Most helpful critical review
157 of 222 people found the following review helpful
on September 12, 2013
A well-written, well-researched book challenging the conventional wisdom on cardiovascular disease could have been powerful, but this is clearly not the book. For starters, there are very few references to peer-reviewed studies, and with the primary source of the book's content being expert quotations called Moments Of Clarity, we're largely forced to accept the claims made by these experts at face value. Personally, I have a hard time doing this when many of the experts are of highly questionable standing (one, Dwight C. Lundell, even lost his medical license due to repeated malpractice ), and additionally, when the experts' opinions are being filtered through a potentially biased editor (Jimmy Moore). Adding to the madness is the fact that many experts hold contradictory opinions about which biomarkers best predict cardiovascular disease- some say triglycerides, some say the total cholesterol/HDL-C ratio, some say the triglyceride/HDL-C ratio, some say ApoB, some say blood sugar, some say oxidized LDL, some say small dense LDL, some say inflammatory markers like CRP. Pretty ironic for a book entitled "Cholesterol Clarity" I must say.
The two most legitimate experts in the book, Thomas Dayspring and Ronald Krauss, seem underutilized, especially Dayspring. If you know Dayspring, you know that he advocates testing for LDL particle number (LDL-P) over LDL cholesterol (LDL-C), and thinks that, contrary to the popular rumor about large LDLs being benign, these LDLs are in fact atherogenic . Dayspring is on firm ground in thinking this. Large LDLs have been linked to atherosclerosis in the MESA Study, in the CARE Study, in subjects with familial hypercholesterolemia, and in non-human primates . Yet despite stating on his website that Dayspring would get to make his case about LDL particle size in Cholesterol Clarity, Moore left his readers with the impression that large LDLs are benign, and limited Dayspring's input into the chapter on LDL particle size to:
"The least accurate way of estimating your atherogenic risk on a standard cholesterol panel would be to look at total cholesterol or LDL cholesterol."
... which in and of itself is questionable. Even though LDL-P is *probably* a better predictor of risk than LDL-C (particularly in the insulin resistant, where LDL-C tends to underestimate LDL-P), a recent study by Wayne State University found lifelong LDL-C values to be highly predictive of cardiovascular events .
As far as Ronald Krauss is concerned, Krauss recently participated in a study (left undiscussed in Cholesterol Clarity) showing that a diet very in red meat and saturated fat drove the production of small, dense LDLs . This means that even if small, dense LDLs were the only dangerous type of LDL, Moore's dietary regimen still comes off as potentially dangerous. This isn't the only study to raise red flags about diets very high in meat and saturated fat when it comes to cardiovascular health. In a study by Keogh et al., flow-mediated dilatation, a measure of arterial health, was impaired by a high saturated fat diet, but not a high carbohydrate diet . In a year long study by Richard Fleming, subjects consuming a high meat diet experienced an overall 39.7% progression in coronary artery disease, with a worsening of numerous risk factors including Lp(a), CRP, and fibrinogen . And in a study by Miller et al., the Atkins diet raised ApoB (largely interchangeable with LDL-P), raised CRP, and worsened flow-mediated dilatation, whereas the South Beach and Ornish diets improved the aforementioned biomarkers . Moore is skeptical of Ornish's Lifestyle Heart Trial since it didn't test nutrition alone, and also employed stress management, exercise, and smoking cessation. But the Miller et al. study tested nutrition alone, and found the Ornish diet to be beneficial. And although a controversial 2010 meta-analysis found no association between saturated fat and cardiovascular disease, its methodologies have been critiqued [9, 10, 11], and other meta-analyses have found benefit to replacing saturated fat with polyunsaturated fat [12, 13, 14, 15], which does not appear to be pro-inflammatory contrary to the assertions of the book .
Moore downplays the cardiovascular concerns about low carbohydrate, high saturated fat diets by pointing out that they raise HDL-C and lower triglycerides. However, a meta-analysis of 108 randomized controlled trials found virtually no evidence that raising HDL-C reduced the rate of coronary heart disease, and concluded that existing evidence favors reductions in LDL-C as the primary goal of therapy . One reason HDL-raising can backfire is that (surprise, surprise) saturated fat consumption impairs its anti-inflammatory properties . And while keeping triglycerides low is prudent, a low carbohydrate diet is not necessary to do this- complex carbohydrate based diets supplemented with omega 3s are also highly effective (more effective than a diet high in saturated fat according to my reference) .
This book tries to scare you away from diets which lower serum cholesterol by, among other things, pointing out that the brain is rich in cholesterol, and pointing out associations between low serum cholesterol, cancer, and depression. However, virtually all brain cholesterol is synthesized within the brain since lipoproteins can't cross the blood-brain barrier . And even if there are studies showing an association between low serum cholesterol and cancer or depression, that doesn't necessarily mean those associations are causal. Multiple studies support the contention that it's cancer which causes low serum cholesterol, not the other way around [21, 22]. And if it's so clear that low cholesterol causes depression, then why is depression uncommon among hunter-gatherers and Asian cultures [23, 24] who tend to have low serum cholesterol [25, 26]? The book takes the fearmongering a step further by discussing the rare, genetic disorder Smith-Lemli-Opitz Syndrome (SLOS). SLOS results from a deficiency in an enzyme called 7-Dehydrocholesterol reductase, which is involved in cholesterol synthesis. This disorder isn't relevant to the average person since the average person possesses this enzyme, and can therefore synthesize cholesterol properly on a cellular level. A deficiency in 7-Dehydrocholesterol reductase has the additional effect of causing a toxic buildup of 7-Dehydrocholesterol . Chris Masterjohn failed to mention this, leaving readers with the false impression that the symptoms of SLOS result from cholesterol deficiency alone. Masterjohn discusses one half of the treatment for SLOS, a cholesterol-rich diet (yes, dietary cholesterol can be absorbed into the body, regardless of what some stubbornly think), but fails to mention the other half: a statin . The reason for this is that statins blunt the production of the cholesterol precursor mevalonate, which in SLOS patients, will eventually become trapped as 7-Dehydrocholesterol .
SLOS is not the only disorder in which statins have proven beneficial. Prior to the invention of statins, subjects with familial hypercholesterolemia aged 20-39 had 100x the cardiovascular mortality, and 10x the all cause mortality of the general public . In a meta-analysis of 5 randomized, double-blind, placebo-controlled trials encompassing 30,817 patients, statins reduced the incidence of major coronary events 31% and all cause mortality 21% . Yet if you went by some of the opinions in this book, you'd think that statins are practically worthless and don't save lives. Yes, statins can have adverse side effects in some people, especially if not taken in conjunction with CoQ10, but I find it ironic for Moore that many of these same symptoms, including muscle cramps, constipation, headache, rash, and general weakness have been reported on very low carbohydrate diets . I also find it ironic that given the contempt Moore has for statins, he would attack Dr. Ornish, who successfully reverses heart disease without statins.
This book wants you to think of cholesterol as a "firefighter" which shows up to repair inflamed and damaged arteries. Why then is it well-documented that statins reduce inflammation and improve endothelial function while simultaneously lowering cholesterol [33, 34, 35, 36, 37]? And if cholesterol is just part of the body's damage control formula, what would the well-established fact that saturated fat raises cholesterol  mean, if not that saturated fat is inherently damaging? The reason saturated fat raises cholesterol is actually quite well-known. Certain saturated fatty acids, chiefly palmitic, myristic, and lauric acid, down-regulate LDL receptors in the liver, reducing LDL clearance from the blood (dietary cholesterol can also do this) [39, 40, 41]. Fred Pescatore evidently never got the memo, as he states:
"I don't think medical science has any idea why LDL-P would rise above 2,000 or even 3,000 in some people who eat a low-carb diet."
We see a variation on the "cholesterol is just a firefighter" theme with Dr. Ravnskov, who states:
"Cholesterol is used to stabilize the tissue after an infection. All scars in the body are rich in cholesterol, including those in the arterial wall. In my view atherosclerotic lesions are just scars after previous infections."
This idea is actually backwards, since infections appear to have an *anti* atherosclerotic effect. Doenhoff et al. worked with two groups of mice made genetically susceptible to atherosclerosis by knocking out the apolipoprotein E gene. Both groups were given the same diet, but one was infected with Schistosoma mansoni, which like many parasites, is capable of stealing cholesterol from the host's gut. The infected mice did not develop atherosclerosis, while the control mice did - the exact opposite of what Ravnskov's hypothesis would predict. A high prevalence of parasitic infections  coupled with the low saturated fat content of wild game  likely explain the low cholesterol of hunter-gatherers- who, once again, in contradiction of Ravnskov, do not ordinarily develop atherosclerosis .
As one final note, this book manages to grossly mislead about Ancel Keys, who is vilified by the low carbers for putting saturated fat on the map as a contributor to cardiovascular disease. Moore states:
"In the 1950s, nutritional health scientist Ancel Keys began investigating why American businessmen were experiencing high rates of heart disease; he surmised it had something to do with higher cholesterol. Out of this came his infamous Seven Countries Study, which concluded that those nations with diets lower in animal fat had lower rates of heart disease, while those nations with diets higher in animal fat had higher rates of heart disease. The results seemed so neat and clean, and yet it was a totally bogus study. Although Keys could have included a total of twenty-two countries in his research data- including countries where people ate more fat with very little heart disease and countries where people ate less fat with more heart disease- he chose to leave those statistics out of his conclusions. They simply didn't fit his theory about saturated fat: that it raises cholesterol levels, which leads to heart disease."
Moore has made a common mistake, which is confusing the Seven Countries Study with Keys' 1953 paper "Atherosclerosis: A Problem In Newer Public Health." The data about twenty-two countries pertains to the 1953 paper, not to the Seven Countries Study, which began in 1958 . Moore also fails to mention that the two researchers who chastised Keys for not using data from all 22 countries in his 1953 paper, Jacob Yerushalmy and Herman Hilleboe, were pointing out that other food categories correlated with heart disease more strongly than percentage of calories from fat, namely total calories from animal protein. Total calories from carbohydrates did not correlate with heart disease, while total calories from vegetable fat and vegetable protein correlated inversely with heart disease . While these data may not in and of themselves "prove" that animal protein causes heart disease, or that vegetable fat and protein are protective (especially when many of the countries had methodological issues with their data, which was Keys' stated reason for excluding them) it doesn't change the fact that Moore is bungling the history and omitting important details.
Moore would also have you believe that, per Keys' sinister influence, Americans "dutifully cut their fat intake," resulting in the obesity epidemic. Yet data I found from the USDA shows fat consumption steadily increasing since the 1950s, mainly from added fats and oils . And while the data shows an increase in carbohydrate consumption, it's primarily from high fructose corn syrup, which practically no one other than the Corn Refiner's Association would argue is healthful. Early 20th century Americans ate a comparable amount of carbohydrates to those eaten today (primarily from grains and potatoes), and did not share our epidemic of obesity . It's also worth pointing out that Keys advocated the Mediterranean diet (one detail this book manages to get right), and although their eating habits have deteriorated somewhat in recent years, Mediterranean countries like Spain and Italy have never had obesity rates close to those of the United States .
I could continue exposing the problems with this book, but hopefully you see by now why it should be taken with a grain of salt. It's biased, full of factual errors, and seems designed to "preach to the choir" and convince people already following the low carb lifestyle that they're not damaging their arteries in any way. It seems unlikely to win over any new converts owing the lack of proper citations, easily demonstrable falsehoods, and dubious cast of "experts."
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