Selection criteria for probiotic supplements

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

* Capsules add another layer of insulation against the potential for contamination, moisture and oxygen related damage, etc. Consumers and health professionals alike prefer capsules due to convenience and viability.

* Chewable Tablets are a good choice for children, elderly patients who have difficulty swallowing and even those seeking to benefit the upper digestive tract. This may be for halitosis, (bad breath), for the esophagus (GIRD), or sim. Imre Zs.Nagy's Membrane Theory of Aging; (9-12) and more recently, Aubrey DeGrey's Mitochondrial Free Radical Theory of Aging (13) and Reductive Hotspot Hypothesis of Aging (14) are all free radical-related theories. It should be noted that none of these theories are mutually exclusive - rather, they complement each other, for the most part.

The theories generally focus on the possible mechanisms by which mitochondria can become dysfunctional and contribute to aging and age-related diseases as shown in the schematic in Fig. 3.

A unique property of mitochondria is that they have their own DNA (deoxyribonucleic acid). DNA is the stuff of which genes and chromosomes are made. Mitochondrial DNA (mtDNA) is quite different from nuclear DNA (nDNA) in several respects. First, mtDNA is not associated with histones. Histones are positively charged "storage" proteins around which nuclear DNA is wound (like thread on a spool) which are vital for the protection of DNA. MtDNA lacks this protective mechanism. Second, most of the complex DNA repair mechanisms that correct damage to nuclear DNA are missing from mitochondria. Therefore, mtDNA lacks both protective and repair mechanisms.

Mitochondrial DNA (mtDNA) is located in the mitochondrial matrix, near the inner mitochondrial membrane (where both energy and free radicals are produced). Since mtDNA lacks protective proteins, it is even more vulnerable to free radical attack.

Mitochondrial dysfunction begins with a less-than-perfect electron transport system. Even under ideal conditions, some electrons "leak" from the electron transport chain. These leaking electrons interact with oxygen to produce superoxide radicals. Because mtDNA is close to the site of the production of superoxide, hydroxyl, or perhydroxyl radicals, and because it lacks protective and repair mechanisms, it is highly susceptible to free radical-induced mtDNA deletions (damage). In fact, the relatively unprotected and unrepaired mtDNA suffers more than ten times the damage that nuclear DNA does. (7,8,15)

Unfortunately, with mitochondrial dysfunction, leakage of electrons can increase significantly, and a vicious cycle can be created. These electrons (free radicals) can damage the mitochondrial membrane, resulting in a loss of membrane fluidity and alteration in its permeability. This can lead to further mitochondrial dysfunction, disruption of cellular energy production, and accelerated cellular aging. (6)

Lipid peroxide damage to mitochondrial membranes increases in a linear fashion, and mtDNA mutations increase exponentially with age. Barrientos speculated that changes in membrane lipid composition could be a cause of age-related decreased membrane fluidity. (16)