Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms

Any extracts used in the following article are for non commercial research and educational purposes only and may be subject to copyright from their respective owners.

Background

Definition:

“Statins, also known as HMG-CoA reductase inhibitors, are a class of lipid-lowering medications that reduce illness and mortality in those who are at high risk of cardiovascular disease. They are the most common cholesterol-lowering drugs.[1]

Low-density lipoprotein (LDL) carriers of cholesterol play a key role in the development of atherosclerosis and coronary heart disease via the mechanisms described by the lipid hypothesis. Statins are effective in lowering LDL cholesterol and so are widely used for primary prevention in people at high risk of cardiovascular disease, as well as in secondary prevention for those who have developed cardiovascular disease.[2][3][4]”

https://en.wikipedia.org/wiki/Statin

---

In contrast to the definition above of what Pharma would like you to think the lipid hypothesis has long since been debunked, and Satans, sorry Statins debunked along with it. For editorial balance they do have some antioxidant properties, but it is more than cancelled out by other pro-oxidant consequences long term.

The fallacies of the lipid hypothesis (2008)

Abstract

“Most researchers to-day consider that a high intake of saturated fat and elevated LDL cholesterol are the most important causes of atherosclerosis and coronary heart disease. The lipid hypothesis has dominated cardiovascular research and prevention for almost half a century although the number of contradictory studies may exceed those that are supportive. The harmful influence of a campaign that ignores much of the science extends to medical research, health care, food production and human life. There is an urgent need to draw attention to the most striking contradictions, many of which may be unknown to most doctors and researchers.”

Keywords: Cholesterol saturated fat cardiovascular disease

https://www.tandfonline.com/doi/full/10.1080/14017430801983082

Docs tried to get me on these, no lifestyle or dietary advice, naturally. Thanks as ever to Dr Mercola I knew about long term Q10 & K2 depletion. I just found this paper on the subject. Its actually much worse than I could have ever imagined.👇 Instead I changed my diet to be cardiovascular friendly & antioxidant with natural sources of K2: grass fed dairy butter, camembert, gouda, edam, jarlsberg, chicken. Black grapes, red wine, spinach, potassium enriched salt, fish oils, tree nuts, dark chocolate, green tea, C, D, Zinc, Mag, glucosamine and multivit/min. Quercetin via onions and several of the above. My BP naturally came back down to normal and my circulation was restored within months. How do I know? I had warm feet for the first time!

---

Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms (2015)

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.

https://pubmed.ncbi.nlm.nih.gov/25655639/

---

If long term data could be fully factored in I suspect the efficacy here would be negative:

https://www.thennt.com/nnt/statins-persons-low-risk-cardiovascular-disease/