Don’t Let STATINS Break Your Heart!

Despite the fact that statins are currently prescribed to around 100 Million people worldwide for the prevention of heart disease these medications, somewhat ironically, actually damage the heart. This damage occurs through a number of different mechanisms.

Statins damage the heart in the following major ways:

  • Statins block Coenzyme Q10 (CoQ10), which is essential for all cellular energy production. The heart contains the most CoQ10 since the heart has the greatest requirements for energy production. Statins block CoQ10 because they act very high up in the mevalonate pathway. The mevalonate pathway is the biochemical step by step process used by the body to create a wide range of essential compounds. Statins inhibit this process - that’s how they lower cholesterol levels and also lower CoQ10 levels.

Statins have the effect of lowering LDL levels (so called ‘bad cholesterol’). However, LDLs provide the main transport mechanism for moving CoQ10 around the body. Therefore, this is another way that statins reduce the availability of CoQ10.

Low levels of CoQ10 weaken the heart and can cause or contribute to heart failure.

Incidentally, LDLs also provide the transport mechanism for a number of other vital nutrients such as vitamin E, and various carotenoids such as beta-carotene.


  • Statins increase the amount of calcified plaque in the arteries. Atherosclerosis is a hardening and narrowing of the arteries. The process involves calcification. The confirm registry found that statin use is associated with an increased number and extent of calcified coronary plaques.

Other studies have shown that statins do not reduce coronary artery calcium, and that the disease continues regardless of the statin use.

The Veteran Affairs Diabetes Trial found that statin use was linked with the progression of coronary artery calcification despite the fact that the statin users had significantly lower and nearly optimal LDL ‘cholesterol' levels.

  • Statins inhibit vitamin K2 and selenium, both of which normally have a protective effect on the heart and blood vessels.


  • Statins increase the risk of Type 2 Diabetes and Diabetes increases the risk of heart disease death by up to 400%.


  • Statins block the response to exercise. After exercise, the heart normally gets stronger as part of the normal adaptation process. Statins hinder this process. This means that the benefits of exercise cannot be obtained by people who take statins. The response to exercise is important for everyone however, it is particularly importance for anyone recovering from a cardiac event.  


The video above has been created to create more awareness of these issues and to encourage people to think carefully before starting statins. T-shirts and posters are also available as part of this campaign to help spread the message.



Nakazato R, Gransar H, Berman DS, et al. Statins use and coronary artery plaque composition: Results from the International Multicenter Confirm Registry. Atherosclerosis. 2012;225(1):148–153.

Raggi P, Davidson M, Callister TQ, et al.. Aggressive versus moderate lipid-lowering therapy in hypercholesterolemic postmenopausal women: beyond endorsed lipid lowering with EBT scanning (BELLES). Circulation. 2005;112(4):563–571. doi:10.1161 /CIRCULATIONAHA.104.512681

Schmermund A, Achenbach S, Budde T, et al. Effect of intensive versus standard lipid-lowering treatment with atorvastatin on the progression of calcified coronary atherosclerosis over 12 months: a multicenter randomized, double-blind trial. Circulation. 2006;113(3):427–437. doi:10.1161/CIRCULATIONAHA.105.568147

Saremi R, Bahn G, Reaven PD, et al. Progression of vascular calcication is increased with statin use in the Veterans Affairs Diabetes Trial (VADT). Diabetes Care. 2012;35(11):2390–2392. doi:10.2337 /dc12-0464

Crandall JP, Mather K, Rajpathak SN on behalf of the Diabetes Prevention Program(DPP) Research Group, et al Statin use and risk of developing diabetes: results from the Diabetes Prevention Program BMJ Open Diabetes Research and Care 2017;5:e000438. doi: 10.1136/bmjdrc-2017-000438

Sattar N  et al. Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet 2010;375:735–42.doi:10.1016/S0140-6736(09)61965-6

Thakker D et al. Statin use and the risk of developing diabetes: a network meta-analysis. Pharmacoepidemiol Drug Saf 2016;25:1131–49.doi:10.1002/pds.4020

Thakker D et al. Statin use and risk of developing diabetes in cardiovascular disease: systematic literature review and meta-analysis. Value Health 2014;17:A478.doi:10.1016/j.jval.2014.08.1378

Ridker PM et al. Cardiovascular benefits and diabetes risks of statin therapy in primary prevention: an analysis from the JUPITER trial. Lancet 2012;380:565–71.doi:10.1016/S0140-6736(12)61190-8

Culver AL et al. Statin use and risk of diabetes mellitus in postmenopausal women in the Women’s Health Initiative. Arch Intern Med 2012;172:144–52.doi:10.1001/archinternmed.2011.625

Mills EJ et al. Efficacy and safety of statin treatment for cardiovascular disease: a network meta-analysis of 170,255 patients from 76 randomized trials. QJM 2011;104:109–24.doi:10.1093/qjmed/hcq165

Baker WL et al. Differing effect of statins on insulin sensitivity in non-diabetics: a systematic review and meta-analysis. Diabetes Res Clin Pract 2010;87:98–107.doi:10.1016/j.diabres.2009.10.008

Nakata M et al. Effects of statins on the adipocyte maturation and expression of glucose transporter 4 (SLC2A4): implications in glycaemic control. Diabetologia 2006;49:1881–92.doi:10.1007/s00125-006-0269-5

Chamberlain LH. Inhibition of isoprenoid biosynthesis causes insulin resistance in 3T3-L1 adipocytes. FEBS Lett 2001;507:357–61.doi:10.1016/S0014-5793(01)03007-1

Mikus CR, Boyle LJ, Borengasser SJ, et al. Simvastatin impairs exercise training adaptations. J Am Coll Cardiol. 2013;62(8):709–714