Infant deaths and old age deaths are very different. The former are mostly due to severe congenital malformations of one or a small number of specific organs. On the contrary, old age deaths are largely the outcome of a long process of deterioration which starts in the 20s and affects almost all organs. In terms of age-specific death rates, there is also a clear distinction: the infant death rate falls off with age, whereas the adult and old age death rate increases exponentially with age in conformity with Gompertz’s law. An additional difference is that whereas aging and old age death have been extensively studied, infant death received much less attention. To our knowledge, the two effects have never been inter-connected. Clearly, it would be satisfactory to explain the two phenomena as being two variants within the same explanatory framework. In other words, a mechanism providing a combined explanation for the two forms of mortality would be welcome. This is the purpose of the present paper. We show here that the same biological effects can account for the two cases provided there is a difference in their severity: death triggered by isolated lethal anomalies in one case and widespread wear-out anomalies in the second. We show that quite generally this mechanism leads indeed, respectively, to a declining and an upgoing death rate. Moreover, this theoretical framework leads to the conjecture that the severity of the death effects, whether in infancy or old age, is higher for organisms which comprised a larger number of organs. Finally, let us observe that the main focus of the paper is the drastic difference of the age-specific death rates (i.e., decreasing versus increasing) because this difference is found in many species, whereas the question of the best fit (e.g., Gompertz versus Weibull) is rather specific to human mortality.

婴儿死亡和老年死亡有很大不同。前者多为某一或少数特定器官的严重先天畸形所致。相反，老年死亡主要是从 20 多岁开始并影响几乎所有器官的长期恶化过程的结果。从年龄别死亡率来看，也有明显的区别：婴儿死亡率随着年龄的增长而下降，而成人和老年死亡率随着年龄的增长呈指数增长，符合Gompertz定律。另一个区别是，虽然衰老和老年死亡已被广泛研究，但婴儿死亡受到的关注要少得多。据我们所知，这两种影响从未相互关联。显然，将这​​两种现象解释为同一解释框架内的两种变体是令人满意的。换句话说，一个为这两种死亡形式提供综合解释的机制将受到欢迎。这就是本文的目的。我们在这里展示了相同的生物学效应可以解释这两种情况，前提是它们的严重程度不同：一种情况是由孤立的致命异常引发的死亡，另一种情况是广泛的磨损异常。我们表明，通常这种机制确实分别导致死亡率下降和上升。此外，这个理论框架导致了这样一种推测，即无论是在婴儿期还是在老年期，死亡效应的严重程度对于包含更多器官的生物体来说都更高。最后，让我们观察一下本文的主要焦点是年龄别死亡率的巨大差异（即，