Cholesterol Lowering Statin Drugs: Morbidity & Mortality
By Amandha Vollmer, BSc., ND intern
“We are now in a position to witness the unfolding of the greatest medical tragedy of all time - never before in history has the medical establishment knowingly created a life threatening nutrient deficiency in millions of otherwise healthy people.” - Peter H. Langsjoen, MD
(relating to statin drug use and CoQ10 reduction from said drug)
I am seeing clients now that are on various drug therapies and I have been concerned with the sheer amount of statins that people are taking, some on very high doses. At this point, I still fail to understand how correlated the dangers of high cholesterol and mortality from cardiac disease are? Is this theory sound? Are we seeing less cardiovascular accidents or death in general when people have their cholesterol controlled with statins (hydroxymethylglutaryl-coenzyme A reductase inhibitors)? My question is “are the studies showing decreased morbidity and mortality rates with patients on statin drug therapy (for dyslipidemia in the prevention of cardiovascular accidents)?
The searching MeSH terms were: statins, side-effects, morbitity, mortality, all-cause mortality& dyslipidemia. The Lancet and JAMA were helpful and I found MANY articles. There were too many articles coming up for diabetic treatment, which I didn’t want so many of, so I used these words together: dyslipidemia morbidity statin and found the best amount of studies in all varieties. Alt Health Watch and Medline were used as well as a few other smaller journals using the LRC database.
Even though I wasn’t interested in many studies involving diabetics, one caught my eye (1). It was a European case controlled study, well executed and substantial enough in numbers that showed an increased risk for polyneuropathy when diabetics are using statins. Another study (2) postulated that statins ‘may affect adversely the muscle's ability to appropriately respond to physical exertion’ a nasty side effect which worsens during physical activity. It appears that muscle complaints are among the morbidity seen in patients taking statins.
A prospective observational study in the UK (3) investigated erectile dysfunction (ED) in males on statin drug therapy and deduced it was higher because of ‘severe endothelial dysfunction’ due to cardiovascular risk factors such as age, smoking and diabetes. This is interesting because the therapy is meant to reduce arterial blockage and so produce better blood flow: should therefore reduce ED, not increase it. So why should patients with atherosclerosis of the penile vasculature become worse off when taking statins? The study seemed to have a challenging time finding out. It didn’t seem to be able to come to a concrete answer in the results, however they ended up saying that it must be diet and lifestyle choices, it couldn’t be the statin! I found this study to be incredibly biased. The researchers assumed since there were some studies done that found measurements in brachial and coronary arteries to improve on some of the drugs, that statins obviously work the way we always thought they did and so it must be something else causing the ED. This was a study showing obvious statin assumption.
I found many valuable studies showing that, in women and elderly persons, there are no or limited total mortality benefits. One JAMA meta-analysis (4) took 13 studies from1966 through December 2003 and found that lipid lowering does not affect total or CHD mortality or total mortality in women and may reduce CHD events only slightly (inconclusive in it’s evidence, however). And in the PROSPER study (5), it was found that elderly patients on 40 mg pravastatin had a decline in blood velocity and wall sheering stress than placebo, however there was no change in mortality. I love how they title this piece of research: “Pravastatin Decreases Wall Shear Stress and Blood Velocity in the Internal Carotid Artery Without Affecting Flow Volume: Results From the PROSPER MRI Study.” Sounds great, doesn’t it? Too bad this decline doesn’t prevent the people from dying! Talk about missing the forest for the trees. Being that the American Heart Association is a front for Big Pharma (like most disease associations) I am not shocked to see studies presented in such a misleading manner like this one.
So far it seems that the studies are not showing decreased rates of morbidity and mortality rates with patients on statin drug therapy. Now I am curious or how high the rates do go.
Upon examining this 28-year study below, known as the Helsinki Businessmen Study (6)(7) it can be seen that the “intervention” group in the chart below was given cholesterol-lowering drugs and diets, the control group no such intervention. This study proved that the use of cholesterol-lowering drugs and diets is risky!
| Helsinki Businessmen Study II Strandberg 1995 Br. Heart J. | Low risk patients | High-risk patients | |
| Control group- | Intervention- cholesterol reduction | ||
| Total cholesterol mg/deciliter | 254 | 284 | 284 |
| Mortality rate per 1000 | 15.2 | 31.1 | 63.7 |
This is a well done study, with solid methodology. It was trying to find out how dangerous it is to lower body cholesterol and what are the outcomes over a long term basis on quality of life, specifically in the elderly. So it seems that not only do statins have very little effectiveness on preventing death and disease while giving many side effects, but lowering cholesterol increases mortality too?
It is interesting to note that even Dr. John Abramson, of Harvard Medical School, in his Lancet article titled "Are Lipid-Lowering Guidelines Evidence-Based?" (8) says that lowering cholesterol in otherwise healthy adults should not be done and he calls for cholesterol treatment guidelines to be revised.
In a paper that needed to be translated in World Review Nutrition Dietetics, Dr. Harumi Okuyam of Nagoya City University in Japan, states that higher total cholesterol levels are closely correlated with lower cancer and all-cause mortality rates (9). He says that Western countries have accepted the cholesterol theory of heart disease and the use of statin drugs, “little benefit seems to result from efforts to limit dietary cholesterol intake or to total cholesterol values to less than approximately 260 mg/decliter.” He sends a warning that the direction of medical practice needs to move away from cholesterol-controlling medications.
I continue to find even more negatives to statin drugs. There are also questions regarding the negative effects of cell-mediated immunity from statins. This may be causing negative clinical cancer outcomes (10). Yet another study (11), this one is a double blind randomized controlled trial, using 102 patients with calcific aortic stenosis and coronary artery calcifications. The researchers found that calcium plaque formation continues to accumulate even with aggressive interventions to reduce cholesterol (using atorvastatin 80 mg daily). So obviously it’s not the excess cholesterol that is causing the real problem, it could be the high inflammatory state of the body, the immune system not functioning properly, the body over calcified and toxic from a toxic lifestyle! I’d say magnesium would play a much better role than any statin drug ever could.
It seems to be common theory to assume that higher levels of HDL and lower levels of LDL are cardioprotective and the goal for most doctors (including many naturopaths) is to toy with these ratios. Well consider this single-blind, placebo-controlled study (12) using the new drug torcetrapib, a drug that raises HDL cholesterol and lowers LDL. In the study, torcetrabip (a cholesteryl ester transfer protein (CETP) inhibitor) increased HDL levels by 46%, and when combined with a statin drug they increased to 61%. Therefore in a dual-day treatment protocol HDL cholesterol is raised by a 106%! LDL amounts were reduced by 17%. It was all ready to be released into the market, there were already articles written and published on how wonderful this drug is, when the manufacturer reported more death and strokes among users than placebos! Oops, people were dying from high HDL and low LDL! I think it is time to take a step back and rethink the theories and pay attention to the vested interests of those parties supporting certain medical theories and ‘corrective’ drugs. Perhaps the lower ‘bad’ cholesterol and increased ‘good’ cholesterol is a symptom of the correction on a deeper level, and changing these ratios with drugs doesn’t do the trick because it’s changing a superficial sign. Perhaps why vitamin C, magnesium and CoQ10 work is because they are regulating many processes and not merely changing a ratio.
REFERENCES:
[1] D. Gaist, U. Jeppesen and M. Andersen et al., Statins and risk of polyneuropathy: a case–control study, Neurology 58 (2002), pp. 1333–1337.
[2] P.D. Thompson, P. Clarkson and R.H. Karas, Statin-associated myopathy, JAMA 289 (2003), pp. 1681–1690.
[3] H. Solomon, Y.P. Samarasinghe and M.D. Feher et al., Erectile dysfunction and statin treatment in high cardiovascular risk patients, Int J Clin Pract 60 (2006), pp. 141–145.
[4] M.E. Walsh and M. Pignone, Drug treatment of hyperlipidemia in women, JAMA 291 (2004), pp. 2243–2252.
[5] J. Shepherd, G.J. Blauw and M.B. Murphy et al., Pravastatin in elderly individuals at risk of vascular disease [PROSPER]: a randomised controlled trial, Lancet 360 (2002), pp. 1623–1630.
[6] Helsinki Businessmen Study II Strandberg 1995 Br. Heart J.
[7] Timo E. Strandberg, MD, PhD*,*, Arto Strandberg, MD*, Kirsi Rantanen, MD
, Veikko V. Salomaa, MD, PhD, K et al. Low cholesterol, mortality, and quality of life in old age during a 39-year follow-up. J Am Coll Cardiol, 2004; 44:1002-1008
[8] J. Abramson, J. Wright. Are lipid-lowering guidelines evidence-based? The Lancet, Volume 369, Issue 9557, Pages 168-169.
[9] The cholesterol hypothesis - its basis and its faults. World Review Nutrition Dietetics 2007; 96:1-17
[10] L. Mascitelli and F. Pezzetta, Statin treatment, reduced T-cell content of atherosclerotic plaques and cancer, J Intern Med 260 (2006), pp. 592–593.
[11] E S Houslay1, S J Cowell1, R J Prescott2, J Reid3, et al. Progressive coronary calcification despite intensive lipid-lowering treatment: a randomised controlled trial. Heart 2006;92:1207-1212.
[12] Margaret E. Brousseau, Ph.D., Ernst J. Schaefer, M.D., Megan L. Wolfe, B.S.,
Et al. Effects of an Inhibitor of Cholesteryl Ester Transfer Protein on HDL Cholesterol. New England Journal Medicine 350(15):1505-15, 2004
Other studies read:
Hasslberger, Sepp. Vitamin C beats statins in cholesterol - heart disease
http://www.newmediaexplorer.org/sepp/2003/11/09/vitamin_c_beats_statins_in_cholesterol_heart_disease.htm. 668, November 09, 2003
| Fonorow, Owen R. CoQ10 and Statins: The Vitamin C Connection. http://www.thecureforheartdisease.com/owen/coq10.htm. 2003 |
M.H. Criqui and B.A. Golomb, Low and lowered cholesterol and total mortality, J Am Coll Cardiol 44 (2004), pp. 1009–1010.
Heart Protection Study Collaborative Group, MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high risk individuals: a randomized placebo controlled trial, Lancet 360 (2002), pp. 7–22.
More:
Modern medicine has never been able to explain why some 45-60 percent of patients with hospital admissions for a heart attack have a “normal level” of cholesterol. [Atherosclerosis 149: 181-90, 2000; Medical Hypotheses 59: 751-56, 2002]
In a study of adults over age 55 years, coronary artery calcifications were ranked by the Agatston scoring method. Blood pressure, cholesterol, smoking and blood sugar, all common risk factors for cardiovascular disease were measured over a 7 year period along with the calcium artery scores. Disturbingly, 29% of the men and 15% of the women who had no cardiovascular symptoms and exhibited no other common risk factors (elevated cholesterol, hypertension, etc.), had extensive coronary artery calcification. [European Heart Journal 25: 48-55, 2004]
posted by Amandha Dawn Vollmer @ 6:40 PM
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