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Kronfeldner makes an important point about the norms that may constrain selection of potential causes for study in population health,1 consistent with the limited set currently in use2 which do not provide a generic, integrated scientific model that explains the past and predicts the future. For example, Kronfeldner highlights how an interest in genetic causes rather than those embedded in the fabric of society may allow us to downplay (or background) social or racial disparities in health; but perhaps because of lack of space, does not mention the large sexual disparity in health whereby men living about 5 years less than women is taken as normal. Notably, despite progress in achieving sexual equality, investigation of such differences has focused on factors controlling women's rather than men's bodies. For example, a substantially higher mortality rate from the leading cause of death, ischaemic heart disease, among men than women was for many years conceptualized as women being protected by estrogen,3 rather than men being vulnerable because of some aspect of maleness. Even today almost exactly 12 years after the Women's Health Initiative trial showed definitively that estrogen does not protect women against ischaemic heart disease or mortality,4 research interest is still focused on hormones in women, whereas the obvious alternative candidate, hormones in men, remains backgrounded, little researched and largely unmentionable.
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Schooling et al. (2014) studied this question.
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