Some years before birth, advertise for a couple of parents
belonging to long-lived families.
—Oliver Wendell Holmes, Sr.
There is great variation in the longevity we see among people. We are all aware that a small percentage of people live to be over 100 years old, living much longer than the vast majority of us. This longevity, taking place in the absence of deliberate actions, is a result of natural functions in these long-lived people.
Scientists have learned about some of the natural factors which allow such people to live so long. This understanding can help us to live a longer, healthier, and more active life.
This chapter lists eight of the more interesting factors which correlate with the natural life span of several mammalian species, including man.
- Brain weight: In general, the greater the brain weight,
the longer the life span. The higher the ratio of brain to body
weight, the longer the species’ average life span. - Body weight: There is not as good a correlation as with
brain weight. A greater species’ body weight does correlate
with longer life span, but a lower individual body weight as
compared to the species average usually seems to increase individual life span, probably due to reduced specific metabolic
rate (see point 3 below). - Specific metabolic rate (SMR)—(food burned per day
per unit of animal body weight). In general, the higher the
SMR, the shorter the life span. Reduced caloric intake means
a lower SMR for the individual. In many short-lived animals,
caloric restriction (lowered SMR) dramatically increases life
span. SMR is an index of how hard the metabolic equipment
in a gram of tissue must work. - Body temperature: The higher the species’ normal
natural body temperature, the greater in general the life
span. (A lower individual body temperature as compared to
the species’ average seems to increase that individual’s life expectancy in cold-blooded species.) Reduction in body temperature results in a lower SMR. Species with higher normal
average body temperatures seem to have more-and/or better
protective and repair enzymes. - The capacity to activate DMBA (an environmental
pollutant, one of the very common class of carcinogens called
polynuclear aromatic hydrocarbons, PAH, found in tobacco
and other combustion tars) to a mutagenic form: DMBA and
many other pollutants, especially the PAH, are not carcinogens in themselves but must be activated, particularly in the
liver, to the metabolites which are carcinogenic. The longer
the life span of the animal, the less the capacity to convert the
pollutants to the carcinogenic form. In other words, in order
to live longer, the damage that would be done to DNA by
such carcinogens as activated PAH must be prevented or
blocked. Blocking of attachment of these carcinogens to DNA
is done more effectively by longer-lived species too. Even in
their metabolized carcinogenic form, these molecules cannot
cause cancer or atherosclerosis unless they bind to the DNA.
In Figure 1, we see the DMBA-induced mutation rate (scale
marked 0 to 700) versus the DMBA concentration. The fibroblast cells of rats suffer a much higher rate of DMBA-induced
mutations than longer-lived animals. Humans; who live longest of all species in this study, show the lowest induced mutation rate. Figure 2 shows the amount of DMBA binding to
DNA (on a scale of 0 to 120) versus time for a number of
mammalian species, including man. You can easily see that
the longer-lived animals bind the least amount of DMBA. Na-
ture seems to be saying that it is necessary (but not sufficient)
for your species to have half the PAH to DNA binding as an-
other species if your species is to live twice as long as another
species. BHT, BHA; selenium, and many other antioxidants
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