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In this paper I would like to present one of the basic ideas of a hypothesis on ageing I have developed, after several years of study of the biochemistry, genetics, ecology and physiology of the process of ageing. My hypothesis introduces the idea that neuronal oxidation damage is directly proportional to the amount of oxygen pressure in the environment. Damage to oxygen sensitive neurons from the dopaminergic system, causes gradual decrease in growth hormone secretion, until total cessation of growth, (which marks the initiation of senescence).
The present oxygen atmospheric concentration is 20.9% (at sea level). From birth, and until the age of 18, this level of oxygen is enough to produce gradual neuronal damage in the dopaminergic system. At the age of 18, the oxygen damage to dopaminergic neurons reaches a certain level that causes a sharp reduction in the secretion of growth hormone. This is the signal for the closure of bone epiphyses which causes the cessation of bone and body growth.
Presently, the source of oxygen we breathe comes from a high atmospheric oxygen pressure of 20.9%. This amount of atmospheric oxygen pressure causes specific levels of neuronal oxidation damage reaching critical levels at the age of 18.
If the atmospheric oxygen pressure is lower than 20.9%, neuronal damage will be less intensive and there will be a delay in reaching the above critical level of dopaminergic neuronal damage. In this case, only at the age of say, 45 years, oxidation damage will cause cessation of growth. If the period of growth continues until the age of 45, that is twice longer than the present average, life span should also increase in a similar ratio. (Figure 3)
The extent of neuronal damage caused by environmental oxygen could be a crucial factor to initiating the process of ageing. In the following critical context of this paper, I shall present a review from different sources, of the biochemical reactions occurring in oxygen sensitive neurons, in conjunction with the endocrine system
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