Cholesterol reducing pills: Do they have a downside?

August 3, 2005

Medications taken against cholesterol may prolong life in the event of arteriosclerosis and perhaps even heart failure. However, new figures seem to indicate that many patients get serious side effects from taking such medications, which side effects could have been avoided had they also taken Co-enzyme Q10.

Millions of people worldwide use cholesterol reducing medicine in the form of statins. These people most often have clogged coronary arteries and the statins are used to protect them against further atherosclerosis, blood clots, and strokes. They work, but to a lesser degree than many people think.

If they are given to one hundred 40-80 year old people who are at high risk due to atherosclerosis or diabetes, they prevent about one coronary blood clot or one stroke per year. In the course of five years, about two deaths are avoided.

Many of the treated meanwhile develop heart failure, which is reduced pump function of the heart, because atherosclerosis damages the heart muscle permanently. They begin to complain of tiredness and increasing shortness of breath.

Is it risky to take cholesterol lowering pills in this situation? There can be debated. The debate is due to the way that the medicine works. It blocks the livers production of mevalonic acid, which is necessary for the production of cholesterol, but it also blocks the production of vital Q10! Not only does the blood’s cholesterol level fall, but also the bloods Q10 level.

Because Q10 is necessary for the tissues to create energy it is easy to imagine that a heart muscle which is weakened by heart failure, is further weakened when Q10 is removed.

Apparently statins work anyway. Statins are believed to lengthen life in heart failure. Not because they lower cholesterol, which may actually be damaging when suffering from heart failure, but because statins have other effects than reducing cholesterol. They are antioxidants and counteract inflammation. In addition they promote the creation of new blood vessels in the heart. None of these effects have anything to do with cholesterol.

Maybe the positive effects of statins outweigh the dramatic Q10 loss that they cause. Nonetheless, it is hard to believe that this loss is completely harmless, especially with heart failure.

The American cardiologist P.H. Langsjoen is one of those who warn that we find ourselves in an epidemic of heart failure with unclear reasons and who believe that statins could be one of the reasons.

At a congress in Los Angeles he put forth data which indicates previously unrecognised side effects. Two thirds of 51 newly referred statin treated patients complained of muscle pain, more than 80% were abnormally tired, and almost 60% had shortness of breath. When they stopped using statins and instead received Q10 (240 mg/day), most became symptom free.

At the same congress a randomised trial showed that muscle pain and tiredness was present in one out of every ten on those treated with statins, but disappeared when they took Q10 (100 mg/day). Just as important, more than half experienced an improved quality of life and many showed improved heart function.

Pills against cholesterol lengthen life, but it is necessary to take Q10 if quality of life also increases so that a longer life is a life worth living.

By: Vitality Council

References:
1. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high-risk individuals: A randomised placebo-controlled trial. Lancet 2002;360:7-22.
2. Langsjoen PH et al. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications. Biofactors. 2003;18(1-4):101-11.
3. Liao JK. Statin therapy for cardiac hypertrophy and heart failure. J Investig Med. 2004 May;52(4):248-53.
4. Bandolier. Statins in heart faikure. http://www.jr2.ox.ac.uk/bandolier/booth/cardiac/statHF.html
5. Fourth Conference of the International Coenzyme Q10 Association. Los Angeles April 14-17 2005.

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