‘Man Up’: the importance and strategy for placing male reproductive health centre stage in the political and research agenda

Men in the United States suffer more severe chronic conditions, have higher death rates for all 15 leading causes of death, and die nearly 7 yr younger than women. Health-related beliefs and behaviours are important contributors to these differences. Men in the United States are more likely than women to adopt beliefs and behaviours that increase their risks, and are less likely to engage in behaviours that are linked with health and longevity. In an attempt to explain these differences, this paper proposes a relational theory of men's health from a social constructionist and feminist perspective. It suggests that health-related beliefs and behaviours, like other social practices that women and men engage in, are a means for demonstrating femininities and masculinities. In examining constructions of masculinity and health within a relational context, this theory proposes that health behaviours are used in daily interactions in the social structuring of gender and power. It further proposes that the social practices that undermine men's health are often signifiers of masculinity and instruments that men use in the negotiation of social power and status. This paper explores how factors such as ethnicity, economic status, educational level, sexual orientation and social context influence the kind of masculinity that men construct and contribute to differential health risks among men in the United States. It also examines how masculinity and health are constructed in relation to femininities and to institutional structures, such as the health care system. Finally, it explores how social and institutional structures help to sustain and reproduce men's health risks and the social construction of men as the stronger sex.

A father's lifetime experiences can be transmitted to his offspring to affect health and development. However, the mechanisms underlying paternal epigenetic transmission are unclear. Unlike in somatic cells, there are few nucleosomes in sperm, and their function in epigenetic inheritance is unknown. We generated transgenic mice in which overexpression of the histone H3 lysine 4 (H3K4) demethylase KDM1A (also known as LSD1) during spermatogenesis reduced H3K4 dimethylation in sperm. KDM1A overexpression in one generation severely impaired development and survivability of offspring. These defects persisted transgenerationally in the absence of KDM1A germline expression and were associated with altered RNA profiles in sperm and offspring. We show that epigenetic inheritance of aberrant development can be initiated by histone demethylase activity in developing sperm, without changes to DNA methylation at CpG-rich regions.