Cholesterol and Heart Disease


dr_duane_graveline_m.d._134By Duane Graveline, M.D., M.P.H.

A healthy 50 year old male ponders this current ad for Lipitor®. "80% of people who have had a heart attack have high cholesterol" it says. This sounds very persuasive yet it is misleading because it all depends upon your definition of high cholesterol.

During my 23 years of general practice, before the era of cholesterol causality, the normal range of cholesterol was 100 to 300. Then overnight it seems, a new disease was created known as hypercholesterolemia and everyone with a cholesterol level of 200 or higher was afflicted with it.

This was the beginning of what I have come to call the cholesterol craze and the drug companies' progressive development of cholesterol lowering drugs, culminating in 1988 with the statins. Since then the acceptable, lower level of cholesterol has fallen from 200 to 170, then 150 and now 130, so this "80% of people who have had heart attacks have high cholesterol" is now true because nearly all people are "caught" by this newest lower value of 130.

At the rate of change seen these past twenty years, soon our acceptable level of cholesterol will be 110 and statin makers will be able to say with complete honesty that almost 100 percent of people who have heart attacks have high cholesterol simply because nearly everyone has high cholesterol if you lower the desirable level sufficiently.

A far more honest statement is that in more than fifty percent of new heart attack cases the cholesterol level is normal or below. Makes a huge difference in your reaction, doesn't it? This is the power of words.

The reality that cholesterol levels are completely normal in more than half of new heart attack cases is what convinced Uffe Ravnskov, MD ( The Cholesterol Myths ) and Kilmer McCully, MD ( The Homocysteine Revolution ) that the theory of cholesterol causation was wrong. It just did not fit the facts.

The debunking of the cholesterol causality theory began in 2003 with the JUPITER study - Justification for the Use of statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (Crestor®). ( Ref 1 ). Investigators began to enroll 17,802 men and women with no evidence of cardiovascular disease and normal to low levels of LDL cholesterol ( low-density lipoprotein ) into a trial. Their cholesterols were all under 130.

The study was to test whether subjects with enhanced inflammatory responses - elevated hsCRP level ( high sensitivity C-reactive protein ) might benefit from taking a statin. At study entry none were considered candidates for statin therapy. However, all trial participants had levels of the inflammatory bio-marker hsCRP equal to or greater than 2 mg/L, putting them at risk for future cardiovascular disease.

So by all existing standards - negative history of heart disease and normal cholesterol levels - these people were not candidates for treatment and ordinarily were not candidates for going on a statin. Half of this group was given a placebo. The other half received a moderate dose of a statin.

Eighteen months later the study was stopped by the ethics committee because of the comparatively high level of heart attacks and strokes in the placebo group. This one study showed the irrelevance of cholesterol to cardiovascular risk and the value of this new inflammatory marker, hsCRP. It also strongly suggested an anti-inflammatory benefit of statins.

Then in January 2008 the results of the ENHANCE trial ( completed in April 2006 ) were finally released. ( Ref 2 ) ENHANCE was a trial that compared one group taking simvastatin ( Zocor® ) with another taking Vytorin® ( simvastatin plus Zetia® ). The thickness and progression of arterial plaque of the participants was monitored for two years.

The addition of Zetia ( a non-statin cholesterol lowering drug ) to the statin simvastatin ( the Vytorin group ), as expected, lowered cholesterol more than in the simvastatin alone group. The endpoint of the trial was the growth of arterial plaque in the two groups.

Surprisingly to those convinced that cholesterol causes arterial plaque, the Vytorin group with the lower LDL cholesterol numbers had slightly increased arterial plaque overall. At best the addition of Zetia to simvastatin had no benefit at all even though total cholesterol was lowered.

In a recent National Institutes of Health ( NIH ) study that was terminated 18 months earlier than planned, 3,414 participants with heart and vascular disease were given either Zocor and a placebo or Zocor and Niaspan® and followed for 32 months. The trial was called AIM-HIGH ( Atherothrombosis Intervention in Metabolic Syndrome with Low HDL / High Triglycerides: Impact on Global Health ) ( Ref 3 ).

The AIM-HIGH trial ended 18 months early because it soon became evident that the addition of Niaspan had no significant benefit on heart attacks and strokes even though it further lowered LDL cholesterol levels ( the so-called "bad" cholesterol ) and raised HDL levels ( the so-called "good" cholesterol ) and it actually seemed to increase slightly the risk of stroke.

Given the conclusions from these studies, even the most steadfast advocate of cholesterol causation has to heed the evidence and rethink their philosophy. Cholesterol it seems is irrelevant to cardiovascular disease.

It is time for drug companies to rethink their strategy for the marketing of statins. Cholesterol is the wrong target in the fight against heart attacks and strokes. Ravnskov, McCully and all the eminently qualified membership of THINCS (The International Network of Cholesterol Skeptics) at www.thincs.org have been saying this for years. It is time to listen.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

Ref 1: http://www.ncbi.nlm.nih.gov/pubmed/18997196
Ref 2: http://www.ccjm.org/content/75/7/497.full
Ref 3: http://www.nih.gov/news/health/may2011/nhlbi-26.htm

June 2011
 

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