Insulin exposure and unifying aging

Background: Absence of a widely agreed upon central paradigm for mammalian aging. Objective: Detailed elaboration of a proposed mammalian aging paradi gm. Methods: Elaboration of a new theoretical model, Results: Hormonal imba lance-growth factor exposure theory (HI-GFE theory) can account for two maj or aging phenomena: (1) decline in mammalian 'reserve capacity' and consequ ent rise of diseases of maintenance, and (2) rise then peaking of most age- associated proliferative diseases. Reserve capacity decline via gradual dec line in mitochondrial maximal energy production (state 3) accounts for the gradual redirection of declined maximal energy production toward survival f unctions like ion pumping to the relative detriment of RNA and protein synt hesis as seen in lesser synthetic rates and slower turnover with consequent gradual cellular impairment. Developmental program triggered, and over-amp le nutritionally driven, growth factor exposure in youth to middle age enco urages promotional events that lead to proliferative diseases that rise coi ncident to rapidly declining reserve capacity and cumulative increased muta tional status of age. Conclusions: Declining mitochondrial state 3 aging en ergy production status is easily and safely reversible with probable conseq uences of greatly postponing the decline in overall 'reserve capacity' whic h may also improve insulin: growth hormone balance and result in lower over all growth factor exposure and consequent longer healthy life of a potentia lly greater magnitude increase in life spans than that seen in calorie-rest ricted animals.