Gary Moller: [DipPhEd PGDipRehab PGDipSportMed(Otago)FCE Certified, Kordel's and Nutra-Life Certified Natural Health Consultant]. ICL Laboratories registered Hair Tissue Mineral Analysis and Medical Nutrition Consultant.

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Wednesday, February 11, 2015

Is this the final nail in the coffin for statin drugs?


This is one of the most damning scientific articles, yet, that confirms what many health experts already knew -  that statins are not "heart healthy".  They are a lie.  

Unfortunately, the billion dollar statin industry has its own momentum and, as we all recognise and accept, businesses are in the business of growth and profit - health promotion is a secondary consideration.  Add the fact that medicine, including in-service medical education, is dominated by the pharmaceutical industry.  It is therefore hardly a surprise that statin sales continue to increase despite the burgeoning scientific evidence that they do a lot of harm and no good.

Please read the article scientific abstract below and then wonder why this has not had any publicity in mainstream media.  Meanwhile I can guarantee you that there will continue to be the weekly drugs industry TV propaganda, dressed up as news, announcing the latest exciting science breakthrough in the search for "The Cure".

There are effective, healthy alternatives to statins: Alternatives that have no nasty side effects other than looking good and feeling great.  Why doesn't your doctor prescribe these instead of harmful drugs?


 2015 Feb 6:1-11. [Epub ahead of print]

Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms.

Abstract
In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and 'heme A', and thereby ATP generation. Statins inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification. Statins inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure, reminiscent of the dilated cardiomyopathies seen with selenium deficiency. Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically reevaluated.

KEYWORDS:

ATP generation; atherosclerosis; coenzyme Q10; heart failure; mitochondrial toxin; selenoprotein; statin; statin cardiomyopathy; vitamin K2

If this is not enough, here are two abstracts about the association of statins with diabetes - not good at all:
 2010 Spring;10(1):16-21.

 2013 Dec;37(6):415-22. doi: 10.4093/dmj.2013.37.6.415.

Diabetogenic effect of statins: a double-edged sword?

Abstract
Statins are widely prescribed cholesterol-lowering agents, which have been demonstrated to significantly reduce cardiovascular morbidity and mortality. However, recent trials have reported that statins cause worsening of hyperglycemia and increase the risk of new-onset diabetes. The association between the diabetogenic effect of statins with intensive dose and accompanying major risk factors for diabetes has been demonstrated. However, statins do not appear to have a class effect on insulin sensitivity in non-diabetic patients. Numerous mechanisms have been suggested to explain how statins cause ╬▓-cell insulin secretory dysfunction and peripheral insulin resistance leading to incident diabetes. According to findings from an aggregate of large clinical trials, the benefits of statin treatment appear to outweigh the risk of new-onset diabetes. Therefore, it would be inappropriate to discontinue the use of statins for prevention of cardiovascular events because of its potential risk for development of incident diabetes. This review addresses the currently available evidence related to statin use and new-onset diabetes from a clinical perspective.

KEYWORDS:

Cardiovascular diseases; Diabetes; Statins

 2013 Jun;13(3):381-90. doi: 10.1007/s11892-013-0368-x.

Do statins cause diabetes?

Abstract
A wealth of evidence has established that cholesterol-lowering statin drugs, widely used for the prevention of cardiovascular disease, do increase the risk of new-onset diabetes, possibly by impairing pancreatic beta cell function and decreasing peripheral insulin sensitivity. Groups at particular risk include the elderly, women, and Asians. The diabetogenic effect of statins appear directly related to statin dose and the degree of attained cholesterol lowering. Statins can cause hyperinsulinemia even in the absence of hyperglycemia and the potential mitogenic effects and implications of prolonged hyperinsulinemia are discussed. Suggestions are made as to how physicians might avert the hyperinsulinemic and diabetogenic effects of statin therapy in clinical practice, and modulate the detrimental effects of these drugs on exercise performance. Finally, long-term studies are needed to determine if the deleterious hyperinsulinemic and diabetogenic effects of statin therapy undermine the beneficial cardiovascular disease risk outcomes in various segments of the population.
PMID:
 
23456437
 
[PubMed - indexed for MEDLINE]
And it has long been known that statins destroy muscles mostly due to coenzyme q10 depletion.  Anybody taking statins drugs, even low dose, should be prescribed high doses of q10:
Coenzyme q10 and statin-induced mitochondrial dysfunction.
Abstract
Coenzyme Q10 is an important factor in mitochondrial respiration. Primary and secondary deficiencies of coenzyme Q10 result in a number of neurologic and myopathic syndromes. Hydroxyl-methylglutaryl coenzyme A reductase inhibitors or statins interfere with the production of mevalonic acid, which is a precursor in the synthesis of coenzyme Q10. The statin medications routinely result in lower coenzyme Q10 levels in the serum. Some studies have also shown reduction of coenzyme Q10 in muscle tissue. Such coenzyme Q10 deficiency may be one mechanism for statin-induced myopathies. However, coenzyme Q10 supplements have not been shown to routinely improve muscle function. Additional research in this area is warranted and discussed in this review.

KEYWORDS:

Coenzyme Q10; mitochondrial dysfunction; myopathy; statins

As an aside, you will note that most scientific abstracts finish with a statement recommending further research!  Of course, this is a reasonable and logical thing for researchers to say.  After all, they rely on securing more funding to keep in business!  I do not have a problem with this, so long as there is some funding to put into action what is already known from research into the "problem".  Sadly, this seldom happens.  The drive for more research funding for finding the next high value patent medicine totally dominates.  Sure, let's continue the search for"The Cure"; but, in the meantime, let's get on with applying what we already know - and we know a lot.




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