Mitochondrial decay
Mitochondrial decay is one major cause of aging, leading to the subsequent death in humans. The mitochondria are the power producing organelles found in every cell of every organ. Their primary job is to generate ATP through various energy cycles that involve nutrients and vitamins. ATP is needed for every movement, thought and action we make. Yet very little ATP can be stored in the body.Under normal conditions the mitochondria generate free radicals during the ATP production process and as a result subject themselves to a lot of free radical damages. As we age, the mitochondria become less efficient, fewer in number and larger. Accordingly, ATP production declines, and this may eventually lead to cell death.
As organs cannot borrow energy from one another, the efficiency of each organ’s mitochondria is essential to its repair processes and functions. If an organ’s mitochondria fail, then so does that organ. Enhancement and protection of mitochondrial function and structure are therefore instrumental in preventing and slowing aging.
Mitochondrial decay is a progressive disruption of mitochondrial structural integrity and functional ability with advancing age, can cause the impairment in cellular energy production and hence the decline in normal function, particularly in organs with high energy consumption such as the brain and the heart. Mitochondrial decay can also lead to the increase in free radical production and thus render the cell more prone to commit suicide (programmed cell death or apoptosis). Some of the age-related diseases, including cardiovascular and neurodegenerative disorders, have been found to involve mitochondrial dysfunction. The maintenance of a youthful mitochondrial functional ability and antioxidant capacity has become a trend in preventive health.
Treatment
This decay, which is a major contributor to aging, can be ameliorated by feeding old rats the normal mitochondrial metabolites acetyl-L-carnitine and lipoic acid at high levels. Many common micronutrient deficiencies, such as iron or biotin, cause mitochondrial decay with oxidant leakage leading to accelerated aging and neural decay.
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