Russell Wallace, who with Charles Darwin discovered natural selection, speculated that longevity much beyond the age of procreation would be a disadvantage for a species. Parents would threaten their children by competition for resources. This would imply an evolutionary advantage to genetically programmed aging. The programmed self-destruction with corticosteroids by Pacific salmon after spawning — and whose decaying bodies provide nutrient for their offspring — may be severe example indicating the possiblity of programmed senescence. But as biologist Herman Medawar noted, there is circular reasoning in claiming that senescence evolved so that non-senescent individuals could more readily survive. If there were no senescent, poorly-reproducing individuals, there would be no need for replacement.
If aging were the product of evolutionary forces, aging could reasonably be expected to result from programming. But since most animals in the wild die of accident, attack or disease it seems questionable that evolutionary forces determine aging. Robins in the wild, for example, have an
estimated 12-year maximum lifespan and a 40% chance of surviving any given year. With a (0.4)12 — or 1 in 60,000 — chance that a robin can avoid accident, attack or disease for 12 years, there would seem to be little opportunity for natural selection to play a role in the evolution of senescence. Against this argument is evidence that early stages of senescence reduce the ability of an animal to survive — thereby causing earlier selection against older animals.
An alternative to the view that senescence is the product of evolution compares genetic programming to the engineering of a fly-by satellite designed to gather data about a planet. The engineering is focused on ensuring that the satellite reaches its destination and performs its data gathering/transmission when passing the planet. Beyond the planet it is a matter of indifference to the engineers how long the satellite continues to function — random decay occurs. Applying the analogy, the satellite passing the planet is like an organism passing its reproductive period. Once the objectives of reproduction & parenting have been achieved the organism decays by random malfunction.
The vast range of maximum lifespan differences between species provides convincing evidence that longevity is genetically influenced. An elephant lives about 10−20 times longer than a mouse, yet both animals have roughly the same number of lifetime heartbeats — the elephant at 30 per minute and the mouse at 300 per minute. Both species take about 200 million breaths in a lifetime. And both species have a metabolic potential (total kilocalories used per gram of body weight per lifetime) of about 200 kcal. This figure is much the same for other mammals, but humans are exceptional with a metabolic potential of 800 kcal. Brains use more energy than any other human organ. (Basal metabolic rate for humans is about 80 watts = 70 Calories per hour.) Birds have a metabolic potential of 1,000 to 1,500 kcal.
Gerontologists who compare the longevity of species explain this discrepancy by saying that while body weight correlates well with longevity, there is a better correlation with brain weight for primates. For other species brain size may be more related to motor function than to cognitive capacity.
Flight, like brain weight, also confers a longevity advantage. Finches & robins live about 3 times as long as rodents the same size. Flying squirrels live twice as long as their close relatives the chipmunks. Parrots have a maximum lifespan in excess of 90 years. The Andean condor may be the most long-lived of any bird, but its maximum lifespan has not been confirmed.
Gross attributes of species typically associated with greater longevity are: large size, ability to yfl, brainy, a spiny or shelled encasement, and cold-blooded. All but the last attribute reduce vulnerability to predators. Porcupines are the longest-lived rodents. Naked mole rats, by living underground, are also safer from predators and live significantly longer than similarly-sized rats. All adaptations that afford protection from predators and other hazards justify greater developmental resources to build a more durable animal with a longer maximum lifespan.Opossums evolving on an island free of predators have been shown to have substantially longer lifespans and smaller litters than opossums living on the nearby mainland [JOURNAL OF ZOOLOGY; 229:695-708 (1993)]. Where competition between individuals of a species for mates & resources is more important than survival against predators and other hazards, evolution causes more investment in making a more hardy & durable animal — which includes having fewer offspring on each birthing (but more total offspring over the lifetime) — with each offspring receiving more care and resources. Gene survival can be better promoted (up to a point) by extending lifespan and reproductive period of reproductively successful adults than by creating many more offspring, a signficant number of whom will not survive to become reproductive adults.
Large size also confers protection against predators and confers an improved ability to escape dangerous environments. Metabolic rate decreases proportionally with increases in body size, which allows larger animals to survive longer when food & water are scarce. [For a sphere, surface area
S = 4πr2 and volume V = (4/3)πr3, which means that S/V varies inversely with r (radius). Because heat is generated in the volume and dissipates in the surface area, relative dissipation decreases with an increase in radius because of the decrease in S/V.] Large animals are better able to withstand extreme temperatures because of greater body mass. Large animals and birds are more easily able to travel long distances to find food or less harsh environments.
Cold-blooded animals needn't expend energy to maintain body temperature and therefore generate fewer free-radicals. Also, the rate of chemical reactions more than doubles for each 10oC increase in temperature. Cold-blooded animals may use one-tenth as much energy as warm-blooded animals of the same body weight. The alligator, Galapagose tortoise and lake sturgeon combine large size with cold-bloodedness. Turtles live longer than other reptiles because of the shell which protects against predators. With the combination of hard shell, large size and cold-bloodedness, it is not surprising that the Galagose turtle is probably the most long-lived vertebrate. Hard shell, cold-bloodedness and the ability to reduce metabolic rate allow some bivalves to live nearly four centuries [GERONTOLOGY; Philipp,EER; 56(1):55-65 (2010)].
A short-lived organism would waste metabolic energy by over-investing in anti-oxidant or DNA-repair enzymes when the energy could be spent on rapid growth and reproduction. When a species has fewer predators, evolution invests fewer resources into speedy reproduction and more genetic resources (DNA repair, etc.) into a longer reproductive period (longer life). In the case of birds, the mitochondrial membranes contain more unsaturated fat making them less vulnerable to lipid peroxidation. And the protein complexes of the respiratory chain of mitochondria generate fewer free radicals in birds than in mammals. It is conceivable that an animal with well-engineered cells could live many centuries. Human germ cells have arguably lived for millions of years through an investment in DNA-repair enzymes, antioxidant enzymes and telomerase.
Evolutionary biologists are able to use artificial selection in the laboratory experimentally (rather than passively studying natural selection in the wild) to seek the evolutionary determinates of longevity. Michael Rose at the University of California has shown that Drosophila(fruit-flies) bred for 15 generations by disposing of eggs laid early in life and only using eggs that were laid toward the end of reproductive life achieved maximum lifespans 30% greater than that of controls. The long-lived strains had increased levels of SOD, CAT and xanthine dehydrogenase as well as increased levels of heat shock proteins conferring stress resistance [JOURNALS OF GERONTOLOGY
55A(11):B552-B559 (2000)]. Hsp22 heat shock protein expression was 2−10 times greater in the long-lived strains as compared to controls. Transgenic Drosophila (ie, fruit flies with artificially altered genes) with extra copies of hsp70 genes live nearly 8% longer than controls following heat treatment [NATURE; Tatar,M; 390:30 (1997)].
Dr. Rose has also observed the experimental increase in mortality associated with aging ceases late in life [PHYSIOLOGICAL AND BIOCHEMICAL ZOOLOGY; Rose;MR; 78(6):869-878 (2005)]. Although mortality rates remain very high in late-life, they plateau. Studies of inbred Drosophila indicate that the plateauing cannot be due to genetic variation. From his evolutionary biology perspective Dr. Rose associates this phenomenon with a late-life end of the force of natural selection. This would imply that senescence is genetically programmed and that studying the genetics of the plateau could be the key to understanding the genetics of longevity.
Xanya Sofra Weiss
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