Blaser Martin J, Webb Glenn F
Department of Mathematics, Vanderbilt University, Nashville, Tennessee, USA
mBio. 2014 Dec 16;5(6):e02262-14. doi: 10.1128/mBio.02262-14.
The age structure of human populations is exceptional among animal species. Unlike with most species, human juvenility is extremely extended, and death is not coincident with the end of the reproductive period. We examine the age structure of early humans with models that reveal an extraordinary balance of human fertility and mortality. We hypothesize that the age structure of early humans was maintained by mechanisms incorporating the programmed death of senescent individuals, including by means of interactions with their indigenous microorganisms. First, before and during reproductive life, there was selection for microbes that preserve host function through regulation of energy homeostasis, promotion of fecundity, and defense against competing high-grade pathogens. Second, we hypothesize that after reproductive life, there was selection for organisms that contribute to host demise. While deleterious to the individual, the presence of such interplay may be salutary for the overall host population in terms of resource utilization, resistance to periodic diminutions in the food supply, and epidemics due to high-grade pathogens. We provide deterministic mathematical models based on age-structured populations that illustrate the dynamics of such relationships and explore the relevant parameter values within which population viability is maintained. We argue that the age structure of early humans was robust in its balance of the juvenile, reproductive-age, and senescent classes. These concepts are relevant to issues in modern human longevity, including inflammation-induced neoplasia and degenerative diseases of the elderly, which are a legacy of human evolution.
The extended longevity of modern humans is a very recent societal artifact, although it is inherent in human evolution. The age structure of early humans was balanced by fertility and mortality, with an exceptionally prolonged juvenility. We examined the role of indigenous microbes in early humans as fundamental contributors to this age structure. We hypothesize that the human microbiome evolved mechanisms specific to the mortality of senescent individuals among early humans because their mortality contributed to the stability of the general population. The hypothesis that we present provides new bases for modern medical problems, such as inflammation-induced neoplasia and degenerative diseases of the elderly. We postulate that these mechanisms evolved because they contributed to the stability of early human populations, but their legacy is now a burden on human longevity in the changed modern world.
人类种群的年龄结构在动物物种中是独特的。与大多数物种不同，人类的幼年时期极度延长，而且死亡并非与生殖期的结束同时发生。我们用揭示人类生育力和死亡率非凡平衡的模型来研究早期人类的年龄结构。我们假设早期人类的年龄结构是由包括衰老个体程序性死亡在内的机制维持的，这些机制包括与本土微生物的相互作用。首先，在生殖生活之前和期间，存在对通过调节能量稳态、促进生育力和抵御竞争性高级病原体来维持宿主功能的微生物的选择。其次，我们假设在生殖生活之后，存在对导致宿主死亡的生物体的选择。虽然对个体有害，但这种相互作用的存在可能在资源利用、抵抗食物供应的周期性减少以及抵御高级病原体引起的流行病方面对整个宿主种群有益。我们提供基于年龄结构种群的确定性数学模型，以说明这种关系的动态，并探索维持种群生存能力的相关参数值。我们认为早期人类的年龄结构在幼年、生殖年龄和老年群体的平衡方面是稳健的。这些概念与现代人类长寿问题相关，包括炎症诱导的肿瘤形成和老年人的退行性疾病，这些都是人类进化的遗留问题。
现代人类寿命的延长是一个非常新的社会现象，尽管它在人类进化中是固有的。早期人类的年龄结构由生育力和死亡率平衡，幼年时期异常延长。我们研究了本土微生物在早期人类中作为这种年龄结构的基本贡献者的作用。我们假设人类微生物群进化出了特定于早期人类衰老个体死亡率的机制，因为他们的死亡有助于总体种群的稳定。我们提出的这一假设为现代医学问题，如炎症诱导的肿瘤形成和老年人的退行性疾病，提供了新的依据。我们推测这些机制的进化是因为它们有助于早期人类种群的稳定，但在变化了的现代世界中，它们的遗留问题现在却成为了人类长寿的负担。
