Hayward Adam D, Rigby Francesca L, Lummaa Virpi
Department of Biological and Environmental Sciences, School of Natural Sciences, University of Stirling, Stirling FK9 4LA, United Kingdom; Institute of Evolutionary Biology, University of Edinburgh, Edinburgh EH9 3FL, United Kingdom;
Department of Animal and Plant Sciences, University of Sheffield, Western Bank, Sheffield S10 2TN, United Kingdom;
Proc Natl Acad Sci U S A. 2016 Aug 9;113(32):8951-6. doi: 10.1073/pnas.1519820113. Epub 2016 Jul 25.
A leading hypothesis proposes that increased human life span since 1850 has resulted from decreased exposure to childhood infections, which has reduced chronic inflammation and later-life mortality rates, particularly from cardiovascular disease, stroke, and cancer. Early-life cohort mortality rate often predicts later-life survival in humans, but such associations could arise from factors other than disease exposure. Additionally, the impact of early-life disease exposure on reproduction remains unknown, and thus previous work ignores a major component of fitness through which selection acts upon life-history strategy. We collected data from seven 18th- and 19th-century Finnish populations experiencing naturally varying mortality and fertility levels. We quantified early-life disease exposure as the detrended child mortality rate from infectious diseases during an individual's first 5 y, controlling for important social factors. We found no support for an association between early-life disease exposure and all-cause mortality risk after age 15 or 50. We also found no link between early-life disease exposure and probability of death specifically from cardiovascular disease, stroke, or cancer. Independent of survival, there was no evidence to support associations between early-life disease exposure and any of several aspects of reproductive performance, including lifetime reproductive success and age at first birth, in either males or females. Our results do not support the prevailing assertion that exposure to infectious diseases in early life has long-lasting associations with later-life all-cause mortality risk or mortality putatively linked to chronic inflammation. Variation in adulthood conditions could therefore be the most likely source of recent increases in adult life span.
一个主流假说是，自1850年以来人类寿命的延长源于儿童期感染暴露的减少，这降低了慢性炎症以及晚年死亡率，尤其是心血管疾病、中风和癌症导致的死亡率。早年队列死亡率常常能预测人类晚年的生存率，但这种关联可能源于疾病暴露之外的因素。此外，早年疾病暴露对生殖的影响仍不明确，因此先前的研究忽略了适应性的一个主要组成部分，而选择正是通过这一组成部分作用于生命史策略。我们收集了来自18世纪和19世纪芬兰的七个人口群体的数据，这些群体的死亡率和生育率自然变化。我们将早年疾病暴露量化为个体前5年期间传染病的去趋势化儿童死亡率，并控制了重要的社会因素。我们发现，没有证据支持早年疾病暴露与15岁或50岁之后的全因死亡风险之间存在关联。我们还发现，早年疾病暴露与 specifically死于心血管疾病、中风或癌症的概率之间没有联系。与生存率无关，没有证据支持早年疾病暴露与生殖表现的几个方面之间存在关联，包括男性和女性的终身生殖成功率和初育年龄。我们的研究结果不支持这样一种普遍观点，即早年接触传染病与晚年全因死亡风险或假定与慢性炎症相关的死亡率存在长期关联。因此，成年期条件的变化可能是近期成人寿命增加的最可能原因。
