For Improved Hearing Function . . .
Hearing Your Mitochondria

Mitochondria are cellular organelles containing genetic material and many enzymes important for cell metabolism, including those responsible for the conversion of food to usable energy.1 They are often referred to as the "powerhouses" of cells, because within them simple food substances such as glucose are broken down into water and carbon dioxide, a process that generates chemical energy. This energy is stored in the form of certain energy-rich molecules, which are used for fuel as needs arise. Surprisingly, according to a recent hypothesis, one of those needs is hearing.

AN ECHO FROM THE PAST
Many millions of years ago, mitochondria existed independently as tiny living organisms that invaded and co-occupied other organisms, ultimately sharing their DNA. Today most living cells contain mitochondria. In an experimental aging model, compounds that stimulate mitochondrial function were tested to determine their impact on hearing and to determine whether they could reduce some of the effects of aging, including hearing loss.

FREE RADICAL METABOLITES
When free radicals wreak their havoc in living organisms, they produce byproduct molecules know as reactive oxygen metabolites (ROMs).2 Continuously generated in vivo (in the living organism), ROMs play a role in at least 100 human clinical conditions with which they have been associated. These include atherosclerosis, arthritis, autoimmune diseases, cancers, heart disease, cerebrovascular accidents, and aging.

Like their free radical progenitors, ROMs are extremely reactive and cause extensive DNA, cellular, and tissue damage. Within the mitochondrial DNA (mtDNA), they cause deletions (the loss of a fragment of genetic information) with increasing frequency as we age and in the presence of presbyacusis, a type of deafness caused by a deterioration of fluid mechanics in the inner ear. With chronic exposure of the mtDNA to ROMs, these deletions cause the cell to become bioenergetically deficient.

MITOCHONDRIAL THEORY OF AGING
Excessive ROM exposure and the damage it causes are the basis of the mitochondrial clock theory of aging, also known as the membrane hypothesis of aging.1 Fortunately, nutrient compounds have been identified that can slow the clock by addressing the problems caused by ROMs, enhancing mitochondrial function, and even reversing several age-related processes. Among these compounds are the mitochondrial metabolites alpha-lipoic acid and acetyl L-carnitine. These two nutrients can have a significant positive effect on age-related hearing loss.

AGE-RELATED HEARING LOSS PREVENTED
Twenty-one Fischer rats (24 months old, which is old for a rat) had their hearing tested by an electrophysiological method. They were divided into three groups and given alpha-lipoic acid, acetyl-L-carnitine, or placebo orally for six weeks.3 Then their hearing was tested again to determine any changes in auditory thresholds.

As expected, the control group demonstrated age-associated threshold deterioration of 3 to 7 decibels, but the rate of hearing loss in the rats treated with alpha-lipoic acid was retarded. Acetyl L-carnitine, by contrast, improved the rats' auditory thresholds during the same time period. In comparison to the control group, the mtDNA deletions associated with aging and presbyacusis were reduced in both of the treated groups.

According to the mitochondrial theory of aging, when mitochondrial metabolites are used for treatment, mitochondrial aging is slowed, and senescence may be delayed. In the study, both acetyl L-carnitine and alpha-lipoic acid were found to reduce age-associated deterioration in auditory sensitivity and to improve cochlear (inner-ear) function. The researchers believe that this was due to the mitochondrial metabolites' ability to protect and repair age-induced damage accumulated in the cochlear mtDNA. At the bottom line, when mitochondrial function is stimulated, its energy-producing capabilities improve.

References

  1. Kowald A. The mitochondrial theory of aging: do damaged mitochondria accumulate by delayed degradation? Exp Gerontol 1999 Aug;34(5):605-12.
  2. Seidman MD. Effects of dietary restriction and antioxidants on presbyacusis. Laryngoscope 2000 May;110(5 Pt 1):727-38.
  3. Seidman MD, Khan MJ, Bai U, Shirwany N, Quirk WS. Biologic activity of mitochondrial metabolites on aging and age-related hearing loss. Am J Otol 2000 Mar;21(2):161-7.

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