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 paradigm.


METHODS
Elaboration of a new theoretical model.


RESULTS
Hormonal imbalance-growth factor exposure theory (HI-GFE theory) can account for two major aging phenomena: (1) decline in mammalian 'reserve capacity' and consequent rise of diseases of maintenance, and (2) rise then peaking of most age-associated proliferative diseases. Reserve capacity decline via gradual decline in mitochondrial maximal energy production (state 3) accounts for the gradual redirection of declined maximal energy production toward survival functions like ion pumping to the relative detriment of RNA and protein synthesis as seen in lesser synthetic rates and slower turnover with consequent gradual cellular impairment. Developmental program triggered, and over-ample nutritionally driven, growth factor exposure in youth to middle age encourages promotional events that lead to proliferative diseases that rise coincident to rapidly declining reserve capacity and cumulative increased mutational status of age.


CONCLUSIONS
Declining mitochondrial state 3 aging energy production status is easily and safely reversible with probable consequences of greatly postponing the decline in overall 'reserve capacity' which may also improve insulin: growth hormone balance and result in lower overall growth factor exposure and consequent longer healthy life of a potentially greater magnitude increase in life spans than that seen in calorie-restricted animals.
Parr
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USC Department of Medicine, University of Southern California, Los Angeles, Calif., USA. 72237.570@compuserve.com
D000375:Aging / Q000502:physiology*; D000818:Animals; D002149:Energy Intake / Q000502:physiology*; D007004:Hypoglycemic Agents / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D008136:Longevity
D007004:Hypoglycemic Agents; D007328:Insulin