Do Hypolipidemic Drugs Lower Medical Expenses?

Joel M. Kauffman, Ph.D.

In a recent review by Tsuyuki and Bungard (1) noncompliance with prescribed hypolipidemic agents was said to have annual associated costs of $25-100 billion in the US alone. How could this be possible? If statin drugs in particular changed the cause of death to sudden fatal hemorrhagic stroke, for example, rather than some form of cardiovascular disease (CVD), then a medical cost saving is possible; but I have not seen such a claim, thus the most that can be expected of statin drugs is to postpone the inevitable. In the CARE trial the relative risk of breast cancer in the treatment group was +1500% (absolute risk +4.2%); but the medical costs of breast cancer are probably comparable with those of CVD. Even if the statin drugs increased lifespan by a number of years, most of the people taking them will eventually die of CVD or cancer anyway, so the largest reduction in cost that could be expected would be a hiatus for a number of years followed by the same costs as before. In addition, the costs of the statin drugs of about $1,000 per year per person for 20-30 years would be added permanently.

Tsuyuki and Bungard wrote that “...numerous randomized controlled trials have conclusively established the efficacy of aggressive cholesterol reduction in decreasing mortality...Despite this robust evidence of efficacy...” How much do statin drugs increase lifespan? In the EXCEL trial of lovastatin, after 1 year the total death rate in the treatment group went up +0.3% absolute. In the 4S trial of simvastatin, after 5.4 years the total death rate went down 3.3%, or -0.6%/year. In the WOSCOPS trial of pravastatin, after 4.4 years, the total death rate went down 0.9%, or -0.2%/year. In the CARE trial of pravastatin, after 5 years, the total death rate went down 0.77%, or -0.15%/year. In the AFCAPS/TexCAPS trial of lovastatin, after 5.2 years, the total death rate went up 0.09%, or +0.02%/year. In the LIPID trial on pravastatin, after 6.1 years, the total death rate went down 3%, or -0.49%/year.2 In the MIRACL trial on atorvastatin for secondary protection, after 2.5 years, there was no change in the total death rate. (3) Taking the mean of these results of these 7 trials, the absolute risk is -0.16%/year. Assuming a 20-30-year treatment period in which the non-CVD deaths do not increase, of which we will know nothing for 10-15 more years, the increase in life expectancy on treatment with statin drugs would be about 4 months.

The assertion or Tsuyuki and Bungard that “Elevated serum cholesterol is well known as a major risk factor for the development of CVD...”[italics added] may be true as written, but cholesterol as a cause of CVD has been disproven decisively. (2,4) It has even been suggested that elevated cholesterol is a protective reaction to elevated homocysteine levels.5 After all, women with the highest cholesterol levels live the longest. (2,4) Two recent reports confirmed that serum cholesterol levels have no predictive value whatever in individuals for the development of calcified plaques in arteries as found by electron beam tomography. (6,7)

Serious consideration should be given to halting the use of the statin drugs, or at least not compensating the costs of their mass adminstration. Statin drugs do not increase lifespan significantly and, with 10-15 more years of trials completed, they might be found to decrease lifespan as the toll in increased cancer rates is exacted. It is actually conceivable that discontinuation of all anticholesterol treatments will actually save $billions/year.

An even more extreme view aired in the United Kingdom is that serum cholesterol level is a relatively poor predictor of CVD, and that the many misclassifications may have damaging psychological effects, and that in most cases, even testing cholesterol level, as well as treating raised concentrations, is a waste of National Health Service resources. (8)

References

1. Tsuyuki RT, Bungard TJ, Poor Adherence with Hypolipidemic Drugs: A Lost Opportunity, Pharmacotherapy 2002:21(5):576-582.

2. Ravnskov U, The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease, New Trends Publishing, Washington, DC, 2000.

3. Schwartz GG et al., JAMA 2001:285:1711-1718.

4. Stehbens WE , Coronary Heart Disease, Hypercholesteremia, and Atherosclerosis I. False Premises and II. Misrepresented Data, Experimental and Molecular Pathology 2001:70:103-119,120-139.

5. McCully KS, “Biomedical Signficance of Homocysteine”, J. Scientific Exploration 2001:15(1):5-20.

6. Hecht HS,Superko HR, Electron Beam Tomographyand National Cholesterol Education Program Guidelines in Asymptomatic Women, J. Amer. College of Cardiology 2001:37:1506-11.

7. P. Raggi, B. Cooil, and T. Q. Callister, Use use of electron beam tomography to develop models for prediction of hard coronary events, Amer Heart J 2001:141:375-82.

8. Sheldon T, Effective Health Care Bulletin 1998:4(1); Kmietowicz Z, BMJ:7 Mar 98.

29 Jun 01

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From the Department of Chemistry & Biochemistry, University of the Sciences in Philadelphia, PA.
Address correspondence to Joel M. Kauffman, Ph. D., Department of Chemistry & Biochemistry, University of the Sciences in Philadelphia, 600 South 43rd St., Philadelphia, PA 19104-4495. FAX 215-895-1100 e-mail kauffman@hslc.org