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Leugens over de rol van verzadigde vetten en cholesterol

Een belangrijk artikel over de onzin van de anti-cholesterol en anti-verzadigd vet industrie en de gevaren hiervan. Mocht iemand dit artikel kunnen vertalen email mij dan even.....

Ron Fonteine


The Cholesterol Theory of Heart Disease is Nonsense

I've been telling people for years that the anti-cholesterol, anti-saturated fat paradigm is not only nonsense but potentially dangerous. The latest confirmation of my stance comes from two recent studies that - in stark contrast to vigorously hyped anti-cholesterol research – have been ignored by the mainstream health media.

The most recent of these studies was published in the November 15, 2009 issue of the New England Journal of Medicine. The ARBITER 6–HALTS trial compared the effects of two combination therapies - either ezetimibe+statins or niacin+statins - on carotid intima-media thickness over a 14-month period. Measurement of carotid artery intima-media thickness is used to indicate the extent of atherosclerosis and for assessing cardiovascular risk.

All of the 363 subjects enrolled in the trial were already taking cholesterol-lowering statin drugs. Statin drugs have become the darlings of the medical establishment due to their ability to lower both total and LDL cholesterol, while ezetimibe has become a popular adjunct to statin treatment thanks to its LDL-lowering actions. The subjects were randomly assigned to receive either extended-release niacin at a target dose of 2000 mg per day or ezetimibe at a dose of 10 mg per day. The niacin was increased from an initial dose of 500 mg at bedtime, by 500 mg every other week, to the maximum tolerated dose (up to 2000 mg at bedtime).

The subjects were men and women (mean age 65) with atherosclerotic cardiovascular disease or a coronary heart disease (CHD) risk equivalent, including diabetes, a 10-year Framingham risk score of 20% or more, or a coronary calcium score above 200 for women or 400 for men.

A total of 208 patients had completed 14 months of treatment when the study was called to a halt. Initial LDL levels were similar in both groups, but etezimibe produced greater reductions in LDL than niacin (-17.6 mg/dl vs -10.0 mg/dl). If you believe the relentless barrage of anti-LDL propaganda emanating from our ever-so-wise, impartial, objective and totally incorruptible health authorities, then this should have produced greater improvements in the etezimibe group.

But it didn't.

When the data was analyzed, it was observed that niacin produced a significant reduction in carotid intima-media thickness at both 8 and 14 months. No significant overall change in carotid intima-media thickness was seen with ezetimibe.

The researchers did however find a significant inverse relationship between changes in LDL cholesterol and carotid intima-media thickness in the ezetimibe group, such that a "paradoxical" increase in the carotid intima-media thickness was seen in patients with greater reductions in LDL cholesterol (rather than simply acknowledge the cholesterol theory is bollocks, researchers invariably label any and every uncomfortable contradiction to this theory a "paradox").

Major adverse cardiovascular events also occurred at a significantly greater rate in the ezetimibe group (9 of 165 patients [5%]) than in the niacin group (2 of 160 patients [1%]).

A peek at the dropout data also reveals some interesting findings. Among 363 patients enrolled in the trial, 44 had left the study by the time it was terminated on June 4, 2009: 16 of 176 (9%) in the ezetimibe group (of whom 9 had been withdrawn and 7 had died) and 28 of 187 (15%) in the niacin group (of whom 27 had been withdrawn and 1 had died). Adverse drug effects were cited as the reason for withdrawal in 3 of 9 patients receiving ezetimibe and 17 of 27 patients receiving niacin. The well-known side effect of flushing was reported in 36% of patients in the niacin group[1].

Bottom line: Ezetimibe produced greater reductions in LDL cholesterol (the so-called "bad" cholesterol) but resulted in no overall improvement in carotid intima-media thickness, while individual results showed greater thickening with greater LDL reductions. The use of etezimibe was also accompanied by a higher number of heart attacks and deaths.

Yep, the "paradoxes" flowed thick and fast in this study. Of course, those of you who have read The Great Cholesterol Con will know that there was absolutely nothing paradoxical about these findings – the cholesterol theory is, and always has been, utter nonsense.

So Popular But So Useless

This is hardly the first time ezetimibe has shown itself to be a dud. The SANDS trial, examining type 2 diabetic American Indians, found that ezetimibe plus statins produced no greater improvement in carotid intima-media thickness than statins alone[2].

In the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) trial, 1873 patients with mild-to-moderate, asymptomatic aortic stenosis (abnormal narrowing of the heart's aortic valve) received either 40 mg of simvastatin plus 10 mg of ezetimibe or placebo daily. During a follow-up of 52.2 months, simvastatin and ezetimibe, as compared with placebo, did not reduce the composite outcome of combined aortic valve events and ischemic events in patients with aortic stenosis.

The simvastatin–ezetimibe group did however experience something that the placebo group did not: an increased cancer risk. A statistically significant excess of incident cancers was observed in the simvastatin– ezetimibe group, with 105 in that group as compared with 70 in the placebo group. In addition, deaths from cancer were more frequent in the simvastatin– ezetimibe group (39 deaths vs. 23 in the placebo group). There was also a significant increase in the number of patients with elevated liver enzyme levels in the simvastatin–ezetimibe group[3].

Increased cancer risk from cholesterol-lowering drugs has been observed previously. In the PROSPER study featuring elderly subjects - the demographic in whom you would most likely expect an increased cancer risk to manifest itself during the relatively short duration of a clinical trial - an increased mortality from malignant causes among those taking pravastatin negated the reduction in cardiovascular deaths[4]. Etezimibe, meanwhile, inhibits the absorption of phytosterols and other phytonutrients linked to protection against cancer[5].

The ENHANCE trial was a double-blind, randomized, 24-month endeavour comparing the effects of 80 mg of simvastatin combined with either with placebo or with 10 mg of ezetimibe daily in 720 patients with familial hypercholesterolemia. Mean levels of LDL cholesterol decreased from 317.8 mg/dl per to 192.7 mg/dl in the simvastatin-only group and from 319.0 mg/dl to 141.3 mg/dl in the combined-therapy group. Despite their significantly greater decrease in LDL levels, the simvastatin+ ezetimibe group experienced no statistically significant greater decrease in carotid intima-media thickness.

Nor was there any advantage in incidence of regression in mean carotid-artery intima–media thickness or new plaque formation. No significant change was observed in mean maximum carotid-artery intima–media thickness, mean measures of the intima–media thickness of the common carotid artery, the carotid bulb, the internal carotid artery, the femoral artery, nor in the average of the mean values for intima–media thickness in the carotid and femoral arteries. Investigator-reported cardiovascular events were noted in seven patients in the simvastatin group (including 1 death from a cardiovascular cause, 2 nonfatal myocardial infarctions, 1 nonfatal stroke, and 5 coronary revascularization procedures) and in 10 patients in the combined-therapy group (including 2 deaths from cardiovascular causes, 3 nonfatal myocardial infarctions, 1 nonfatal stroke, and 6 coronary revascularizations)[6].

Since its introduction in 2002, ezetimibe has become the primary adjunct to statins for reducing "elevated" LDL. This is despite the fact that it has so far shown itself to be totally incapable of actually producing any meaningful health benefit for the people who take it. In today's bizarro drug company-owned health arena, where cholesterol reduction has become a sacred end in itself, a woeful inability to reduce heart attack or death is swept aside as a minor inconvenience. There's money to be made in them thar lipid-lowering drugs, to hell with any profit-destroying notion that they are largely a waste of time and money…

WHO Says the Saturated Fat Theory is Garbage?

A recent special issue of Annals of Nutrition and Metabolism was devoted to "Fats and Fatty Acids in Human Nutrition". This issue was the result of a joint FAO/WHO Expert Consultation held in Geneva, November 2008 and contains "the background papers which have been prepared by a panel of carefully selected experts and have served as the basis for the updated dietary recommendations of FAO and WHO"[7]

One of the papers presented in this special report was a sweeping review of both prospective epidemiological studies and clinical trials examining the relationship between dietary fat and CHD[8]. This review was conducted by researchers from the Department of Human Nutrition at the University of Otago, Dunedin , New Zealand.

I must confess that when I initially pulled up the PDF of this study (which you can freely access from the link below), I was fully expecting more of the same old fat- and cholesterol-phobic hoopla that has regrettably characterized public health recommendations for almost half a century. Instead, I was pleasantly surprised. In fact, pleasantly shocked is a more fitting description. Despite being published under the auspices of one of the world's largest health organizations, the report actually tells…the truth!

After examining 28 prospective epidemiological studies, the researchers reported that:

"Intake of total fat was not significantly associated with CHD mortality..." (p. 175)

"Intake of total fat was also unrelated to CHD events..." (p. 175)

"Intake of TFA [trans fatty acids] was strongly associated with CHD mortality..." (p. 181)

"Intake of SFA [saturated fatty acids] was not significantly associated with CHD mortality...

Similarly SFA intake was not significantly associated CHD events..." (p. 181)

Their pooled analysis of data from randomized controlled clinical trials showed:

"...fatal CHD was not reduced by either the low-fat diets... or the high P/S diets [diets high in polyunsaturated fats and low in saturated fats] ...". (p. 188)

On page 193, they conclude:
"There is probably no direct relation between total fat intake and risk of CHD."

If you were expecting this rare gem of health authority-sanctioned honesty and factual reporting to be reflected in said health authority's dietary recommendations to the public, then you clearly know little about the mechanics of these anachronistic juggernauts. Maintaining the status quo is a self-serving activity of utmost importance to reigning orthodoxies. Changes to currently accepted diet and health recommendations occur almost imperceptibly over time, as small modifications that "advance" the current body of knowledge but never upset the underlying foundational dogma itself. Such modifications typically include the inclusion of politically acceptable discoveries (such as the cardiovascular benefits of omega-3 fatty acids from fish and fish oils). However, the wholesale embrace of politically incorrect findings is unthinkable. As such, the world's health authorities continue to preach the kind of nonsense that rational minds would associate with the ignorant, superstitious thinking of the Dark Ages. Such nonsense includes the belief that cholesterol, an essential life-sustaining substance that Mother Nature saw fit to include in the membranes of all our cells, to protect our nervous systems, and to use as the basis for production of our most important hormones, is in fact toxic and must be lowered at all costs.

And so it is in this case: despite the conclusions of the aforementioned review, WHO are still currently preaching the same old anti-cholesterol/anti-saturate hogwash in their CHD prevention guidelines[9].

Where's Your Head at?

Some of you reading this will do further investigation and will conclude of your own volition that what I have reported above is factual. Some of you will be confused and will not know what to make of what I have just reported; it sounds compelling but at the same time you have great difficulty accepting that so many "prestigious" health authorities, government bodies, medical associations, doctors, journalists, authors, and numerous other assorted talking heads could be so wrong. Such a mindset reveals a rather na´ve understanding of human nature. No matter how prestigious and well-funded the organization or
profession, it is still comprised of fallible human individuals with a deep-rooted evolutionary-programmed tendency to follow the herd and subscribe to groupthink.

A minority of readers will even become angry at what I have just written, offended by my temerity to report facts which so blatantly contradict what they have come to believe. My response to those who fall into this category is…too bad. After years of coming under attack from the disgruntled worshippers of various scientifically untenable nutrition paradigms, I'm totally over trying to reason with the unreasonable. My aim is simply to relay research findings to those who may find the information useful, not to pander to the fragile sensibilities of those who attain emotional solace in certain diet and health beliefs.

Life, if you allow it to be so, is a fascinating voyage of continual discovery. If you wish to make any meaningful progress during this voyage, you will frequently need to re-examine beliefs that you have become comfortable with, and you must be prepared to discard these beliefs if the evidence dictates.

For those prepared to do this, and who would like to further examine the contrarian side of the cholesterol story, may I recommend the following resources:

1.The Great Cholesterol Con by yours truly. Yes, it's my own book and after years of extensive research and effort I would of course be expected to gush on about what a wonderfully ground-breaking, enlightening and beneficial tome it constitutes. So don't listen to me; check out the non-partisan reviews by Amazon customers and folks like Chris Masterjohn, who considers the book "the most well-written and well-researched book on the "skeptic" side of the debate":   http://www.cholesterol-and-health.com/Anthony-Colpo-Great-Cholesterol-Con.html

A review of TGCC by Joel Kauffman can be viewed here: http://www.jpands.org/vol11no4/bookreviews.pdf

The Amazon page for The Great Cholesterol Con can be found here: http://www.amazon.com/Great-Cholesterol-Con-Anthony-Colpo/dp/1430309334

Those of you looking to save some money and wanting instant access to the book can get an ebook version here: http://www.thegreatcholesterolcon.com/

NOTE: To those of you who purchase my book (or already have it), please read Chapter 22 – over and over. Judging by the reviews and comments I have read about my book, that chapter appears to be overlooked by many readers. Yet if you are truly serious about preventing coronary heart disease, it contains the most valuable information you may ever come across.

2.My freely available article on LDL cholesterol, which appeared in the Journal of American Physicians and Surgeons: http://www.jpands.org/vol10no3/colpo.pdf

Also a letter of criticism and my reply:
http://www.jpands.org/vol11no1/correspondence.pdf

3.Fat and Cholesterol are Good for You by Uffe Ravnskov. Don't be fooled by the Atkins-like title; Uffe is a serious and meticulous researcher with dozens of peer-reviewed research papers to his name. I consider his writings essential reading for anyone interested in the cholesterol debate. His book can be obtained here:
http://www.amazon.com/Fat-Cholesterol-are-Good-You/dp/919755538X/ref=pd_sim_b_2

Uffe also heads a group called THINCS, whose website contains various articles and links to resources articulating skeptical views of the cholesterol theory:
http://www.thincs.org/

The website contains some great information; the page devoted to unpublished correspondence (critical letters that were knocked back by the journals they were submitted to) makes for especially interesting reading. Please note this does not constitute a blanket endorsement by myself of THINCS – while I find myself agreeing with almost everything Uffe writes, I don't agree with some of the assertions made by certain other THINCS members/contributors. I would urge readers to be especially wary of authors who make untenable claims about the superiority of isocaloric low-carb diets for weight loss (claims that have been repeatedly disproved in tightly controlled ward studies), and those who claim to have discovered a single unifying cause of CHD whilst ignoring the critical role of such factors as bodily iron stores, nutrition (especially refined carbohydrate intake), vitamin and mineral status (most notably magnesium), infectious disease, omega-3:omega-6 status, physical activity, obesity, and/or stress. 

4.Statin Drugs Side Effects and the Misguided War on Cholesterol by Duane `Spacedoc' Graveline. This former astronaut and physician was a key figure in alerting the public to the little-known statin side effect of transient memory loss, which has since been the subject of peer-reviewed articles and case reports. Those who are being cajoled by their doctors to begin statin drug use would be well advised to read this book:
http://www.amazon.com/Statin-Drugs-Effects-Misguided-Cholesterol/dp/0970081790

All the best,

Anthony Colpo


References

1.Taylor AJ, et al. Extended-release niacin or ezetimibe and carotid intima-media thickness. New England Journal of Medicine, Nov 26, 2009; 361 (22): 2113-2122.
2.Fleg JL, et al. Effect of Statins Alone Versus Statins Plus Ezetimibe on Carotid Atherosclerosis in Type 2 Diabetes. The SANDS (Stop Atherosclerosis in Native Diabetics Study) Trial. Journal of the American College of Cardiology, 2008; 52: 2198-2205.
http://content.onlinejacc.org/cgi/reprint/j.jacc.2008.10.031v1.pdf
3.Rosseb° AB, et al. Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. New England Joural of Medicine, 2008; 359: 1343-1356.
http://content.nejm.org/cgi/reprint/359/13/1343.pdf
4.Shepherd J, et al. PROspective Study of Pravastatin in the Elderly at Risk. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. Lancet, 2002; 360: 1623-1630.
5.Bradford PG, Awad AB. Phytosterols as anticancer compounds. Molecular Nutrition & Food Research, 2007; 51: 161-170.
6.Kastelein JJ, et al. Simvastatin with or without ezetimibe in familial hypercholesterolemia. New England Joural of Medicine, Apr. 3, 2008; 358 (14): 1431-1443.
http://content.nejm.org/cgi/reprint/358/14/1431.pdf
7.Fats and Fatty Acids in Human Nutrition. Annals of Nutrition and Metabolism, 2009; 55 (1-3). Available online: Link
8.Skeaff MC, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence from Prospective Cohort and Randomised Controlled Trials. Annals of Nutrition and Metabolism, 2009; 55: 173–201. Link
9.http://www.fao.org/DOCREP/005/AC911E/ac911e07.htm#bm07.4.3


 

 


 


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