Ubiquitous

u-biq-ui-tous- adjective: existing or being everywhere, esp. at the same time; omnipresent

Coenzyme Q10, also known as ubiquinone, is the Lady Gaga of herbal supplements. New to the scene, kind of different, really interesting, has potential for a lot of great things, but no one seems to know what to make of it.

Ubiquinone has been known to biochemists for years, but the concept of using it as a dietary supplement came about relatively recently.

So... what is coenzyme Q10? The name is appearing more and more in the aisles of pharmacies and health food store and its celebrity as a supplement rivals that of vitamin D. However, coQ 10 is not a vitamin; it is naturally synthesized in the human body (in contrast to a vitamin, which is obtained through diet).

CoQ is a bright orange, lipophilic substance that acts as an antioxidant and plays a major role in oxidative phosphorylation in mitochondria. It resides in the inner layer of the lipid bilayer membrane of mitochondria and accepts electrons from NADH. Protons are then pumped from the mitochondrial matrix into the inter membranous space, creating an electrical gradient. As protons cross back though the membrane, they pass through a proton channel where ATP synthase uses the energy to add a phosphate group to ADP, creating ATP, the energy currency of cells. Coenzyme Q has also been shown to regenerate active forms of the vitamins E and C. Its reduced form, ubiquinol, is present in all tissues.

Circa 1990, it was discovered that HMG-CoA reductase inhibitors (aka statins), designed to inhibit the production of LDL cholesterol, also inhibited the synthesis of coenzyme Q10. Additionally, LDL cholesterol serves as a transporter of coenzyme Q, therefore reductions in LDL would also theoretically reduce the amount of coenzyme Q in blood circulation. As a result, it was hypothesized that repleting CoQ could eliminate some of the side effects associated with statin therapy; namely, myalgias and rhabdomyolysis.

The mechanism for statin induced myalgias is still unknown, but it has been hypothesized that the reduction in coenzyme Q10 may, at least, be a contributing factor. Studies subsequently showed that CoQ supplementation could replete plasma and muscle levels of coenzyme Q, however, they failed to show a reduction in myalgias. Mabuchi et al concluded in 2007 that reduction in CoQ levels was a primary effect of statins and that supplementation with 100 mg/day of CoQ significantly boosted plasma levels. There was, however, no significant difference in myalgias or liver function tests.

In 2007, Marcoff and Thompson’s meta-analysis published in the Journal of the American College of Cardiology, carefully dissected the outcomes of studies and showed that a lot of questions remain unanswered. There have been very few studies specifically looking at muscular levels of coenzyme Q10 in patients with statin induced myalgias, and the question of whether decreased coenzyme Q10 levels can cause mitochondrial dysfunction remains unanswered despite some preliminary studies. Additionally, the meta-analysis failed to demonstrate a clear benefit though the use of coenzyme Q10 supplementation in patients taking a statin.

Despite the plethora of small trials examining coenzyme Q supplementation, larger and better powered trials are needed. As it stands, coenzyme Q is not recommended with statin therapy or as a treatment for statin induced myalgias.

References:
Meisenberg G, Simmons WH. Principles of medical biochemistry. 2nd ed. Mosby-Elsevier 2006.

Mabuchi H et al. Effects of CoQ10 supplementation on plasma lipoprotein lipid, CoQ10 and liver and muscle enzyme levels in hypercholesterolemic patients treated with atorvastatin: a randomized double-bling study. Atherosclerosis 2007;195:e182-e189.

Marcoff L, Thomson MD. The role of coenzyme Q10 in statin-associated myopathy: a systematic review. Journal of the American College of Cardiology 2007;49(23):2231-7.

Wynn RL. The effects of CoQ10 supplements on patients taking statin drugs. General Dentistry 2010;58(3):168-170.