Mutation accumulation  The first modern theory of mammal ageing was formulated by Peter Medawar in 1952. This theory formed in the previous decade with J. B. S. Haldane and his selection shadow concept. The development of human civilization has shifted the selective shadow as the conditions that humans now live in include improved quality of victuals, living conditions, and healthcare. This improved healthcare includes modern medicine such as antibiotics and new medical technology. A few studies in Drosophila have shown that the age of expression of novel deleterious mutations, defines the effects they contribute on mortality. Overall, however; although their frequency increases, their effects and variation decreases with age.   Antagonistic pleiotropy When examining the body-size vs. lifespan relationship, one also observes that predatory mammals tend to live longer than prey mammals in a controlled environment, such as a zoo or nature reserve. The explanation for the long lifespans of primates (such as humans, monkeys, and apes) relative to body size is that their intelligence, and they would have a lower intrinsic mortality.  Diseases
Mutation accumulation Germ line The first modern theory of mammal ageing was formulated by Peter Medawar in 1952. This theory formed in the previous decade with J. B. S. Haldane and his selection shadow concept. The development of human civilization has shifted the selective shadow as the conditions that humans now live in include improved quality of victuals, living conditions, and healthcare. This improved healthcare includes modern medicine such as antibiotics and new medical technology. A few studies in Drosophila have shown that the age of expression of novel deleterious mutations, defines the effects they contribute on mortality. Overall, however; although their frequency increases, their effects and variation decreases with age. Somatic cells A popular idea, that has failed to gain significant experimental support, is that mutation in somatic cells, as distinct from DNA damage in somatic cells, is the primary cause of aging. Mice defective in the mutL homolog Pms2 have about a 100-fold elevated mutation frequency in all tissues, but do not appear to age more rapidly. These mice display mostly normal development and life, except for early onset carcinogenesis and male infertility. Although germline mutations may influence the course of the aging process over many generations (as discussed above), somatic mutations occurring during the lifetime of an organism appear to have little, if any, affect on the aging process. Antagonistic pleiotropy When examining the body-size vs. lifespan relationship, one also observes that predatory mammals tend to live longer than prey mammals in a controlled environment, such as a zoo or nature reserve. The explanation for the long lifespans of primates (such as humans, monkeys, and apes) relative to body size is that their intelligence, and they would have a lower intrinsic mortality. Potential immortality of the germ line Individual organisms are ordinarily mortal; they age and die, while the germlines which connect successive generations are potentially immortal. The basis for this difference is a fundamental problem in biology. The Russian biologist and historian Zhores A. Medvedev 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. In particular, Medvedev considered that the most important opportunities for information maintenance of germ cells are created by recombination during meiosis and DNA repair; he saw these as processes within the germ cells that were capable of restoring the integrity of DNA and chromosomes from the types of damage that cause irreversible ageing in somatic cells. Diseases
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Germ line
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Somatic cells
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A popular idea, that has failed to gain significant experimental support, is that mutation in somatic cells, as distinct from DNA damage in somatic cells, is the primary cause of aging. Mice defective in the mutL homolog Pms2 have about a 100-fold elevated mutation frequency in all tissues, but do not appear to age more rapidly. These mice display mostly normal development and life, except for early onset carcinogenesis and male infertility. Although germline mutations may influence the course of the aging process over many generations (as discussed above), somatic mutations occurring during the lifetime of an organism appear to have little, if any, affect on the aging process.
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Potential immortality of the germ line Individual organisms are ordinarily mortal; they age and die, while the germlines which connect successive generations are potentially immortal. The basis for this difference is a fundamental problem in biology. The Russian biologist and historian Zhores A. Medvedev 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. In particular, Medvedev considered that the most important opportunities for information maintenance of germ cells are created by recombination during meiosis and DNA repair; he saw these as processes within the germ cells that were capable of restoring the integrity of DNA and chromosomes from the types of damage that cause irreversible ageing in somatic cells.