Nineteen studies on the behavioral effects of prenatal exposure to hormones administered for the treatment of at-risk human pregnancy are reviewed. Because the role of prenatal exposure to hormones in the development of human behavioral sex differences is potentially confounded by society's differential treatment of the sexes, comparisons between exposed and unexposed subjects were evaluated and summarized separately for male and female subjects. Therefore, this review focuses on data for individuals whose prenatal hormone environments were atypical relative to what is normal for their own sex.OK, so what were the conclusions?
Overall, it appears that prenatal exposure to androgen-based synthetic progestin exerted a masculinizing and/or defeminizing influence on human behavioral development, whereas prenatal exposure to natural progesterone and progesterone-based synthetic progestin had a feminizing and/or demasculinizing influence, particularly among female subjects. The data on prenatal exposure to synthetic estrogen derive primarily from subjects exposed to diethylstilbestrol (DES). DES-exposed male subjects appeared to be feminized and/or demasculinized, and there is some evidence that exposed female subjects were masculinized.
These findings are discussed in the context of prenatal hormonal contributions to sexually dimorphic behavioral development both within and between the sexes. Recommendations for the conduct of future research in developmental behavioral endocrinology are presented.
Three issues that qualify research in the area of human behavioral endocrinology must be considered in order to appropriately interpret the findings (see Reinisch & Gandelman, 1978, for a more detailed discussion).
The first qualifier relates to the inability to implement true experimental design (i.e., random assignment to treatment conditions) in research on human behavioral endocrinology. Because this area of human research is subject to strict ethical, moral, and legal constraints, true experimental design is precluded when studying potentially harmful interventions in humans.
Consequently, interpretation of the relationship between prenatal hormones and human behavioral development is limited to correlative rather than causal explanation. It is only through thoughtful comparison of conclusions derived from human "experiments of nature" or of medical treatmems with those derived from carefully controlled experimems with laboratory animals that confidence in the former can be attained. The role of hormones in organizing the neural substrate for behavior in nonhuman animals has been clearly established with two basic
experimental paradigms: perinatal androgen administration to genetic females, resulting in defeminization and/or masculinization, and perinatal androgen deprivation of genetic males, resulting in demasculinization and/or feminization, of sexually dimorphic behaviors and gonadotropin secretion in adolescence and adulthood. Extensive reviews of the nonhuman animal literature are provided by Ellis (1982), Hines (1982), and Reinisch (1974; 1983).
The second qualifier relates to the fact that the behavioral repertoires of males and females are not mutually exclusive, but rather, are overlapping. It is rare for one sex to display a behavior that is never exhibited by the other sex (menstruation, gestation, lactation, and impregnation being the notable exceptions). Typically, differences between males and females occur in the average frequency with which particular behaviors are exhibited by each sex. Thus, behavioral sex differences reflect quantitative, not qualitative, differences (Goy, 1970).
The third qualifier relates to the fact that masculinity and femininity are multidimensional. Masculinity and femininity are no longer conceptualized as opposite ends of a single, unidimensional, bipolar continuum (Fig. 2a), but are now understood to be a multidimensional matrix of independent or semi-independent factors.
The orthogonal or independent model (Fig. 2b: Constantinople, 1973; Bem, 1974; Whalen, 1974; Spence & Helmreich, 1978; Heilbrun, 1976; Berzins et al., 1978) and the oblique or correlated model (Fig. 2c: Reinisch, 1976; Reinisch & Sanders, 1987) suggest that masculinity and femininity are, with regard to many behavioral dimensions, relatively independent.
These models imply that an increase in the frequency or strength of masculine behavior (masculinization) is not necessarily associated with a decrease in feminine behavior (defeminization). Conversely, feminization is not necessarily concomitant with demasculinization. Thus, an individual may exhibit high frequencies of both masculine and feminine behavior (androgynous), low levels of both kinds of behavior (undifferentiated), or high levels of one type of behavior and low levels of the other (masculine or feminine).
The difference between the orthogonal and oblique models resides in the extent to which masculinity and femininity are considered to be independent. Whereas the orthogonal model proposes total independence, the oblique model suggests that there is some degree of correlation between masculinization and defeminization and between feminization and demasculinization.
Our review suggests that endogenous hormones present prenatally influence at least some aspects of sexually dimorphic behavioral development in normal male and female subjects, perhaps by establishing particular behavioral predispositions. In general, play-related activities and interests, aggression/assertion, and gender identity/role emerged as the behavioral categories most often affected by prenatal exposure to exogenous hormones. These effects are not simple, however. For example, although prenatally DES-exposed male subjects appear to have been demasculinized in terms of interest in active participation in sports, they were masculinized with regard to interest in passive viewing of sports. Prenatal exposure to some of these hormonal treatments was associated with delayed or diminished sexual maturation and behavior, while in other instances these dimensions were enhanced.Unfortunately, it's behind a paysite firewall, but if your library has access, you should be able to view it. I'm accessing it at home using my ANU library privileges, as both PhD candidate and lecturer.
Another reason why I want a career in academe.