Revival: Biological Effects of Low Level Exposures to Chemical and Radiation (1992)

10 BIOLOGICAL EFFECTS OF LOW LEVEL EXPOSURES

This hypothesis naturally leads to the question of how advantageous
pharmacologic agents enhance longevity. For example, it is well established
that administration of antihypertensive agents to individuals with high
blood pressure reduces population mortality. Viewed in the context of this
discussion, antihypertensive agents do not slow senescence, but rather mod­
ulate senescent symptoms in a positive, life-enhancing fashion. In other
words, senescent toxicity is still present, but its maleficent manifestations,
which in turn could elicit further injury and destruction (e.g., stroke,
myocardial infarction, etc.), are temporarily held in abeyance. This concept
also seems to apply to drugs that lower cholesterol in humans. The author’s
unpublished Gompertz analysis of the data from Anderson et al.48 demon­
strates that the population with elevated serum cholesterol had Gompert-
zians upwardly displaced in a near-parallel fashion relative to subjects with

normal cholesterol. As discussed previously,514 this indicates reversible tox­
icity. Serum cholesterol-lowering drugs presumably return the patient to a
senescent state that he or she would be at in the absence of elevated serum
cholesterol; that is, cholesterol lowering drugs modulate senescent symp­
toms, manifestations, and cascading effects, but not senescence itself.
The skeptic, justifiably, would take strong exception to this view. Ulti­
mately, however, most disagreements come full circle, returning to the
thorny issue of just what constitutes aging! As Huber Warner, chief of the
molecular and cell biology branch at the U.S. National Institute on Aging
put it, “If you ask what’s normal aging, we still can’t tell you.”49 Restated
poetically in metaphor:

There was the Door to which I found no Key:

There was the Veil through which I could not see:

Some little talk awhile of Me and Thee

There was —and then no more of Thee and Me.

Rubaiyat of Omar Khayyam29

The approach taken here, admittedly arbitrary, is that biological disor­

der, cell dysdifferentiation, variations in constraints, etc., produce aging,

and that disease is a manifestation of aging, not aging itself.

Hypothesis VIII: Relative to other eutherian mammalian species, humans’

enhanced longevity (e.g., maximum life span potential) is due to a neote-

nous slowing of orthodox mammalian aging, as opposed to a qualitatively

distinct aging process.

Applying allometric scaling principles to the entire class Mammalia,50-53

and assuming a body mass of 70 kg for humans, our species should have a

gestation time of 6.08 months, a maximum life span of 26.9 years, and a

brain mass of 269 g. Realistic values of these variables are 9.0 months, 114

years, and 1400 g, respectively.50*54 The sizable deviation of these human