Oxidative damage of cell structures by free radicals is thought to play an important role in the functional declines that accompany aging (5). If not neutralized by antioxidants, the highly reactive molecules may damage mitochondria over time, causing them to function less efficiently.
Coenzyme Q10 plays an important role in mitochondrial energy synthesis and functions as an antioxidant in mitochondrial membranes. Moreover, tissue levels of coenzyme Q10 have been reported to decline with age (6). One of the hallmarks of aging is a decline in energy metabolism in many tissues, especially liver, heart, and skeletal muscle. It has been proposed that age-associated declines in tissue coenzyme Q10 levels may play a role in this decline (7).
One study showed that coenzyme Q10 supplementation attenuates the age-related increase in DNA damage (8).
Presently, there is no scientific evidence that coenzyme Q10 supplementation prolongs life or prevents age-related functional declines in humans.
Oxidative modification of fat-transporting proteins (‘low-density lipoproteins’, LDL) in arterial walls is thought to represent an early event leading to the development of atherosclerosis. Coenzyme Q10 supplementation increases its concentration in human LDL (9), potentially inhibiting the damaging oxidation of LDL (4).
Animal studies found that coenzyme Q10 supplementation significantly inhibited the formation of atherosclerotic lesions (10).
Interestingly, co-supplementation with vitamin E (alpha-tocopherol) and coenzyme Q10 was more effective in inhibiting atherosclerosis than supplementation with either vitamin E or coenzyme Q10 alone (11).
Coenzyme Q10 supplementation shows promise as an inhibitor of LDL oxidation and atherosclerosis; however more research is needed to determine its role in disease prevention.
Authored by Dr Peter Engel in 2010, reviewed and revised by Dr. D. Raederstorff on 18.04.2017