Dilman V M
J Theor Biol. 1986 Jan 7;118(1):73-81. doi: 10.1016/s0022-5193(86)80009-1.
It is known that increased mortality due to environmental hazards results, in the course of natural selection, in the shortening of maximum life span and acceleration of sexual maturation in a population subjected to an intensified pressure from external environment. As a consequence, the prereproductive period/maximum life span ratio appears to be approximately the same in each species. Mechanisms responsible for this are not clear yet. Since maximum life span is limited by both ageing and formation of certain diseases (in humans, the so-called main noninfectious diseases), the paper discusses four possible models of development of ageing and age-linked disease--ecological, genetic, degenerative (metabolic) and ontogenetic. It was found that it is the ontogenetic model only that can adequately account for the development of moderate shifts in the duration of both sexual maturation and maximum life span. It also provides the rationale for the pleotropic activity of genes during the development of the organism, its ageing and formation of age-connected diseases.
众所周知,在自然选择过程中,由于环境危害导致的死亡率增加会使受到外部环境压力增强的种群的最大寿命缩短,并加速其性成熟。因此,每个物种的生殖前期/最大寿命比似乎大致相同。造成这种情况的机制尚不清楚。由于最大寿命受到衰老和某些疾病形成(在人类中,即所谓的主要非传染性疾病)的限制,本文讨论了衰老和与年龄相关疾病发展的四种可能模型——生态模型、遗传模型、退行性(代谢)模型和个体发育模型。研究发现,只有个体发育模型能够充分解释性成熟持续时间和最大寿命的适度变化的发展。它还为基因在生物体发育、衰老以及与年龄相关疾病形成过程中的多效性活动提供了理论依据。