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The Cholesterol Wars: The Cholesterol Skeptics vs the Preponderance of Evidence 1st Edition

by Daniel Steinberg (Author)

3.5 7 ratings

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Today, in the era of the statins (cholesterol lowering drugs), there is no longer any doubt about the value of lowering blood cholesterol levels. The Cholesterol Wars chronicles the controversy that swirled around the 'lipid hypothesis' of atherosclerosis for so many years. In fact, 'the lower the better' is the position of many clinicians. However, getting to this point has been a long uphill battle marked by heated debate and sometimes violent disagreement. The history of this controversy is told here for its own sake and because remembering it may help us avoid similar mistakes in the future.

Dr. Steinberg and his colleagues have published over 400 papers relating to lipid and lipoprotein metabolism and atherosclerosis reflecting the prominence these authors have in the community
Chronicles the miraculous power of the statins to prevent heart attacks and save lives, of great interest to the many manufacturers of these drugs
Discusses new targets for intervention based on a better understanding of the molecular basis of atherosclerosis

Review

Presents an analytic history of a major controversy in biomedical research and the lessons it offers in dealing with future controversies.

ISBN-10

0123739799
ISBN-13

978-0123739797
Edition

1st
Publisher

Academic Press
Publication date

August 6, 2007
Language

English
Dimensions

6.45 x 0.79 x 9.11 inches
Print length

240 pages
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Product details

Publisher ‏ : ‎ Academic Press; 1st edition (August 6, 2007)
Language ‏ : ‎ English
Hardcover ‏ : ‎ 240 pages
ISBN-10 ‏ : ‎ 0123739799
ISBN-13 ‏ : ‎ 978-0123739797
Item Weight ‏ : ‎ 1.28 pounds
Dimensions ‏ : ‎ 6.45 x 0.79 x 9.11 inches

Best Sellers Rank: #3,447,446 in Books (See Top 100 in Books)
- #348 in Biochemistry (Books)
- #524 in History of Medicine (Books)
- #733 in Cardiology (Books)

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3.5 7 ratings

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lhfang2008

I love this book.

Reviewed in the United States on January 21, 2012

I read this book twice. It recalled the history of lipid hypothesis in athero. It really gives me a lot of insight and guidance in my future work.
True, any hypothesis is not perfect, but it works for the majority of people without genenetic disorer.
Nowadays, I guess anyone who refuses to obey the cholesterol/lipid lowering rule can do 3 things. One is to pray that you have a superstrong genetic construction, 2 is to exercise extremely, and 3 is to buy higher medical insurance.

8 people found this helpful

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Dr. Richard D. Feinman

Still Skeptical

Reviewed in the United States on December 17, 2009

Verified Purchase

The most remarkable thing about this book is that it may be the only one of its kind. The number of books attacking the lipid or diet-heart hypothesis (some listed on people who bought the book) is large and growing -- there are two called The Cholesterol Con yet this appears to be the only answer to what are very serious criticisms. Chapter 1 is a shock right off: "...the hypothesis relates to blood lipids, not dietary lipids, as the putative directly causative factor. Although diet, especially dietary lipid, is an important determinant...." What? We haven't been hearing for thirty years that a low fat diet is the key player? Of course, throughout the book, saturated fat is made to appear a major if not overriding factor and the same lack of hard proof that saturated fat causes CVD is missing. The description of the big studies is remarkably different thatn as described by the skeptics. The big save of the diet-heart hypothesis are the statins but the demonstration that there is improvement in risk because of lowered LDL is still not reliable. The book is nonetheless well researched (within the bias) and worth reading but the title tells you that this is, by analogy with a court of law, a civil suit. The cholesterol hypothesis is not established beyond a reasonable doubt.

35 people found this helpful

Helpful

Zahc

Beware

Reviewed in the United States on June 10, 2014

Steinberg at the beginning mentions "exaggerated skepticism" and "totality of the evidence". The suggestion is that those who do not believe in the lipid hypothesis were overly cautious and have not looked at the totality of the evidence, which is not true at all. One has to keep high standards, but not so high as to stifle the growth of knowledge. On the other hand, standards cannot be so low such that almost anything goes, which is the case with Steinberg. He is rarely critical of anything that seems to support his case even if it may be of poor quality, but is critical of anything that he does not agree with.

Steinberg starts with the animal evidence where there is the obvious problem of extrapolating the evidence to humans, which he realizes. There have been numerous studies in a variety of animal models using a variety of treatments that show major reductions in atherosclerosis that are independent of cholesterol, and even in the presence of severe hypercholesterolemia (1). What this shows is that the amount of damage caused by increased cholesterol levels in animal models depends strongly on the conditions under which it is placed. It is not as simple as similar cholesterol levels implying similar atherosclerosis, or higher cholesterol levels implying greater atherosclerosis. It should be noted also that hypercholesterolemia induces oxidative stress and other factors in these models (which can be reduced without reducing cholesterol), so it is not a case of simply having high cholesterol levels. This is the most that can be said without drifting into speculation about mechanisms.

Observationally, the total/HDL ratio seems to be the most reliable predictor of cardiovascular outcomes. In the elderly, the relation between total cholesterol, LDL cholesterol, and cardiovascular events is inconsistent and much less clearer (2-6). Of course, it does not mean that these associations are causal. For example, HDL-C is one of the most robust predictors of CV events (admitted by Steinberg), and many researchers naively thought that such relation was probably causal, but today the trial evidence says otherwise and researchers are now claiming that HDL function is important. In other words, let's not forget that correlation does not imply causation.

It is amazing to see how Steinberg dismisses the low cholesterol-high mortality relation as not causal, but readily accepts any high-cholesterol relations as being casual without any criticism. Nevertheless, he cites one study which apparently (it's speculation) supports his claim, while ignoring other studies saying otherwise. For example, he could have cited the later Honolulu Heart Program (7) which referred to the very study Steinberg cites. The authors based on their data explicitly stated that the Iribarren hypothesis was "implausible", and even found an "inverse trend" between cholesterol and CV mortality. This is not by any means an isolated finding, as numerous large studies (8-18) have repeatedly confirmed what is found in reviews (19-21). Dismissing this relation is even more absurd when one considers that there is little benefit to be gained from lowering cholesterol, contrary to what Steinberg will have you believe.

With regard to the trial evidence, Steinberg cites some early dietary trials to support his case, but leaves out some important facts:

To anyone who has read the Oslo Diet Heart Study (22), would realize this involved massive dietary changes. The experimental group increased their EPA/DHA and vitamin D intake through seafood and cod liver oil, reduced their intake of trans fat dramatically, increased their nut, fruit, vegetable intake and restricted their intake of refined grains and sugar. Yet Steinberg ignores all this and claims that it was the drop in cholesterol level that was responsible for the protective effect. With regard to all-cause mortality Steinberg claims that a larger number of subjects would be needed to find a statistically significant decrease in all-cause mortality. A better explanation for the lack of a larger difference in mortality was the excessive intake of omega-6 consumption in the intervention group.

Steinberg to his credit realizes that the primary endpoint of the LA Veterans was not statistically significant (23). The only statistically significant result was a post-hoc pooled endpoint. Despite no significant difference in the primary endpoint including CHD death and total mortality, Steinberg states that it "stands as one of the most important and persuasive studies of the prestatin era". Even if it were successful it would not have provided evidence for cholesterol lowering since there was a combination of confounders in favor of the experimental group such as less heavy smokers, less trans fat, higher n-3 intake, and higher vitamin E status.

Steinberg goes on to cite the Finnish Mental Hospitals Study, and contrary to what he says, it is in fact one of the worst dietary trials ever conducted. In fact, some meta-analyses exclude it because of its inappropriate design (never to be seen again) and large confounding (24, 25). He also attempts to dismiss the Minnesota CS trial (26) because of its short duration which he would have no doubt accepted if the result had went his way. Nevertheless, despite its short duration, the Minnesota CS actually provided a large number of events, and the overall analysis found no reduction whatsoever in CHD or mortality events. In fact, there were non-significantly more CHD events and overall deaths in the lower cholesterol group suggesting that maybe it is a good thing the trial was not longer, since these results are consistent with longer studies employing a similar intervention (omega-6 rich oils) suggesting even larger increases in CHD events and mortality (27, 28). So its likely that if the study was longer it would have ended up in disaster, not benefit as Steinberg seems to believe.

There are other trials cited by Steinberg which don't make much sense. For example, Steinberg cites the non-randomized/non-blinded Anti-Coronary Club (29) which not only employed multiple interventions, but also found a greater number of deaths from all causes and deaths from CHD in the lower cholesterol group. Of course, imbalances between the groups could have played a part in such a non-randomized study, but it is absurd to claim a result as "positive" when there are more deaths in the intervention group. This should not be dismissed, as we are talking about total mortality, which is the most reliable endpoint in any study, especially in a non-blinded trial. Nevertheless, Steinberg rightly acknowledges that the study was "seriously flawed". In the Medical Research Council (30), which Steinberg rightly calls a "negative study" there were non-significant differences between the groups, including strikingly similar rates in the harder endpoints of CHD/CVD/overall death. Steinberg also claims that the St. Vincent's Hospital study was "a case-control study, not a randomized trial", but fails to mention that it did originally have a randomized comparison with five years follow-up. Maybe Steinberg does not mention this better controlled comparison because the results were not in accord with his beliefs (92).

What we have then is a multitude of negative trials: La Veterans (23), Medical Research Council (30), Minnesota CS (26), Rose Corn Oil Trial (32), Sydney Diet-Heart Study (28), DART fat arm (31), WHI (33), St. Vincent's Hospital Study (92), and the Research Committee low-fat trial (34). In fact, if some of the better controlled fat replacement trials ("modiﬁed fat intake") are pooled in an analysis (23,26,28,30,32,90), there is a non-significant 5% increase in total mortality for unsaturated diets (91). In others words, the evidence from dietary trials does not support Steinberg, and in reality argues against his position. This is even clearer when one considers that many of these trials may have had confounders that favored the lower cholesterol groups e.g. less trans fat, less processed foods. Steinberg should also take note that the most successful dietary trials ever conducted had little to no reductions in cholesterol levels (in comparison to the control group of course), and achieved benefits in short time, suggesting together with the negative trials, that reductions in cholesterol are irrelevant (31, 35-37).

Speaking of the LRC-CPPT trial (38), Steinberg claims that the use of the one-tailed test was appropriate. However, the issue here is not really a one-tailed test, but the fact that it was never prespecified and used such a low standard (one-tailed at 0.05 rather than 0.025). Using conventional statistics, the primary endpoint of the trial was not statistically significant, and the decrease in CHD death was nowhere near statistical significance including no decrease in the objective endpoint of total mortality. Also, although less studied than other drugs, resins may actually have pleiotropic effects (39-42). Despite all of this Steinberg somehow finds the results convincing as evidence to lower cholesterol. Steinberg also mentions the POSCH trial (43), but nowhere does he mention that the surgery resulted in weight loss (among other effects), already recognized by others (44), and neither does he mention that the results were not statistically significant at the formal end and instead cites an observational follow-up.

Steinberg apparently thinks that fibrates and niacin are effective drugs even though fibrates fail to lower CHD/CV mortality and total mortality (45,46,93), and niacin fails to lower these same endpoints (47-50,93). This is despite the fact that these drugs "improve" numerous lipid markers and also have pleiotropic effects. Claiming that niacin in the Coronary Drug Project (48) was a success is ridiculous, since there was no reduction in its primary endpoint of total mortality including CHD/CV mortality at the end of the formal trial, which is all you really need to know. Instead, Steinberg cherry-picks a few lesser important secondary endpoints, and an observational follow-up, which is problematic as already pointed out by others (51,52). Other drugs that lower cholesterol have also failed miserably such as hormones (53-58), CETP inhibitors (59-61,93), and ezetimibe (99). Note carefully: fibrates, niacin, hormones, resins, CETP (and sPLA2) inhibitors, and ezetimibe, all fail to reduce CHD/CV death and total mortality despite "favorable effects" on cholesterol markers.

What about statins? In the section about statins Steinberg asks: Is the effect of the statins on coronary event rates all due to the extent to which they lower LDL? Or do their so-called pleiotropic effects (i.e. effects independent of cholesterol lowering) also play a significant role? The implication with these questions is that the pleiotopic effects may be responsible for only part (not all) of the benefits. The problem is that Steinberg (or anyone) has never proved that the benefits of statins are due to LDL lowering per se in the first place, and so there is the third possibility that the pleiotropic effects are responsible for all the benefits.

Even though the modest benefits of statins are probably due to its pleiotropic effects, the so called benefits of statins are without doubt, greatly exaggerated. Steinberg states that "The 4S study showed, for the first time in any cholesterol-lowering trial, a significant decrease in all-cause mortality". What Steinberg does not mention is that this is also the last time such a reduction in mortality was seen. The trial has never been replicated, was stopped based on an interim analysis, and had major conflicts of interest (62). The mortality reduction seen in LIPID (63) was not seen in a similar population in CARE (64), the latter being the better designed study, and HPS (65) failed to report results for all groups involved (factorial design), and claimed mortality benefits for numerous subgroups, which was not confirmed in later studies.

There is controversy with regard to statin use in primary prevention, and meta-analyses only show mortality reductions of around 10%, some not statistically significant. Also, without going into detail, most of these studies are of poor quality, resulting in uncertainty as to whether statins should be used this population (66,67).

Statins have also failed to lower mortality in the elderly (68), failed to lower CHD/CV death and total mortality in hypertensive patients (69,70), failed to lower coronary events, CV/cardiac death, and total mortality in heart failure patients (71,72), failed to lower CHD death, CV/cardiac death, and total mortality in kidney patients (73-76), failed to lower CV death and total mortality in aortic stenosis patients (77), failed to lower CV/cardiac death and total mortality in stroke patients (78), failed to lower CV events, CHD/CV mortality and total mortality in diabetic patients (73, 79-82), and have failed to lower CHD death and total mortality in secondary prevention patients using intensive treatment (83,84).

In short, even with all the "favorable effects" of statins, both lipid and non-lipid (pleiotropic), these drugs are next to useless. Of course, corruption and a lack of transparency are major problems in the pharmaceutical industry (94-98), and another reason why one should not place too much weight on such research, especially the earlier statin trials (88,89).

One other thing you would notice from those supporting cholesterol lowering (including Steinberg) is that they often refer to non-randomized analyses e.g. a graph of many studies apparently showing that the greater the reduction in cholesterol the greater the reduction in risk, or analyses claiming that "each 1 mmol/L reduction in LDL...". Do not be fooled by this, as these analyses are non-randomized and inevitably problematic, as already pointed out by researchers before (85,86). What you have to look at is the randomized comparison, which is the whole purpose trials are set up in the first place.

In the end, there is no "preponderance of evidence", and to support Steinberg's view you have to selectively cite the evidence, selectively interpret the evidence, and create a bunch of unproven ad hoc hypotheses to explain away a massive amount of the data. You get the impression that in Steinberg's mind, cholesterol was already guilty before he reviewed the evidence, and he interprets the evidence based on this belief rather than looking at the evidence objectively. Given the utter failure of cholesterol lowering treatments to lower CHD/CV mortiality and total mortality in almost every study, maybe it is really time for a reappraisal of the idea that cholesterol is to blame (87-89).

As another reviewer stated, most of the information in this book is already available in Steinberg's Thematic review series available on the net for free. If you decide to get this book be sure to pick up other books for balance: my recommendations would be "The Great Cholesterol Con" by Anthony Colpo, "Cholesterol is Not the Culprit: A Guide to Preventing Heart Disease" by Fred Kummerow, and "Cholesterol and statins: Sham science and bad medicine" by Michel de Lorgeril.

References

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57) Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results From the Women's Health Initiative randomized controlled trial. JAMA. 2002;288(3):321-33.
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Tim Josling

Disappointing, one sided and shallow

Reviewed in the United States on May 27, 2019

The author claims that he presents the totality of evidence including large amounts of evidence that you will not read about in the many sceptical books.

What I found was a very one-sided presentation and nothing that was new.

All the studies that support his point of view are ground breaking, solid, convincing etc. The studies that do not are ignored or subjected to selective demands for rigor.

There is very little by way of real and deep insight into the processes underlying heart disease. This was the most disappointing aspect - after reading the book I felt I had learned very little and that I had wasted my time.

You could summarise the book very succinctly as "shut up and take statins". Yes statins reduce LDL and according to industry sponsored studies they reduce the risk of dying of a heart attack somewhat. Is this purported effect because they reduce LDL? Who knows. No-one reading the book will be significantly enlighted on this or any other point.

You would read this book thinking that statins only have rare and/or minor side-effects. Tell that to people taking it.

This is not the book we are looking for. We really need a stronger rebuttal of the sceptic case, assuming that is possible.

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Mr burn

Industry funded crap

Reviewed in the United States on October 13, 2019

industry funded crap.
When I was in med school total cholesterol levels of < 300 with LDL < 200 were acceptable.
Now, through the drug company funded oversight groups, and studies, multiple mandates have lowered the levels time and again to suit their sales quotas.
Misinformation and disinformation.

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Eva Terry

Biased and unbalanced

Reviewed in the United States on March 10, 2011

The author carefully builds his argument that the lipid hypothesis is valid. However, he ignores the mountain of evidence that argues against the lipid hypothesis. He also ignores the clinical studies that demonstrate the futility of lowering LDL as a means to combat cardiovascular disease.

Overall, this books contains nothing but justifications and rationalizations to cling onto an outdated concept.

To save money, read his Thematic Review series: The Pathogenesis of Atherosclerosis, An Interpretive history of the cholesterol controversy from the Journal of lipid Research.

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