New research published in the journal PLoS indicates that the use of the cholesterol-lowing class of drugs known as statins is associated with an increased prevalence of microalbuminuria, a well-known marker of vascular dysfunction, affecting both cardiovascular and kidney disease risk.
Statins Harm The Heart
Microalbuminuria is known to double the risk for a cardiovascular event in patients with type 2 diabetes mellitus and is a marker for endothelial function; endothelial dysfunction may, in fact, be far more significant than elevated blood lipids in determining cardiovascular disease risk. This new finding therefore calls into question the justification for using statin drugs for primary prevention of cardiovascular disease, which is presently the standard of care in the drug-base conventional medical model.
According to the study:
Microalbuminuria (MAU) is considered as a predictor or marker of cardiovascular and renal events. Statins are widely prescribed to reduce cardiovascular risk and to slow down progression of kidney disease. But statins may also generate tubular MAU. The current observational study evaluated the impact of statin use on the interpretation of MAU as a predictor or marker of cardiovascular or renal disease…Use of statins is independently associated with MAU, even after adjusting for bias by indication to receive a statin.
This study confirms a growing body of research indicating that statin drugs are cardiotoxic. Examples of this cardiotoxicy are as follows:
- Atorvastatin has been found to worsen ventricular diastolic function
- Lovastatin has been found to make LDL cholesterol more susceptible to oxidation
- Simvastatin-induced heart failure has been reported
- Simvastatin-induced atrial fibrillation has been reported
- Statin induced myocardial ischemia has been reported in animal studies
A review published in the journal Biofactors in 2004 found that the use of statin drugs may be resulting in coenzyme q10 depletion, and raised the possibility that this could be behind the congestive heart failure epidemic presently afflicting those in the United States.
Another more recent study published in the journal of Clinical Cardiology demonstrated that statin drugs weaken the heart muscle in humans.
OBJECTIVES: The purpose of this study was to evaluate the effects of statin therapy on myocardial function as measured with echocardiography with tissue Doppler imaging (TDI) and strain imaging (SI) independent of its lipid-lowering effect. BACKGROUND: Statin use is known to improve outcomes in the primary and secondary prevention of ischemic heart disease, but their use is also associated with myopathy, muscle weakness and in rare cases, rhabdomyolysis. We sought to evaluate whether TDI and SI is able to identify changes in myocardial function associated with statin use. METHODS: Myocardial function was evaluated in 28 patients via echocardiography with TDI and SI. We identified 12 patients (5 females) without overt cardiovascular disease (including hypertension, smoking, and diabetes) that were on statin therapy and compared their echocardiographic findings with 16 (12 females) age, sex, and cholesterol-profile-matched controls. Tissue Doppler imaging parameters of diastolic (E(‘)/A(‘) and E/E(‘)) and systolic (S’) function were measured. Regional systolic function was obtained by SI in 4-chamber, 2-chamber, long axis, and average global views. RESULTS: There was no significant difference in myocardial function as measured by Doppler and minor differences as measured via TDI among the 2 groups. There was significantly better function noted with SI in the control group vs the statin group in the 4-chamber (-19.05% +/- 2.45% vs -16.47% +/- 2.37% P = 0.009), 2-chamber (-20.30% +/- 2.66% vs -17.45% +/- 4.29% P = 0.03), long axis (-17.63% +/- 3.79% vs -13.83% +/- 3.74% P = 0.01), and average global (-19.0% +/- 2.07% vs -15.91% +/- 2.81% P = 0.004) views. CONCLUSION: Statin therapy is associated with decreased myocardial function as evaluated with SI.
A growing body of clinical research now indicates that the cholesterol-lowering class of drugs known as statins, are associated with over 300 adverse health effects — research boldly flying in the face of national health policy, medical insurance premium guidelines, statin drug manufacturer advertising claims, and the general sentiment of the public, with approximately 1 in every 4 adult Americans over 45 currently using these drugs to “prevent heart disease.”
The Cholesterol Myth
For well over 40 years, statin drugs have successfully concretized a century old myth about the primary cause of heart disease: namely, that cholesterol “causes” plaque build up in the arteries, ultimately leading to obstruction of blood flow, and subsequent morbidity and mortality.
Indeed, the medical establishment and drug companies have been singing the praises of this “cholesterol myth,” to the tune of 25 billion dollars in statin drug sales, annually.
While it is true that oxidized low-density lipoprotein is found within the atheromatous plaque that is found in damaged arteries, it is less likely a cause than an effect of heart disease. The underlying damage to the lining of the artery, which could be infectious, chemical, stress and/or nutritionally-related, comes before the immune response that results in plaque buildup there. Blaming LDL cholesterol for causing heart disease, is like blaming the scab for the injury that caused it to form, or, like blaming the band-aid for the scab it is covering — this is, after all, the inborn and fatal flaw of allopathic medicine which focuses only on symptoms of disease, which it then — fool-heartedly — attempts to suppress by any chemical means necessary.
Death By Statins?
No one can deny that statins do exactly what they are designed to do: suppress cholesterol production and reduce measurable blood serum levels. The question is, rather, at what price do they accomplish this feat, and for what ultimate purpose?
With the National Cholesterol Education Program Guidelines, having been designed by “experts” on the payroll of statin drug manufacturers, requiring ultra-low levels to obtain a strictly theoretical and numerical definition of “health,” statin drugs are guaranteed to receive first-line treatment status in the goal of the preventing and treating heart disease through lipid suppression.
What is at question here, is whether the unintended, adverse effects of this chemical class of drugs are less, the same or worse than the purported “cardiovascular” benefits they provide?
Fundamentally, statin drugs damage the muscles and nerves in the body — so much so that a dose as low as 5 mg a day (albeit in rare cases) can kill a human. There are well over 100 studies demonstrating the myotoxic, or muscle-harming effects of these drugs, and over 80 demonstrating the effects of nerve damage, as well. When you consider that a vast proportion of our body is comprised of muscles and coordinating nerve systems, this drug has the potential to cause damage to the entire body, and undoubtedly does so universally, differing only in the matter of degree — the damage occurring acutely in those at the tip of the iceberg, asymptomatically in the majority of others at the base.
Moreover, statin myotoxicity is not exclusive to skeletal muscle. If you consider that the heart is also a muscle, in fact, is our most tireless muscle, an obvious red flag should go up. It is a remarkable fact that it took over 40 years before the biomedical research and publishing fields were able to produce a human study, like the one published in the Journal of Clinical Cardiology in Dec. 2009, showing that statin drugs, despite billions of advertising/marketing dollars to the contrary, actually weaken the heart muscle.
These results, while disturbing, are to be expected given the well-known problem associated with statin drug use, namely, the inhibition of the mevalonate pathway necessary to produce the heart-essential nutrient coenzyme Q10. Coenzyme Q10 deficiency itself may be a major contributing cause to heart disease. There is also research that statin drugs deplete the body of the cardioprotective minerals (and associated mineral-protein complexes) zinc and selenium. This finding may also explain why rates of heart failure may be increasing in the general population given these drugs.
While the discovery that statin drugs, instead of preventing heart disease, likely contribute to it, is surprising and counterintuitive, it should not distract from the more disturbing discovery that they contribute to over 300 disease and/or adverse health effects.
Millions of statin drugs users around the globe are risking their lives on a bad bet that taking a magic chemical pill will reduce their risk of dying of a disease that is not caused by a lack of the drug. What is more likely to happen, however, is that the quality and duration of their lives will be reduced, profoundly, along with billions of dollars of squandered cash that could have been spent on authentically medicinal and cardioprotective foods, nutrients, minerals and vitamins.
In light of these findings, a very serious question is raised: are those who are party to the manufacture, promotion, administration and/or prescribing of this chemical class of drugs, in violation of the medical ethical principle of informed consent? And is this ethical violation, insofar as it results in injury to those who have been mislead and/or coerced to take these drugs, also a legal/criminal one?