Testosterone

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The chemical structure of testosterone.

Testosterone (T) 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 conversion to DHT, which exhibits far stronger affinity for the AR in these tissues) 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 women, particularly the libido.[1]

Testosterone and estrogen are nearly identical in terms of their chemical structure, and in men, estrogen is produced via the conversion of T to estrogen via the process of aromatization. Estrogen is important to men's general health due to estrogen's enhancing effects on libido, bone health and its neuroprotective nature. In men that are particularly sensitive to estrogen, aromatization may result in feminizing effects such as the development of breast tissue (gynecomastia).

Greater prenatal exposure to androgens, in particular, seem to play a prominent role in driving male-typical cognition and behavior,[2] though the extent to which androgens play a direct role in driving these differences is still in doubt.[3] The influence of androgens in driving these changes does not seem limited to the prenatal environment or puberty (periods when the organism is particularly sensitive to the masculinizing effects of T). 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,[4] with the notable exception of the dramatic effects anabolic steroid use can have on the promotion of lean tissue growth.[5][6]

In humans (and other animals), testosterone plays a role in driving increased aggression, violent behavior, and status drive.[7]

One should take studies on the effects of testosterone on driving certain psychological changes should be taken with a grain of salt, as many studies that examine the effects of testosterone (and other hormones) on psychology are deeply flawed. A large amount of these kinds of studies 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 body's response to testosterone in adulthood. Adult T-levels are also substantially affected by lifestyle factors[8][9] such as age, smoking, body fat percentage and general health, which is likely another confounding factor in such studies.

Secular decline in T-levels of Western men[edit | edit source]

There has been a secular decline in male serum T levels in Western countries that is independent of factors such as population aging and increased obesity,[10] a finding which has lead to sensationalist headlines regarding rampant 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.[11] If this finding proves robust, this reduction in SHBG would result in less negative feedback being exerted on men's hypothalamic-pituitary-gonadal axis (HPG axis), which would lead to the body downregulating T production as it essentially needs less to produce the desired effects. Meaning the secular decrease in T wouldn't be particularly relevant in driving any practical differences in population level masculinization. One reason why SHBG is lowering is likely due to increasing obesity, meaning that obese men would often have lower T levels (due to higher aromatization of T to estrogen, as the fat cells contain the aromatase enzyme[12]) but would also be more sensitive to the testosterone they do produce. Serum testosterone levels are far less clinically relevant than levels of unbound (free) testosterone, so what is important to establish a real decline in T levels would be to prove that levels of free-testosterone are falling. This is crucial, as some men have high serum T levels because their level of SHBG is high, which means most of the T they produce is effectively useless. Generally the body tries to maintain strong homeostasis when it comes to hormones.

Cross-national and cross-temporal difference in diet and general lifestyle also likely play much of a role in determining the hormonal profile of men from said countries and periods. For example, intakes of dietary protein in wealthy Western countries are generally higher than in developing countries,[13] which together with dietary fibre intake also being negatively correlated with country level economic development,[14] would result in lower levels of SHBG in the bloodstream, which would again lead to the bodies of Western individuals being generally more sensitive to the effects of T compared to people in developing countries.[15] These are all factors that need to be taken into account when trying to examine cohort level differences in hormonal profiles.

Another flaw with many of these studies is that they do not control for the fact that smoking has massively decreased in Western countries,[16] with cigarette consumption peaking in the 1950s and falling to low levels in the modern era.[17] This is important because smoking is correlated with higher free and total serum testosterone levels,[18] a link that is not known to be casual (it could be due to T being linked to impulsiveness and risk taking etc.), though it likely is to some degree as nicotine and other compounds found in tobacco have moderate anti-aromatase properties.[19] The inhibition of the aromatase enzyme would lead to increased T levels as the body would tend to compensate for the lower estrogen levels by increasing testosterone production.[20]

T and social dominance[edit | edit source]

In many animals, testosterone has a positive relationship to male dominance status.[21][22] 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,[23][24] though it does seem to be linked with dominant behavior and heightened attentiveness (or lowered in some instances) to social cues pertaining to dominance rank to some degree.[25][26][27][28][29] These null results are likely due to many contextual factors such as respective culture/ethnicity,[30] age of the male,[31] and the male's own level of social status[32] that serve to moderate the influence of testosterone in driving such behavior.

Higher 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.[33] This is similar to the conclusions of research into male facial-width-to-height ratio, another trait linked to status drive and dominance, which has discovered that this characteristic is only linked to violence in men of lower socio-economic status.[34] Likely the major way T-levels would contribute to dominance rank (and sexual success) in such contexts would via the favorable effects T levels have on lean body mass, as free testosterone levels seem quite strongly linked to men's amount of upper and lower body muscle mass, especially when comparing low T men to men with T levels in the normal range.[35] Not surprisingly, a man's level of muscularity is a major factor in other men's determinations of that man's level of social dominance, social threat and capacity for violence. Muscularity also seems to be strongly linked to mating success in certain social contexts, such as among university students in fraternities, an effect that appears mediated by other men's perceptions of muscular men's physical dominance.[36]

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. Some research has indicated that children that have received higher levels of exposure to prenatal androgens had lower quality social relationships and more restricted interests (boys only in this sample) essentially implicating higher neurological masculization in the development of (sub-clinical) autistic traits,[37] in line with the extreme male brain theory of autism. As even subclinical autistic traits seem to be linked to less social connectedness and loneliness[38] it therefore likely that exposure to excess levels of testosterone in the prenatal environment is associated with lower social status, less romantic success and other negative social outcomes, suggesting that this trait is subject to significant balancing selection in modern society.

Together with the general feminization of post-industrial Western society, this may result in evolutionary mismatches wherein excess levels of masculinity and (certain) testosterone-related traits may be generally associated with lower social status. Other research has indicated that the broader autism phenotype (BAP) may have had certain adaptive qualities that were evolutionarily selected for in the past, suggesting that neurological masculinzation may previously benefited males reproductive success.[39] Some traits that are linked to higher levels of testosterone exposure in the womb, such as systematizing, may also promote the attainment of social status and wealth, leading to higher fitness and reproductive success. It is plausible that a shift from mating systems based around arranged marriage and female economic dependence on men towards greater female mate choice together with a greater tendency towards hierarchies being based around likability sheer competence in modern service economies has resulted in lowered sexual success for men that are prone towards systematizing, thus leading to yet another potential evolutionary mismatch.

Another potential factor that serves to mask effects in research that examines the link between status and testosterone is that these studies often do not take into account the effects that the release of short bursts of T may play in mediating to outcome of dominance contests. However, a growing literature on the "challenge hypothesis" of testosterone does. The challenge hypothesis states that testosterone will rise in men in contexts where male intersexual competition is particularly salient, such as during or after male dominance contests or in the presence of fertile females.[40] Evidence for this hypothesis in human samples is mixed, but does generally support the thesis that male testosterone levels are reactive in response to male intrasexual competition related cues, particularly in response to victory in status competitions.[41]

It is very likely that testosterone does not mediate any of these status-seeking behaviors on its own to a substantial degree, as interactions with other hormones such as cortisol,[42] estrogen, prolactin, and various neurotransmitters such as serotonin[43] appear crucial in driving many of the behaviors linked to "high-T" in the popular imagination.

T and sexual behavior[edit | edit source]

Testosterone does seem to generally drive greater reproductive effort in males, and it is a highly replicable finding that men in committed relationships tend to have lower testosterone levels (though the effect is generally weak[44]), possibly to promote greater pair-bonding in males.[45] Part of this link between lower T and being in a committed relationship may not be casual. Instead, it may stem from the apparent fact that lower testosterone men may be more pro-social, more generous to their female partners and that men with higher testosterone seem to have larger levels of conflict in their relationships, particularly in egalitarian societies that seek to reduce status competition among males.[46] Thus men in committed relationships may be partly selected for low-T. Higher testosterone is very weakly positively related to mating success (but not reproductive success) in men (at least in modern WEIRD samples), which may simply be explicable by the fact that testosterone levels are linked to libido (and thus likely greater mating effort).

A link between testosterone (and physical masculinization) and non-committal sexual strategies indicates that T is generally linked to a fast life history strategy based around maximizing mating effort and minimizing parental care, a strategy that many high-T men seem unable to operationalize effectively in light of these weak effects for sexual success and T.

Dual hormone hypothesis[edit | edit source]

The dual hormone hypothesis states that testosterone substantially interacts with the stress hormone cortisol in order to exert its assumed affects on dominance behavior and mating drive. Cortisol is thought to inhibit these effects when levels are high, and androgens generally have the effect of inhibiting cortisol release. Thus the ratio between the two hormones is thought to be more important than levels of either one on their own, in terms of driving behaviors such as approach/avoidance, status seeking, violence, and sex drive.

For example, some evidence shows 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 presence of lower levels of the stress hormone cortisol and suppressed when higher levels of this hormone are present.[47]

This effect extends to Empathy[48], Bargaining Power[49] and Visualization[50].

This hypothesis also demonstrated that attractiveness and dominance are not orthogonal, according to studies[51] demonstrating purely testosterone (no cortisol) mediates attractiveness, whereas dominance is affected by both testosterone and cortisol.

Testosterone Reactivity as the Alternate Axis[edit | edit source]

There are other research[52][53] that demonstrates that temporal testosterone levels have less bearing on dominance than "Testosterone Reactivity". Jointly, T-Reactivity and Cortisol levels are better predictors of attractiveness and dominance than temporal T-levels. Also T-Reactivity has been demonstrated[54][55] to be a good correlation to anxiety.

Weirdly enough other research[56] have shown that testosterone is inversely correlated to T-levels, and that higher T-Reactivity (and lower Alpha/Stability traits) is correlated to father's avoidance of children (absent fatherhood). It is possible that there is a genetic or hormonal component (e.g. Digit Ratio) to testosterone reactivity.

Alternatively, research on masturbation[57] demonstrated that high male dominance and low female dominance is correlated to desire for masturbation.

See also[edit | edit source]

References[edit | edit source]

  1. https://www.sciencedirect.com/science/article/abs/pii/S2213858715002843
  2. https://journals.lww.com/environepidem/Fulltext/2019/10001/Prenatal_Sex_Hormones_and_Behavioral_Outcomes_in.267.aspx
  3. https://royalsocietypublishing.org/doi/abs/10.1098/rstb.2008.0282
  4. https://pubmed.ncbi.nlm.nih.gov/27347894/
  5. https://www.strongerbyscience.com/much-steroids-increase-hypertrophy/
  6. https://www.strongerbyscience.com/steroids-and-strength-differences/
  7. https://web.archive.org/web/20160109111144/http://www.homepage.psy.utexas.edu/HomePage/faculty/josephs/pdf_documents/Arch_Chall_NBR.pdf
  8. https://academic.oup.com/jcem/article/92/2/549/2566787?login=true
  9. https://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.1019.6064&rep=rep1&type=pdf
  10. https://academic.oup.com/jcem/article/92/1/196/2598434?login=true
  11. https://academic.oup.com/jcem/article/92/12/4696/2597312?login=true
  12. https://pubmed.ncbi.nlm.nih.gov/11399122/
  13. https://www.wri.org/data/people-are-eating-more-protein-they-need-especially-wealthy-regions
  14. https://www.robertbarrington.net/fibre-intake-various-countries/
  15. https://academic.oup.com/jcem/article/85/1/293/2854619?login=true
  16. https://ncci.canceraustralia.gov.au/prevention/smoking-prevelance/smoking-prevalence-adults
  17. https://ourworldindata.org/smoking
  18. https://pubmed.ncbi.nlm.nih.gov/31528824/
  19. https://www.researchgate.net/publication/232974519_Potential_Contribution_of_Aromatase_Inhibition_to_the_Effects_of_Nicotine_and_Related_Compounds_on_the_Brain
  20. https://www.getroman.com/health-guide/anastrozole-improve-testosterone/
  21. https://onlinelibrary.wiley.com/doi/abs/10.1002/ajpa.20387
  22. https://www.sciencedirect.com/science/article/abs/pii/S0018506X0800161X
  23. https://www.sciencedirect.com/science/article/pii/S0306453016301780
  24. https://www.sciencedirect.com/science/article/abs/pii/S0191886910001406
  25. https://link.springer.com/article/10.1007/s40750-014-0020-2#Sec3
  26. https://www.sciencedirect.com/science/article/abs/pii/S1364661311000787
  27. https://www.sciencedirect.com/science/article/abs/pii/S0018506X20301975
  28. https://www.sciencedirect.com/science/article/abs/pii/S0018506X16305050
  29. https://www.sciencedirect.com/science/article/abs/pii/S0306453016304292
  30. https://www.amazon.com/Behave-Biology-Humans-Best-Worst/dp/1594205078
  31. https://www.sciencedirect.com/science/article/abs/pii/S1054139X14002250
  32. https://www.sciencedirect.com/science/article/abs/pii/S0306453019312934
  33. https://www.tandfonline.com/doi/abs/10.1080/19485565.2006.9989114
  34. https://pubmed.ncbi.nlm.nih.gov/30412629/
  35. https://www.sciencedirect.com/science/article/abs/pii/S0039128X16301052
  36. https://incels.wiki/w/Scientific_Blackpill#Among_male_university_students.2C_only_cues_of_physical_dominance_over_other_men_predicted_their_mating_success
  37. https://pubmed.ncbi.nlm.nih.gov/15679528/
  38. https://link.springer.com/article/10.1007/s10803-018-3812-6
  39. https://www.proquest.com/openview/3b780f7e3a7306b98c528f5dcea7bc46/1?pq-origsite=gscholar&cbl=18750
  40. https://www.sciencedirect.com/science/article/abs/pii/S0018506X08002183
  41. https://www.sciencedirect.com/science/article/abs/pii/S0018506X16300198
  42. https://www.sciencedirect.com/science/article/abs/pii/S030645301500400X
  43. https://link.springer.com/article/10.1007/s11031-011-9264-3
  44. https://www.sciencedirect.com/science/article/pii/S0306453019301271
  45. https://www.sciencedirect.com/science/article/abs/pii/S0018506X19300030
  46. https://www.nature.com/articles/s41598-020-70958-3
  47. https://psyarxiv.com/42t6e/
  48. https://link.springer.com/content/pdf/10.1007/s40750-014-0017-x.pdf
  49. http://www.spelab.org/uploads/2/7/8/4/27842457/mehta%2C_mor%2C_yap%2C_prasad%3B_2015.pdf
  50. https://www.frontiersin.org/articles/10.3389/fnbeh.2018.00101/full
  51. https://link.springer.com/article/10.1007/s40750-018-0098-z
  52. https://link.springer.com/article/10.1007/s40750-018-0098-z
  53. https://www.sciencedirect.com/science/article/pii/S2352154615000571
  54. https://www.sciencedirect.com/science/article/pii/S0306453020300317
  55. https://www.epanlab.nl/wp-content/uploads/2021/01/Hutschemaekers-et-al.-2020.pdf
  56. https://core.ac.uk/download/pdf/287614716.pdf
  57. https://doi.org/10.1007/s10508-018-1231-6

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