Ricklefs R E
Department of Biology, University of Missouri at St. Louis, St. Louis, Missouri 63121-4499, USA.
Am Nat. 1998 Jul;152(1):24-44. doi: 10.1086/286147.
Evolutionary considerations predict that rate of aging should vary in direct relation to the mortality rate of presenescent young adults (extrinsic mortality rate) independently of differences in physiology, such as rate of metabolism. This prediction emerges from theory irrespective of the particular genetic mechanisms responsible for variation in aging. Yet this critical relationship has not been confirmed in comparative studies of natural populations. In the present analysis, rate of aging is estimated by the rate of increase in mortality rate (mx) with age (x). Comparisons between natural and captive populations of birds suggest that the Weibull model (mx = m0 + alphaxbeta) provides a better description of aging than the Gompertz model (mx = m0esigmax). Rate of aging is quantified by the parameter omega (dimension: 1/time), which is calculated from the Weibull parameters alpha and beta (omega = alpha1/(beta+1)). In this analysis, rate of aging in birds and mammals is directly related to extrinsic mortality (estimated by the initial mortality rate, m0) independently of taxonomic group and of variation in body size and, by implication, metabolic rate. When time is expressed in years, rate of senescence is related to initial mortality rate by omega = 0.294m0(0.367). This result implies that natural selection in response to variation among taxa in m0 has resulted in the evolutionary modification of factors that influence the rate of aging in natural populations. The potential strength of selection on factors that could further reduce rate of aging is indicated by the proportion of deaths due to aging-related causes. Although species with low initial mortality rates also exhibit reduced rates of increase in mortality rate with age (i.e., delayed senescence), the relatively high proportion of aging-related deaths in such species suggests that further evolutionary responses leading to long life are severely constrained. This argues against mutation accumulation and antagonistic pleiotropy as genetic mechanisms underlying senescence and suggests, instead, that rate of aging represents a balance between wear and tear, on the one hand, and genetically controlled mechanisms of prevention and repair, on the other. Evidently, remedies for extreme physiological deterioration in old age either are not within the range of genetic variation or are too costly to be favored by selection.
进化方面的考虑预测，衰老速率应与衰老前年轻成年个体的死亡率（外在死亡率）直接相关，而与生理差异无关，比如代谢速率。这一预测源于理论，与导致衰老差异的特定遗传机制无关。然而，在对自然种群的比较研究中，这一关键关系尚未得到证实。在本分析中，衰老速率通过死亡率（mx）随年龄（x）的增加速率来估计。对鸟类自然种群和圈养种群的比较表明，威布尔模型（mx = m0 + alphaxbeta）比冈珀茨模型（mx = m0esigmax）能更好地描述衰老。衰老速率由参数ω（单位：1/时间）量化，它由威布尔参数α和β计算得出（ω = α1/(β + 1)）。在本分析中，鸟类和哺乳动物的衰老速率与外在死亡率直接相关（由初始死亡率m0估计），与分类群以及体型变化无关，进而也与代谢速率无关。当时间以年表示时，衰老速率与初始死亡率的关系为ω = 0.294m0(0.367)。这一结果意味着，针对不同分类群中m0差异的自然选择导致了影响自然种群衰老速率的因素发生进化改变。与衰老相关原因导致的死亡比例表明了对可能进一步降低衰老速率的因素进行选择的潜在强度。尽管初始死亡率低的物种也表现出死亡率随年龄增加的速率降低（即衰老延迟），但这类物种中与衰老相关死亡的比例相对较高，这表明导致长寿的进一步进化反应受到严重限制。这反对将突变积累和拮抗多效性作为衰老的遗传机制，相反，这表明衰老速率一方面代表磨损与损耗，另一方面代表基因控制的预防和修复机制之间的平衡。显然，针对老年时极端生理衰退的补救措施要么不在遗传变异范围内，要么成本过高而无法受到选择青睐。
