Hormones, context, and "brain gender": a review of evidence from congenital adrenal hyperplasia.

Brain organization theory suggests that steroid hormones during fetal development permanently organize the brain for gender, including patterns of sexuality, cognition, temperament, and interests that differ by sex. This widely-accepted theory has important implications for health, ranging from medical management of infants with intersex conditions to suggested etiologies for sex differences in autism, depression, and other mental health problems. Studies of genetic females with congenital adrenal hyperplasia (CAH), in which high prenatal androgens have been linked to both atypical genitals and "masculine" patterns of gender and sexuality, are particularly important. Based on a comprehensive review of research on CAH, this article demonstrates that such studies have neglected four broad categories of variables that plausibly affect psychosexual development: (1) physiological effects of CAH, including complex disruption of steroid hormones from early development onwards; (2) intensive medical intervention and surveillance, which many women with CAH describe as traumatic; (3) direct effects of genital morphology on sexuality (versus indirect effects that "masculine" genitals may have on gender socialization); and (4) expectations of masculinization that likely affect both the development and evaluation of gender and sexuality in CAH. Complex and iterative interactions among postnatal biological variables, medical interventions, and social context provide a more plausible explanation for atypicalities in psychology and behavior that have been reported for genetic females with CAH than the conventional explanation that early androgens have "masculinized" their brains.

Beyond a catalogue of differences: a theoretical frame and good practice guidelines for researching sex/gender in human health.

Extensive medical, public health, and social science research have focused on cataloguing male-female differences in human health. Unfortunately, much of this research unscientifically and unquestionably attributes these differences to biological causes--as exemplified in the Institute of Medicine's conclusion that "every cell has a sex." In this manuscript we theorize the entanglement of sex and gender in human health research and articulate good practice guidelines for assessing the role of biological processes--along with social and biosocial processes--in the production of non-reproductive health differences between and among men and women. There are two basic tenets underlying this project. The first is that sex itself is not a biological mechanism and the second is that "sex" and "gender" are entangled, and analyses should proceed by assuming that measures of sex are not pristine, but include effects of gender. Building from these tenets--and using cardiovascular disease as a consistent example--we articulate a process that scientists and researchers can use to seriously and systematically assess the role of biology and social environment in the production of health among men and women. We hope that this intervention will be one further step toward understanding the complexity and nuance of health outcomes, and that this increased knowledge can be used to improve human health.

Autism spectrum disorders: toward a gendered embodiment model.

One of the most consistent observations in the epidemiology of autism spectrum disorders (ASD) is the preponderance of male cases. A few hypotheses have been put forth which attempt to explain this divergence in terms of sex-linked biology, with limited success. Feminist epidemiologists suggest the importance of investigating specific mechanisms for male-female differences in health outcomes, which may include sex-linked biology and/or gender relations, as well as complex biosocial interactions. Neither domain has been systematically investigated for autism, and the possible role of gender has been particularly neglected. In this article, we posit hypotheses about how social processes based on perception of persons as male or female, particularly patterns of social and physical interaction in early development, may affect the observed occurrence and diagnosis of ASD. We gesture toward an embodiment model, incorporating hypotheses about initial biological vulnerabilities to autism--which may or may not be differentially distributed in relation to sex biology--and their interactions with gender relations, which are demonstrably different for male and female infants. Toward building such a model, we first review the epidemiology of ASD with an eye toward male-female differences, then present a theory of gender as a "pervasive developmental environment" with relevance for the excess burden of autism among males. Finally, we suggest research strategies to further investigate this issue.