Evolution of ageing
In 1889, he theorized that ageing was part of life's program to make room for the next generation in order to sustain the turnover that is necessary for evolution.
[citation needed] Natural selection is a process that allows organisms to better adapt to the environment, it is the survival of the fittest which are predicted to produce more offsprings.
Natural selection acts on life history traits in order to optimize reproductive success and lifetime fitness.
[citation needed] There is no theory that explains how these deleterious mutations affect fitness on different ages and the evolution of senescence.
Therefore, there is not much reason why the body should remain fit for the long haul because selection pressure is low for traits that would maintain viability past the time when most animals would have died anyway.
Metabolic diseases come along due to the low demand for physical activity in modern civilization compared to times where humans had to forage in the wild for survival.
Why did selection not find and favor mutations in ways that allow us, for example, to regenerate our cells, or to not produce toxic metabolism?
Most people have already reproduced before any disease manifest; this means that parents will pass their alleles to their offsprings before they show any fitness problems, and it is therefore "too late" for selection.
[8] The non-adaptive theory assumes that the evolutionary deterioration of human age occurs as a result of accumulation of deleterious mutations in the germline.
[8] These deleterious mutations start expressing themselves late in life, by the time we are weak/wobbly and have already reproduced, this means that Natural selection cannot act on them because reproduction has ended.
Studies done on Drosophila melanogaster have shown an inverse relationship between the mean optimal age at maturity and mutation rates per gene.
Research has shown that this is not true for all genes and may be thought of as partial validation of the theory, but it cuts the core premise: that genetic trade-offs are the root cause of ageing.
This concept focuses on the evolutionary pressure to reproduce in a set, optimal time period that is dictated by age and ecological niche.
Apoptosis or programmed cell death is associated with gradual degradation of the immune system, skeletal muscle, and aging-associated malfunction.
Naked mole rats have high telomerase activity, they live long, and were thought by some to never get cancer; and therefore possibly be an exception to this hypothesis.
Longer-lived species possess many mechanisms for offsetting damage due to causes such as oxidation, telomere shortening, and other deteriorative processes.
Shorter-lived species, having earlier ages of sexual maturity, have less need for longevity and thus did not evolve or retain the more-effective repair mechanisms.
This supports the idea that the force of natural selection declines as a function of age, which was first introduced by Peter B. Medewar and J.B.S Haldane.
The model also supports Medewars' theory that due to dangerous and unpredicted conditions in the environment such as diseases, climate changes and predators, many individuals die not too long after sexual maturation.
[41] Often also postreproductive individuals make intergenerational transfers: bottlenose dolphins and pilot whales guard their grandchildren; there is cooperative breeding in some mammals, many insects and about 200 species of birds; sex differences in the survival of anthropoid primates tend to correlate with the care to offspring; or an Efe infant is often attended by more than 10 people.
[citation needed] Skulachev (1997)[43] has suggested that programmed ageing assists the evolution process by providing a gradually increasing challenge or obstacle to survival and reproduction, and therefore enhancing the selection of beneficial characteristics.
The explanation for the long lifespans of primates (such as humans, monkeys, and apes) relative to body size is that they manage to achieve lower extrinsic mortality due to their intelligence.
[citation needed] Individual organisms are ordinarily mortal; they age and die, while the germlines which connect successive generations are potentially immortal.
The Russian biologist and historian Zhores A. Medvedev[47] considered that the accuracy of genome replicative and other synthetic systems alone cannot explain the immortality of germ lines.
Rather Medvedev thought that known features of the biochemistry and genetics of sexual reproduction indicate the presence of unique information maintenance and restoration processes at the different stages of gametogenesis.
Lamin A promotes genetic stability by maintaining levels of proteins that have key roles in non-homologous end joining and homologous recombination.
[55] In HGPS, the inability to adequately repair DNA damages due to defective A-type lamin may cause aspects of laminopathy-based premature aging.
There are four common traits of Werner's syndrome: cataracts in both eyes, changes in skin similar to scleroderma, short stature, and early graying and loss of hair.
[59] Bloom syndrome is a rare autosomal recessive disorder that is characterized by short stature, chromosomal instability, predisposition to cancer, and sun-sensitive skin.
[61] Cockayne syndrome is a homozygous or heterozygous mutation that results in short stature, abnormalities in head size, and slow growth and development.
