Zum einen eine aus einer Störung der Geschlechtsidentität ("Wer bin ich?") rührende Scham. Ein Mann schämt sich für das, was er ist. Er denkt, er sei nicht Mann genug und fühlt sich anderen Männern unterlegen.
Zweitens unbefriedigte männliche Bedürfnisse. Hierunter fallen zum einen die Anerkennung des Sohnes durch den Vater oder die Bestätigung der männlichen Identität. Weiterhin fallen hierunter die männliche körperliche Zuneigung - von Vater zum Sohn, zwischen Gleichaltrigen oder zwischen Männern im Allgemeinen.
Letztlich gibt es auch noch das, was man im weitesten Sinn als genetisch veranlagt bezeichnen kann. Das heißt nun nicht zwangsweise, dass es ein "schwules Gen" gibt (dieses wurde bisher nicht gefunden. Selbst wenn es so etwas aber geben sollte, ist das noch kein Kriterium für "moralisch akzeptabel", "normal" oder auch "gut" oder "schlecht", "natürlich" oder was auch immer. Auch würde dies keineswegs bedeuten, dass man zwangsweise so leben muss oder dass Gott einen so gemacht hat und man somit keine Wahl mehr hätte. Hat man sehr wohl). Genetisch veranlagt kann z.B. bedeuten, dass man bestimmte Charakterzüge oder Eigenschaften hat, die es einem erleichtern, unter bestimmten zusätzlichen gesellschaftlichen und/oder familiären Bedingungen gleichgeschlechtliche Neigungen zu entwickeln und/oder sie auszuleben. Ein Vergleich zur Verdeutlichung: Ein erfolgreicher Fußballer wird vielleicht mit bestimmten genetischen Voraussetzungen geboren, die es ihm ermöglichen, schnelle und geschickte Spielzüge zu machen. Das heißt aber nicht, dass es ein "Fußball-Gen" gibt!
(siehe auch: http://www.saintjoe.com/)
Biology and Sexual Orientation
The relationship between biology and sexual orientation is a subject of research. While scientists do not know the exact cause of sexual orientation, they theorize that it is caused by a complex interplay of genetic, hormonal, and environmental influences. Hypotheses for the impact of the post-natal social environment on sexual orientation, however, are weak, especially for males.
Biological theories for explaining the causes of sexual orientation are favored by scientists. These factors, which may be related to the development of a sexual orientation, include genes, the early uterine environment (such as prenatal hormones), and brain structure.
Scientific research and studies
Fetal development and hormones
The influence of hormones on the developing fetus has been the most influential causal hypothesis of the development of sexual orientation. In simple terms, the developing fetal brain begins in a "female" typical state. The presence of the Y-chromosome in males prompts the development of testes, which release testosterone, the primary androgen receptor-activating hormone, to masculinize the fetus and fetal brain. This masculinizing effect pushes males towards male typical brain structures, and most of the time, attraction to females. It has been hypothesized that gay men may have been exposed to little testosterone in key regions of the brain, or had different levels of receptivity to its masculinizing effects, or experienced fluctuations at critical times. In women, it is hypothesized that high levels of exposure to testosterone in key regions may increase likelihood of same sex attraction. Supporting this are studies of the finger digit ratio of the right hand, which is a robust marker of prenatal testosterone exposure. Lesbians on average, have significantly more masculine digit ratios, a finding which has been replicated numerous times in studies cross-culturally. While direct effects are hard to measure for ethical reasons, animal experiments where scientists manipulate exposure to sex hormones during gestation can also induce lifelong male-typical behavior and mounting in female animals, and female-typical behavior in male animals.
Maternal immune responses during fetal development are strongly demonstrated as causing male homosexuality and bisexuality. Research since the 1990s has demonstrated that the more male sons a woman has, there is a higher chance of later born sons being gay. During pregnancy, male cells enter a mother's bloodstream, which are foreign to her immune system. In response, she develops antibodies to neutralize them. These antibodies are then released on future male foetuses and may neutralize Y-linked antigens, which play a role in brain masculinization, leaving areas of the brain responsible for sexual attraction in the female-typical position, or attracted to men. The more sons a mother has will increase the levels of these antibodies, thus creating the observed fraternal birth order effect. Biochemical evidence to support this effect was confirmed in a lab study in 2017, finding that mothers with a gay son, particularly those with older brothers, had heightened levels of antibodies to the NLGN4Y Y-protein than mothers with heterosexual sons. J. Michael Bailey has described maternal immune responses as "causal" of male homosexuality. This effect is estimated to account for between 15 and 29% of gay men, while other gay and bisexual men are thought to owe sexual orientation to genetic and hormonal interactions.
Socialization theories, which were dominant in the 1900s, favored the idea that children were born "undifferentiated" and were socialized into gender roles and sexual orientation. This led to medical experiments in which newborn and infant boys were surgically reassigned into girls after accidents such as botched circumcisions. These males were then reared and raised as females without telling the boys, which, contrary to expectations, did not make them feminine nor attracted to men. All published cases providing sexual orientation grew up to be strongly attracted to women. The failure of these experiments demonstrate that socialization effects does not induce feminine type behavior in males, nor make them attracted to men, and that the organizational effects of hormones on the fetal brain prior to birth have permanent effects. These are indicative of 'nature', not nurture, at least with regards to male sexual orientation.
The sexually dimorphic nucleus of the preoptic area (SDN-POA) is a key region of the brain which differs between males and females in humans and a number of mammals (e.g., sheep/rams, mice, rats), and is caused by sex differences in hormone exposure. The INAH-3 region is bigger in males than in females, and is thought to be a critical region in sexual behavior. Dissection studies found that gay men had significantly smaller sized INAH-3 than heterosexual males, which is shifted in the female typical direction, a finding first demonstrated by neuroscientist Simon LeVay, which has been replicated. Dissection studies are rare, however, due to lack of funding and brain samples.
Long-term studies of domesticated sheep lead by Charles Roselli have found that 6-8% of rams have a homosexual preference through their life. Dissection of ram brains also found a similar smaller (feminized) structure in homosexually oriented rams compared to heterosexually oriented rams in the equivalent brain region to the human SDN, the ovine sexually dimorphic nucleus (oSDN). The size of the sheep oSDN has also been demonstrated to be formed in utero, rather than postnatally, underscoring the role of prenatal hormones in masculinization of the brain for sexual attraction.
Other studies in humans have relied on brain imaging technology, such as research lead by Ivanka Savic which compared hemispheres of the brain. This research found that straight men had right hemispheres 2% larger than the left, described as modest but "highly significant difference" by LeVay. In heterosexual women, the two hemispheres were the same size. In gay men, the two hemispheres were also the same size, or sex atypical, while in lesbians, the right hemispheres were slightly larger than the left, indicating a small shift in the male direction.
A model proposed by evolutionary geneticist William R. Rice argues that a misexpressed epigenetic modifier of testosterone sensitivity or insensitivity that affected development of the brain can explain homosexuality, and can best explain twin discordance. Rice et al. propose that these epimarks normally canalize sexual development, preventing intersex conditions in most of the population, but sometimes failing to erase across generations and causing reversed sexual preference. On grounds of evolutionary plausibility, Gavrilets, Friberg and Rice argue that all mechanisms for exclusive homosexual orientations likely trace back to their epigenetic model. Testing this hypothesis is possible with current stem cell technology.
Multiple genes have been found to play a role in sexual orientation. Scientists caution that many people misconstrue the meanings of genetic and environmental. Environmental influence does not automatically imply that the social environment influences or contributes to the development of sexual orientation. Hypotheses for the impact of the post-natal social environment on sexual orientation are weak, especially for males. There is, however, a vast non-social environment that is non-genetic yet still biological, such as prenatal development, that likely helps shape sexual orientation.: 76
A number of twin studies have attempted to compare the relative importance of genetics and environment in the determination of sexual orientation. In a 1991 study, Bailey and Pillard conducted a study of male twins recruited from "homophile publications", and found that 52% of monozygotic (MZ) brothers (of whom 59 were questioned) and 22% of the dizygotic (DZ) twins were concordant for homosexuality. 'MZ' indicates identical twins with the same sets of genes and 'DZ' indicates fraternal twins where genes are mixed to an extent similar to that of non-twin siblings. In a study of 61 pairs of twins, researchers found among their mostly male subjects a concordance rate for homosexuality of 66% among monozygotic twins and a 30% one among dizygotic twins. In 2000, Bailey, Dunne and Martin studied a larger sample of 4,901 Australian twins but reported less than half the level of concordance. They found 20% concordance in the male identical or MZ twins and 24% concordance for the female identical or MZ twins. Self reported zygosity, sexual attraction, fantasy and behaviours were assessed by questionnaire and zygosity was serologically checked when in doubt. Other researchers support biological causes for both men and women's sexual orientation.
A 2008 study of all adult twins in Sweden (more than 7,600 twins) found that same-sex behaviour was explained by both heritable genetic factors and unique environmental factors (which can include the prenatal environment during gestation, exposure to illness in early life, peer groups not shared with a twin, etc.), although a twin study cannot identify which factor is at play. Influences of the shared environment (influences including the family environment, rearing, shared peer groups, culture and societal views, and sharing the same school and community) had no effect for men, and a weak effect for women. This is consistent with the common finding that parenting and culture appears to play no role in male sexual orientation, but may play some small role in women. The study concludes that genetic influences on any lifetime same-sex partner were stronger for men than women, and that "it has been suggested individual differences in heterosexual and homosexual behavior result from unique environmental factors such as prenatal exposure to sex hormones, progressive maternal immunization to sex-specific proteins, or neurodevelopmental factors", although does not rule out other variables. The use of all adult twins in Sweden was designed to address the criticism of volunteer studies, in which a potential bias towards participation by gay twins may influence the results:
Biometric modeling revealed that, in men, genetic effects explained .34–.39 of the variance [of sexual orientation], the shared environment .00, and the individual-specific environment .61–.66 of the variance. Corresponding estimates among women were .18–.19 for genetic factors, .16–.17 for shared environmental, and .64–.66 for unique environmental factors. Although wide confidence intervals suggest cautious interpretation, the results are consistent with moderate, primarily genetic, familial effects, and moderate to large effects of the nonshared environment (social and biological) on same-sex sexual behavior.
Chromosome linkage studies
Chromosome linkage studies of sexual orientation have indicated the presence of multiple contributing genetic factors throughout the genome. In 1993, Dean Hamer and colleagues published findings from a linkage analysis of a sample of 76 gay brothers and their families. Hamer et al. found that the gay men had more gay male uncles and cousins on the maternal side of the family than on the paternal side. Gay brothers who showed this maternal pedigree were then tested for X chromosome linkage, using twenty-two markers on the X chromosome to test for similar alleles. In another finding, thirty-three of the forty sibling pairs tested were found to have similar alleles in the distal region of Xq28, which was significantly higher than the expected rates of 50% for fraternal brothers. This was popularly dubbed the "gay gene" in the media, causing significant controversy. Sanders et al. in 1998 reported on their similar study, in which they found that 13% of uncles of gay brothers on the maternal side were homosexual, compared with 6% on the paternal side.
A later analysis by Hu et al. replicated and refined the earlier findings. This study revealed that 67% of gay brothers in a new saturated sample shared a marker on the X chromosome at Xq28. Two other studies (Bailey et al., 1999; McKnight and Malcolm, 2000) failed to find a preponderance of gay relatives in the maternal line of homosexual men. One study by Rice et al. in 1999 failed to replicate the Xq28 linkage results. Meta-analysis of all available linkage data indicates a significant link to Xq28, but also indicates that additional genes must be present to account for the full heritability of sexual orientation.
Mustanski et al. (2005) performed a full-genome scan (instead of just an X chromosome scan) on individuals and families previously reported on in Hamer et al. (1993) and Hu et al. (1995), as well as additional new subjects. In the full sample they did not find linkage to Xq28.
Results from the first large, comprehensive multi-center genetic linkage study of male sexual orientation were reported by an independent group of researchers at the American Society of Human Genetics in 2012. The study population included 409 independent pairs of gay brothers, who were analyzed with over 300,000 single-nucleotide polymorphism markers. The data strongly replicated Hamer's Xq28 findings as determined by both two-point and multipoint (MERLIN) LOD score mapping. Significant linkage was also detected in the pericentromeric region of chromosome 8, overlapping with one of the regions detected in the Hamer lab's previous genomewide study. The authors concluded that "our findings, taken in context with previous work, suggest that genetic variation in each of these regions contributes to development of the important psychological trait of male sexual orientation". Female sexual orientation does not seem to be linked to Xq28, though it does appear moderately heritable.
In addition to sex chromosomal contribution, a potential autosomal genetic contribution to the development of homosexual orientation has also been suggested. In a study population composed of more than 7000 participants, Ellis et al. (2008) found a statistically significant difference in the frequency of blood type A between homosexuals and heterosexuals. They also found that "unusually high" proportions of homosexual males and homosexual females were Rh negative in comparison to heterosexuals. As both blood type and Rh factor are genetically inherited traits controlled by alleles located on chromosome 9 and chromosome 1 respectively, the study indicates a potential link between genes on autosomes and homosexuality.
The biology of sexual orientation has been studied in detail in several animal model systems. In the common fruit fly Drosophila melanogaster, the complete pathway of sexual differentiation of the brain and the behaviors it controls is well established in both males and females, providing a concise model of biologically controlled courtship. In mammals, a group of geneticists at the Korea Advanced Institute of Science and Technology bred a female mice specifically lacking a particular gene related to sexual behavior. Without the gene, the mice exhibited masculine sexual behavior and attraction toward urine of other female mice. Those mice who retained the gene fucose mutarotase (FucM) were attracted to male mice.
In interviews to the press, researchers have pointed that the evidence of genetic influences should not be equated with genetic determinism. According to Dean Hamer and Michael Bailey, genetic aspects are only one of the multiple causes of homosexuality.
In 2017, Scientific Reports published an article with a genome wide association study on male sexual orientation. The research consisted of 1,077 homosexual men and 1,231 heterosexual men. A gene named SLITRK6 on chromosome 13 was identified. The research supports another study which had been done by the neuroscientist Simon LeVay. LeVay's research suggested that the hypothalamus of gay men is different from straight men. The SLITRK6 is active in the mid-brain where the hypothalamus is. The researchers found that the thyroid stimulating hormone receptor (TSHR) on chromosome 14 shows sequence differences between gay and straight men. Graves' disease is associated with TSHR abnormalities, with previous research indicating that Graves' disease is more common in gay men than in straight men. Research indicated that gay people have lower body weight than straight people. It had been suggested that the overactive TSHR hormone lowered body weight in gay people, though this remains unproven.
In 2018, Ganna et al. performed another genome-wide association study on sexual orientation of men and women with data from 26,890 people who had at least one same-sex partner and 450,939 controls. The data in the study was meta-analyzed and obtained from the UK Biobank study and 23andMe. The researchers identified four variants more common in people who reported at least one same-sex experience on chromosomes 7, 11, 12, and 15. The variants on chromosomes 11 and 15 were specific to men, with the variant on chromosome 11 located in an olfactory gene and the variant on chromosome 15 having previously been linked to male-pattern baldness. The four variants were also correlated with mood and mental health disorders; major depressive disorder and schizophrenia in men and women, and bipolar disorder in women. However, none of the four variants could reliably predict sexual orientation.
In August 2019, a genome-wide association study of 493,001 individuals concluded that hundreds or thousands of genetic variants underlie homosexual behavior in both sexes, with 5 variants in particular being significantly associated. Some of these variants had sex-specific effects, and two of these variants suggested links to biological pathways that involve sex hormone regulation and olfaction. All the variants together captured between 8 and 25% of the variation in individual differences in homosexual behavior. These genes partly overlap with those for several other traits, including openness to experience and risk-taking behavior. Additional analyses suggested that sexual behavior, attraction, identity, and fantasies are influenced by a similar set of genetic variants. They also found that the genetic effects that differentiate heterosexual from homosexual behavior are not the same as those that differ among nonheterosexuals with lower versus higher proportions of same-sex partners, which suggests that there is no single continuum from heterosexual to homosexual preference, as suggested by the Kinsey scale.
A study suggests linkage between a mother's genetic make-up and homosexuality of her sons. Women have two X chromosomes, one of which is "switched off". The inactivation of the X chromosome occurs randomly throughout the embryo, resulting in cells that are mosaic with respect to which chromosome is active. In some cases though, it appears that this switching off can occur in a non-random fashion. Bocklandt et al. (2006) reported that, in mothers of homosexual men, the number of women with extreme skewing of X chromosome inactivation is significantly higher than in mothers without gay sons. 13% of mothers with one gay son, and 23% of mothers with two gay sons, showed extreme skewing, compared to 4% of mothers without gay sons.
Blanchard and Klassen (1997) reported that each additional older brother increases the odds of a man being gay by 33%. This is now "one of the most reliable epidemiological variables ever identified in the study of sexual orientation". To explain this finding, it has been proposed that male fetuses provoke a maternal immune reaction that becomes stronger with each successive male fetus. This maternal immunization hypothesis (MIH) begins when cells from a male fetus enter the mother's circulation during pregnancy or while giving birth. Male fetuses produce H-Y antigens which are "almost certainly involved in the sexual differentiation of vertebrates". These Y-linked proteins would not be recognized in the mother's immune system because she is female, causing her to develop antibodies which would travel through the placental barrier into the fetal compartment. From here, the anti-male bodies would then cross the blood/brain barrier (BBB) of the developing fetal brain, altering sex-dimorphic brain structures relative to sexual orientation, increasing the likelihood that the exposed son will be more attracted to men than women. It is this antigen which maternal H-Y antibodies are proposed to both react to and 'remember'. Successive male fetuses are then attacked by H-Y antibodies which somehow decrease the ability of H-Y antigens to perform their usual function in brain masculinization.
In 2017, researchers discovered a biological mechanism of gay people who tend to have older brothers. They think Neuroligin 4 Y-linked protein is responsible for a later son being gay. They found that women had significantly higher anti-NLGN4Y levels than men. In addition, mothers of gay sons, particularly those with older brothers, had significantly higher anti-NLGN4Y levels than did the control samples of women, including mothers of heterosexual sons. The results suggest an association between a maternal immune response to NLGN4Y and subsequent sexual orientation in male offspring.
The fraternal birth order effect, however, does not apply to instances where a firstborn is homosexual.
In 2004, Italian researchers conducted a study of about 4,600 people who were the relatives of 98 homosexual and 100 heterosexual men. Female relatives of the homosexual men tended to have more offspring than those of the heterosexual men. Female relatives of the homosexual men on their mother's side tended to have more offspring than those on the father's side. The researchers concluded that there was genetic material being passed down on the X chromosome which both promotes fertility in the mother and homosexuality in her male offspring. The connections discovered would explain about 20% of the cases studied, indicating that this is a highly significant but not the sole genetic factor determining sexual orientation.
Research conducted in Sweden has suggested that gay and straight men respond differently to two odors that are believed to be involved in sexual arousal. The research showed that when both heterosexual women and gay men are exposed to a testosterone derivative found in men's sweat, a region in the hypothalamus is activated. Heterosexual men, on the other hand, have a similar response to an estrogen-like compound found in women's urine. The conclusion is that sexual attraction, whether same-sex or opposite-sex oriented, operates similarly on a biological level. Researchers have suggested that this possibility could be further explored by studying young subjects to see if similar responses in the hypothalamus are found and then correlating these data with adult sexual orientation.
Studies of brain structure
A number of sections of the brain have been reported to be sexually dimorphic; that is, they vary between men and women. There have also been reports of variations in brain structure corresponding to sexual orientation. In 1990, Dick Swaab and Michel A. Hofman reported a difference in the size of the suprachiasmatic nucleus between homosexual and heterosexual men. In 1992, Allen and Gorski reported a difference related to sexual orientation in the size of the anterior commissure, but this research was refuted by numerous studies, one of which found that the entirety of the variation was caused by a single outlier.
Research on the physiologic differences between male and female brains are based on the idea that people have male or a female brain, and this mirrors the behavioral differences between the two sexes. Some researchers state that solid scientific support for this is lacking. Although consistent differences have been identified, including the size of the brain and of specific brain regions, male and female brains are very similar.
Sexually dimorphic nuclei in the anterior hypothalamus
LeVay also conducted some of these early researches. He studied four groups of neurons in the hypothalamus called INAH1, INAH2, INAH3 and INAH4. This was a relevant area of the brain to study, because of evidence that it played a role in the regulation of sexual behaviour in animals, and because INAH2 and INAH3 had previously been reported to differ in size between men and women.
He obtained brains from 41 deceased hospital patients. The subjects were classified into three groups. The first group comprised 19 gay men who had died of AIDS-related illnesses. The second group comprised 16 men whose sexual orientation was unknown, but whom the researchers presumed to be heterosexual. Six of these men had died of AIDS-related illnesses. The third group was of six women whom the researchers presumed to be heterosexual. One of the women had died of an AIDS-related illness.
The HIV-positive people in the presumably heterosexual patient groups were all identified from medical records as either intravenous drug abusers or recipients of blood transfusions. Two of the men who identified as heterosexual specifically denied ever engaging in a homosexual sex act. The records of the remaining heterosexual subjects contained no information about their sexual orientation; they were assumed to have been primarily or exclusively heterosexual "on the basis of the numerical preponderance of heterosexual men in the population".
LeVay found no evidence for a difference between the groups in the size of INAH1, INAH2 or INAH4. However, the INAH3 group appeared to be twice as big in the heterosexual male group as in the gay male group; the difference was highly significant, and remained significant when only the six AIDS patients were included in the heterosexual group. The size of INAH3 in the homosexual men's brains was comparable to the size of INAH3 in the heterosexual women's brains.
William Byne and colleagues attempted to identify the size differences reported in INAH 1–4 by replicating the experiment using brain sample from other subjects: 14 HIV-positive homosexual males, 34 presumed heterosexual males (10 HIV-positive), and 34 presumed heterosexual females (9 HIV-positive). The researchers found a significant difference in INAH3 size between heterosexual men and heterosexual women. The INAH3 size of the homosexual men was apparently smaller than that of the heterosexual men, and larger than that of the heterosexual women, though neither difference quite reached statistical significance.
Byne and colleagues also weighed and counted numbers of neurons in INAH3 tests not carried out by LeVay. The results for INAH3 weight were similar to those for INAH3 size; that is, the INAH3 weight for the heterosexual male brains was significantly larger than for the heterosexual female brains, while the results for the gay male group were between those of the other two groups but not quite significantly different from either. The neuron count also found a male-female difference in INAH3, but found no trend related to sexual orientation.
LeVay has said that Byne replicated his work, but that he employed a two-tailed statistical analysis, which is typically reserved for when no previous findings had employed the difference. LeVay has said that "given that my study had already reported a INAH3 to be smaller in gay men, a one tailed approach would have been more appropriate, and it would have yielded a significant difference [between heterosexual and homosexual men]".: 110
J. Michael Bailey has criticized LeVay's critics – describing the claim that the INAH-3 difference could be attributable to AIDS as "aggravating", since the "INAH-3 did not differ between the brains of straight men who died of AIDS and those who did not have the disease".: 120 Bailey has further criticized the second objection that was raised, that being gay might have somehow caused the difference in INAH-3, and not vice-versa, saying "the problem with this idea is that the hypothalamus appears to develop early. Not a single expert I have ever asked about LeVay's study thought it was plausible that sexual behavior caused the INAH-3 differences.": 120
The SCN of homosexual males has been demonstrated to be larger (both the volume and the number of neurons are twice as many as in heterosexual males). These areas of the hypothalamus have not yet been explored in homosexual females nor bisexual males nor females. Although the functional implications of such findings still have not been examined in detail, they cast serious doubt over the widely accepted Dörner hypothesis that homosexual males have a "female hypothalamus" and that the key mechanism of differentiating the "male brain from originally female brain" is the epigenetic influence of testosterone during prenatal development.
A 2010 study by Garcia-Falgueras and Swaab stated that "the fetal brain develops during the intrauterine period in the male direction through a direct action of testosterone on the developing nerve cells, or in the female direction through the absence of this hormone surge. In this way, our gender identity (the conviction of belonging to the male or female gender) and sexual orientation are programmed or organized into our brain structures when we are still in the womb. There is no indication that social environment after birth has an effect on gender identity or sexual orientation."
The domestic ram is used as an experimental model to study early programming of the neural mechanisms which underlie homosexuality, developing from the observation that approximately 8% of domestic rams are sexually attracted to other rams (male-oriented) when compared to the majority of rams which are female-oriented. In many species, a prominent feature of sexual differentiation is the presence of a sexually dimorphic nucleus (SDN) in the preoptic hypothalamus, which is larger in males than in females.
Roselli et al. discovered an ovine SDN (oSDN) in the preoptic hypothalamus that is smaller in male-oriented rams than in female-oriented rams, but similar in size to the oSDN of females. Neurons of the oSDN show aromatase expression which is also smaller in male-oriented rams versus female-oriented rams, suggesting that sexual orientation is neurologically hard-wired and may be influenced by hormones. However, results failed to associate the role of neural aromatase in the sexual differentiation of brain and behavior in the sheep, due to the lack of defeminization of adult sexual partner preference or oSDN volume as a result of aromatase activity in the brain of the fetuses during the critical period. Having said this, it is more likely that oSDN morphology and homosexuality may be programmed through an androgen receptor that does not involve aromatisation. Most of the data suggests that homosexual rams, like female-oriented rams, are masculinized and defeminized with respect to mounting, receptivity, and gonadotrophin secretion, but are not defeminized for sexual partner preferences, also suggesting that such behaviors may be programmed differently. Although the exact function of the oSDN is not fully known, its volume, length, and cell number seem to correlate with sexual orientation, and a dimorphism in its volume and of cells could bias the processing cues involved in partner selection. More research is needed in order to understand the requirements and timing of the development of the oSDN and how prenatal programming effects the expression of mate choice in adulthood.
Childhood gender nonconformity
Childhood gender nonconformity is a strong predictor of adult sexual orientation that has been consistently replicated in research, and is thought to be strong evidence of a biological difference between heterosexual and non-heterosexuals. A review authored by J. Michael Bailey states: "childhood gender nonconformity comprises the following phenomena among boys: cross-dressing, desiring to have long hair, playing with dolls, disliking competitive sports and rough play, preferring girls as playmates, exhibiting elevated separation anxiety, and desiring to be—or believing that one is—a girl. In girls, gender nonconformity comprises dressing like and playing with boys, showing interest in competitive sports and rough play, lacking interest in conventionally female toys such as dolls and makeup, and desiring to be a boy". This gender nonconformist behavior typically emerges at preschool age, although is often evident as early as age 2. Children are only considered gender nonconforming if they persistently engage in a variety of these behaviors, as opposed to engaging in a behavior on a few times or on occasion. It is also not a one-dimensional trait, but rather has varying degrees.
Children who grow up to be non-heterosexual were, on average, substantially more gender nonconforming in childhood. This is confirmed in both retrospective studies where homosexuals, bisexuals and heterosexuals are asked about their gender typical behavior in childhood, and in prospective studies, where highly gender nonconforming children are followed from childhood into adulthood to find out their sexual orientation. A review of retrospective studies that measured gender nonconforming traits estimated that 89% of homosexual men exceeded heterosexual males level of gender nonconformity, whereas just 2% of heterosexual men exceeded the homosexual median. For female sexual orientation, the figures were 81% and 12% respectively. A variety of other assessments such as childhood home videos, photos and reports of parents also confirm this finding. Critics of this research see this as confirming stereotypes; however, no study has ever demonstrated that this research has exaggerated childhood gender nonconformity. J. Michael Bailey argues that gay men often deny that they were gender nonconforming in childhood because they may have been bullied or maltreated by peers and parents for it, and because they often do not find femininity attractive in other gay males and thus would not want to acknowledge it in themselves. Additional research in Western cultures and non-Western cultures including Latin America, Asia, Polynesia, and the Middle East supports the validity of childhood gender nonconformity as a predictor of adult non-heterosexuality.
This research does not mean that all non-heterosexuals were gender nonconforming, but rather indicates that long before sexual attraction is known, non-heterosexuals, on average, are noticeably different from other children. There is little evidence that gender nonconforming children have been encouraged or taught to behave that way; rather, childhood gender nonconformity typically emerges despite conventional socialization. Medical experiments in which infant boys were sex reassigned and reared as girls did not make them feminine nor attracted to males.
Boys who were surgically reassigned female
Between the 1960s and 2000, many newborn and infant boys were surgically reassigned as females if they were born with malformed penises, or if they lost their penises in accidents.: 72–73 Many surgeons believed such males would be happier being socially and surgically reassigned female. In all seven published cases that have provided sexual orientation information, the subjects grew up to be attracted to females. Six cases were exclusively attracted to females, with one case 'predominantly' attracted to females. In a review article in the journal Psychological Science in the Public Interest, six researchers including J. Michael Bailey state this establishes a strong case that male sexual orientation is partly established before birth:
This is the result we would expect if male sexual orientation were entirely due to nature, and it is opposite of the result expected if it were due to nurture, in which case we would expect that none of these individuals would be predominantly attracted to women. They show how difficult it is to derail the development of male sexual orientation by psychosocial means.
They further argue that this raises questions about the significance of the social environment on sexual orientation, stating, "If one cannot reliably make a male human become attracted to other males by cutting off his penis in infancy and rearing him as a girl, then what other psychosocial intervention could plausibly have that effect?" It is further stated that neither cloacal exstrophy (resulting in a malformed penis), nor surgical accidents, are associated with abnormalities of prenatal androgens, thus, the brains of these individuals were male-organized at birth. Six of the seven identified as heterosexual males at follow up, despite being surgically altered and reared as females, with researchers adding: "available evidence indicates that in such instances, parents are deeply committed to raising these children as girls and in as gender-typical a manner as possible." Bailey et al. describe these sex reassignments as 'the near-perfect quasi-experiment' in measuring the impact of 'nature' versus 'nurture' with regards to male homosexuality.
'Exotic becomes erotic' theory
Daryl Bem, a social psychologist at Cornell University, has theorized that the influence of biological factors on sexual orientation may be mediated by experiences in childhood. A child's temperament predisposes the child to prefer certain activities over others. Because of their temperament, which is influenced by biological variables such as genetic factors, some children will be attracted to activities that are commonly enjoyed by other children of the same gender. Others will prefer activities that are typical of another gender. This will make a gender-conforming child feel different from opposite-gender children, while gender-nonconforming children will feel different from children of their own gender. According to Bem, this feeling of difference will evoke psychological arousal when the child is near members of the gender which it considers as being 'different'. Bem theorizes that this psychological arousal will later be transformed into sexual arousal: children will become sexually attracted to the gender which they see as different ("exotic"). This proposal is known as the "exotic becomes erotic" theory. Wetherell et al. state that Bem "does not intend his model as an absolute prescription for all individuals, but rather as a modal or average explanation."
Two critiques of Bem's theory in the journal Psychological Review concluded that "studies cited by Bem and additional research show that [the] Exotic Becomes Erotic theory is not supported by scientific evidence." Bem was criticized for relying on a non-random sample of gay men from the 1970s (rather than collecting new data) and for drawing conclusions that appear to contradict the original data. An "examination of the original data showed virtually all respondents were familiar with children of both sexes", and that only 9% of gay men said that "none or only a few" of their friends were male, and most gay men (74%) reported having "an especially close friend of the same sex" during grade school. Further, "71% of gay men reported feeling different from other boys, but so did 38% of heterosexual men. The difference for gay men is larger, but still indicates that feeling different from same-sex peers was common for heterosexual men." Bem also acknowledged that gay men were more likely to have older brothers (the fraternal birth order effect), which appeared to contradict an unfamiliarity with males. Bem cited cross-cultural studies which also "appear to contradict the EBE theory assertion", such as the Sambia tribe in Papua New Guinea, which ritually enforced homosexual acts among teenagers; yet once these boys reached adulthood, only a small proportion of men continued to engage in homosexual behaviour - similar to levels observed in the United States. Additionally, Bem's model could be interpreted as implying that if one could change a child's behavior, one could change their sexual orientation, but most psychologists doubt this would be possible.
Neuroscientist Simon LeVay said that while Bem's theory was arranged in a "believable temporal order",: 65 that it ultimately "lacks empirical support".: 164 Social psychologist Justin Lehmiller stated that Bem's theory has received praise "for the way it seamlessly links biological and environmental influences" and that there "is also some support for the model in the sense that childhood gender nonconformity is indeed one of the strongest predicators of adult homosexuality", but that the validity of the model "has been questioned on numerous grounds and scientists have largely rejected it."
Sexual orientation and evolution
Sexual practices that significantly reduce the frequency of heterosexual intercourse also significantly decrease the chances of successful reproduction, and for this reason, they would appear to be maladaptive in an evolutionary context following a simple Darwinian model (competition amongst individuals) of natural selection—on the assumption that homosexuality would reduce this frequency. Several theories have been advanced to explain this contradiction, and new experimental evidence has demonstrated their feasibility.
Some scholars have suggested that homosexuality is indirectly adaptive, by conferring a reproductive advantage in a non-obvious way on heterosexual siblings or their children, a hypothesised instance of kin selection. By way of analogy, the allele (a particular version of a gene) which causes sickle-cell anemia when two copies are present, also confers resistance to malaria with a lesser form of anemia when one copy is present (this is called heterozygous advantage).
Brendan Zietsch of the Queensland Institute of Medical Research proposes the alternative theory that men exhibiting female traits become more attractive to females and are thus more likely to mate, provided the genes involved do not drive them to complete rejection of heterosexuality.
In a 2008 study, its authors stated that "There is considerable evidence that human sexual orientation is genetically influenced, so it is not known how homosexuality, which tends to lower reproductive success, is maintained in the population at a relatively high frequency." They hypothesized that "while genes predisposing to homosexuality reduce homosexuals' reproductive success, they may confer some advantage in heterosexuals who carry them". Their results suggested that "genes predisposing to homosexuality may confer a mating advantage in heterosexuals, which could help explain the evolution and maintenance of homosexuality in the population". However, in the same study, the authors noted that "nongenetic alternative explanations cannot be ruled out" as a reason for the heterosexual in the homosexual-heterosexual twin pair having more partners, specifically citing "social pressure on the other twin to act in a more heterosexual way" (and thus seek out a greater number of sexual partners) as an example of one alternative explanation. The study acknowledges that a large number of sexual partners may not lead to greater reproductive success, specifically noting there is an "absence of evidence relating the number of sexual partners and actual reproductive success, either in the present or in our evolutionary past".
The heterosexual advantage hypothesis was given strong support by the 2004 Italian study demonstrating increased fecundity in the female matrilineal relatives of gay men. As originally pointed out by Hamer, even a modest increase in reproductive capacity in females carrying a "gay gene" could easily account for its maintenance at high levels in the population.
Gay uncle hypothesis
The "gay uncle hypothesis" posits that people who themselves do not have children may nonetheless increase the prevalence of their family's genes in future generations by providing resources (e.g., food, supervision, defense, shelter) to the offspring of their closest relatives.
This hypothesis is an extension of the theory of kin selection, which was originally developed to explain apparent altruistic acts which seemed to be maladaptive. The initial concept was suggested by J. B. S. Haldane in 1932 and later elaborated by many others including John Maynard Smith, W. D. Hamilton and Mary Jane West-Eberhard. This concept was also used to explain the patterns of certain social insects where most of the members are non-reproductive.
Vasey and VanderLaan (2010) tested the theory on the Pacific island of Samoa, where they studied women, straight men, and the fa'afafine, men who prefer other men as sexual partners and are accepted within the culture as a distinct third gender category. Vasey and VanderLaan found that the fa'afafine said they were significantly more willing to help kin, yet much less interested in helping children who are not family, providing the first evidence to support the kin selection hypothesis.
The hypothesis is consistent with other studies on homosexuality, which show that it is more prevalent amongst both siblings and twins.
Vasey and VanderLaan (2011) provides evidence that if an adaptively designed avuncular male androphilic phenotype exists and its development is contingent on a particular social environment, then a collectivistic cultural context is insufficient, in and of itself, for the expression of such a phenotype.
Biological differences in gay men and lesbian women
Some studies have found correlations between physiology of people and their sexuality; these studies provide evidence which suggests that:
Gay men and straight women have, on average, equally proportioned brain hemispheres. Lesbian women and straight men have, on average, slightly larger right brain hemispheres.
The suprachiasmatic nucleus of the hypothalamus was found by Swaab and Hopffman to be larger in gay men than in non-gay men; the suprachiasmatic nucleus is also known to be larger in men than in women.
Gay men report, on average, slightly longer and thicker penises than non-gay men.
The average size of the INAH 3 in the brains of gay men is approximately the same size as INAH 3 in women, which is significantly smaller, and the cells more densely packed, than in heterosexual men's brains.
The anterior commissure was found to be larger in gay men than women and heterosexual men, but a subsequent study found no such difference.
The functioning of the inner ear and the central auditory system in lesbians and bisexual women are more like the functional properties found in men than in non-gay women (the researchers argued this finding was consistent with the prenatal hormonal theory of sexual orientation).
The startle response (eyeblink following a loud sound) is similarly masculinized in lesbians and bisexual women.
Gay and non-gay people's brains respond differently to two putative sex pheromones (AND, found in male armpit secretions, and EST, found in female urine).
The amygdala, a region of the brain, is more active in gay men than non-gay men when exposed to sexually arousing material.
Finger length ratios between the index and ring fingers have been reported to differ, on average, between non-gay and lesbian women.
Gay men and lesbians are significantly more likely to be left-handed or ambidextrous than non-gay men and women; Simon LeVay argues that because "[h]and preference is observable before birth... [t]he observation of increased non-right-handness in gay people is therefore consistent with the idea that sexual orientation is influenced by prenatal processes," perhaps heredity.
A study of over 50 gay men found that about 23% had counterclockwise hair whorl, as opposed to 8% in the general population. This may correlate with left-handedness.
Gay men have increased ridge density in the fingerprints on their left thumbs and little fingers.
Length of limbs and hands of gay men is smaller compared to height than the general population, but only among white men.
J. Michael Bailey has argued that the early childhood gender nonconforming behavior of homosexuals, as opposed to biological markers, are better evidence of homosexuality being an inborn trait. He argues that gay men are "punished much more than rewarded" for their childhood gender nonconformity, and that such behavior "emerges with no encouragement, and despite opposition", making it "the sine qua non of innateness".
Whether genetic or other physiological determinants form the basis of sexual orientation is a highly politicized issue. The Advocate, a U.S. gay and lesbian newsmagazine, reported in 1996 that 61% of its readers believed that "it would mostly help gay and lesbian rights if homosexuality were found to be biologically determined". A cross-national study in the United States, the Philippines, and Sweden found that those who believed that "homosexuals are born that way" held significantly more positive attitudes toward homosexuality than those who believed that "homosexuals choose to be that way" or "learn to be that way".
Equal protection analysis in U.S. law determines when government requirements create a “suspect classification" of groups and therefore eligible for heightened scrutiny based on several factors, one of which is immutability.
Evidence that sexual orientation is biologically determined (and therefore perhaps immutable in the legal sense) would strengthen the legal case for heightened scrutiny of laws discriminating on that basis.
The perceived causes of sexual orientation have a significant bearing on the status of sexual minorities in the eyes of social conservatives. The Family Research Council, a conservative Christian think tank in Washington, D.C., argues in the book Getting It Straight that finding people are born gay "would advance the idea that sexual orientation is an innate characteristic, like race; that homosexuals, like African-Americans, should be legally protected against 'discrimination;' and that disapproval of homosexuality should be as socially stigmatized as racism. However, it is not true." On the other hand, some social conservatives such as Reverend Robert Schenck have argued that people can accept any scientific evidence while still morally opposing homosexuality. National Organization for Marriage board member and fiction writer Orson Scott Card has supported biological research on homosexuality, writing that "our scientific efforts in regard to homosexuality should be to identify genetic and uterine causes... so that the incidence of this dysfunction can be minimized.... [However, this should not be seen] as an attack on homosexuals, a desire to 'commit genocide' against the homosexual community... There is no 'cure' for homosexuality because it is not a disease. There are, however, different ways of living with homosexual desires."
Some advocates for the rights of sexual minorities resist what they perceive as attempts to pathologise or medicalise 'deviant' sexuality, and choose to fight for acceptance in a moral or social realm. The journalist Chandler Burr has stated that "[s]ome, recalling earlier psychiatric "treatments" for homosexuality, discern in the biological quest the seeds of genocide. They conjure up the specter of the surgical or chemical "rewiring" of gay people, or of abortions of fetal homosexuals who have been hunted down in the womb." LeVay has said in response to letters from gays and lesbians making such criticisms that the research "has contributed to the status of gay people in society".
1) Frankowski BL (June 2004). "Sexual orientation and adolescents". Pediatrics. 113 (6): 1827–32. doi:10.1542/peds.113.6.1827. PMID 15173519.
2) Lamanna MA, Riedmann A, Stewart SD (2014). Marriages, Families, and Relationships: Making Choices in a Diverse Society. Cengage Learning. p. 82. ISBN 978-1305176898. Retrieved February 11, 2016. "The reason some individuals develop a gay sexual identity has not been definitively established – nor do we yet understand the development of heterosexuality. The American Psychological Association (APA) takes the position that a variety of factors impact a person's sexuality. The most recent literature from the APA says that sexual orientation is not a choice that can be changed at will, and that sexual orientation is most likely the result of a complex interaction of environmental, cognitive and biological factors...is shaped at an early age...[and evidence suggests] biological, including genetic or inborn hormonal factors, play a significant role in a person's sexuality (American Psychological Association 2010)."
3) Stuart GW (2014). Principles and Practice of Psychiatric Nursing. Elsevier Health Sciences. p. 502. ISBN 978-0323294126. Retrieved February 11, 2016. "No conclusive evidence supports any one specific cause of homosexuality; however, most researchers agree that biological and social factors influence the development of sexual orientation."
4) Bailey JM, Vasey PL, Diamond LM, Breedlove SM, Vilain E, Epprecht M (September 2016). "Sexual Orientation, Controversy, and Science". Psychological Science in the Public Interest. 17 (2): 45–101. doi:10.1177/1529100616637616. PMID 27113562.
5) Bailey JM, Vasey PL, Diamond LM, Breedlove SM, Vilain E, Epprecht M (September 2016). "Sexual Orientation, Controversy, and Science". Psychological Science in the Public Interest. 17 (2): 45–101. doi:10.1177/1529100616637616. PMID 27113562. S2CID 42281410.
6) Balthazart J (August 2011). "Minireview: Hormones and human sexual orientation". Endocrinology. 152 (8): 2937–47. doi:10.1210/en.2011-0277. PMC 3138231. PMID 21693676.
7) Breedlove SM (August 2017). "Prenatal Influences on Human Sexual Orientation: Expectations versus Data". Archives of Sexual Behavior. 46 (6): 1583–1592. doi:10.1007/s10508-016-0904-2. PMC 5786378. PMID 28176027.
8) Roselli CE (July 2018). "Neurobiology of gender identity and sexual orientation". Journal of Neuroendocrinology. 30 (7): e12562. doi:10.1111/jne.12562. PMC 6677266. PMID 29211317.
9) Balthazart J (January 2018). "Fraternal birth order effect on sexual orientation explained". Proceedings of the National Academy of Sciences of the United States of America. 115 (2): 234–236. doi:10.1073/pnas.1719534115. PMC 5777082. PMID 29259109.
10) Bogaert AF, Skorska MN, Wang C, Gabrie J, MacNeil AJ, Hoffarth MR, et al. (January 2018). "Male homosexuality and maternal immune responsivity to the Y-linked protein NLGN4Y". Proceedings of the National Academy of Sciences of the United States of America. 115 (2): 302–306. doi:10.1073/pnas.1705895114. PMC 5777026. PMID 29229842.
11) Bailey JM (January 2018). "The Fraternal Birth Order Effect Is Robust and Important". Archives of Sexual Behavior. 47 (1): 17–19. doi:10.1007/s10508-017-1115-1. PMID 29159754. S2CID 35597467.
12) Blanchard R (January 2018). "Fraternal Birth Order, Family Size, and Male Homosexuality: Meta-Analysis of Studies Spanning 25 Years". Archives of Sexual Behavior. 47 (1): 1–15. doi:10.1007/s10508-017-1007-4. PMID 28608293. S2CID 10517373.
13) LeVay S (2016-08-01). Gay, Straight, and the Reason Why: The Science of Sexual Orientation. Oxford University Press. pp. 107–110. ISBN 978-0-19-029739-8.
14) LeVay S (2016-08-01). Gay, Straight, and the Reason Why: The Science of Sexual Orientation. Oxford University Press. ISBN 978-0-19-029739-8.
15) Rice WR, Friberg U, Gavrilets S (December 2012). "Homosexuality as a consequence of epigenetically canalized sexual development". The Quarterly Review of Biology. 87 (4): 343–68. doi:10.1086/668167. JSTOR 10.1086/668167. PMID 23397798. S2CID 7041142.
16) Gavrilets S, Friberg U, Rice WR (January 2018). "Understanding Homosexuality: Moving on from Patterns to Mechanisms" (PDF). Archives of Sexual Behavior. 47 (1): 27–31. doi:10.1007/s10508-017-1092-4. PMID 28986707. S2CID 33422845.
17) Rice WR, Friberg U, Gavrilets S (September 2013). "Homosexuality via canalized sexual development: a testing protocol for a new epigenetic model". BioEssays. 35 (9): 764–70. doi:10.1002/bies.201300033. PMC 3840696. PMID 23868698.
18) Bailey JM, Pillard RC (December 1991). "A genetic study of male sexual orientation". Archives of General Psychiatry. 48 (12): 1089–96. doi:10.1001/archpsyc.1991.01810360053008. PMID 1845227.
19) Whitam FL, Diamond M, Martin J (June 1993). "Homosexual orientation in twins: a report on 61 pairs and three triplet sets". Archives of Sexual Behavior. 22 (3): 187–206. doi:10.1007/bf01541765. PMID 8494487. S2CID 8941681.
20) Bailey JM, Dunne MP, Martin NG (March 2000). "Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample". Journal of Personality and Social Psychology. 78 (3): 524–36. CiteSeerX 10.1.1.519.4486. doi:10.1037/0022-35126.96.36.1994. PMID 10743878.
21) Hershberger, Scott L. 2001. Biological Factors in the Development of Sexual Orientation. Pp. 27–51 in Lesbian, Gay, and Bisexual Identities and Youth: Psychological Perspectives, edited by Anthony R. D’Augelli and Charlotte J. Patterson. Oxford, New York: Oxford University Press. Quoted in Bearman and Bruckner, 2002.
22) Långström N, Rahman Q, Carlström E, Lichtenstein P (February 2010). "Genetic and environmental effects on same-sex sexual behavior: a population study of twins in Sweden". Archives of Sexual Behavior. 39 (1): 75–80. doi:10.1007/s10508-008-9386-1. PMID 18536986. S2CID 11870487.
23) Hamer DH, Hu S, Magnuson VL, Hu N, Pattatucci AM (July 1993). "A linkage between DNA markers on the X chromosome and male sexual orientation". Science. 261 (5119): 321–7. Bibcode:1993Sci...261..321H. doi:10.1126/science.8332896. PMID 8332896.
24) Wilson G, Rahman Q (2008). Born Gay: The Psychobiology of Sex Orientation (2nd ed.). Peter Owen Publishers. ISBN 9780720613094.
25) Hu S, Pattatucci AM, Patterson C, Li L, Fulker DW, Cherny SS, et al. (November 1995). "Linkage between sexual orientation and chromosome Xq28 in males but not in females". Nature Genetics (Submitted manuscript). 11 (3): 248–56. doi:10.1038/ng1195-248. PMID 7581447. S2CID 721490.
26) Vilain E (2000). "Genetics of sexual development". Annual Review of Sex Research. 11: 1–25. PMID 11351829.
27) Hamer DH, Rice G, Risch N, Ebers G (1999). "Genetics and Male Sexual Orientation". Science. 285 (5429): 803. doi:10.1126/science.285.5429.803a.
28) Mustanski BS, Dupree MG, Nievergelt CM, Bocklandt S, Schork NJ, Hamer DH (March 2005). "A genomewide scan of male sexual orientation" (PDF). Human Genetics. 116 (4): 272–8. doi:10.1007/s00439-004-1241-4. PMID 15645181. S2CID 206989147. Archived from the original (PDF) on 2005-04-15.
29) Sanders AR, Martin ER, Beecham GW, Guo S, Dawood K, Rieger G, et al. (May 2015). "Genome-wide scan demonstrates significant linkage for male sexual orientation". Psychological Medicine. 45 (7): 1379–88. doi:10.1017/S0033291714002451. PMID 25399360. S2CID 4027333.
30) Ngun TC, Vilain E (2014). The Biological Basis of Human Sexual Orientation: Is There a Role for Epigenetics? (PDF). Advances in Genetics. 86. pp. 167–84. doi:10.1016/B978-0-12-800222-3.00008-5. ISBN 9780128002223. ISSN 0065-2660. PMID 25172350. Archived from the original (PDF) on 2016-03-31. Retrieved 20 March 2016.
31) Ellis L, Ficek C, Burke D, Das S (February 2008). "Eye color, hair color, blood type, and the rhesus factor: exploring possible genetic links to sexual orientation". Archives of Sexual Behavior. 37 (1): 145–9. doi:10.1007/s10508-007-9274-0. PMID 18074215. S2CID 8303331.
32) Poiani A (2010). Animal Homosexuality: A Biosocial Perspective. Cambridge University Press. pp. 55–96. ISBN 978-1139490382.
33) Pavlou HJ, Goodwin SF (February 2013). "Courtship behavior in Drosophila melanogaster: towards a 'courtship connectome'". Current Opinion in Neurobiology. 23 (1): 76–83. doi:10.1016/j.conb.2012.09.002. PMC 3563961. PMID 23021897.
34) Park D, Choi D, Lee J, Lim DS, Park C (July 2010). "Male-like sexual behavior of female mouse lacking fucose mutarotase". BMC Genetics. 11: 62. doi:10.1186/1471-2156-11-62. PMC 2912782. PMID 20609214.
35) Connor S (31 October 1995). "The 'gay gene' is back on the scene". The Independent.
36) Knapton S (13 February 2014). "Being homosexual is only partly due to gay gene, research finds". The Telegraph. Telegraph Media Group. Archived from the original on February 14, 2014.
37) Sanders AR, Beecham GW, Guo S, Dawood K, Rieger G, Badner JA, et al. (December 2017). "Genome-Wide Association Study of Male Sexual Orientation". Scientific Reports. 7 (1): 16950. Bibcode:2017NatSR...716950S. doi:10.1038/s41598-017-15736-4. PMC 5721098. PMID 29217827.
38) LeVay S (August 1991). "A difference in hypothalamic structure between heterosexual and homosexual men". Science. 253 (5023): 1034–7. Bibcode:1991Sci...253.1034L. doi:10.1126/science.1887219. PMID 1887219. S2CID 1674111.
39) Frisch M, Nielsen NM, Pedersen BV (January 2014). "Same-sex marriage, autoimmune thyroid gland dysfunction and other autoimmune diseases in Denmark 1989-2008". European Journal of Epidemiology. 29 (1): 63–71. doi:10.1007/s10654-013-9869-9. PMID 24306355. S2CID 11819672.
40) Deputy NP, Boehmer U (August 2010). "Determinants of body weight among men of different sexual orientation". Preventive Medicine. 51 (2): 129–31. doi:10.1016/j.ypmed.2010.05.010. PMID 20510272.
41) Blanchard R, Bogaert AF (December 1996). "Biodemographic comparisons of homosexual and heterosexual men in the Kinsey Interview Data". Archives of Sexual Behavior. 25 (6): 551–79. doi:10.1007/BF02437839. PMID 8931880. S2CID 23951518.
42) Price M (2018-10-19). "Giant study links DNA variants to same-sex behavior". Science | AAAS. Retrieved 2019-01-21.
43) Ganna A, Verweij KJ, Nivard MG, Maier R, Wedow R, Busch AS, et al. (August 2019). "Large-scale GWAS reveals insights into the genetic architecture of same-sex sexual behavior". Science. 365 (6456): eaat7693. doi:10.1126/science.aat7693. PMC 7082777. PMID 31467194.
"Genetics of Sexual Behavior". Genetics of Sexual Behavior. geneticsexbehavior.info. 28 February 2018. Retrieved 30 August 2019.
44) Bocklandt S, Horvath S, Vilain E, Hamer DH (February 2006). "Extreme skewing of X chromosome inactivation in mothers of homosexual men". Human Genetics. 118 (6): 691–4. CiteSeerX 10.1.1.533.4517. doi:10.1007/s00439-005-0119-4. PMID 16369763. S2CID 1370892. Archived from the original on 2007-06-09.
45) Blanchard R, Klassen P (April 1997). "H-Y antigen and homosexuality in men" (PDF). Journal of Theoretical Biology. 185 (3): 373–8. Bibcode:1997JThBi.185..373B. CiteSeerX 10.1.1.602.8423. doi:10.1006/jtbi.1996.0315. PMID 9156085. Archived from the original (PDF) on 2012-09-15.
46) Wade N (10 April 2007). "Pas de Deux of Sexuality Is Written in the Genes". The New York Times.
47) Blanchard R (1997). "Birth order and sibling sex ratio in homosexual versus heterosexual males and females". Annual Review of Sex Research. 8: 27–67. PMID 10051890.
48) Bogaert AF, Skorska M (April 2011). "Sexual orientation, fraternal birth order, and the maternal immune hypothesis: a review". Frontiers in Neuroendocrinology. 32 (2): 247–54. doi:10.1016/j.yfrne.2011.02.004. PMID 21315103. S2CID 45446175.
49) Cantor, Blanchard, Paterson, & Bogaert, 2002; Blanchard & Bogaert, 2004
50) Blanchard, 2011; Rieger et al., 2012
51) Camperio-Ciani A, Corna F, Capiluppi C (November 2004). "Evidence for maternally inherited factors favouring male homosexuality and promoting female fecundity". Proceedings. Biological Sciences. 271 (1554): 2217–21. doi:10.1098/rspb.2004.2872. PMC 1691850. PMID 15539346.
52) Camperio Ciani A, Cermelli P, Zanzotto G (June 2008). "Sexually antagonistic selection in human male homosexuality". PLOS ONE. 3 (6): e2282. Bibcode:2008PLoSO...3.2282C. doi:10.1371/journal.pone.0002282. PMC 2427196. PMID 18560521.
53) Savic I, Berglund H, Lindström P (May 2005). "Brain response to putative pheromones in homosexual men". Proceedings of the National Academy of Sciences of the United States of America. 102 (20): 7356–61. Bibcode:2005PNAS..102.7356S. doi:10.1073/pnas.0407998102. PMC 1129091. PMID 15883379.
54) Wade, Nicholas. (May 9, 2005). "Gay Men Are Found to Have Different Scent of Attraction." New York Times.
55) Swaab DF, Hofman MA (December 1990). "An enlarged suprachiasmatic nucleus in homosexual men" (PDF). Brain Research. 537 (1–2): 141–8. doi:10.1016/0006-8993(90)90350-K. PMID 2085769. S2CID 13403716.
56) Allen LS, Gorski RA (August 1992). "Sexual orientation and the size of the anterior commissure in the human brain". Proceedings of the National Academy of Sciences of the United States of America. 89 (15): 7199–202. Bibcode:1992PNAS...89.7199A. doi:10.1073/pnas.89.15.7199. PMC 49673. PMID 1496013.
57) Byne W, Parsons B (March 1993). "Human sexual orientation. The biologic theories reappraised". Archives of General Psychiatry. 50 (3): 228–39. doi:10.1001/archpsyc.1993.01820150078009. PMID 8439245.
58) Byne W, Tobet S, Mattiace LA, Lasco MS, Kemether E, Edgar MA, et al. (September 2001). "The interstitial nuclei of the human anterior hypothalamus: an investigation of variation with sex, sexual orientation, and HIV status". Hormones and Behavior. 40 (2): 86–92. doi:10.1006/hbeh.2001.1680. PMID 11534967. S2CID 3175414.[permanent dead link]
59) Lasco MS, Jordan TJ, Edgar MA, Petito CK, Byne W (May 2002). "A lack of dimorphism of sex or sexual orientation in the human anterior commissure". Brain Research. 936 (1–2): 95–8. doi:10.1016/s0006-8993(02)02590-8. PMID 11988236. S2CID 7774361.
60) Cahill, 2006; Lenroot and Giedd, 2010; McCarthy et al., 2009; Sakuma, 2009
61) Jäncke, L., Mérillat, S., Liem, F., & Hänggi, J. (2015). Brain size, sex, and the aging brain. Human Brain Mapping, 36(1), 150–169. https://doi.org/10.1002/hbm.22619, Berenbaum and Beltz, 2016.
62) LeVay S (2016-08-01). Gay, Straight, and the Reason Why: The Science of Sexual Orientation. Oxford University Press. ISBN 978-0-19-029738-1.
63) Bailey J (2003-03-10). The Man Who Would Be Queen. ISBN 978-0-309-08418-5.
64) Swaab DF, Gooren LJ, Hofman MA (1992). "Gender and sexual orientation in relation to hypothalamic structures". Hormone Research (Submitted manuscript). 38 Suppl 2 (2): 51–61. doi:10.1159/000182597. hdl:20.500.11755/7cb8b769-4329-407a-b0ee-13e011017f68. PMID 1292983.
65) Garcia-Falgueras A, Swaab DF (2010). "Sexual Hormones and the Brain: An Essential Alliance for Sexual Identity and Sexual Orientation". Pediatric Neuroendocrinology. Endocr Dev. Endocrine Development. 17. pp. 22–35. doi:10.1159/000262525. ISBN 978-3-8055-9302-1. PMID 19955753.
66) Roselli CE, Stormshak F (March 2009). "Prenatal programming of sexual partner preference: the ram model". Journal of Neuroendocrinology. 21 (4): 359–64. doi:10.1111/j.1365-2826.2009.01828.x. PMC 2668810. PMID 19207819.
67) Bailey JM, Vasey PL, Diamond LM, Breedlove SM, Vilain E, Epprecht M (September 2016). "Sexual Orientation, Controversy, and Science". Psychological Science in the Public Interest. 17 (2): 45–101. doi:10.1177/1529100616637616. PMID 27113562. S2CID 42281410.
68) Bailey JM (2003-03-10). The Man Who Would Be Queen: The Science of Gender-Bending and Transsexualism. Joseph Henry Press. p. 80. ISBN 978-0-309-08418-5.
69) Bem DJ (December 2000). "Exotic becomes erotic: interpreting the biological correlates of sexual orientation" (PDF). Archives of Sexual Behavior. 29 (6): 531–48. doi:10.1023/A:1002050303320. PMID 11100261. S2CID 12078658. PDF Archived 2007-04-11 at the Wayback Machine
70) Wetherell M, Talpade Mohanty C (2010). The SAGE Handbook of Identities. Sage Publications. p. 177. ISBN 978-1446248379.
71) Peplau LA, Garnets LD, Spalding LR, Conley TD, Veniegas RC (April 1998). "A critique of Bem's "Exotic Becomes Erotic" theory of sexual orientation" (PDF). Psychological Review. 105 (2): 387–94. doi:10.1037/0033-295X.105.2.387. PMID 9577243.
72) Lehmiller JJ (2017-12-26). The Psychology of Human Sexuality. John Wiley & Sons. pp. 156–157. ISBN 978-1-119-16471-5.
73) MacIntyre F, Estep KW (1993). "Sperm competition and the persistence of genes for male homosexuality". Bio Systems. 31 (2–3): 223–33. doi:10.1016/0303-2647(93)90051-D. PMID 8155854.
74) Baker, Robin (1996) Sperm Wars: The Science of Sex, p.241 ff.
75) "Gender bending". The Economist. 2008-10-23.
76) Zietsch B, Morley K, Shekar S, Verweij K, Keller M, Macgregor S, et al. (November 2008). "Genetic factors predisposing to homosexuality may increase mating success in heterosexuals". Evolution and Human Behavior. 29 (6): 424–433. doi:10.1016/j.evolhumbehav.2008.07.002.
77) Hamer, D., Copeland, P. The Science of Desire: The Search for the Gay Gene and the Biology of Behavior (Simon and Schuster, 1994) ISBN 0-684-80446-8
78) Moskowitz C (11 February 2010). "How Gay Uncles Pass Down Genes". livescience.com. Retrieved 22 July 2020.
79) Mayr, E. (1982). The Growth of Biological Thought: Diversity, Evolution, and Inheritance. Cambridge: Harvard University Press. p 598.
80) Vanderlaan, Doug P. (2011). The development and evolution of male androphilia in Samoan fa'afafine (Thesis).
81) "Study Supports Gay Super Uncles Theory". 2010-02-05.
82) Vasey PL, VanderLaan DP (February 2012). "Sexual orientation in men and avuncularity in Japan: implications for the kin selection hypothesis". Archives of Sexual Behavior. 41 (1): 209–15. doi:10.1007/s10508-011-9763-z. PMID 21656333. S2CID 33348533.
83) "BBC NEWS - Health - Scans see 'gay brain differences'". 2008-06-16.
84) Panzica GC, Aste N, Viglietti-Panzica C, Ottinger MA (March 1995). "Structural sex differences in the brain: influence of gonadal steroids and behavioral correlates". Journal of Endocrinological Investigation. 18 (3): 232–52. doi:10.1007/BF03347808. PMID 7615911. S2CID 10435075.
85) Swaab DF, Zhou JN, Ehlhart T, Hofman MA (June 1994). "Development of vasoactive intestinal polypeptide neurons in the human suprachiasmatic nucleus in relation to birth and sex". Brain Research. Developmental Brain Research. 79 (2): 249–59. doi:10.1016/0165-3806(94)90129-5. PMID 7955323.
86) Roughgarden J (2004). Evolution's Rainbow: Diversity, Gender, and Sexuality in Nature and People. Berkeley, CA: University of California Press. p. 245. ISBN 9780520240735.
87) Bogaert AF, Hershberger S (June 1999). "The relation between sexual orientation and penile size". Archives of Sexual Behavior. 28 (3): 213–21. doi:10.1023/A:1018780108597. PMID 10410197. S2CID 42801275.
88) Lasco MS, Jordan TJ, Edgar MA, Petito CK, Byne W (May 2002). "A lack of dimorphism of sex or sexual orientation in the human anterior commissure". Brain Research. 936 (1–2): 95–8. doi:10.1016/S0006-8993(02)02590-8. PMID 11988236. S2CID 7774361.
89) McFadden D (February 2002). "Masculinization effects in the auditory system". Archives of Sexual Behavior. 31 (1): 99–111. doi:10.1023/A:1014087319682. PMID 11910797. S2CID 2743338.
90) Rahman Q, Kumari V, Wilson GD (October 2003). "Sexual orientation-related differences in prepulse inhibition of the human startle response". Behavioral Neuroscience. 117 (5): 1096–102. doi:10.1037/0735-7044.117.5.1096. PMID 14570558.
91) Savic I, Berglund H, Gulyas B, Roland P (August 2001). "Smelling of odorous sex hormone-like compounds causes sex-differentiated hypothalamic activations in humans". Neuron. 31 (4): 661–8. doi:10.1016/S0896-6273(01)00390-7. PMID 11545724. S2CID 2547202.
92) Berglund H, Lindström P, Savic I (May 2006). "Brain response to putative pheromones in lesbian women". Proceedings of the National Academy of Sciences of the United States of America. 103 (21): 8269–74. Bibcode:2006PNAS..103.8269B. doi:10.1073/pnas.0600331103. PMC 1570103. PMID 16705035.
93) Safron A, Barch B, Bailey JM, Gitelman DR, Parrish TB, Reber PJ (April 2007). "Neural correlates of sexual arousal in homosexual and heterosexual men". Behavioral Neuroscience. 121 (2): 237–48. doi:10.1037/0735-7044.121.2.237. PMID 17469913.. The authors of the study caution that any interpretation of this finding must take into account that the group difference in brain activation between heterosexual men and homosexual men in the amygdala region is not large and that the most robust finding is that both heterosexual and homosexual men used the same areas when they reacted to sexually preferred stimuli. "For the most part, homosexual and heterosexual men showed very similar patterns of activation (albeit to different erotic stimuli). One possible exception was the amygdala, in which homosexual men showed greater activational differences between preferred and nonpreferred erotic stimuli compared with heterosexual men. However, this difference was not hypothesized a priori, was not large, and was the only group difference found out of many tested. Thus, this finding needs replication."(Debra A. Hope (editor), What is Sexual Orientation and Do Women Have One? (presentation by J.M. Bailey), Nebraska Symposium on Motivation, Volume 54 p. 47, Springer Science, 2009.)
94) Williams TJ, Pepitone ME, Christensen SE, Cooke BM, Huberman AD, Breedlove NJ, et al. (March 2000). "Finger-length ratios and sexual orientation" (PDF). Nature. 404 (6777): 455–6. Bibcode:2000Natur.404..455W. doi:10.1038/35006555. PMID 10761903. S2CID 205005405. Archived from the original (PDF) on 2015-06-26.
95) Tortorice JL (2002), Written on the body: butch vs. femme lesbian gender identity and biological correlates of low digit ratio, Rutgers University, OCLC 80234273
96) 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. S2CID 1743441.
97) Rahman Q, Wilson GD (April 2003). "Sexual orientation and the 2nd to 4th finger length ratio: evidence for organising effects of sex hormones or developmental instability?". Psychoneuroendocrinology. 28 (3): 288–303. doi:10.1016/S0306-4530(02)00022-7. PMID 12573297. S2CID 21071741.
98) Putz DA, Gaulin SJ, Sporter RJ, McBurney DH (May 2004). "Sex hormones and finger length: What does 2D:4D indicate?" (PDF). Evolution and Human Behavior. 25 (3): 182–99. doi:10.1016/j.evolhumbehav.2004.03.005. Archived from the original (PDF) on 2010-01-07.
99) Rahman Q (May 2005). "Fluctuating asymmetry, second to fourth finger length ratios and human sexual orientation". Psychoneuroendocrinology. 30 (4): 382–91. doi:10.1016/j.psyneuen.2004.10.006. PMID 15694118. S2CID 39896938.
100) Kraemer B, Noll T, Delsignore A, Milos G, Schnyder U, Hepp U (2006). "Finger length ratio (2D:4D) and dimensions of sexual orientation". Neuropsychobiology. 53 (4): 210–4. doi:10.1159/000094730. PMID 16874008. S2CID 201838.
101) 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. S2CID 6324765.
102) Grimbos T, Dawood K, Burriss RP, Zucker KJ, Puts DA (April 2010). "Sexual orientation and the second to fourth finger length ratio: a meta-analysis in men and women". Behavioral Neuroscience. 124 (2): 278–87. doi:10.1037/a0018764. PMID 20364887. S2CID 2777884.[permanent dead link]
103) Hiraishi K, Sasaki S, Shikishima C, Ando J (June 2012). "The second to fourth digit ratio (2D:4D) in a Japanese twin sample: heritability, prenatal hormone transfer, and association with sexual orientation". Archives of Sexual Behavior. 41 (3): 711–24. doi:10.1007/s10508-011-9889-z. PMID 22270254. S2CID 14974103.
104) 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.
105) Mustanski BS, Bailey JM, Kaspar S (February 2002). "Dermatoglyphics, handedness, sex, and sexual orientation". Archives of Sexual Behavior. 31 (1): 113–22. doi:10.1023/A:1014039403752. PMID 11910784. S2CID 29217315.
106) Lippa RA (April 2003). "Handedness, sexual orientation, and gender-related personality traits in men and women". Archives of Sexual Behavior. 32 (2): 103–14. doi:10.1023/A:1022444223812. PMID 12710825. S2CID 4196223.
107) Hepper PG, Shahidullah S, White R (1991). "Handedness in the human fetus". Neuropsychologia. 29 (11): 1107–11. doi:10.1016/0028-3932(91)90080-R. PMID 1775228. S2CID 12123306.
108) France D (18 June 2007). "The Science of Gaydar". New York Magazine.
109) Bailey J (2003-03-10). The Man Who Would Be Queen. p. 123. ISBN 978-0-309-08418-5.
110) The Advocate (1996, February 6). Advocate Poll Results. p. 8.
111) Ernulf KE, Innala SM, Whitam FL (December 1989). "Biological explanation, psychological explanation, and tolerance of homosexuals: a cross-national analysis of beliefs and attitudes". Psychological Reports. 65 (3 Pt 1): 1003–10. doi:10.2466/pr0.19188.8.131.523. PMID 2608821. S2CID 34025486.
112) Whitley B. E. Jr (1990). "The relationship of heterosexuals' attributions for the causes of homosexuality to attitudes toward lesbians and gay men". Personality and Social Psychology Bulletin. 16 (2): 369–377. doi:10.1177/0146167290162016. S2CID 145507505.
113) Leslie CR (2017). "The Geography of Equal Protection" (PDF). Minnesota Law Review. 101 (4): 1580. Archived from the original (PDF) on 2018-12-23. Retrieved 2019-12-22. "Thus, because the level of scrutiny is often outcome determinative, the probability of courts protecting gay Americans from discrimination is often a function of whether judges conclude that sexual orientation is a suspect classification. To determine this, courts generally consider four factors: whether the members of the group: (1) have historically been subjected to discrimination; (2) share a defining characteristic unrelated to their ability to perform or contribute to society; (3) share a defining immutable characteristic; and (4) lack political power."
114) Balog K (2005–2006). "Equal Protection for Homosexuals: Why the Immutability Argument is Necessary and How it is Met". Cleveland St. L. Rev.: 545–573.
115) Talbot M (25 January 2010). "Is Sexuality Immutable?". The New Yorker.
116) "Prop. 8 trial: defenders of gay-marriage ban make their case". Christian Science Monitor. 2010-01-26. Retrieved 27 January 2010.
117) What Makes People Gay? By Neil Swidey. The Boston Globe. Published August 14, 2005. Accessed June 18, 2009.
118) Card OS (August 7, 2008). "Science on gays falls short". Deseret Morning News. Archived from the original on December 4, 2010. Retrieved June 12, 2010.
119) Burr C (June 2007). "Homosexuality and Biology". The Atlantic Monthly.
"Doubt cast on 'gay gene'". BBC News. 23 April 1999.
Byne W (May 1994). "The biological evidence challenged". Scientific American. 270 (5): 50–5. Bibcode:1994SciAm.270e..50B. doi:10.1038/scientificamerican0594-50. PMID 8197445.
Muscarella F, Fink B, Grammer K, Kirk-Smith M (December 2001). "Homosexual orientation in males: evolutionary and ethological aspects" (PDF). Neuro Endocrinology Letters. 22 (6): 393–400. PMID 11781535. Archived from the original (PDF) on 2018-10-05.
Rahman Q (2005). "The neurodevelopment of human sexual orientation". Neuroscience and Biobehavioral Reviews. 29 (7): 1057–66. doi:10.1016/j.neubiorev.2005.03.002. PMID 16143171. S2CID 15481010.
Rines JP, vom Saal FS (June 1984). "Fetal effects on sexual behavior and aggression in young and old female mice treated with estrogen and testosterone". Hormones and Behavior. 18 (2): 117–29. doi:10.1016/0018-506X(84)90037-0. PMID 6539747. S2CID 37946760.
Veniegas RC, Conley TD (2000). "Biological Research on Women's Sexual Orientations: Evaluating the Scientific Evidence". Journal of Social Issues. 56 (2): 267–282. doi:10.1111/0022-4537.00165.
Ryan BC, Vandenbergh JG (October 2002). "Intrauterine position effects". Neuroscience and Biobehavioral Reviews. 26 (6): 665–78. doi:10.1016/S0149-7634(02)00038-6. PMID 12479841. S2CID 27722357.
LeVay S, Hamer DH (May 1994). "Evidence for a biological influence in male homosexuality". Scientific American. 270 (5): 44–9. Bibcode:1994SciAm.270e..44L. doi:10.1038/scientificamerican0594-44. PMID 8197444.
vom Saal FS (July 1989). "Sexual differentiation in litter-bearing mammals: influence of sex of adjacent fetuses in utero". Journal of Animal Science. 67 (7): 1824–40. doi:10.2527/jas1989.6771824x. PMID 2670873.[permanent dead link]
vom Saal FS, Bronson FH (May 1980). "Sexual characteristics of adult female mice are correlated with their blood testosterone levels during prenatal development". Science. 208 (4444): 597–9. Bibcode:1980Sci...208..597V. doi:10.1126/science.7367881. PMID 7367881.
(Source: https://en.wikipedia.org/wiki/Biology_and_sexual_orientation. October 24th, 2021)
Interessante wissenschaftliche These: "Schwul geboren" worden zu sein, heißt nicht automatisch, ein "schwules Gen" zu haben...
Es ist grundfalsch, die Ursache für gleichgeschlechtliche Neigungen alleine in biologischen Vorgängen sehen zu wollen. Wer dabei psychologische Aspekte sowie prägende Aspekte aus der Lebensgeschichte ignoriert, handelt nicht wissenschaftlich.
Die Tatsache, dass sich die Lebensläufe der Betroffenen in so vielen Punkten überproportional gleichen (bei Männern etwa ein gestörtes oder nicht vorhandenes Verhältnis zum Vater, Identitätsstörungen, Missbrauchserfahrungen, psychische Erkrankungen etc.), kann nicht einfach als unwichtig vom Tisch gewischt werden.
Damit würde man weder der Wissenschaft noch den Betroffenen einen Gefallen tun.
There is no general answer to that question. Are evil spirits or is “the evil” still active today? Can people be “possessed”? Definitely yes. To say otherwise would be both naïve and dangerous. However, before we talk about evil spirits, we need to make sure that we are not confusing that with a mental disorder. Also let’s keep in mind that many different factors contribute to the development of human sexuality. Even in the very rare cases that there definitely is demonic activity involved, deliverance from evil through a deliverance prayer or in extreme cases through an exorcism would not solve all the other problems and it would certainly not meet the underlying relational, emotional and spiritual needs. You might chase the demon out, but the problem with your dad is still very much alive and kicking.
Some might also – consciously or subconsciously – take that as an excuse that keeps them from being active as to taking steps for recovery and being responsible for present thoughts and actions. It is so much easier to blame an evil spirit than to address the underlying core issues!
Others might seek the “quick fix” through deliverance instead of going the hard road of recovery and healing. In other words: We don’t have to beg God to “take it away from us” – we already free through Christ’s atoning death on the Cross that broke the power of sin! All that keeps us from true recovery is the belief that it can be done!
Looking back on those hard years since I left the gay life in 2004 there is one thing I can definitely confirm: If you gave me the choice between the “quick fix” (like through deliverance) and those years where I had to learn to trust and believe in Him, I would always go for the last one. Yes, there were hard and painful moments, but also moments of joy and true satisfaction of coming home to the One in whose image I was created! To compare it with an image: Think of a father that teaches his son how to ride a bike. First, the son will be scared when dad takes off the crutches. Dad will still hold his sonny at first to give him some confidence and courage, but step by step he will let him ride on his own. Little sonny might take the whole street trying to ride straight ahead and sometimes he will also fall and scratch his knee, but dad will always be there with him, teaching him everything he needs to know for riding his little bike. Imagine the joy the little boy will experience once he manages to handle his bike – and how proud his daddy will be of him! That was pretty much how God taught me to live another life. He also rewarded me with an extra: He brought many great friends into my life, godly men that stand with me in good and bad.
None of that I’d have ever gotten through a snip of the finger that turned me from gay to straight” in a second. And boy am I grateful it happened the way it did.