ann Intern Med. 2017 Aug 15;167(4): 281-282.
Butter nonsense: the rise of the cholesterol deniers
Nissen Calls Statin Denialism A Deadly Internet-Driven Cult
The Movie “Cholesterol: The Great Bluff” Is an Exercise in Denialism
Demasi, M; Lustig R. H; Malhotra A. (2017). “The cholesterol and calorie hypotheses are both dead — it is time to focus on the real culprit: insulin resistance”. The Pharmaceutical Journal doi:10.1211/CP.2017.20203046.
Expert reaction to new report on statins and the cholesterol hypothesis
Dr. James Stein Speaks Out Against “Statin Denialism”
Tim Noakes called a ‘cholesterol denialist’