Is human brain masculinization estrogen receptor-mediated? Reply to Luoto and Rantala.
Level 5 - mechanism / opinion, no new human data
Commentary/expert opinion and narrative rebuttal with no original empirical data
PubMed 28818501 · doi:10.1016/j.yhbeh.2017.07.018
What was done
This commentary responded to arguments regarding the role of estrogen receptors in human brain masculinization. The authors synthesized existing literature comparing human and rodent sex differentiation, analyzed human genetic conditions (such as androgen receptor and estrogen receptor functioning), and reviewed findings from genetic females prenatally exposed to synthetic estrogens like diethylstilbestrol (DES).
What was found
The abstract provides no quantitative data or effect sizes. The authors argue that functional androgen receptors, rather than testosterone aromatization or estrogen receptors, are necessary for male-typical behavior in genetic males. Furthermore, they note that the totality of evidence from females exposed to DES in utero indicates little to no effect of estrogens on sexuality, supporting the view that estrogen plays a limited role in masculinizing human brain and behavior.
Why it matters
Rodent models demonstrate a critical aromatase- and estrogen-mediated pathway for brain masculinization; this commentary clarifies why those mechanisms do not readily generalize to human sexual differentiation, where androgen receptor pathways dominate.
Limits
This is an opinion letter without a systematic search methodology, meta-analysis, or new primary empirical data. Specific sample sizes, effect estimates, and statistical certainty cannot be evaluated from the abstract.
Cited by
- contradicts During fetal development, estrogen plays an essential role in masculinizing regions of the male brain.