Cohen Alan A
Groupe de recherche PRIMUS, Department of Family Medicine, University of Sherbrooke, 3001 12e Ave, N, Sherbrooke, QC, J1H 5N4, Canada.
Curr Aging Sci. 2015;8(1):14-23.
The longstanding debate about whether aging may have evolved for some adaptive reason is generally considered to pit evolutionary theory against empirical observations consistent with aging as a programmed aspect of organismal biology, in particular conserved aging genes. Here I argue that the empirical evidence on aging mechanisms does not support a view of aging as a programmed phenomenon, but rather supports a view of aging as the dysregulation of complex networks that maintain organismal homeostasis. The appearance of programming is due largely to the inadvertent activation of existing pathways during the process of dysregulation. It is argued that aging differs markedly from known programmed biological phenomena such as apoptosis in that it is (a) very heterogeneous in how it proceeds, and (b) much slower than it would need to be. Furthermore, the taxonomic distribution of aging across species does not support any proposed adaptive theories of aging, which would predict that aging rate would vary on a finer taxonomic scale depending on factors such as population density. Thus, while there are problems with the longstanding non-adaptive paradigm, current evidence does not support the notion that aging is programmed or that it may have evolved for adaptive reasons.
关于衰老是否可能因某些适应性原因而进化的长期争论,通常被认为是将进化理论与一些实证观察相对立,这些实证观察表明衰老作为生物体生物学的一个程序性方面,特别是保守的衰老基因。在此我认为,关于衰老机制的实证证据并不支持将衰老视为一种程序性现象的观点,而是支持将衰老视为维持生物体稳态的复杂网络失调的观点。程序性的表象很大程度上是由于在失调过程中现有通路的意外激活。有人认为,衰老与已知的程序性生物学现象如细胞凋亡明显不同,因为(a)其进展方式非常异质,且(b)比所需的速度要慢得多。此外,衰老在物种间的分类学分布并不支持任何提出的衰老适应性理论,这些理论会预测衰老速率会在更精细的分类学尺度上因诸如种群密度等因素而有所不同。因此,虽然长期存在的非适应性范式存在问题,但目前的证据并不支持衰老具有程序性或它可能因适应性原因而进化的观点。