ABSTRACT
It has been proposed that aging occurs because of a failure of the pineal gland to produce melatonin from serotonin each day beginning at sunset and throughout the night. This lack leads to a nighttime deficiency of melatonin both absolutely and also relatively to serotonin. As melatonin has wide-spread integrative and regenerative effects, its lack may lead to disturbances normally associated with aging. The present paper reviews the pertinent literature which appeared since our first publication, but earlier articles are also included. Evidence is presented for a role of melatonin and serotonin in controlling the neuroendocrine and immune networks and in inhibiting the development of ischemic heart and Alzheimer's disease, tumor formation and other degenerative processes associated with aging. The possible role of melatonin in the favourable effects of dietary restriction on aging is also discussed. This paper provides additional evidence that a melatonin deficiency, especially in relation to serotonin, may be responsible for the promotion of aging in the organism.
Subject(s)
Aging/physiology , Melatonin/physiology , Serotonin/physiology , Animals , Cell Division/physiology , Circadian Rhythm/physiology , Humans , Neoplasms/physiopathology , Pineal Gland/physiopathology , Secretory Rate/physiologyABSTRACT
The hypothesis presented in this paper defines aging as a pathological process originating in the pineal gland. This results in a diminished output of melatonin, along with a diminished melatonin to serotonin ratio, leading to a decline in adaptive processes and a predictable syndrome manifested by the "diseases of the aged" (DOA) and subsequent death of the organism. That is, aging is a syndrome of relative melatonin deficiency resulting from the gradual failure of the pineal gland.
