http://en.wikipedia.org/wiki/DNA_repairLongevity and caloric restriction
Most lifespan influencing genes affect the rate of DNA damageA number of individual genes have been identified as influencing variations in lifespan within a population of organisms. The effects of these genes is strongly dependent on the environment, particularly on the organism's diet. Caloric restriction reproducibly results in extended lifespan in a variety of organisms, likely via nutrient sensing pathways and decreased metabolic rate. The molecular mechanisms by which such restriction results in lengthened lifespan are as yet unclear (see[27] for some discussion); however, the behavior of many genes known to be involved in DNA repair is altered under conditions of caloric restriction.
For example, increasing the gene dosage of the gene SIR-2, which regulates DNA packaging in the nematode worm Caenorhabditis elegans, can significantly extend lifespan.[28] The mammalian homolog of SIR-2 is known to induce downstream DNA repair factors involved in NHEJ, an activity that is especially promoted under conditions of caloric restriction.[29] Caloric restriction has been closely linked to the rate of base excision repair in the nuclear DNA of rodents,[30] although similar effects have not been observed in mitochondrial DNA.[31]
Interestingly, the C. elegans gene AGE-1, an upstream effector of DNA repair pathways, confers dramatically extended lifespan under free-feeding conditions but leads to a decrease in reproductive fitness under conditions of caloric restriction.[32]
This observation supports the pleiotropy theory of the biological origins of aging, which suggests that genes conferring a large survival advantage early in life will be selected for even if they carry a corresponding disadvantage late in life.mielenkiintoista juttua kyllä. evoluutiotakaan ei kiinnosta vanhat ihmiset. vievät vaan resursseja ja parempi, että kuolevat, eivätkä pyöri jaloissa.
tämä siis evoluution mielipide ei minun.
