Since the early reports in the Western media about coronavirus and the question of its mortality risk, the significance of age has been highlighted.
Unlike other flu-like viruses, it seemed, COVID-19 selectively harmed the oldest of those who became infected. Infants, children and young adults seemed, if not immune, then at least relatively unaffected. Early accounts of the outcome of those adults admitted to hospitals in Wuhan city, the assumed starting point of the pandemic, indicated that older age, chronic disease and multiple organ failure were each independent risk factors for subsequent mortality (Zhou et al., 2020).
These findings have provided the basis for most national public health warnings for who was most at risk and who most needs to ’self-isolate’. Age has most often and most loudly been highlighted as the vector distinguishing between the ‘vulnerable’ and the ‘invulnerable’. Otherwise, it seemed, we were all in this together. The governor of New York even claimed that Coronavirus was ‘the great equalizer’.
Survival or death are not random outcomes, whatever the circumstances. With increasing age, people are increasingly likely to die, whether or not they are infected by a potentially deadly viral infection. The well-known Gompertz curve showing mortality exponentially rising with age has long served as a marker distinguishing ageing from the sheer passage of time. At the same time, what has also become increasingly evident is that factors other than age play their part in defining life expectancy and shaping the arc of mortality, including the various social divisions we have recently shown reflect a widening heterogeneity of the unitary category of old age (Gilleard and Higgs, 2020).
Gender has proved a major division; older men are at least a third more likely to die after becoming infected than are older women, with evidence of this gender divide emerging consistently in several countries, from China to Italy, and from Spain to the UK. Equally, if not more noticeable, is the divide evident in US data on COVID-19 mortality associated with ‘race’. In various states and counties where such data has been released, African Americans are reportedly dying from the viral infection twice or even three times as often as their white Euro-American peers (Ball, 2020; Onder, Rezza and Brusaferro, 2020; Thebault, Ba Tran and Williams, 2020).
Since one must assume that the virus does not change its shape or structure, after attaching itself to the cells of men and women, Black and White people or young and old people, the locus for the mortality effect must lie with differences in the host, that is in either their social or biological characteristics. What is notable is that these patterns of difference in response to COVID-19 seem to directly mirror differences in late life expectancy, in general. After the age of sixty five, men have shorter life expectancies, African Americans have shorter life expectancies and people with co-morbidity have shorter life expectancies. It seems a reasonable hypothesis to suggest that COVID-19 is like a magnifying glass, amplifying but not fundamentally altering the chronology of life and death nor the impact of social divisions.
Chris Gilleard is Visiting Senior Research Fellow in the Department of Social and Policy Sciences at the University of Bath and the Division of Psychiatry at University College London.
Paul Higgs is Professor of the Sociology of Ageing at University College London.
Bristol University Press newsletter subscribers receive a 35% discount – sign up here. Please note that only one discount code can be used at a time.
The views and opinions expressed on this blog site are solely those of the original blog post authors and other contributors. These views and opinions do not necessarily represent those of the Policy Press and/or any/all contributors to this site.