Neuroscience and sexual orientation: Difference between revisions

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The chances of being left-handed may be increased in homosexual populations. According to one hypothesis, same-sex orientation may be due to generalized developmental factors (i.e., non-hormonal environmental or genetic factors) that shift erotic preferences away from the species-typical pattern of opposite-sex attraction during the neurodevelopment of the fetus. If this logic is correct, one would expect that male and female homosexuality should be associated with other signs of developmental instability such as increased fluctuating asymmetry (e.g., in dermatoglyphics, and the lengths of ears, wrists, fingers and feet).<ref name="number6"/><ref name=QRborngay/>
The chances of being left-handed may be increased in homosexual populations. According to one hypothesis, same-sex orientation may be due to generalized developmental factors (i.e., non-hormonal environmental or genetic factors) that shift erotic preferences away from the species-typical pattern of opposite-sex attraction during the neurodevelopment of the fetus. If this logic is correct, one would expect that male and female homosexuality should be associated with other signs of developmental instability such as increased fluctuating asymmetry (e.g., in dermatoglyphics, and the lengths of ears, wrists, fingers and feet).<ref name="number6"/><ref name=QRborngay/>


However, several studies have found no significant differences in fluctuating asymmetry between heterosexuals and homosexuals,<ref name="number6"/><ref name="Rahman2005">{{cite journal|author1=Rahman Q|title=Fluctuating asymmetry, 2nd to 4th finger length ratios and human sexual orientation.|journal=Psychoneuroendocrinology.|date=May 2005|volume=30|issue=4|pages=382–91|doi=10.1016/j.psyneuen.2004.10.006|pmid=15694118|publisher=Elsevier Inc.}}</ref><ref name="Mustanskietal2002">{{cite journal|author1=Mustanski BS|author2=Bailey JM|author3=Kaspar S|title=Dermatoglyphics, handedness, sex, and sexual orientation.|journal=Arch. Sex. Behav.|date=Feb 2002|volume=31|issue=1|pages=113–22|doi=10.1023/A:1014039403752|pmid=11910784}}</ref> suggesting that a homosexual orientation is not a 'less than optimal' phenotypic sexual orientation.<ref name="number6"/> On the contrary, it has been found that gay men and lesbian women actually show ''less'' fluctuating asymmetry (and thus, less developmental instability) than heterosexual men or women, not more. In other words, heterosexuals have a weaker genomic ability than homosexuals to successfully buffer development to achieve a normal [[phenotype]] under imperfect environmental conditions.<ref name="RSasymmetryLeVay">{{cite book|author1=Simon LeVay|title=Gay, Straight, and the Reason Why: The Science of Sexual Orientation.|date=2010|publisher=Oxford University Press|isbn=0199752966|pages=230–5}}</ref> Additionally, it has been found that heterosexual male-to-female (MtF) transsexuals (i.e., MtF transsexuals who are attracted to women) exhibited greatest fluctuating asymmetry in comparison to homosexual and control groups, which shows that developmental instability may account for variations in [[gender identity]] but not sexual orientation per se.<ref name=QRborngay /> It has also been found that homosexual men are stereotypically considered more attractive than heterosexual men, homosexual men are actually rated as more attractive than heterosexual men (even when the raters do not know the men's sexual orientations), and in childhood, independent raters describe gender atypical boys as more attractive than gender-typical boys.<ref name=QRborngay /> Thus, something in the physiognomy of homosexual children and adults marks them out as more attractive. It has been suggested that this is due to the fact that homosexual men have low fluctuating asymmetry, which is known to be [[Fluctuating asymmetry#Fluctuating asymmetry in sexual selection|associated with greater attractiveness]].<ref name=QRborngay /><ref>{{cite journal|author1=Thornhill R|author2=Gangestad SW|title=Facial attractiveness|journal=Trends Cogn Sci|date=Dec 1999|volume=3|issue=12|pages=452–460|doi=10.1016/S1364-6613(99)01403-5|pmid=10562724}}</ref>
However, several studies have found no significant differences in fluctuating asymmetry between heterosexuals and homosexuals,<ref name="number6"/> suggesting that a homosexual orientation is not a 'less than optimal' phenotypic sexual orientation.<ref name="number6"/> On the contrary, it has been found that gay men and lesbian women actually show ''less'' fluctuating asymmetry (and thus, less developmental instability) than heterosexual men or women, not more. In other words, heterosexuals have a weaker genomic ability than homosexuals to successfully buffer development to achieve a normal [[phenotype]] under imperfect environmental conditions.<ref name="RSasymmetryLeVay">{{cite book|author1=Simon LeVay|title=Gay, Straight, and the Reason Why: The Science of Sexual Orientation.|date=2010|publisher=Oxford University Press|isbn=0199752966|pages=230–5}}</ref> Additionally, it has been found that heterosexual male-to-female (MtF) transsexuals (i.e., MtF transsexuals who are attracted to women) exhibited greatest fluctuating asymmetry in comparison to homosexual and control groups, which shows that developmental instability may account for variations in [[gender identity]] but not sexual orientation per se.<ref name=QRborngay /> It has also been found that homosexual men are stereotypically considered more attractive than heterosexual men, homosexual men are actually rated as more attractive than heterosexual men (even when the raters do not know the men's sexual orientations), and in childhood, independent raters describe gender atypical boys as more attractive than gender-typical boys.<ref name=QRborngay /> Thus, something in the physiognomy of homosexual children and adults marks them out as more attractive. It has been suggested that this is due to the fact that homosexual men have low fluctuating asymmetry, which is known to be [[Fluctuating asymmetry#Fluctuating asymmetry in sexual selection|associated with greater attractiveness]].<ref name=QRborngay /><ref>{{cite journal|author1=Thornhill R|author2=Gangestad SW|title=Facial attractiveness|journal=Trends Cogn Sci|date=Dec 1999|volume=3|issue=12|pages=452–460|doi=10.1016/S1364-6613(99)01403-5|pmid=10562724}}</ref>


Hence, the general mechanism proposed by the developmental instability account of Lalumiere et al. for both male and female homosexuality is incompatible with the variance suggested by the evidence for different pathways to male versus female homosexuality.<ref name="number6"/> The developmental instability hypothesis has also been criticized for being too domain general and for being unclear on exactly what developmental mechanisms are supposedly disrupted.<ref name=QRborngay /> Thus, the canalization of the sexual orientation trait is more likely due to specific neurodevelopmental mechanisms (which may include the actions of prenatal androgens) rather than general-purpose neurodevelopmental mechanisms (such as developmental instability).<ref name="number6"/>
Hence, the general mechanism proposed by the developmental instability account of Lalumiere et al. for both male and female homosexuality is incompatible with the variance suggested by the evidence for different pathways to male versus female homosexuality.<ref name="number6"/> The developmental instability hypothesis has also been criticized for being too domain general and for being unclear on exactly what developmental mechanisms are supposedly disrupted.<ref name=QRborngay /> Thus, the canalization of the sexual orientation trait is more likely due to specific neurodevelopmental mechanisms (which may include the actions of prenatal androgens) rather than general-purpose neurodevelopmental mechanisms (such as developmental instability).<ref name="number6"/>

Revision as of 13:23, 5 October 2018

Sexual orientation
Sexual orientations
Related terms
Research
Animals
Related topics

Sexual orientation is an enduring pattern of romantic or sexual attraction (or a combination of these) to persons of the opposite sex or gender, the same sex or gender, or to both sexes or more than one gender.[1][2] The ultimate causes and mechanisms of sexual orientation development in humans remain unclear and many theories are speculative and controversial. However, advances in neuroscience explain and illustrate characteristics linked to sexual orientation. Studies have explored structural neural-correlates, functional and/or cognitive relationships, and developmental theories relating to sexual orientation in humans.

Developmental neurobiology

Many theories concerning the development of sexual orientation involve fetal neural development, with proposed models illustrating prenatal hormone exposure, maternal immunity, and developmental instability. Other proposed factors include genetic control of sexual orientation. No conclusive evidence has been shown that environmental or learned effects are responsible for the development of non-heterosexual orientation.[3]

Prenatal androgen model

Sexual dimorphisms in the brain and behavior among vertebrates are accounted for by the influence of gonadal steroidal androgens as demonstrated in animal models over the past few decades. The prenatal androgen model of homosexuality describes the neuro-developmental effects of fetal exposure to these hormones.[3] In 1985, Geschwind and Galaburda proposed that homosexual men are exposed to high androgen levels early in development, explaining their tendency to be less right-handed and by extension the hyper-masculinized traits observed in this population.[3] It is currently argued that temporal and local variations in androgen exposure to a fetus's developing brain is a factor in the pathways determining homosexuality. Recently research has moved on to finding somatic markers for prenatal hormonal exposure that can be easily, and non-invasively, explored in otherwise endocrinologically normal populations. As these somatic markers are known to be influenced by prenatal sex hormones, showing variation in these features between homosexuals and heterosexuals can provide a 'window' into the early neurodevelopment of sexual orientation under the influence of prenatal hormones. Various somatic markers (including 2D:4D finger ratios, auditory evoked potentials, fingerprint patterns and eye-blink patterns) have since been found to show variation based on sexual orientation in healthy adult individuals.[3][4]

Other evidence supporting the role of testosterone and prenatal hormones in sexual orientation development include observations of male subjects with cloacal exstrophy who were sex-assigned as female during birth only later to declare themselves male. This supports the theory that the prenatal testosterone surge is crucial for gender identity development. Additionally, females whose mothers were exposed to diethylstilbestrol (DES) during pregnancy show higher rates of bi- and homosexuality.[5]

2D:4D digit ratio

The best non-invasive marker of prenatal hormone exposure is the digit ratio of the second and fourth finger lengths (2D:4D ratio), a known sexually dimorphic measure (males showing lower ratios than females). Patients with androgen over-exposure (such as in congenital adrenal hyperplasia) show lower 2D:4D ratios,[6][7] providing evidence linking prenatal androgen exposure as key to this feature. XY individuals with androgen insensitivity syndrome due to a dysfunctional gene for the androgen receptor present as women and have feminine digit ratios, as would be predicted if androgenic hormones affect digit ratios. This finding also demonstrates that the sex difference in digit ratio is unrelated to the Y chromosome per se.[8] Additionally, the 2D:4D ratio has been shown to be affected by variation in the androgen receptor gene in men.[9] The ratio of testosterone to estrogen in amniotic fluid has also been found to be negatively correlated with the 2D:4D ratio.[3]

Independent studies indicate that homosexual women have masculinized (lower) digit ratios,[10][11][12][13][14][15][16] and homosexual men show either hyper-masculinized or feminized ratios. These findings reinforce the prenatal androgen model that non-typical prenatal hormone exposure is related to the development of human homosexuality.[3]

Auditory evoked potentials

Studies of the central nervous system processing of auditory sensation, aspects of which has been linked to prenatal androgen exposure, to click-stimuli have shown that homosexual women have masculinized responses while homosexual men have hyper-masculinized responses.[3]

Fraternal birth order effect

Studies show that homosexual men have higher numbers of older brothers than heterosexual men.[17] This finding led to the discovery of the fraternal birth order effect, according to which the more older brothers a man has from the same mother, the greater the probability is that he will have a homosexual orientation. Estimations indicate that there is a 33% increase in chances of homosexuality in a male child with each older brother.[3] The fraternal birth order effect holds true only for biological brothers and the chances of male homosexuality is not increased by the number of older stepbrothers or adopted siblings.[18] It is estimated that one-seventh of all homosexual males owe their sexual orientation to the fraternal birth order effect.[19][20][21] As the effect is contingent on handedness and handedness is a prenatally determined trait, the fraternal birth order effect is understood to be biological, rather than psychosocial, in nature and is known to operate prenatally.[18]

The exact biological mechanism by which the effect operates during prenatal life is currently unconfirmed. The proposed mechanism by which the effect is believed to operate states that a mother develops an immune response against a substance important in male fetal development during pregnancy, and that this immune effect becomes increasingly likely with each male fetus gestated by the mother. This immune effect is thought to cause an alteration in (some) later born males' prenatal brain development. The target of the immune response may be molecules (i.e., Y-linked proteins) on the surface of male fetal brain cells, including in sites of the anterior hypothalamus (which has been linked to sexual orientation in other research). Antibodies produced during the immune response are thought to cross the placental barrier and enter the fetal compartment where they bind to the Y-linked molecules and thus alter their role in sexual differentiation, leading some later born males to be attracted to men as opposed to women. To date, the proposed mechanism has only indirect evidence to support it. It is also the only plausible mechanism proposed so far to explain how the fraternal birth order effect may operate in utero.[18] The fraternal birth order effect does not apply to the development of female homosexuality.[18]

Developmental instability and handedness

Developmental instability refers to an organism's degree of vulnerability to environmental and genetic stresses during development.[3][22][23] Measures of this instability provide some insight into the developmental history of the organism. Asymmetry in bilateral features of the body, known as fluctuating asymmetry, is often employed in research as a proxy measure of developmental instability. Consistent non-right handedness is also said to constitute a measure of developmental instability.[22]

The chances of being left-handed may be increased in homosexual populations. According to one hypothesis, same-sex orientation may be due to generalized developmental factors (i.e., non-hormonal environmental or genetic factors) that shift erotic preferences away from the species-typical pattern of opposite-sex attraction during the neurodevelopment of the fetus. If this logic is correct, one would expect that male and female homosexuality should be associated with other signs of developmental instability such as increased fluctuating asymmetry (e.g., in dermatoglyphics, and the lengths of ears, wrists, fingers and feet).[3][22]

However, several studies have found no significant differences in fluctuating asymmetry between heterosexuals and homosexuals,[3] suggesting that a homosexual orientation is not a 'less than optimal' phenotypic sexual orientation.[3] On the contrary, it has been found that gay men and lesbian women actually show less fluctuating asymmetry (and thus, less developmental instability) than heterosexual men or women, not more. In other words, heterosexuals have a weaker genomic ability than homosexuals to successfully buffer development to achieve a normal phenotype under imperfect environmental conditions.[24] Additionally, it has been found that heterosexual male-to-female (MtF) transsexuals (i.e., MtF transsexuals who are attracted to women) exhibited greatest fluctuating asymmetry in comparison to homosexual and control groups, which shows that developmental instability may account for variations in gender identity but not sexual orientation per se.[22] It has also been found that homosexual men are stereotypically considered more attractive than heterosexual men, homosexual men are actually rated as more attractive than heterosexual men (even when the raters do not know the men's sexual orientations), and in childhood, independent raters describe gender atypical boys as more attractive than gender-typical boys.[22] Thus, something in the physiognomy of homosexual children and adults marks them out as more attractive. It has been suggested that this is due to the fact that homosexual men have low fluctuating asymmetry, which is known to be associated with greater attractiveness.[22][25]

Hence, the general mechanism proposed by the developmental instability account of Lalumiere et al. for both male and female homosexuality is incompatible with the variance suggested by the evidence for different pathways to male versus female homosexuality.[3] The developmental instability hypothesis has also been criticized for being too domain general and for being unclear on exactly what developmental mechanisms are supposedly disrupted.[22] Thus, the canalization of the sexual orientation trait is more likely due to specific neurodevelopmental mechanisms (which may include the actions of prenatal androgens) rather than general-purpose neurodevelopmental mechanisms (such as developmental instability).[3]

A significant problem with the measurement of fluctuating asymmetry is that many of the anatomical features that are used for the measurement of fluctuating asymmetry also display some degree of directional asymmetry (i.e., developmentally normal deviation from symmetry that is in the same direction in most individuals, such as the position of the heart on the left side of the chest), and the direction and magnitude of the directional asymmetry can vary between the sexes and between homosexuals and heterosexuals (homosexuals have comparatively more directional asymmetry than heterosexuals).[24] If this directional asymmetry is not carefully assessed and removed from the data for each group of subjects, the measure of fluctuating asymmetry is likely to be incorrect. When datasets from previously published studies (that appeared to show increased fluctuating asymmetry in homosexuals) were reanalyzed in light of this issue, it was found that homosexual men and women actually show less fluctuating asymmetry than heterosexual men or women. This suggests that homosexual people experience less developmental instability than heterosexual people.[24]

Functional differences

Recent studies have begun exploring the functional and cognitive substrates of sexual orientation, ultimately a behavioral manifestation. Neural processing in response to specific stimuli and sexually-biased cognitive tasks have been found to be correlated with an individual's sexual orientation.

Functional cerebral asymmetry

Differences in neural processing and cognitive tasks have been found in relation to sexual orientation. In a 1997 review on cognition, cerebral lateralization, and sexual orientation, Sanders and Ross-Field suggested that prenatal hormonal events would lead to functional cerebral asymmetries related to sexual orientation.[26]

Related studies

Various animal and insect models have been used to explore sexual orientation and brain characteristics. One experiment involved genetically altering male Drosophila causing them to have feminized brain structures involved in processing sexually dimorphic contact pheromones. Transformed males showed increase homosexual courtship behaviors to wild-type male flies, and there a correlation was found between the courtship behavior and the expression of the altered gene in the sexually related brain regions.[27]

Future studies

The development of sexual orientation is a far from complete subject. While neuroscience has made advancements shedding light on the mechanisms and relationships between the human brain and sexual orientation, much more further research should be conducted.

Areas for future research include:[3]

  • finding markers for sex steroid levels in the brains of fetuses that highlight features of early neuro-development leading to certain sexual orientations
  • determine the precise neural circuitry underlying direction of sexual preference
  • use animal models to explore genetic and developmental factors that influence sexual orientation
  • further population studies, genetic studies, and serological markers to clarify and definitively determine the effect of maternal immunity
  • neuroimaging studies to quantify sexual-orientation-related differences in structure and function in vivo
  • neurochemical studies to investigate the roles of sex steroids upon neural circuitry involved in sexual attraction

Notes

References

  1. ^ "Sexual orientation, homosexuality and bisexuality". American Psychological Association. Archived from the original on August 8, 2013. Retrieved August 10, 2013.
  2. ^ "Sexual Orientation". American Psychiatric Association. Archived from the original on July 22, 2011. Retrieved January 1, 2013.
  3. ^ a b c d e f g h i j k l m n o Rahman, Q (2005). "The neurodevelopment of human sexual orientation". Neuroscience & Biobehavioral Reviews. 29 (7): 1057–66. doi:10.1016/j.neubiorev.2005.03.002. PMID 16143171.
  4. ^ Williams TJ; Pepitone ME; Christensen SE; Cooke BM; Huberman AD; Breedlove NJ; Breedlove TJ; Jordan CL; Breedlove SM (Mar 2000). "Finger-length ratios and sexual orientation" (PDF). Nature. 404 (6777): 455–6. doi:10.1038/35006555. PMID 10761903. Retrieved 17 August 2016.
  5. ^ Swaab DF (December 2004). "Sexual differentiation of the human brain: relevance for gender identity, transsexualism and sexual orientation". Gynecological Endocrinology. 19 (6): 301–12. doi:10.1080/09513590400018231. PMID 15724806.
  6. ^ Brown et al. 2002
  7. ^ Okten et al. 2002
  8. ^ Berenbaum SA, Bryk KK, Nowak N, Quigley CA, Moffat S (November 2009). "Fingers as a marker of prenatal androgen exposure". Endocrinology. 150 (11): 5119–24. doi:10.1210/en.2009-0774. PMC 2775980. PMID 19819951.
  9. ^ Manning, John T.; Bundred, Peter E.; Newton, Darren J.; Flanagan, Brian F. (2003). "The second to fourth digit ratio and variation in the androgen receptor gene". Evolution and Human Behavior. 24 (6): 399–405. doi:10.1016/S1090-5138(03)00052-7.
  10. ^ Williams, T. J.; Pepitone, ME; Christensen, SE; Cooke, BM; Huberman, AD; Breedlove, NJ; Breedlove, TJ; Jordan, CL; Breedlove, SM (March 2000). "Finger-length ratios and sexual orientation" (PDF). Nature. 404 (6777): 455–456. doi:10.1038/35006555. PMID 10761903.
  11. ^ Tortorice, J.L. (2002). "Written on the body: butch/femme lesbian gender identity and biological correlates". Rutgers Ph.D. Dissertation.
  12. ^ McFadden D, Shubel E (December 2002). "Relative lengths of fingers and toes in human males and females". Hormones and Behavior. 42 (4): 492–500. doi:10.1006/hbeh.2002.1833. PMID 12488115.
  13. ^ Hall LS, Love CT (February 2003). "Finger-length ratios in female monozygotic twins discordant for sexual orientation". Archives of Sexual Behavior. 32 (1): 23–8. doi:10.1023/A:1021837211630. PMID 12597269.
  14. ^ Csathó A, Osváth A, Bicsák E, Karádi K, Manning J, Kállai J (February 2003). "Sex role identity related to the ratio of second to fourth digit length in women". Biological Psychology. 62 (2): 147–56. doi:10.1016/S0301-0511(02)00127-8. PMID 12581689.
  15. ^ Putz, D; Gaulin, Steven J.C.; Sporter, Robert J.; McBurney, Donald H. (2004). "Sex hormones and finger lengthWhat does 2D:4D indicate?" (PDF). Evolution and Human Behavior. 25 (3): 182–199. doi:10.1016/j.evolhumbehav.2004.03.005. Archived from the original (PDF) on 2010-01-07. {{cite journal}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  16. ^ Wallien MS, Zucker KJ, Steensma TD, Cohen-Kettenis PT (August 2008). "2D:4D finger-length ratios in children and adults with gender identity disorder". Hormones and Behavior. 54 (3): 450–4. doi:10.1016/j.yhbeh.2008.05.002. PMID 18585715.
  17. ^ Bogaert AF (July 2006). "Biological versus nonbiological older brothers and men's sexual orientation". Proceedings of the National Academy of Sciences of the United States of America. 103 (28): 10771–4. doi:10.1073/pnas.0511152103. PMC 1502306. PMID 16807297.
  18. ^ a b c d Bogaert AF; Skorska M (2011). "Sexual orientation, fraternal birth order, and the maternal immune hypothesis: a review". Front Neuroendocrinol. 32 (2): 247–54. doi:10.1016/j.yfrne.2011.02.004. PMID 21315103.
  19. ^ Cantor JM, Blanchard R, Paterson AD, Bogaert AF (February 2002). "How many gay men owe their sexual orientation to fraternal birth order?". Arch Sex Behav. 31 (1): 63–71. doi:10.1023/A:1014031201935. PMID 11910793.
  20. ^ Blanchard R, Bogaert AF (January 1996). "Homosexuality in men and number of older brothers". Am J Psychiatry. 153 (1): 27–31. doi:10.1176/ajp.153.1.27. PMID 8540587.
  21. ^ Blanchard R; Bogaert AF (2004). "Proportion of homosexual men who owe their sexual orientation to fraternal birth order: An estimate based on two national probability samples". Am J Hum Biol. 16 (2): 151–7. doi:10.1002/ajhb.20006. PMID 14994314.
  22. ^ a b c d e f g Rahman Q; Wilson GD (2003). "Born gay? The psychobiology of human sexual orientation". Personality and Individual Differences. 34. Elsevier: 1337–1382. doi:10.1016/s0191-8869(02)00140-x.
  23. ^ Lalumière ML, Blanchard R, Zucker KJ (July 2000). "Sexual orientation and handedness in men and women: a meta-analysis". Psychological Bulletin. 126 (4): 575–92. doi:10.1037/0033-2909.126.4.575. PMID 10900997.
  24. ^ a b c Simon LeVay (2010). Gay, Straight, and the Reason Why: The Science of Sexual Orientation. Oxford University Press. pp. 230–5. ISBN 0199752966.
  25. ^ Thornhill R; Gangestad SW (Dec 1999). "Facial attractiveness". Trends Cogn Sci. 3 (12): 452–460. doi:10.1016/S1364-6613(99)01403-5. PMID 10562724.
  26. ^ Sanders G, Wright M (October 1997). "Sexual orientation differences in cerebral asymmetry and in the performance of sexually dimorphic cognitive and motor tasks". Archives of Sexual Behavior. 26 (5): 463–80. doi:10.1023/A:1024551704723. PMID 9343633.
  27. ^ Ferveur JF, Störtkuhl KF, Stocker RF, Greenspan RJ (February 1995). "Genetic feminization of brain structures and changed sexual orientation in male Drosophila". Science. 267 (5199): 902–5. doi:10.1126/science.7846534. PMID 7846534.
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