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While fitness level is certainly a factor in the EOMD so commonly detected in the individual who is over 50 years old, it can hardly explain the EOMD observed in the young and health conscious.
A recent publication helps to illustrate the point that EOMD is not simply a function of fitness.
Statistical studies are repeatedly showing that moderate exercise seems to have a more beneficial effect than intense exercise, secondary to the excessive free radical activity induced when subjects with EOMD exercise beyond their aerobic capacity.
EOMD: The Primary Cause of Mitochondrial Decay, Aging, and Degenerative Disease
(2-5,19,54) EOMD occurs in the young before any signs or evidence of mitochondrial decay.
This vicious cycle is really brought home in an article entitled, "Oxidative damage and mutation to mitochondrial DNA and age-dependent decline of mitochondrial respiratory function." In this article the authors are depicting EOMD when they describe the "gradual impairment of respiratory function" which increases with age.
However, four of the factors leading to EOMD mentioned previously--methylation disorders, nutritional deficiencies, hormonal deficiencies, and decreased levels of fitness--also result in the decrease of available ADP, resulting in greater ROS formation.
The point here is that many of my patients with EOMD, even those with values for serum TSH, T3, and T4, which are in range, show a decrease in their resting ATP production as well as a decrease in maximal ATP production.
This observation has made me believe that sub-clinical hypothyroidism is much more common than it is currently thought to be, and may be a particularly onerous component of EOMD. It also serves to explain why one recently published animal study demonstrated that mice in the upper quartile of resting ATP production lived 36% longer than those in the lowest quartile.
They go on further to state, "The patterns of cellular damage from ischemic/hypoxic insult, which have been well studied, parallel those seen following inhibition of cellular ATP production ..." Inhibition of cellular ATP production is what we are seeing in EOMD, and Levine and Kidd state that from a pathological perspective, it is tantamount to classical hypoxia.
In essence, the terms "impaired oxygen utilization," "functional hypoxia," and "EOMD" are identical in implication.
1) Degenerative disease and aging are preceded by early onset mitochondrial dysfunction (EOMD), which occurs long before actual mitochondrial decay, and commonly occurs in the young and asymptomatic.
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