6,453
edits
No edit summary |
No edit summary |
||
Line 1: | Line 1: | ||
'''Testosterone''' is a steroid and male sex hormone (androgen). | '''Testosterone''' is a steroid and the primary male sex hormone (androgen). Its effects on the body result from the direct activation of the androgen receptors found in various tissues across the body or via its metabolism to other androgens, most notably via the actions of the enzyme 5-α-reductase, which converts testosterone to the far more potent androgen dihydrotestosterone (DHT). | ||
In humans, testosterone and other androgens are crucial for the development and maintenance of several male sexually dimorphic traits, such as men's greater bone density and muscle mass compared to women, and (mainly via the process of aromatization to DHT) the development of fixed masculine traits during puberty, such as androgenic body hair, enlargement of the male sex organs, and greater vocal depth. Despite the common perception of it as a male hormone, it is also produced by women in much smaller amounts (in ovaries and the adrenal glands), and it seems to play an essential role in the maintenance of several vital physiological functions in them, particularly the [[sex drive|libido]].<ref>https://www.sciencedirect.com/science/article/abs/pii/S2213858715002843</ref> | |||
Greater prenatal exposure to androgens, in particular, seem to play a prominent role in driving male-typical cognition and behavior,<ref>https://journals.lww.com/environepidem/Fulltext/2019/10001/Prenatal_Sex_Hormones_and_Behavioral_Outcomes_in.267.aspx</ref> though the extent to which androgens play a direct role in driving these differences is still in doubt.<ref>https://royalsocietypublishing.org/doi/abs/10.1098/rstb.2008.0282</ref> | |||
The influence of androgens in driving these changes does not seem limited to the prenatal environment or puberty. However, most of the physiological, cognitive, and behavioral effects resulting from the administration of exogenous sex hormones to adults seem small apart from the specific cases regarding the administration of opposite sex hormones to transgenders.<ref>https://pubmed.ncbi.nlm.nih.gov/27347894/</ref> | |||
In humans (and other animals), testosterone plays a role in driving increased aggression, violent behavior, and status drive.<ref>https://web.archive.org/web/20160109111144/http://www.homepage.psy.utexas.edu/HomePage/faculty/josephs/pdf_documents/Arch_Chall_NBR.pdf</ref> | |||
In many animals, testosterone has a positive relationship to [[dominance hierarchy|male dominance status]].<ref>https://onlinelibrary.wiley.com/doi/abs/10.1002/ajpa.20387</ref><ref>https://www.sciencedirect.com/science/article/abs/pii/S0018506X0800161X</ref> | |||
In humans the link between testosterone and male dominance status is more tenuous, with several studies finding no link between T levels and achieved social rank, <ref>https://www.sciencedirect.com/science/article/pii/S0306453016301780</ref><ref>https://www.sciencedirect.com/science/article/abs/pii/S0191886910001406</ref> though it does seem to be linked with dominant behavior and heightened attentiveness to social cues pertaining to dominance rank to some degree.<ref>https://link.springer.com/article/10.1007/s40750-014-0020-2#Sec3</ref><ref>https://www.sciencedirect.com/science/article/abs/pii/S1364661311000787</ref><ref>https://www.sciencedirect.com/science/article/abs/pii/S0018506X20301975</ref><ref>https://www.sciencedirect.com/science/article/abs/pii/S0018506X16305050</ref><ref>https://www.sciencedirect.com/science/article/abs/pii/S0306453016304292</ref> | |||
These null results are likely due to many contextual factors such as respective culture/ethnicity,<ref>https://www.amazon.com/Behave-Biology-Humans-Best-Worst/dp/1594205078</ref> age of the male,<ref>https://www.sciencedirect.com/science/article/abs/pii/S1054139X14002250</ref> and the male's own level of social status,<ref>https://www.sciencedirect.com/science/article/abs/pii/S0306453019312934</ref> moderating the effect of testosterone in driving such behavior. | |||
T levels may be more strongly related to the attainment of dominance in social milieus based around violent domination as opposed to ones based around social consensus, competence, and likability.<ref>https://www.tandfonline.com/doi/abs/10.1080/19485565.2006.9989114</ref> | |||
These null findings pertaining to testosterone and actual status attainment (despite testosterone driving competitiveness and social dominance related behaviors) may also imply that the excess possession of certain testosterone-related traits may be ''harmful'' to attain social status in specific social contexts. Together with the general [[feminization]] of post-industrial Western society, this may result in [[evolutionary mismatch|evolutionary mismatches]] wherein high levels of masculinity and testosterone-related traits may be generally associated with lower social status. Still, these traits would have been generally rewarded in the more violent and unstable contexts where they were evolutionarily selected. | |||
Testosterone also very likely does not mediate any of these status-seeking behaviors on its own to a substantial, as interactions with other hormones such as cortisol,<ref>https://www.sciencedirect.com/science/article/abs/pii/S030645301500400X</ref> estrogen, prolactin, and various neurotransmitters such as serotonin<ref>https://link.springer.com/article/10.1007/s11031-011-9264-3</ref> appear crucial in driving many of the behaviors linked to "high-T" in the popular imagination. | |||
Many studies that examine the effects of testosterone (and other hormones) on psychology are deeply flawed as they do not take these inter-hormone interactions into account, do not use particularly reliable measures of testosterone, have low sample sizes, do not take into account interindividual differences in sensitivity to androgens and do not take into account the effects prenatal and pubertal 'priming' may have on shaping the bodies response to testosterone in adulthood. Adult T-levels are also substantially related to lifestyle factors <ref>https://academic.oup.com/jcem/article/92/2/549/2566787?login=true</ref><ref>https://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.1019.6064&rep=rep1&type=pdf</ref> such as age, smoking, body fat percentage and general health. | |||
There has been a secular decline in testosterone in Western countries,<ref>https://academic.oup.com/jcem/article/92/1/196/2598434?login=true</ref> leading to sensationalist headlines regarding rampant [[soyboy|feminization]] of men being driven by this factor alone. However, other longitudinal studies have found concurrent evidence that sex-hormone-binding globulin (SHBG), a protein that binds to testosterone and makes it inert in the body, has also been decreasing on a population and cohort level.<ref>https://academic.oup.com/jcem/article/92/12/4696/2597312?login=true</ref> | |||
If this finding proves robust, this reduction in SHBG results in less negative feedback being exerted on men's hypothalamic-pituitary-gonadal axis (HPG axis), which would result in the body downregulating T production as it essentially needs less to produce the desired effects. Meaning the secular decrease in T wouldn't be relevant in driving any practical differences in population level masculinization. | |||
==Dual hormone hypothesis== | ==Dual hormone hypothesis== | ||
The fact that increased | Many people associate Testosterone with male sex drive, however, increased Testosterone shows no relation to increased male sexual desire (with the concurrent presence of high cortisol levels). | ||
The fact that increased Testosterone alone doesn't increase male sex drive provides some support for the dual hormone hypothesis. It is said some effects of Testosterone become potentiated in the prescence of lower levels of the stress hormone cortisol and suppressed when higher levels of this hormone are present. Thus the two hormones interact to produce the effects commonly seen to be associated with Testosterone alone.<ref>https://psyarxiv.com/42t6e/</ref> | |||
==See also== | ==See also== | ||
Line 16: | Line 35: | ||
<references /> | <references /> | ||
{{ | {{B}} |
edits