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Monday, January 4, 2010

The Cholesterol Theory of Heart Disease is Nonsense

Anthony Colpo who I have learned much from especially back in the days he was regularly putting out good analysis of many health items on The Omnivore.com. Here is a new newsletter I just saw published on the_omnivore@yahoogroups.com. I've provided it in full here. It is a bit long but thorough as I have found him to be. Thank You Anthony!
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The Cholesterol Theory of Heart Disease is Nonsense
Posted by: "theomnivorenewsletter" ac.theomnivore@gmail.com theomnivorenewsletter
Sun Jan 3, 2010 4:30 pm (PST)


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 naïve 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-Co\
n.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.

1. 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


1. 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.

2. 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/0970\
081790


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. Rossebø 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:
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=showproducts&se\
archWhat=books&ProduktNr=251867

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.
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&Artikel\
Nr=229002&Ausgabe=250361&ProduktNr=223977&filename=229002.pdf

9. http://www.fao.org/DOCREP/005/AC911E/ac911e07.htm#bm07.4.3


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**DISCLAIMER**
The information in this email is for information purposes only and is
not to be construed as medical advice. The author accepts no liability
for any harm , real or imagined, associated with the use of this
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