part two Cholesterol and mortality

[Guest guest]

RESEARCH REPORT

Cholesterol – A Review: Part II

by William R. Ware, PhD

CHOLESTEROL AND MORTALITY

"To arrive at a contradiction is to confess an error in one’s thinking; to maintain a contradiction is to

abdicate one’s mind and to evict oneself from the realm of reality" Ann Rand

As discussed in Part I, mainstream medicine regards the cholesterol-heart disease connection as an established

fact. It has been elevated almost to a sacred belief. Anyone who questions the foundations of this hypothesis

runs the risk of being branded a heretic or someone who is unable to appreciate the wisdom and beauty of one

of medical science’s outstanding achievements. Many careers have been built on the Cholesterol Hypothesis,

careers replete with high profile medical academic positions, drug company supported lectureships and

consulting and financial support for research. Any medical professional who openly expresses serious doubts

runs the risk of being ostracized by his or her peers. But there are indeed deniers and skeptics, and it seems

important that Newsletter readers are aware of their views [1,2]. Avid readers of the British journals The Lancet,

the Quarterly Journal of Medicine and the British Journal of Medicine are probably among those most keenly

aware of these voices crying in the wilderness. Such criticism or questioning is rare in North American Journals.

But science thrives and progresses on dissent, controversy and attempts to falsify hypotheses, a fact that seems

underappreciated by those who guard the conventional wisdom. Some would argue that this does a profound

disservice to the progress of medical science and the ultimate discovery of so-called truth.

Painting cholesterol and in particular LDL as demons, sort of on a par with toxic substances or even pathogenic

bacteria, is unfortunate since this almost totally obscures the fact that cholesterol is essential for our wellbeing. It

is involved in ensuring the integrity of cell walls and in the synthesis of testosterone, estrogen,

dehydroepiandrosterone (DHEA), progesterone, cortisol, and last but not least, vitamin D by photosynthesis from

the exposure to skin to ultraviolet light. We produce cholesterol in the liver, and in general, high dietary

consumption results in lower endogenous production, and many feeding studies have found virtually no

dependence of serum levels on dietary intake [3]. This is obviously inconsistent with the conventional wisdom

which suggests limiting the dietary intake of cholesterol, a recommendation which the food industry picked up on

and has played to the limit. Finally, the Cholesterol Hypothesis has resulted in widespread screening and a vast

amount of anxiety, stress and pharmaceutical intervention over cholesterol levels labeled elevated and declared

dangerous and even life-threatening.

 

What we will call the Cholesterol Hypothesis simply states that that high levels of total cholesterol, i.e. TC and

LDL cholesterol (LDL), cause atherosclerosis and are associated with elevated risk of developing coronary heart

disease. The word cause is important in this context because cause is relatively difficult to establish in many

human disorders and CHD appears to be one of them. The reason in part is the extraordinary complexity of the

sequence of events associated both with the development of atherosclerosis and the events leading to an acute

coronary episode, e.g. a heart attack. One thing that appears clear is that the simplistic view of cholesterol

clogging up ones arteries (the kitchen drain analogy) is just that—simplistic. The evidence against the

Cholesterol Hypotheses as regards cholesterol-causing atherosclerosis was reviewed in Part I.

STUDIES CONCERNING CHOLESTEROL AND MORTALITY

Part II of this review series will deal with the question of cholesterol levels and both overall mortality and

coronary heart disease mortality in men and women of all ages who are free of coronary heart disease as

evidenced by the absence of chronic or acute angina, a history of a heart attack intervention to open an artery or

insert a stent or coronary artery bypass. One frequently sees the concern put forward in the medical literature

that some intervention or procedure has not been proven to favorably influence mortality and thus its value is

questionable until this aspect is settled in randomized trials. In fact, critics of screening frequently use this as a

"gold standard." Some consider the impact on mortality to be an important if not essential factor in the riskbenefit

equation and in addition, there is always the possibility that an intervention or procedure actually

increases mortality. In addition, impact on mortality is viewed by some as important in judging risk factors.

Overall mortality is a relatively easily established endpoint because there is little room for debate since the

patient is dead, but disease specific mortality is another matter since in may not always be clear as to what was

actually the cause of death and death certificates can be inaccurate or even simply wrong about this.

One of the largest and most recent studies to address the mortality issue was published in 2004 and involved

almost 150,000 Austrian men and women ages 20 to 95 years [4]. The study involved multiple evaluations of

total cholesterol over a 15-year period between 1985 and 1999. Overall (all-cause) mortality and CHD mortality

were evaluated by comparing the lowest and highest quartiles of TC with the middle quartiles used as reference.

The following results are of particular interest.

• For men, there was no statistically significant association between all-cause mortality and high TC ( >

248 mg/dL) for age > 50 years. For high TC, there was a weak association for ages < 49 years. For low

TC (<187 mg/dL) there was an increase in the mortality rate.

• For women, there was no statistically significant association between high TC (> 244 mg/dL) and allcause

mortality at any age. For low TC (< 184 mg/dL), there was an increased risk of all-cause

mortality for ages >49 years of age.

• For men, high TC was significantly associated with CHD mortality for the age group 20-49 years, and a

weak positive association was also found for those ≥ 65 years.

• For women, high TC was associated with weakly elevated CHD risk only in the age group 20-49.

However, some studies discussed below failed to find this enhanced risk.

• For both men and women, there was no association between either high or low TC and stroke mortality,

but low TC was associated with increased risk of cancer mortality in men 50-64 years and women of

>50 years of age.

Thus for overall mortality, high TC was not a significant issue for men over 50 or for women at any age, but in

fact there was evidence of increased overall mortality associated with low cholesterol. For men under 50 years of

age, overall mortality exhibited a U-shaped curve vs. TC. For women, the mortality rate curve which has been

seen in many studies is more or less flat at high to intermediate TC levels and then slopes upward indicating

increased mortality associated with low TC.

The weak positive association between CHD mortality and high TC for men over 65 is inconsistent with a large

number of earlier studies. Ravnskov has summarized these studies in a recent commentary [5]. His review

summarized 13 studies, the largest 4 of which involved over 12,000 men and women, where 7 studies found that

the lower the TC or LDL, the higher the mortality, and all 13 studies found that high TC or LDL did not predict

increased mortality in this age group. Seven of these studies had subjects in the age group 60-65 years and

one exhibited an inverse relationship where increasing TC decreased coronary mortality (this was actually part of

the famous Framingham Study).

Similar results related to elderly men were reported for the Honolulu Heart Program follow-up study which

involved over 3500 men followed for a maximum of 20 years [6]. The age range was 71-93 years. Mean

cholesterol levels for the quartiles were 149, 178, 199, and 231 mg/dL. When the lowest quartile for TC was

used as reference, the relative risk for all-cause mortality decreased (0.72, 0.60 and 0.65) as TC levels

increased. Thus there was benefit rather than risk associated with high TC as it relates to all-cause mortality.

When results from the first year of follow-up were excluded, similar risk reduction with increasing TC were found.

This argues against the low levels being due to preexisting illness. In addition, the long-term follow-up in this

study, in the opinion of the authors, renders the hypothesis untenable that the low TC effect is due to

undiagnosed preexisting conditions that reduced TC levels. The authors state that, "We have been unable to

explain our results." This could be translated into a statement that the results are not in accord with the

conventional wisdom.

continued at: http://www.yourhealthbase.com/ihn183mx.pdf

 

for part one and other good reading see:

 

Issue 182...November 2007....16th Year

 

 

EDITORIAL

THIS MONTH's TOPICS

Multiple benefits of krill oil Omega-3 fatty acids and ADHD Omega-3 better than Ritalin More positive research for vitamin D Are high doses of vitamin D safe? Childhood sun exposure and MS Vitamin D and cardiovascular risk

NEWSBRIEFS Food additives and hyperactive behaviour in children Waist-to-hip ratio and atherosclerosis Magnesium intake and risk of type 2 diabetes Coenzyme Q10 and high blood pressure Vitamin B6 and colorectal cancer

RESEARCH REPORT Cholesterol - A Review: Part I By William R. Ware, PhD

 

The Prostate Monitor

EDITORIAL Modifiable risk factors for BPH Micronutrients and prostate cancer risk Early vs. deferred hormonal treatment of locally advanced prostate cancer

 

 

THE AFIB REPORT

 

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