Selection criteria for probiotic supplements

Townsend Letter for Doctors and Patients, Feb-March, 2003 by Dr. S.K. Dash

Approaches to Resuscitate Aging Mitochondria

Understanding the proposed mechanisms by which mitochondrial dysfunction can contribute to aging and aging-related diseases suggests several potential interventions. These include 1) maintenance of optimal Krebs' cycle and respiratory chain efficiency, 2) restoration of mitochondrial membrane fluidity, and 3) reduction in deleterious free radical activity.

Many nutrients play indispensable roles in mitochondrial energy production and provide vital antioxidant protection against the free radicals generated by oxidative phosphorylation. The substances in Table I have been shown to have generally positive effects on mitochondrial dysfunction-related conditions in a number of animal and human studies. These substances have alleviated a number of mitochondrial-induced diseases, including Parkinson's disease, diabetes, and fatigue.

Improving Mitochondrial Function

As evidence implicating mitochondrial dysfunction in the aging process continues to accumulate, the question becomes: What -- if anything -- can we do about it?

Fortunately, a growing body of research suggests that a number of interventionist strategies may help to reduce mitochondrial damage, enhance mitochondrial repair, and restore mitochondrial energy-producing processes to more youthful levels. These strategies include lifestyle changes, such as diet and exercise, as well as supplementation with nutritional and pharmaceutical substances that may minimize age-related mitochondrial changes and enhance mitochondrial function.

DMAE

Zs.-Nagy believes that the best approaches to counteract the ravages of free radical-induced membrane damage are to use antioxidant membrane stabilizers like dimethylaminoethanol (DMAE) or centrophenoxine. (17) DMAE is an efficient OH- radical scavenger that is incorporated into the cell membrane of neurons where it may provide site-specific radical protection in nerve cells. It not only prevents the accumulation of lipofuscin (the pigment that accumulates in cells with age and which causes the well known "age-spots" that occur in many older people), but also often causes the spots to completely disappear. Finally, it is a mild cerebral stimulant, which has been used to treat both Attention Deficit Disorder and Alzheimer's disease. It is a safe, effective cognitive enhancer in normal adults, as well.

CoQ10

Coenzyme Q10 is probably the most widely used cofactor for treating mitochondrial-related diseases. CoQ10 functions as the electron carrier in the inner mitochondrial membrane, transferring electrons from complexes I and II to complex Ill. In addition to increasing biosynthesis of ATP (the universal energy molecule), and acting as a potent free radical scavenger, CoQ10 also reduces lactic acid levels, improves muscle strength, and decreases muscle fatigability. (18)

Idebenone

Idebenone is a CoQ10 analog that, while sharing some of CoQ10's properties, offers unique mitochondrial-protective benefits of its own. Idebenone is a powerful mitochondrial free radical quencher that reduces the ever-increasing damage to mitochondrial DNA that occurs with age. Idebenone has also been shown to be more effective than CoQ10 in the electron transport chain. Studies show that when cellular oxygen levels are low -- a condition that may occur periodically over a lifetime -- idebenone is actually superior to CoQ10 for preventing free radical damage while helping cells maintain relatively normal ATP levels -- a property that is especially beneficial to brain and heart cells that may be rapidly damaged during low ATP production due to poor tissue oxygenation. (19)