Hmmmm.... 1. Only given an abstract 2. Abstract is riddled with typos 3. Admits no causation, only correlation 4. Started in 1938, a time where ethical considerations in science were at their peak /s Let's read a full study that displays awareness of its limitations! TL;DR--Let's not pretend it has anything to do with penis size. Differing levels of hormones have been found to be linked to both genitalia and sexuality, but it doesn't mean that anything has any causation, only correlation. I think it's important to keep these particulars in mind so we can avoid unfairly stereotyping gay men.The evidence supports a role for prenatal testosterone exposure in the development of sex-typed interests in childhood, as well as in sexual orientation in later life, at least for some individuals. It appears, however, that other factors, in addition to hormones, play an important role in determining sexual orientation. These factors have not been well-characterized, but possibilities include direct genetic effects, and effects of maternal factors during pregnancy. Although a role for hormones during early development has been established, it also appears that there may be multiple pathways to a given sexual orientation outcome and some of these pathways may not involve hormones.
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According to the classical model of hormonal influences on mammalian sexual differentiation, prenatal or neonatal exposure to testicular hormones causes male-typical development, whereas female-typical development occurs in the absence of testicular hormones. A corollary of this formulation is that ovarian steroids are not required for female-typical development, a point to which we will return. The empirical record generally supports this model for a wide range of brain regions and behaviors that differ on the average for male and female animals. For example, treating female rodents with testosterone early in life decreases their female-typical behavior in adulthood, and increases their male-typical behavior. Similarly, castrating male rodents early in life leads to decreased male-typical, and increased female-typical, behavior subsequently [54]. The same manipulations produce neural changes as well. Early testosterone treatment of female rats increases the volume of sexually-dimorphic nucleus of the preoptic area (SDN-POA), a region of the anterior hypothalamic preoptic area that is larger in male than in female rats [50;51], and castration of male rats early in life reduces the volume of the same nucleus [50;80].
Shit, I straight up do not understand hubski. I feel like when I try to joke around shit gets completely ignored, probably because it's either not funny, or no effort went into it. On the flip side, it seems like trying to dig deeper into a post only makes me look like a moron. W/e, I need to lurk more.
I'm not sure about the point of your comment, or how you managed to get anything anti-gay out of the post title or the linked abstract. This part of the paper you linked is interesting though, and it does address my other comment Similarly, testosterone acts on the external genitalia largely following conversion to DHT, but may require conversion to estradiol before exerting some of its neurobehavioral effects. This last difference could even explain the apparent paradox of larger penises, suggesting greater DHT exposure, in homosexual than in heterosexual men. If more of the testosterone these men produce is converted to DHT in the periphery, less could be available for conversion to estradiol in the brain, thus leading to greater masculinization of the external genitalia, but reduced neurobehavioral masculinization. This possibility is highly speculative, however, but the point that genital masculinization and neurobehavioral masculinization need not parallel one another, because of the varied downstream mechanisms involved in testosterone’s effects on development, is important.