It has become a well-known fact that men universally die younger than women. Less common knowledge, however, is the complexity underlying this gendered life-expectancy difference (GLED).
Though men are physically stronger than women, by virtue of significantly greater endogenous levels of testosterone, the GLED estimates tend to range from 5-7 years in favour of females. Females can thus be considered ‘biologically stronger’ than males.
However, it would be reductionistic to solely blame biological differences. Male-female behavioural disparities also account for the non-trivial GLED that transcends the world.
From a social standpoint, men consistently demonstrate greater risk-taking behaviours during adolescence and emerging adulthood. While higher relative levels of testosterone is associated with these social determinants, and can be explained in part for the higher incidence of preventable deaths in males, conformity to hegemonic expressions of masculinity may also pose a contributing factor.
In other words, even in men that may have low-normal levels of testosterone, perceived social pressure to intimate hegemonic forms of masculinity may alter male behaviour to the detriment of lifespan. Further, hegemonic masculinities are attributable to toxic degrees of stoicism, delayed help-seeking and suicide risk. Overall, a dynamic interplay exists between individual and social determinants of male life expectancy.
The research pertaining to testosterone levels and male healthspan is equivocal. An inverted U curve is an appropriate visual representation of this relationship, in that too little and too much testosterone appears inimical to healthspan.
It is important to distinguish healthspan from lifespan. Healthspan is a more recent term that denotes expected quality years of life, whereas lifespan is merely the chronological extent to which someone lives (which could be an existence host to severe and various co-morbidities).
Healthy levels of testosterone confer many benefits, including but not limited to lean body mass, physical strength, protection against mental health disease. On the other hand, male sex hormones may suppress the immune system and be a factor in cardiovascular disease (CVD) representing the primary cause of male deaths worldwide.
Previous research that has investigated the effects of castration suggests that the relative absence of testosterone confers extended lifespan. A 2012 Korean paper specifically looked at eunuchs, males that were castrated at a young age, and observed an increase in life expectancy of 14.4-19.1 years when compared with uncastrated men of homogenous socioeconomic status. In this instance, ‘lifespan’ would seem more apt than ‘healthspan’ given male sex hormones enhance the overall quality of a man’s life.
Given the complexity and equivocality of testosterone, it may not directly be culpable for the higher incidence of CVD and associated GELD. Oestrogen, which women possess to a considerably higher degree than men (especially during reproductive years), does exert protective effects against CVD. CVD is nevertheless the leading cause of female deaths too, albeit at a reduced absolute incidence.
In short, science and expert analyses has not yet struck an unwavering consensus as to the reasons underpinning men’s shorter life expectancy. We can be confident in saying that social determinants related to male behaviour, and the relatively greater oestrogen levels in women, are notable factors in the entrenched GELD.