Although male pattern balding isnot necessarily tied to old age, it is very definitely due to a clock. If you transplant hairs from the balding area onto another part of the head, these hairs fall out right on schedule with the others remaining in the balding area. If you transplant hairs from nonbalding areas to the balding area, the hairs will keep right on growing, even while the hairs around them are falling out.
Common male pattern balding seems to involve hormonal messages sent to the internal cellular clocks in the hair follicles in specific areas, such as
the top of the head. Balding can be halted by castrating the balding male individual, thereby interrupting the hormone clock run signal. Therefore we know that balding depends to a degree on male hormones, and to some measure on the anatomic site. Testosterone causes hair to grow in other areas, such as the beard and moustache zones. We know that dihydrotestosterone, produced by the action of the enzyme testosterone-5-alpha-reductase on testosterone, causes some hair follicles to go into the resting (non-growing) phase. Only those cells which have a genetic susceptibility will be affected. These follicles are not usually immediately killed in the process, even though they no longer grow hairs large enough to
be easily visible to the naked eye.
It is possible to reinstate menstrual cycling in most non-cycling older female rodents and in some human females with the drug bromocriptine (Parlodel®, made by Sandoz). Bromocriptine is a stimulant of the dopaminergic nervous system in the brain, which in turn stimulates the release by the pituitary gland of hormone-releasing factors (necessary for sex hormone production) and growth hormone (necessary for proper immune system function). The dopaminergic tract is one of the brain’s systems showing the sharpest decline in activity with age—it is especially vulnerable to oxidative damage and accumulates lipofuscin throughout life. It is not yet understood just how bromocriptine reinstates menstrual
cycling—resetting the clock—but it apparently involves increasing the level of dopaminergic stimulation to the hypothalamus and pituitary to the higher levels found in youth.
A clock, the one that programs the developmental stages of life, appears to be responsible for the finding that rats and mice can live much longer life spans if their caloric intake is restricted early in life. In rodents, reproduction can be delayed if conditions, especially the availability of food, are not supportive. It seems likely that the extended life span is due
to putting the animals “on hold” by retarding development and delaying reproduction until food becomes more available. If food is fed ad lib (at the animal’s chosen level) to these calorie-restricted animals, they rapidly mature and reproduce. In effect, the restricted food supply stalls the animals at an immature level of their development—and hence their reproduction—until more food becomes available. If severe caloric restriction during development is attempted with higher animals such as monkeys, which take several years to reach reproductive maturity, brain damage occurs and the animals do not live extended life spans.
It is possible to greatly extend the life spans of some insects by depriving their developing larvae of food and water. The larvae then become smaller in size and regress to an earlier larval development stage, failing to develop into adult insects. Given food and water again, the larvae proceed to develop normally. If deprived once again, the larvae again retrogress. Manipulating the maturation of the beetle Trogoderma glabrum in this manner, Drs. Beck and Bharadwaj (1972) produced larvae that lived over two years. The insect’s normal life span (from egg to death of the adult) is only eight weeks. By two years of age, very extensive genetic damage
had accumulated in these incredibly long-lived insect larvae, since they did not possess the quantities of protective and repair enzymes found in animals that normally live two years.
Aging clocks can turn off protective mechanisms essential to maintaining an animal’s life. After spawning, salmon rapidly peroxidize and die. Major protective mechanisms that they have against peroxidation before spawning cease to function afterwards, leaving them defenseless against the release by the adrenal glands of massive amounts of pro-oxidant hor-
mones. The “turning off’ is thought to be due to a hyperactivity of the adrenals triggered by the spawning. If you prevent the fish from spawning by castration, by removal of the pituitary, or by hormone treatments, they live for many more years, whereas the spawning salmon die in hours. A
similar phenomenon occurs with eels. This clock mechanism is an example where the interests of the genes (to make copies of themselves) conflicts with the interests of the individual animal. Yet another example: Female octopuses die soon after they hatch their young. But if you remove’the preoptic gland (their version of the pituitary), they won’t mate and will live
on for years.
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