Men, on average, live shorter lives than women. Globally, men born in 2009 can expect to live 64.3 years compared to 68 years for women (Central Intelligence Agency of the United States of America, 2010). Reliable vital statistics kept over long periods of time show, moreover, that this male longevity deficit has been persistent and pervasive (Human Mortality Database, 2010).
The nearly ubiquitous observation of the deficit suggests that it arises from fundamental biological mechanisms conserved by natural selection. The “mother” and “grandmother” hypotheses, for example, assume that women have looked after infants and “provisioned” children over much of human history (O’Connell et al., 1999 and Peccei, 2001). Women who lived long enough to help their children and grand children survive to reproductive age presumably had more grandchildren and great-grandchildren than women who died relatively young (Lahdenpera, Lummaa, Helle, Tremblay, & Russell, 2004). These assumptions imply that natural selection would conserve mutations that confer longevity on women more than men (Madrigal and Melendez-Obando, 2008 and Shanley et al., 2007).
Other literature claims that reproductive success among men depends on the ability to compete successfully for women (Clutton-Brock & Isvaran, 2007). Natural selection would, therefore, conserve mutations that aid this competition (Moller, Fincher, & Thornhill, 2009). Mutations that make males more competitive may, however, also reduce lifespan. Metabolism that yields rapid growth, for example, confers the advantage of size and strength but also apparently accelerates aging (Kawahara & Kono, 2010). Competition itself, moreover, can lead to trauma that shortens life (Moller, Fincher et al., 2009).
Not all mechanisms that increase fitness in males also shorten life span. Males hardy enough to father children late in life through, for example, serial monogamy should yield more grandchildren than less robust men (Jokela et al., 2010 and Lahdenpera, Russell et al., 2007). The literature suggests, however, that natural selection conserved more, or more powerful, life extending mechanisms in women than in men.
These arguments may parsimoniously explain the emergence and persistence of the male longevity deficit. But the deficit has exhibited frequent and sizeable changes over time. Conserved differences such as those described briefly above do not suggest intuitively appealing explanations of this temporal variability. Researchers have, therefore, typically attributed it to phenomena such as war (Elder, Clipp, Brown, Martin, & Friedman, 2009), improvements in obstetric practices (Pavard, Koons, & Heyer, 2007), gender roles (Courtenay, 2000), and social reforms (Nobles, Brown, & Catalano, 2010) that differentially affect male and female mortality and appear more in the realm of the social than biological sciences. I, however, speculate that selection in utero, a mechanism both conserved by natural selection and affected by social processes, could induce variability over time in the male longevity deficit. I describe the mechanism and offer an empirical test of its possible effect among Swedes – a population with the longest continuous record of sex-specific longevity in annual birth cohorts. I also replicate the test in a shorter, more complex set of data from England and Wales. Results support the hypothesis that selection in utero may explain part of the difference in longevity between males and females in modern populations.
