Sexual Orientation: Born This Way?

Abstract

The origin of sexual orientation has been a topic of extreme debate between the church, the homosexual community, and beyond. Homosexual rights activists argue that if there is a moderate to strong biological determinism reinforcing a homosexual orientation, then homosexual couples should receive the same rights as heterosexual couples. They also argue that homosexual behavior is not sinful because it is predicated on uncontrollable homosexual desires and therefore should be accepted in the church and the broader culture. Additionally, documents such as the DSM-V and other APA publications take the stance that homosexual orientation is not a pathological condition and should not be treated nor changed. This paper will demonstrate that scientific evidence has shown that homosexual orientation does not have a moderate or strong biologically deterministic character. The first section will review the genetic evidence for a homosexual gene, as well as the concordance studies of twins to ascertain if certain loci determine sexual orientation. The second section will examine the evidence for the possibility of hormonal control of orientation. The third section will investigate whether or not sexual dimorphism of the brain contributes to sexual orientation. The fourth section will examine evidence that sexual orientation is mutable and thus not completely under the influence of biological factors. The analysis of this paper will show that genes, hormones, and brain structure only indirectly contribute to determining sexual orientation. Thus, the argument that homosexuality is purely biological cannot justifiably be used to argue for equal rights in society, acceptance in the church, or as proof of the immutability of orientation.

Introduction

John Smid was already married when he first developed intense homosexual attractions.[1] This desire eventually led him to seek a divorce from his pregnant wife. He reported that he “had been wrestling with increasing homosexual desires and fantasies for some time, and [he] had no idea how or where [he] was going to get satisfaction” within the confines of his marriage.[2]

Biological determinists who ascribe to compatibilism would argue that John’s homosexual orientation was biologically determined and entirely out of his control.[3] Additionally, many would argue that despite his wife’s desire to change him, no such attempts should be made.[4] Advocates argue that John’s sexual orientation should legally protect him and allow him to pursue the satisfaction he desires. However, groups like the Family Research Council (FRC) hold a different framework for sexuality. In their view, homosexual orientation may have some biological roots, but is predominantly influenced by social, environmental, and individual factors.[5] As such, homosexual orientation is not necessarily something that is permanent, but could be curbed or eliminated. From the biological perspective, there was no hope for reconciliation within John’s marriage, but within the FRC framework, there would at least have been a chance at change. This paper attempts to analyze the biological determinism framework to understand whether or not it accurately represents reality such that decisions, laws, and therapies can be based on it.

Prior to the analysis of the scientific literature, the terms “homosexual identity,” “homosexual orientation,” and “homosexual behavior” are defined and expounded upon to facilitate the discussion of their usage within the articles cited in this paper. Additionally, some evidence indicating that sexual orientation can change is presented in support of the theory that orientation is not solely biologically determined. Section one examines benchmark twin studies on the inheritability of orientation and the presence of a gay gene, as well as subsequent studies that have attempted to show that homosexual orientation is passed along the family line. Section two examines the hypothesis that either adult or fetal sex hormones imprint sexual orientation on the brain. The third section addresses whether or not sexually dimorphic brain structures determine sexual orientation. The final section contains an examination of whether or not one can change one’s sexual orientation. If orientation were mutable, it would be evidence that it is not wholly biologically determined. An examination of the evidence demonstrates that biology can account for the presence of factors that indirectly place a person in a path that promotes homosexuality. However, the evidence also shows that biological factors do not moderately or strongly influence a person’s sexual orientation.

Initial Considerations

Background Definitions

Before analyzing specific articles and determining if they contribute to our understanding of the causes and origin of sexual orientation, it is important to define exactly what the concepts “sexual identity,” “sexual behavior,” and “sexual orientation” mean. Sexual behavior includes all of the physical things people do related to sex, influenced by arousal and attraction.[6] Sexual identity has been a term that has included various components depending on the researcher; while one’s concept of sexual identity is highly individualistic, this paper relies on the holistic definition presented by Raymond Berger who defined sexual identity as a matter of “overt behavior, covert behavior, and self-image.”[7] Berger’s definition is useful in that it represents a view balanced by his work in the mental health clinical setting, alongside his research as a professor of social work. Additionally, he emphasizes that sexual identity is influenced by – “life experiences, cultural and religious values, social reaction, self-attribution, and association with others.”[8]

Sexual orientation has been difficult to define; however, in his book Sexual Identity, Mark Yarhouse provides a concise and easy to understand definition. He defines sexual orientation as “the direction of a person’s attractions.”[9] Attractions are the seemingly innate, sexually-oriented mental and physiological reactions people experience in response to sensory and social stimuli.[10] The ambiguity around their origin is one of the main reasons that people feel as if they have no control over the subjects of their attraction.[11] There are two predominant theories about the origin of sexual attraction.  The first is the strictly deterministic view that these attractions are entirely biological in nature, either through genetics, hormones, or brain structures.[12] The second is that environmental, social, and cultural situations condition us be attracted to certain people.[13]

These three terms are often used interchangeably; research articles commonly commit the philosophical error of conflating of one or more of these terms. In many of the articles prior to 2000, sexual behavior is seen to be synonymous with sexual orientation. This conflation of terms stems from the historical use of mouse models to study homosexual behavior. These studies were necessarily limited to behavioral analysis, with no ability to comment on the identity or orientation of the mice. Therefore, when orientation studies were conducted on human subjects, observation of homosexual behavior was emphasized in an attempt to replicate studies in which behavior was seen in non-human test subjects.[14] In line with the naturalist view of human anthropology, homosexual behavior was assumed to be an indicator of homosexual attraction and orientation. For example, in his study on INAH 3, LeVay says that he tested whether or not the “nuclei exhibit a size dimorphism … with sexual orientation,” even though the study is partially based on rat studies where “variability in the size [of brain structure] is strongly correlated with the amount of male-typical sexual behavior shown.”[15]

A second common conflation is that a homosexual identity is presumed if a research subject has any homosexual attraction or behavior. Many research articles use the Kinsey Scale combined with questionnaires and interviews to ascertain subjects’ sexual orientation.[16] This scale is defined as:

Rating| Description

0| Exclusively heterosexual

1| Predominantly heterosexual, only incidentally homosexual

2| Predominantly heterosexual, but more than incidentally homosexual

3| Equally heterosexual and homosexual

4| Predominantly homosexual, but more than incidentally heterosexual

5| Predominantly homosexual, only incidentally heterosexual

6| Exclusively homosexual

X| No socio-sexual contacts or reactions

Though this scale contains many subdivisions, it is clear that 0-1 are heterosexual, 2-4 are bisexual (a condition that was excluded from the scale out of many researcher’s desire for a binary state), and 5-6 are homosexual. Unfortunately, many studies group Kinsey scale 1 or 2 subjects (which at best could be labeled bisexual) alongside strict homosexuals. This often led to inflated results and undermined the integrity of many studies.

Finally, it is important to keep in mind that while it is necessary to use explicit definitions for identity, orientation, and behavior in individual papers such as this one, the academic community has not accepted universal scientific or sociological definitions of these terms.[17] Thus, the importance and explanatory power of all articles concerning sexual orientation are assessed differently depending on the biases and beliefs of individual researchers.

Philosophical Presuppositions

Prior to engaging with the scientific evidence, it is also important to discuss the main philosophical views that back biological determinism and the opposing view that sexual  orientation is a matter of circumstance and choice. First, hard determinism is the view that all events are philosophically necessary and caused by prior events.[18] Hard determinists deny that free will exists thus orientation is not chosen. However, a different brand of determinism, called soft determinism, asserts that free will is compatible with determinism.[19] Also called hard compatibilism, this second view argues that events necessitate specific human actions and yet the human being is still said to “choose” to act.[20] In opposition to hard determinism and hard compatibilism is libertarian freedom: the view that human beings are agents that act as prime movers and choose independently of external forces, even though they are influenced by them.[21]

One of the leading proponents of biological determinism of sexual orientation is Jacques Balthazart. Determinists like Balthazart argue that there is a direct causal link between “every human action” and all events that led to that action.[22] Thus, homosexual orientation must be the result of a specific set of genes which produce proteins that affect brain structures and hormones, eliciting same-sex feelings and desires. These feelings and desires would by nature be difficult if not impossible to change by personal decision, due to their biological origin.

To the compatibilist, the “choice” to engage in homosexual behavior is the natural outcome of these desires and feelings. The hard determinist argues that biological events such as protein interactions, influence of hormones, and neuronal impulses directly produce homosexual feelings and orientation. The hard compatibilist’s view is similar, however, they argue that some part of the human being does make a choice but that choice is dictated by the biological interactions. One bias that both hard determinists and hard compatibilists are prone to is the association and equation of homosexual behavior to homosexual orientation due to the direct link their philosophy enforces.

The non-determinist view is backed by a libertarian understanding of freedom. In this view, some combination of biological, psychological, societal, and personal factors lead to the development of homosexual feelings and desires. However, at the juncture where the decision to engage in homosexual behavior is made, feelings and desires do not necessarily dictate the behavior because “causal power rests in the agent.”[23] A person therefore bases their choice on feelings, desires, and other inputs which may or may not result in homosexual behavior. Under this view, behavior and orientation are not causally connected; orientation influences but does not cause behavior. Proponents of this view call all animal research on this topic into question because it is impossible to test the feelings and desires of animals, so by necessity, experiments can only investigate outward behavior.

In one sense, the purpose of this paper is to provide evidence for evaluating which of the preceding views is the correct philosophical background for understanding homosexual orientation. This paper presents evidence that biological inputs alone are not enough to create a fully formed sexual orientation. Thus, as a philosophy, biological determinism is an insufficient foundation for the study of sexual orientation. It is possible that hard compatibilism is sufficient, as long as it accounts for the wider range of environmental and societal inputs that affect people’s lives. However, the evidence presented in the final section of this paper demonstrates that people who want to choose a different orientation can have success in doing so. Therefore, some form of libertarian freedom is an equally viable philosophical framework to explain sexual orientation.

Genetic Research

A large portion of research into the biological determination of sexual orientation has been centered on the hypothesis that a gene or group of genes determines the inheritance of the homosexual orientation. Many foundational studies examined the genetic code of subjects who experience homosexual attraction in an attempt to identify shared genes or genetic regions. Though early genetic studies seemed to implicate certain genes in the control of sexual orientation, these were typically filled with flaws and refuted by later studies.

Gay Gene Research

The concept of the existence of a “gay-gene” can be traced back to one article, “A Linkage Between DNA Markers on the X-Chromosome and Male Sexual Orientation” by Dean Hamer, et. al.[24] In a survey of homosexual people, Hamer and team found that homosexuality was isolated to maternal uncles and male cousins. They conducted a sex-linked gene map analysis of homosexual brothers and their mothers (when available). They found a statistically significant linkage in a subtelomeric region of the X chromosome in 33 out of 40 brother pairs who were tested.[25] As a result, Hamer argued that the maternally sex-linked Xq28 locus most likely contains a gene that is involved with sexual orientation.[26]

Hamer’s research study seems promising until the following are considered. First, the 40 sibling pairs were selected “because they had a homosexual brother and no indication of transmission through fathers or to females.”[27] Candidate subjects with homosexual fathers or paternal uncles and cousins were excluded from the study.[28] This type of exclusion severely compromises the results. In addition, heterosexual brothers, maternal uncles, and cousins were not tested. It is therefore entirely possible that the heterosexual members of these families also inherited the Xq28 locus but showed no sign of homosexual orientation. Therefore, this study did not contain an adequate control group to make a definitive declaration on Xq28’s involvement in orientation.

Second, the authors point out that their findings rule out the possibility of a definitive “gay” gene passed on through simple Mendelian inheritance.[29] At best, from this study, one could argue that sexual orientation is akin to something like skin color, which has multiple genes involved in its determination. To say that Xq28 contains the “gay” gene is far from appropriate.

Third, Xq28 is not actually a gene, but a locus containing over eight million base pairs and multiple genes.[30] In light of this, the authors also admit that it would be very difficult to further isolate any specific gene from this region due to issues arising from the small sample size.[31] The study’s small size already teeters dangerously close to being insufficient to make generalized conclusions. In order to further narrow the nucleotide ranges, sample sizes would have to be sought that may not be physically possible.

Fourth, as previously mentioned, Hamer selectively excluded subjects in which a maternal sex-linkage was not already suspected.[32] This leads to two potential problems. First, by limiting their study to the X-linked inheritance, the researchers ruled out the possibility of discovering a pattern of autosomal inheritance. Second, by neglecting to study any heterosexual brothers of the homosexual subjects, the researchers failed to include a proper control group to test the relevance of any loci of significance. If Xq28 had been found in heterosexual brothers, the result would provide evidence against Xq28’s involvement in sex-linked homosexual orientation. Therefore, Hamer was forced to admit from the outset that Xq28 must be at best only one of many possible genetic inputs resulting in a homosexual orientation.[33] Additionally, he conceded that his results indicated that “environmental, experiential, social, and cultural factors” must also contribute to orientation.[34]

Fifth, the authors admit that, like all studies of this nature, “replication and confirmation of [these] results is essential.”[35] Unfortunately for Hamer, this replication and confirmation has not been forthcoming. For example, George Rice’s study of the same locus contained a larger sample size and better controls, and was unable to reproduce Hamer’s results.[36]

Sixth, a fundamental issue of linking complex human behavior to specific genes is that a link does not necessarily imply deterministic control over the behavior.[37] For example, in the case of homosexual orientation, it is within the realm of theoretical possibility that a gene exists that causes a person to have a feminine voice or other kinds of feminine characteristics. If a male had this gene it is entirely possible that he would be treated differently (bullied or outcast) as a result of having this sociologically determined effeminate physical characteristic. This in turn could put him into environmental or social situations that could promote homosexual exploration and lead to the development of a homosexual orientation. In this case, the gene is not deterministic at all, but in the presence of certain sociological or environmental factors, it contributes to exposure to homosexuality and demonstrates higher penetrance into the homosexual community. Removing the cultural factors would remove the gene’s influence on orientation, thus removing any link to homosexuality. Though this situation is not real, it could equally account for all the data that Hamer provides, thus his conclusion is not the only reasonable one.

Seventh, a number of further studies refute Hamer’s findings on the Xq28 locus. Mustanski authored one vital study that attempted to scan the entire human genome for genes that contribute to male sexual orientation.[38] Their study did identify three loci that showed a minimal level of potential co-inheritance which were marked for further study by the authors.[39] Yet, their results were far from conclusively showing any meaningful relationship. On the topic of Xq28 and the possibility of sex linkage, this study agreed with other modern studies in that neither this gene nor sex chromosomes have a significant impact on sexual orientation.[40] In fact, there was not a single gene in the entire genome that passed Lander and Kruglyak’s “criteria for genomewide significance,” ruling out autosomal inheritance as well.[41] The importance of this genome-wide study cannot be understated. That not a single gene in the entire human genome had even moderate determinacy over sexual orientation is a serious strike against any form of biological determination at all, as genes impact hormone levels, enzymes, developmental pathways, and the majority of the human form.[42]

In 2012, Drabant et. al. conducted a study using the 23andMe database, which includes over 180,000 individuals, to determine if any genes in the human genome influence sexual orientation.[43] Their work was ground-breaking in scope as it is the largest genetic study on sexual orientation to date. In their survey of the human genome, the search for genes influencing sexual orientation “did not identify any genetic loci reaching genome-wide significance at p < 5 x 10^-8 among men or women.”[44]

In another study, Hamer himself hypothesized that the Y chromosome, which is responsible for “the conversion of androgens into estrogens … and plays an important role in the sexual differentiation of the brain,” likely determines sexual orientation.[45] He and his co-authors, Michael DuPree and Brian Mustanski, conducted a study in which they brought together a sample of 439 people for single-point and multi-point linkage analyses to look for unique inheritance patterns in the homosexual community.[46] In spite of the large sample size and thorough linkage analysis, they found that there was “no relationship” of the CYP19 gene to orientation at all.[47] Additionally, they confirmed this finding with a follow-up RNA expression study that corroborated these results.[48]

The importance of the CYP19 study goes beyond this single gene. CYP19 is one of the most logical genes to have a connection to sexual orientation. In fact, the researchers cite mouse knockout studies that demonstrate that this gene plays a direct role in sexual behavior and desire levels of mating.[49] The fact that the human equivalent of this gene has virtually no impact on sexual orientation leads to the natural question: If not this then what? Researchers have found it difficult to identify many such candidate genes, and must fall back on less promising candidates as each is ruled out.

All of the major gene studies, including genome-wide studies, turn up empty handed when trying to find direct genetic linkage to orientation. Due to severe methodological flaws, Hamer was unable to demonstrate either sex-linked or autosomal inheritance patterns with regard to sexual orientation. Additionally, one major genome-wide study failed to identify any loci that were strongly or moderately significant in determining sexual orientation. It is important to note that the inability of genome-wide studies to identify significant loci directly impacts the likelihood that studies on hormones and brain structures will produce positive results. Genes regulate both hormones and brain structures, and thus one would expect these regulatory pathways to have been identified in the genetic studies. Having examined studies that focused primarily on genes, it is also important to analyze the body of twin studies on homosexual orientation.

Genetic Twin Studies

Twin studies are the second type of genetic study that has been conducted to investigate the biological influence on sexual orientation. The primary advantages of twin studies are that they allow for the examination of genetically identical people with potentially different lives. If homosexual orientation is genetically inherited, researchers would expect to see a high level of concordance regarding the sexual orientation of monozygotic (MZ) twin brothers, combined with decreasing levels of concordance connecting dizygotic (DZ) twin brothers, and nearly no concordance between adoptive brothers. Though the earliest twin studies showed this pattern, they are fraught with faulty methodology and interpretation. These early studies have been refuted by nearly all modern twin studies.

It is important to note that biological determinists do not theorize that sexual orientation is a Mendelian-level trait; Mendelian-controlled phenotypes are typically controlled by one or very few proteins, which authoritatively enforce them. In twin studies, this type of inheritance would yield 100% concordance rates. Instead, most determinists hold that genetics are a requirement and a primary factor leading to the development of a homosexual orientation in a complex process that can be influenced by other factors.[50] According to this theory, orientation more resembles alcoholism, which has a large genetic component, but environmental factors account for the incomplete concordance between monozygotic twins. A study by Kaij found that monozygotic twins had a pairwise concordance rate of 71% for alcoholism.[51]

One of the earliest studies, conducted in 1952 by Dr. Kallmann, found that in a small population sample, brothers and non-identical twins of homosexual men self-reported homosexuality at a rate of 11.5% when limited to Kinsey Scale ratings of 5 and 6.[52] However, Kallmann found that all of the homosexual men with identical twins he studied reported their twin was also homosexual.[53] Having found 100% concordance in monozygotic twins, Kallmann initially believed that his study demonstrated a strong genetic determination of sexual orientation. However, this and the following study, discussed later, both exhibit many issues that virtually nullify their results.

Another of the most predominant twin studies on the nature of homosexual orientation was conducted by Bailey and Pillard in 1991. As twin registries were not yet available, they used selective advertising to recruit subjects for their study.[54] Their subjects fell into three groups: monozygotic twins, dizygotic twins, and adoptive brothers. These groupings are particularly interesting to compare because MZ twins share all genetics, pre-natal conditions, and social/environmental conditions. In contrast, DZ twins share some genetics and all pre-natal and environmental factors, and adoptive brothers share no genetics or pre-natal conditions but all environmental factors. This allows for the isolation of genetics from social and environmental factors in the attempt to determine the causes of homosexual orientation.

Bailey and Pillard administered three sets of questionnaires to the subjects to determine 1) the subject’s sexual orientation, 2) whether the subjects adhered to normative gender roles in childhood, and 3) the zygosity of the twin pairs.[55] The authors found that, from the group of individuals whom they could confirm the sexual orientation, MZ twins showed a 50% probandwise concordance, DZ twins showed a 24% probandwise concordance, and adoptive brothers showed a 19% probanwise concordance for homosexual orientation.[56]

These results indicate that there is a moderate direct genetic influence on sexual orientation; however, there are several skewing flaws and philosophical errors with this study. First, the method they used to determine zygosity was a questionnaire with a known 5-10% error rate.[57] Factoring that error into the results could change them substantially, especially considering the small sample sizes.

Second, the questionnaires regarding childhood behaviors and interests were administered to both heterosexual and homosexual college students. The study found that heterosexual college subjects scored significantly more gender normative on the scale than the homosexual probands.[58] However, the ranges for these two groups showed a moderate overlap and considerable margin of error, nullifying the statistical and clinical significance of the test. This damages the argument that a genetic cause of sexual orientation would manifest early in the form of non-gender normative behavior. As the authors admit, they found “no evidence that the presence of gender nonconformity increases the likelihood of finding homosexual relatives.”[59] Without continual exhibition throughout life, it is less likely that orientation is genetically determined.

A third flaw arises when the authors reveal their bias by postulating that heterosexual people whom their hypothesis would predict to be homosexuals had simply not yet realized they were homosexual.[60] Additionally, this bias crept into their methodology in that their presentation of the results is skewed toward results that match their hypothesis. For example, the results section reports that 25 out of 50 MZ scored a 0 or 1 on the Kinsey scale and 7 out of 50 scored as bisexual, leaving only 18 with a Kinsey score of 5 or 6, which is strict homosexuality.[61] However, the abstract of the paper lumps these two groups together as “homosexual” claiming a 52% rate of homosexuality among MZ co-twins. Though the authors are not deceptive, it would have been better had they given a robust reason for their groupings.

Fourth, with these studies, and most studies completed prior to 2000, use of the probandwise concordance method led to seriously misleading results.[62] Probandwise concordances are calculated by (2C)/(2C+D), whereas pairwise concordances are calculated by C/(C+D).[63] For example, if five out of ten pairs meet the criteria for concordance, then under pairwise calculations the concordance would be the intuitive 50%, whereas with the probandwise calculation their concordance would be 66%.[64] Authors use probands because it allows them to count both homosexuals as data points in a situation where both twins are homosexual. However, this is a confusion of data: the calculation determines whether, given that one sibling is homosexual, the other sibling is also homosexual. This allows twin pairs in which both brothers are homosexual to be counted twice: to correct for this the twins should be taken as pairs not as individuals. Additionally, the homosexual brother in the case where the twin is heterosexual is not counted anywhere in the probandwise calculation. Thus, there is a substantial discrepancy in how the data are presented due to artificial weighting via statistical methods.

A fifth source of substantial error in early twin studies was “volunteer error.” Many of the researchers used “convenience samples” where subjects were selected from places “conveniently accessible to the researcher.”[65] Sample bias therefore arose as the subjects were recruited specifically to take part in homosexual research. Subjects were pooled from prisons, HIV clinics and hospitals, and homosexual groups.[66] This selective recruitment biased their subject groups toward twins with higher levels of concordance. Later studies eliminated this selection bias by pulling subjects at random from twin registries.

Sixth, early twin studies also break many of the “rules” of twin studies.[67] One of the most egregious examples is the expansion of the definition of “genetic” to refer to the following inclusively: 1) actual shared DNA, 2) pre-natal biological interactions, and 3) the social/physical environment in which the children were reared.[68] Essentially, the majority of these studies ignore the substantial impact that nurture can have on genetic expression. Family history is usually not taken into context regarding mitigating circumstances which could have the effect of encouraging a person toward a homosexual orientation. Thus, true genetic impact has the high potential of being overstated.[69]

Finally, a study like Bailey and Pillard’s is only as strong as other researchers’ ability to reproduce it. Many researchers have attempted to utilize twin studies to replicate this work, but have been unable to produce the same findings. One of the premier modern twin studies was conducted by Bailey, Dunn, and Martin using an Australian twin registry to examine both male and female homosexuals. As a result of the large sample size and twin registry, their research avoided many of the problems of the earlier studies. Their sample size was one of the largest at the time with N = 4,901.[70] Although this study used the probandwise calculation that inflates the percentages, the authors limited themselves to a strict definition of homosexual orientation and found that male MZ twins demonstrated a 20% concordance and female MZ twins demonstrated a 24% concordance.[71] Dizygotic male twins showed a surprising 0% concordance, with female twins showing 10.5%.[72] The importance of this finding cannot be overstated. At the reported percentages of probandwise concordance, genetic and fetal biological factors have been shown to only slightly increase the prevalence of a homosexual orientation over the general population.

The way in which the authors presented their evidence allows it to be misinterpreted as strong evidence for the biological determinism of homosexuality, because they address variation not causation. For example, they stated in their results that 45% of the variation in heritability in male homosexuality can be attributed to genetic causes.[73] This does not mean that homosexuality has a moderate or even strong level of determinism. Rather, it simply means that in the traits that homosexuals express, 45% of the diversity exhibited comes from genes.[74] However, there are several factors regarding this statistic that are cause for concern. First, the confidence interval for the heritability of male homosexuality is .00 to .71.[75] Promoting results of this kind as evidence for anything is somewhat irresponsible and akin to saying one has a 95% confidence Chicago is somewhere in the Western Hemisphere. The statement is true, but it does not add much knowledge about Chicago. Similarly, male homosexuality most likely does have some heritability, but concluding that it has between 0% and 71% really does not add much to the discussion. Additionally, the researchers’ value for the variation in heritability of female homosexuality was only 8%, vastly lower than in males.[76] It is interesting that the reported confidence interval for women was similar to the men: .00 to .67.[77] Either the mechanism for inheritance of homosexuality is significantly different between men and women, or something is skewing the results of this study.

Another issue with how the researchers report their findings is that they claim statistical significance for their results and allow readers to assume that these results are clinically significant.[78] However, as the authors of the study themselves admit, their study “did not provide statistically significant support for the importance of genetic factors” in determining sexual orientation.[79]

One final note on this study is the methodology does not ensure that heritability is measured rather than mere correlation. The authors of a review article note that using these methods, a study of women in the early 1900’s could conclude that earrings are heritable.[80] In reality though, earring use is cultural and only correlated with genetics. Similarly, the childhood gender nonconformity associated with male homosexual orientation could be attributed to family patterns correlated to, but not caused by genetics. Thus, even the assessment of genetic heritability is suspect to cultural bias.[81]

Additionally, other reviewers provide a fresh way of interpreting twin study data, utilizing the full definition of “genetic,” taking into account all twin study factors.[82] When the authors of the aforementioned twin studies reported an 11% concordance, they were saying that “the practical effect of genes, other shared pre-natal biological factors, and a shared home environment, is weak.”[83] Therefore, 89% of the contributing factors to homosexual orientation of the dizygotic twin data is a result of individual responses to chance-oriented environmental, social, or cultural stimuli. In other words, an 11% concordance is not simply a weak concordance, but positive strong evidence for environmental or social factors.

One possible complaint that could be raised against this evidence is that all of these studies were done with twins raised in the same household; however, there is one small study that factored out the issues that come with twins being raised together. In this paper, Eckert et. al. found six MZ twins that were raised apart in which at least one member claimed to be a homosexual.[84] They found that all female twins were discordant for homosexuality, leading the authors to admit that homosexual orientation is most likely an “acquired trait.”[85] There were only two male twin pairs with a homosexual brother and only one of the two was also homosexual. At best, this demonstrates that genetics do not deterministically enforce sexual orientation in men while allowing for some small interaction. A larger sample would be needed to ascertain this definitively.

Using the Minnesota Twin Registry, Scott Hershberger conducted an exemplary twin study to follow-up earlier work by other researchers. His study examined the “genetic effects on sexual orientation for a large sample of both male and female twins.”[86] Unlike earlier reports, he found that “the same set of genes was responsible for sexual orientation in the sexes.”[87] This result contradicts the belief that orientation is a sex-linked trait for men and is induced by a fundamentally different apparatus in women. The study also found that the minor effects that were demonstrated were greater in women than in men, which is another finding counter to prior articles like Hamer’s article on Xq23. Overall, Hershberger makes the significant conclusion that his data demonstrates that environmental effects were “more important in the aggregate than genetic effects for every phenotype.”[88]

Even more recent is Langstrom’s study involving 3,826 twin pairs.[89] His proband results indicated an 18% concordance for male MZ twins and 22% concordance for female MZ twins, confirming the more recent data that indicates a lack of genetic determination in orientation.[90] He also found that genetic factors accounted for .34-.39 of the variance in heritability among men and .18-.19 of the variance in heritability among women. This study also confirmed that individual environmental factors could account for the majority of the variation seen in sexual orientation (.61-.66 for men and .64-.66 for women).[91]

In alignment with Langstrom’s idea that individual-specific environmental factors have the strongest input into sexuality, Bearman and Bruckner also found in their study of adolescents that “the pattern of concordance (similarity across pairs) of same-sex preference for sibling pairs does not suggest genetic influence independent of social context.”[92] In fact, they go on to assert that “less gendered socialization in early childhood and preadolescence shapes same-sex romantic preferences.”[93]

In conclusion, though earlier studies implicated genetic inheritance as the primary driver of sexual orientation, the combination of their methodological flaws and refutations by later studies pointed otherwise. The studies of Kallman, and Bailey and Pillard boasted impressive results; however, low sample size, biased recruitment methods, imbalanced statistical methods, and faulty underlying assumptions about the nature of genetic influence all rendered their studies invalid. The influence of genetics on orientation was further denounced by the studies of Bailey, Dunn and Martin, as well as Hershberger; these studies used larger sample sizes and rigorous control groups and found that environment and social events have the greatest effect in determining sexual orientation. Taken together with the lack of genome evidence as discussed above, it is quite clear that scientific studies have thus far failed to demonstrate a moderate or substantial role of genetics in the determination of sexual orientation.

Hormonal Influence on Sexual Orientation

After genetics, the most likely candidates for controlling sexual orientation are the sex hormones of the neuroendocrine system. Sex hormones, or androgens, such as testosterone and estrogen, are responsible for controlling the formation of primary and secondary sex characteristics, control of sexual cycles, and regulation of sex drive.[94] As such, researchers have spent considerable time in examining whether sex hormones demonstrate any level of control over sexual orientation. There are two predominant theories on how hormones could influence orientation: (1) influence of hormones in the adult and (2) influence of hormones during fetal development.

Adult Sex Hormones

Prior to fetal hormone studies, researchers tested the theory that abnormal adult hormone ratios were the leading cause of homosexual orientation. In line with this theory, hormone adjustment therapy was suggested as a method that would allow a person to switch their sexual orientation.[95] This theory stemmed from previous work in mouse models that strongly linked hormone levels to sexual behavior.[96] It was assumed by researchers, doctors, and practitioners that sexual orientation in humans might also be controlled by the same mechanism.[97] However, practitioners found that adjusting the sex-hormone levels or ratios in adults did not have any effect on the behavior or orientation of the patient. For example, Dr. Rosenzweig reports the hospitalization of a homosexual male who underwent seven different hormone adjustment treatments over a seven-month period, but was unable to detect differences in the behavior or personality of the patient.[98]

Another study looked at testosterone, androstenedione, and cortisol in seven lesbian women and seven heterosexual women of similar age and socioeconomic status.[99] The theory was that the presence of male hormones in the female body is the primary cause of a sexual orientation directed toward other females. Downey et. al. found that there were no significant differences of any kind in hormone levels between the women tested.[100] In fact, the heterosexual and homosexual women “reported quite similar sexual behavior patterns except for the difference of sex partner.”[101]

The results of this study are important for a number of reasons. First, the findings indicate that adult sex hormones do not control sexual orientation. This corroborates Rosenzweig’s and others’ findings that sex hormone therapies are relatively ineffective at helping to curb a person’s homosexual attractions.[102] Second, although studies in rats have previously found that hormone levels play a regulatory role in sexual behavior, this study demonstrated that there is a discontinuity between hormones and orientation in human women.

These studies failed to yield any substantial results, finding that sexual orientation is not controlled through adult hormones. Thus, research in this area has nearly ceased, and few modern studies have been conducted. However, with the increased understanding of developmental biology, researchers began to investigate the effect of fetal sex hormone levels on orientation.

Fetal Sex Hormones

It is hypothesized that “male heterosexuality and female homosexuality result from prenatal exposure to high levels of testicular hormones, while homosexual males and heterosexual females are exposed to lower levels.”[103] This hypothesis is based on the theory that some species of animals develop an initially “female” brain that undergoes masculinization at some point during fetal development as a result of sex hormone ratios.[104] Studies have shown that some animals do exhibit sex differential behavior as a result of exposure to various sex hormones at young developmental stages.[105]  However, one interesting note from studies on hormonal influence of behavior is that “a rigid dichotomy” of male/female brain types “does not actually exist.”[106]

Prior to analyzing research studies, it is important to note that one of the fundamental philosophical problems with the fetal hormone theory is that it conflates behavior with attraction. By the definition of homosexual orientation provided in the introduction of this thesis, homosexual orientation is the pervasive feelings of attraction a person feels toward either males or females. The theory however, was based on the sexual behavior of rats, not the feelings rats have for one another. Sexual behavior focuses on the physical acts and instincts involved therein, whereas orientation focuses on the psychological aspects of sexuality.[107] Thus, there is not scientific reason to expect there to be a connection between hormones and orientation.

A second philosophical issue with the hormone theory is presented by the clear evidence of properly functioning sex hormones in homosexuals, namely the secondary sex characteristics. In attempting to define homosexuality, sociologist Raymond Berger asserts that homosexuality is primarily an issue of the mind and “self-image,” not one’s genitalia and sex characteristics.[108] It seems unlikely that the proposed hormone imbalances could affect psychological sexual orientation, given that they did not change physical sex characteristics in the slightest.

With these philosophical considerations set in place, individual research studies can be analyzed in the context of this framework. The fetal hormone hypothesis rests on a proposed imbalance of hormones.[109] If abnormally low levels of androgens during development did lead to a feminized brain in male homosexuals, one would expect to observe a female response to changes in hormone levels. One way to test this hypothesis is to see whether homosexual men respond to increased estrogen concentrations by exhibiting a luteinizing hormone (LH) spike, as occurs during the female monthly cycle.[110] This line of thinking garnered attention as Dorner published an article demonstrating just such a link in 1975. In his study, he administered estrogens intravenously to a small sample of heterosexual, bisexual, and homosexual men.[111] He found that bisexual men and heterosexual men exhibited only a decrease in LH, whereas the homosexual men exhibited both an initial decrease in LH followed by an LH spike shortly thereafter.[112] This LH spike is in line with the typical female response to estrogens. The authors concluded that this response to estrogens in homosexual men was a result of a feminized brain.[113] They also postulated that the feminization occurred as a result of testosterone deficiency in the fetal male.[114] Additionally, his findings were initially replicated by Gladue in 1984.[115]

However, there were several methodological flaws with Dorner’s study including the assumption that rat hormonal control of sexual behavior was similar to primate/human hormonal control of sexual orientation. This assumption proved unreliable as a 1973 study using rhesus monkeys as test subjects found that increased estrogen concentrations produced LH spikes in healthy males.[116] This demonstrated that LH spikes in adult males is not indicative of imbalanced hormones during the fetal stage.

Additionally, the entire body of evidence was overturned when Gooren demonstrated “that although males and females may have different patterns of LH secretion, this is because they have different levels of hormones in circulation and not because they have differently organized brain[s].”[117] By demonstrating that the LH spike was not controlled by the activity of the brain, Gooren revealed that the prior studies were ineffective in determining whether or not fetal hormones had an impact on orientation. The action of fetal hormones on the brain had no correlation with the adult hormones that controlled the LH spike, and as demonstrated in the previous section, adult hormones do not impact sexual orientation.[118] Gooren, using a larger sample size than earlier studies, found that his results did “not indicate that estrogen response can discriminate between heterosexual and homosexual men.”[119] His reasoning came from the finding that in certain biochemical environments, LH spikes were invoked in men of any sexual persuasion.[120] Gooren concluded his study with a severe caution against any “premature linking” of sexual orientation and sex hormones.[121]

Similarly, Meyer-Bahlburg conducted a study on the effects of prenatal estrogens on women in an attempt to link hormones to orientation.[122] Until 1971, women with high risk pregnancies were prescribed a synthetic estrogen called DES as a preventative treatment.[123] Unfortunately, this drug caused cancer and other issues in female children and so was banned in 1971.[124] The use of DES provides a sample of women who were exposed in utero to a female androgen that did not change primary or secondary sex characteristics.[125] It is significant that the DES-exposed women do not exhibit abnormal physical sex characteristics.[126] Therefore, if orientation was correlated with DES exposure, the researchers could be certain that fetal hormones were the cause.[127]

The study looked at a number of behaviors, emotions, and decisions among DES-exposed women and found that when taken together there was a significant difference between DES and control women.[128] However, when factors regarding sexual orientation alone were examined, the researchers demonstrated that pre-natal DES had a minimal, non-significant effect.[129]

In conclusion, the issue is not whether or not hormones have any effect whatsoever on orientation, but whether or not there is a strong or even moderate determinism of prenatal sex hormones on orientation. The studies mentioned all fail to demonstrate either type of correlation. In fact, the authors of one study expressly state in their conclusion that a single biological factor cannot possibly fully determine sexual orientation, which is a complex behavior.[130] Additionally, they noted that most of the DES-exposed patients were heterosexual.[131]

Sex Hormone Disease Studies

Another way that researchers attempt to demonstrate hormonal influence over sexual orientation is through the study of people with diseases that affect sex hormone production in the early stages of life. One such disease is Congenital Adrenal Hyperplasia (CAH) in which the developing fetus has abnormally large adrenal glands which over-produce androgens.[132] The overproduction of androgens leads to “ambiguous genitalia” in females and early sexual secondary sex differentiation in both males and females.[133] Given that the fetal hormone imbalance is strong enough in these conditions to cause opposite sex physical characteristics, these cases present an opportunity to study the effect of fetal hormones on sexual orientation.

Dittmann et. al. conducted a study of 34 females with CAH using surveys and interviews that asked a variety of questions about each individual’s sexual behavior, sexual experience, and sexual orientation.[134] They found that the type and severity of CAH was correlated with different sexual behavior.[135] The authors hypothesized that this was not due to the fetal hormones however, but the fact that women with CAH felt less comfortable with their bodies, because they had more masculine features, and malformations of their genitalia made sex with men more difficult and uncomfortable.[136] They concluded that “prenatal hormone effects do not determine the sexual orientation of an individual” even though they may “play a significant predispositional role” along with a wide variety of other biological, environmental and social factors.[137]

This is an important result because it points out a potential pathway for the development of sexual orientation. This article lends support to the idea that sexual orientation forms based on a person’s reactions to their biology and environment. For example, the biological drive for sexual interaction is based in part on sex hormone cycles in the body. For a CAH person who has difficulty interacting with men, it is conceivable that such a person might turn to more fulfilling sexual relations with another female, which could foster the development of a homosexual orientation. However, it is important to note that even with these hormonal and morphological influences “a majority of patients develop a heterosexual orientation.”[138]

A second disease that is useful in examining the effects of abnormal fetal response to sex hormones is Androgen Insensitivity Syndrome (AIS). In this case, the proportions of hormones are not the issue; instead, genetically male people are deficient in a protein receptor and therefore testosterone cannot bind and exert its effects.[139] This disease is especially useful in factoring out the effect of genetics with relationship to hormones. Genetic males with AIS have fully female bodies and are typically attracted to males.[140] This disease potentially lends evidence for a hormonal basis for orientation, but it is nearly impossible to factor out the confounding variables, such as the effect that having a female body and being raised as female would have on the psychology of an individual. Interestingly, this group of female-presenting males offer a compelling case against any genetic basis for sexual orientation. Aono et. al. conducted a study in which AIS patients were exposed to estrogen in order to initiate a LH spike.[141] The researchers found that it was impossible to initiate a LH spike in these subjects, leading them to believe that “insensitivity of the hypothalamus to androgen in TFS patients [does] not affect the sex differentiation of the hypothalamus.”[142] In other words, fetal hormones seem to have no feminizing effect on the brain, thus calling the fetal hormone hypothesis into doubt. Additionally, if homosexual orientation was controlled by genetics, unless the specific receptor involved in AIS happened to be the genetic basis for homosexuality, one would expect ~98% of AIS males to be attracted to women, as dictated by their genetics. That AIS males are overwhelmingly attracted to males instead strongly supports the social/environmental hypothesis of sexual orientation.[143]

A third disease that could shed some light on this topic is 5-Alpha Reductase Deficiency. People with this disease are genetic males that, at birth, present with ambiguous genitalia more in line with females. At puberty, they exhibit strong male primary and secondary sex characteristics.[144] Imperato-McGinley conducted a study on a small sample of people in the Dominican Republic who were suffering from this disease. Eighteen of the children in her study with 5ARD were unambiguously raised as having a female gender until puberty.[145] Imperato-McGinley found that all of her subjects had a sexual orientation directed toward females and all but one had completely switched their gender to male upon puberty.[146] This seems to indicate that hormones might have an impact on orientation. However, there are cultural issues that prevent such a small and culturally-dependent study from providing definitive evidence. First, there is extreme cultural pressure in the Dominican Republic toward being male. The children involved “may have been pressured to behave as males in puberty no matter what their sexual preferences might have been.”[147] Second, it is again difficult to separate their upbringing from their hormonal influence. Thus, more studies would be needed to demonstrate hormonal interaction in their sexual orientation.

In conclusion, neither adult nor fetal sex hormones have been satisfactorily shown to exert a moderate or strong effect on sexual orientation. While adult hormones have been completely ruled out, fetal hormones may impact orientation in two ways. First, fetal hormones may affect orientation indirectly through the presentation of sex characteristics that incur a socio-environmental response that pressure the individual into a homosexual orientation. Second, as indicated by disease studies, hormones may have a minor direct role. However, further and larger studies need to be conducted in order to make any determination. Finally, it should be noted that even if sex hormones are demonstrated to influence orientation, “the vast majority of homosexuals do not have a history of atypical endocrinological development.”[148] At this point, it is safe to say that hormones are at best indirectly involved in determining sexual orientation.

Brain Structure and Sexual Orientation

The third area of research into the biological origin of sexual orientation is concerned with differential brain structures between men and women. It is hypothesized that brain structures generally associated with sexual behavior will vary according to sexual orientation.[149] The assumption is that a homosexual male’s brain will more closely resemble a female’s brain. Given that no evidence of genetic or hormonal control of sexual orientation has yet been found, it seems unlikely that investigation into the development of homosexual brain structures that are controlled by genetics and hormones will yield positive results. However, there is a third mechanism by which a homosexual male’s brain might begin to resemble a female’s brain. The brain can be very flexible: a brain cancer survivor can regain lost function after surgery when neighboring brain structures expand to take on unaccustomed functions. Similarly, it is possible that a homosexual’s brain might undergo change due to repeated behaviors in light of environmental and social stimuli. Therefore, each research study must be analyzed in the context of understanding whether the differential brain structures recorded have their origin in genetics or environmental stimuli.

Interstitial Nucleus of the Anterior Hypothalamus 3 (INAH 3)

One of the most cited articles on dimorphic brain structures was conducted by researcher Simon LeVay in his paper on the hypothalamus’s potential role in homosexuality. LeVay argued that the third (of four) interstitial nucleus of the anterior hypothalamus (INAH 3) was on average two times larger for heterosexual men than for homosexual men or heterosexual women.[150] This would seem to indicate that it is dimorphic with sexual orientation. However, there are serious concerns with this study that limit the conclusions one can draw regarding the question of biology and sexual orientation.

First, there are methodological flaws in how the size of INAH 3 was determined. None of the four INAH’s have well demarcated boundaries and the researchers did not attempt to measure cell density recordings or cell counts due to the difficulty of working with such an ill-defined region.[151] Though they did conduct their sampling in a blind test environment, the lack of specific data surrounding these small brain areas could lead to a substantial amount of error in their recordings.[152] This error could potentially refute all of their findings.

Second, the researchers mention but pass over the importance of the fact that there were exceptions to their study. They did find heterosexual men with small INAH 3s and homosexual men with larger INAH 3s.[153] This could simply be an indicator of the complexity of the biology of homosexual orientation, but more likely it is reflective of INAH 3’s inability to directly affect orientation. If there is any interaction, it is more likely that differences in INAH 3 cause unrelated phenotypes to be expressed, which could trigger cultural or social pressures leading to a homosexual orientation. This hypothesis would explain why the size of INAH 3 is not expressly deterministic.

Third, LeVay acknowledged a serious issue resulting from the use of cadavers as research subjects: the inability to definitively determine sexual orientation.[154] LeVay notes that two of the subjects who died of AIDS complications had denied homosexuality in life; additionally, any subjects for whom no information on sexual orientation was available were presumed to be heterosexual.[155] Thus, LeVay did not obtain adequate information on the research subjects and many subjects of his already small sample size ought to have been excluded from the study. Unfortunately, this sample size is too small to adequately determine correlation.

Fourth, the potential impact of AIDS on the homosexual male’s brain structure cannot be ignored. LeVay mentions this issue but dismisses it saying, (i) “the size difference in INAH 3 was apparent even when comparing the homosexual men with heterosexual AIDS patients, (ii) there was no effect of AIDS on the volumes of the three other nuclei examined (INAH 1, 2, and 4), and (iii) in the entire sample of AIDS patients there was no correlation between the volume of INAH 3 and the length of survival from the time of diagnosis.”[156] However, the lack of a control group eliminates his first point since no true comparison can be made. LeVay’s second point is also suspect because if his research is correct, there would be a substantial differentiating factor between INAH 1, 2, 4 and INAH 3. This difference could result in a different susceptibility to the AIDS virus. Finally, AIDS is known to manifest with widely different latency periods among patients, and medications can dramatically affect its ability to ravage the immune system. Combined with the fact that AIDS causes a general increase in susceptibility to diseases of all kinds, it does not make sense to talk about a correlation between INAH 3 size and AIDS diagnosis time. This type of correlation would not be easy to determine, even if it did exist.

Fifth, a general issue with studies of this kind is that the attempt to link genetics with complex, will-governed behavior is highly suspect.[157] LeVay raises the issue without recognizing it when he makes the comparison of mice to humans. In mice, destruction of this area does indeed reduce male-typical sexual behavior, but it does not induce homosexual behavior.[158] However, mice operate primarily on instinct whereas humans make behavior-level decisions based on a combination of biological, hormonal, cultural, social, environmental, and mental factors. Thus, these behaviors are not really referring to orientation in mice and are not directly comparable.[159]

In conclusion, LeVay’s research has too many methodological flaws to make any solid claims regarding the relationship of INAH 3 and sexual orientation. He used a population sample that was too small, obtained an ill-defined medical and social history of subjects, and he did not use accurate nor adequate measurement techniques to determine the size of INAH 3. Thus, more research would need to be done on this brain structure before making any conclusions.

Anterior Commissure

A second brain structure implicated in determining sexual orientation is the anterior commissure, which connects the two hemispheres of the brain. In 1992, Laura Allen and Roger Gorski produced a paper that claimed to demonstrate a statistically significant size difference in the anterior commissure between homosexual and heterosexual males, and heterosexual females. In their study, they found that, on average “the midsagittal plane of the anterior commissure in homosexual men was 18% larger than in heterosexual women and 34% larger than in heterosexual men.”[160] This level of differentiation in a sexually dimorphic area of the brain could provide evidence of a biological basis of sexual orientation. However, there are substantial issues with the study that cast the results into doubt.

First, the authors specifically selected out the brains of people who were known to be bisexual.[161] This presents an interesting issue in that one way of viewing bisexuality is the simultaneous presence of both a heterosexual and homosexual orientation. The recognition of this group of people makes biological determination of sexual orientation difficult since most traits examined are binary (larger than or smaller than). Thus, expressing a behavior that would require the full expression of both binary states would lessen the reality of the studied trait’s involvement in determining sexual orientation.

Second, the authors’ use of average structure size is somewhat misleading. The overwhelming majority of homosexual male, heterosexual male, and heterosexual female anterior commissures fall within the same basic range and in fact would seem to exhibit no dimorphism at all.[162] The researchers would need a substantially larger sample size and a greater deviation between each grouping for any utilization of the average to be of scientific use. They partially admit this in the article, but then argue that a smaller sample size affirmed their results.[163] Unfortunately, smaller sample sizes do not help their case.

Third, the authors made a curious adjustment to the data. They noted that “AC size did not correlate with brain weight,” but they adjusted their measurements by brain weight anyway because female brains weighed less than male brains.[164] This type of transformation would artificially inflate any AC size differentiation between male and female brains in a way that is not necessarily justified. This structure, along with the corpus callosum, connects the two hemispheres of the brain together. Therefore, male and female brains can have different weights without dimorphism in the size of the anterior commissure. It is akin to two roads with differing numbers of houses built on them. The road, like the AC, would not necessarily need to change much even with increased “housing” or neurons on each side.

Fourth, the authors cite differences such as handedness, visual-spatial abilities, and verbal scores as example of differences between men and women that might be affected by the AC; however, none of those are complex behaviors like sexual orientation.[165] Thus, the comparison is invalid.

Finally, a study conducted in 2002 by Mitchell S. Lasco also examined the anterior commissure using a sample of cadavers with “no known psychiatric, endocrinological or neurodegenerative disorders.”[166] This study used advanced imaging techniques that allowed them to ascertain size differences with a high degree of accuracy.[167] The authors concluded by failing “to detect any variation in the size of the [anterior commissure] with either sex or sexual orientation.”[168] Thus, the link between the AC and orientation is not necessarily as clear cut as Allen and Gorski would like to believe.[169]

Suprachiasmatic Nucleus

The suprachiasmatic nucleus (SCN) has also been implicated in determining sexual orientation. This brain structure is known to regulate biological clocks such as various reproductive cycles.[170] Swaab and Hofman reported that on average homosexual males had a SCN that was “1.73 times larger” than heterosexual males and that “contained 2.09 times as many cells.”[171] The authors did note that the SCN is not actually sexually dimorphic, so it is unclear exactly how a larger SCN would contribute to sexual orientation. One thought the authors offer is that neuronal apoptosis does not occur in homosexual men and so their childhood numbers of SCN neurons remain into adulthood. The retention of these neurons could cause a hormone imbalance, similar to women who suffer from Prader-Willi syndrome.[172] Finally, the authors argued that their paper did not support the idea that “homosexual men have a female brain.”[173] This refutes a number of earlier articles, including the INAH 3 study.

In conclusion, though some brain structures may potentially have an impact on sexual orientation, there is no available research to demonstrate either a strong or moderate correlation. Either the studies use suspect statistical methodologies, or their results are inconclusive. Additionally, it is important to remember that environment and behavior can affect the brain as well as genetics and hormones.

Sexual Orientation and Psychological Therapy

Finally, any evidence that sexual orientation can change would also contribute to a non-biological understanding of sexual orientation. In the example given in the introduction, Mr. Smid must decide if homosexuality is biologically “normative” before considering whether or not to embrace his homosexual desires. However, in that assessment there is a hidden confounding variable. Biological determinism and the mutability of sexual orientation are not by necessity overlapping questions. The American Psychiatric Association assumes that orientation is biologically determined in the same way as eye color, and that sexual orientation is impossible, or at best extremely difficult or potentially damaging to change.[174] However, the opposite is not necessarily true. It is entirely possible that social and environmental factors, rather than biological factors, act on a young child to irrevocably cause the development of a homosexual orientation that proves extremely resistant to change. It is also equally plausible that sexual orientation is fluid and that by changing one’s social and environmental situation, orientation can be adjusted. The scope of this paper is not to judge whether sexual orientation is mutable. However, given that the results of this paper indicate that biology does not authoritatively determine orientation, the door remains open to the possibility that sexual orientation is changeable.

In their book, Ex Gays: A Longitudinal Study of Religiously Mediated Change in Sexual Orientation, Jones and Yarhouse conducted careful research on the possibility that sexual orientation can be changed.[175] First, they present a thorough, historical literature review which contains 29 articles claiming that 696 individuals in total had either experienced a positive outcome in their attempt to treat their homosexuality or were experiencing some level of progress in the treatment.[176] These initial findings encouraged Jones and Yarhouse to conduct a study that attempted to curtail many of the methodological pitfalls that hinder orientation therapy studies.[177] It is important to note that none of their results indicate that changing one’s sexual orientation is an easy process, or that a “high percentage” of people have been able to make the change.[178] Additionally, they comment that no research has shown that it is possible for everyone in every situation to change their orientation.[179]

The Jones and Yarhouse study is multifaceted and extensive. In one branch of the study, they followed 73 subjects, after sample erosion, who were undergoing therapy to either change their sexual orientation or trying to remain chaste in a homosexual identity.[180] Throughout the course of the subjects’ treatments, those who experienced a lessened homosexual orientation “were consistently in the large effect size range,” while those who experienced a developing heterosexual orientation “were consistently in the medium to small effect size range.”[181] It is interesting to note that the greatest changes were consistently found in the subpopulation that qualified as “Truly Gay,” meaning that they met a “rigorous standard” that confirmed they were not simply entertaining the idea that they might be gay.[182]

Qualitatively, Jones and Yarhouse found that 15% of their subjects experienced success in the form of complete conversion from homosexuality to heterosexuality, 23% experienced success in the form of chastity, and 29% experienced positive change but not complete success.[183] Only 27% experienced no change or a negative change.[184] These results, combined with the quantitative data, indicate that while it is impossible to say that everyone can change their orientation or that change can be achieved easily, it is difficult to sustain the idea that orientation is always immutable (unlike eye color or skin color).

One of the more well-rounded critiques of Jones and Yarhouse comes from Patrick Chapman, a biological anthropologist and author of Thou Shalt Not Love. First, he raises the point that 41 of the individuals in the study were in a sexual orientation change program at the time of their recruitment to the study.[185] Thus, the amount of change that they experienced through the program was not measured by a comparison of a true initial self-report to a final self-report. Instead, the authors had to rely on retrospection for those subjects. As the reviewer states, this could bias the results. Though it is possible that the results were biased, Jones and Yarhouse never claim that their study is the definitive work, requiring no further analysis. Additionally, Jones commented in a follow up article that although 41 individuals had already started the process of therapy, they were near the beginning of the process so the retrospective period was the “immediate past.”[186] At most, the reviewer’s comment is a good point that should be accounted for in further analysis.

Additionally, the reviewer raises the issue that multiple testimonies from the individuals in the study reported negative and potentially harmful effects of going through therapy. He charges Jones and Yarhouse with “ignoring the statements” of these participants in their conclusion that homosexual therapy is not harmful.[187] The reviewer also points out that multiple people have committed suicide after not having been able to change their orientation. He ends his critique asking, how many deaths does it take to say something is harmful? Though it seems like this is a substantial critique, the ultimate cause of those suicides is unknown. Was it the inability to undergo orientation change? Or was it the co-morbidity with depression that pushed someone to commit suicide? Jones and Yarhouse carefully designed their study to isolate orientation therapy from all other factors and therefore their assertion that therapy has a no-to-low risk of causing harm is warranted.[188] Thus, despite objections, Jones and Yarhouse’s study is good evidence for the mutability of sexual orientation and concomitantly provides evidence that strict biological determinism is deficient in explaining the origin and maintenance of sexual orientation.

Conclusion

The scientific evidence concerning the genetic, hormonal, structural, and immutable determinism of sexual orientation shows that biological factors do not strongly or moderately enforce a homosexual orientation. First, genetic and twin studies demonstrate that no single gene or group of genes deterministically sets a person’s sexual orientation. Second, though some hormonal diseases may impact sexual orientation, no all-inclusive theory has been able to strongly or moderately connect a homosexual orientation to fetal hormone imbalances. Third, though some research has implicated dimorphic brain structures in determining sexual orientation, the evidence is inconclusive at best, and often countered by later studies. Fourth, Yarhouse’s longitudinal study indicates that orientation is, to some degree and for some people, mutable and thus not entirely under biological control.

These results have far reaching implications for the church, legal, and therapeutic fields. To the person who is struggling with a homosexual orientation and wants to change, these results may be encouraging, and it is at least feasible to think that with different environmental and social factors, one could work on changing one’s orientation or gaining a degree of celibacy. Additionally, these findings give the church more room to take a stance against the full acceptance of homosexuality as a normative and acceptable behavior. Given the lack of evidence that the homosexual orientation is wholly deterministic, the church would be justified in conducting research on methods of counseling that might prove helpful, rather than simply giving up hope for those who desire to be free of a homosexual orientation. Finally, current research demonstrates that homosexual orientation is not the same as skin color, race, or other genetic differentiators (which are immutable) and thus should not be grouped in with them concerning the equal protection clause of the constitution. In conclusion, modern research is increasingly showing that homosexual orientation is a complex phenomenon that is not moderately or strongly determined by biology, but rather the consequence of a mixture of biological, social, environmental, and personal influences.

[1] Bob Davies and Lela Gilbert, Portraits of Freedom: 14 People Who Came Out of Homosexuality, (Downers Grove, IL: InterVarsity Press, 2001), 132.

[2] Bob Davies and Lela Gilbert, Portraits of Freedom: 14 People Who Came Out of Homosexuality, 130.

[3] Jacques Balthazart, The Biology of Homosexuality, (New York: Oxford University Press, 2012), ix.

[4] American Psychiatric Association, “Position Statement on Psychiatric Treatment and Sexual Orientation, 2000,” https://www.camft.org/ias/images/PDFs/SOCE/APA_Position_Statement.pdf (accessed March 4, 2017).

[5] Peter Sprigg and Timothy Dailey, ed. “Getting it Straight: ‘What Causes Homosexuality?’” What the Research Shows about Homosexuality, (Washington, DC: Family Research Council, 2004), 29-34.

[6] Balthazart, The Biology of Homosexuality, 4.

[7] Raymond Berger, “What is a Homosexual?: A Definitional Model,” Social Work 28, no. 2 (March-April 1983): 133.

[8] Ibid., 135.

[9] Mark A. Yarhouse and Lori A. Burkett, Sexual Identity: A Guide to Living in the Time Between the Times, (Lanham, MD: University Press of America, Inc., 2003), 5.

[10] Balthazart, The Biology of Homosexuality, 4-5.

[11] Davies and Gilbert, Portraits of Freedom: 14 People Who Came Out of Homosexuality, 25, 134, 155-156.

[12] Balthazart, The Biology of Homosexuality, 101, 118.

[13] Stanton L. Jones and Mark A. Yarhouse, Homosexuality: The Use of Scientific Research in the Church’s Moral Debate, (Downer’s Grove, IL: InterVarsity Press, 2000), 527-591, Kindle.

[14] Balthazart, The Biology of Homosexuality, 47-60.

[15] Simon LeVay, “A Difference in Hypothalamic Structure Between Heterosexual and Homosexual Men,” Science 253.5023 (August 1991): 1034+, emphasis mine.

[16] The Kinsey Institute, Indiana University. “The Kinsey Scale.” https://kinseyinstitute.org/research/publications/kinsey-scale.php (accessed March 15, 2017).

[17] Lawrence S. Mayer, M.B., M.S., Ph.D. and Paul R. McHugh, M.D., “Sexuality and Gender: Findings from the Biological, Psychological and Social Sciences” New Atlantis: A Journal of Technology and Society, (Fall 2016): 24.

[18] J. P. Moreland and William Lane Craig, Philosophical Foundations for a Christian Worldview, (Downer’s Grove, IL: IVP Academic, 2003), 268.

[19] Ibid.

[20] Ibid., 269.

[21] Ibid., 270.

[22] Ibid., 269.

[23] Ibid., 270.

[24] Dean Hamer, Stella Hu, Victoria A. Magnuson, Nan Hu, and Angela M. L. Pattatucci, “A Linkage Between DNA Markers on the X Chromosome and Male Sexual Orientation,” Science 261.5119 (July 16, 1993): 321+, Academic OneFile, http://go.galegroup.com/ps/i.do?p=AONE&sw=w&u=biola_main&v=2.1&it=r&id=GALE%7CA14360599&asid=9723c28a467466f08c9247c39fbe8a3b (accessed March 18, 2017).

[25] Ibid., 321+.

[26] Ibid., 321+.

[27] Ibid., 321+.

[28] Ibid., 321+.

[29] Ibid., 321+.

[30] A. De Sario, E. M. Geigl, G. Palmieri, M. D’Urso, and G. Bernardi, “A Compositional Map of Human Chromosome Band Xq28,” Proceedings of the National Academy of Sciences U.S.A. 93, no. 3 (Feb 6, 1996): 1298.

[31] Hamer, et. al., “A Linkage Between DNA Markers on the X Chromosome and Male Sexual Orientation,” 321+.

[32] Ibid., 321+.

[33] Ibid., 321+.

[34] Ibid., 321+.

[35] Ibid., 321+.

[36] George Rice, Carol Anderson, Neil Risch, and George Ebers, “Male Homosexuality: Absence of Linkage to Microsatellite Markers at Xq28,” Science 284.5414 (April 23, 1999): 665.

[37] W. Byne and B. Parsons, “Biology and Human Sexual Orientation,” Harvard Mental Health Letter 10, no. 8 (1994): 5-7.

[38] Brian S. Mustanski, Michael G. DuPree, Caroline M. Nievergelt, Sven Bocklandt, Nicholas J. Schork, and Dean H. Hamer, “A Genomewide Scan of Male Sexual Orientation,” Human Genetics 116 (January 12, 2005): 272.

[39] Ibid., 275.

[40] Ibid., 273.

[41] E. Lander and L. Kruglyak, “Genetic Dissection of Complex Traits:

Guidelines for Interpreting and Reporting Linkage Results,” Natural Genetics 11 (1995): 241–247.

[42] Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walter, Molecular Biology of the Cell, 4th ed., (New York, NY: Garland Science, 2002), 27.

[43] E. M. Drabant, A. K. Kiefer, N. Eriksson, J. L. Mountain, U Francke, J. Y. Tung, D. A. Hinds, and C. B. Do, “Genome Wide Association Study of Sexual Orientation in a Large Web-Based Cohort,” (Mountain View, CA: 23andME, 2012).

[44] Ibid.

[45] Michael Dupree, Brian Mustanski, Sven Bocklandt, Caroline Nievergelt, and Dean Hamer, “A Candidate Gene Study of CYP19 (Aromatase) and Male Sexual Orientation,” Behavior Genetics 34, no. 3 (May, 2004): 243.

[46] Ibid., 245-246.

[47] Ibid., 248.

[48] Ibid., 247-248.

[49] Ibid., 244.

[50] Boris Tabakoff and Paula L. Hoffman, “Genetics and Biological Markers of Risk for Alcoholism,” Public Health Reports (1974-) 103, no. 6 (Nov. – Dec., 1988): 690, 692.

[51] L. Kaij, Alcoholism In Twins: Studies on the Etiology and Sequelae of Abuse of Alcohol, (Stockholm, Sweden: Winkell Publishers, 1960), as cited in Boris Tabakoff and Paula L. Hoffman, “Genetics and Biological Markers of Risk for Alcoholism,” 691.

[52] Franz J. Kallmann, “Twin and Sibship Study of Overt Male Homosexuality,” American Journal of Human Genetics 4, no. 2 (June, 1952): 143.

[53] Ibid., 140.

[54] J. Michael Bailey and Richard C. Pillard, “A Genetic Study of Male Sexual Orientation,” Archives of General Psychiatry 48 (December 1991): 1090.

[55] Ibid., 1092.

[56] Ibid., 1092.

[57] Ibid., 1091.

[58] Ibid., 1094.

[59] Ibid., 1093.

[60] Ibid., 1092.

[61] Ibid., 1092.

[62] Neil Whitehead and Briar Whitehead, My Genes Made Me Do It!: A Scientific Look at Sexual Orientation, (Lafayette, LA: Huntington House Publishers, 1999), 178.

[63] Gregory Carey, “Twin Concordance Rates,” (Boulder, CO: Department of Psychology and Neuroscience at the University of Colorado Boulder, 2000): 1-2, http://psych.colorado.edu/~carey/hgss/hgssadvanced/TwinConcordance.pdf (accessed on March 18, 2017).

[64] Jones and Yarhouse, Ex Gays: A Longitudinal Study of Religiously Mediated Change in Sexual Orientation, 1458, Kindle.

[65] Lawrence S. Mayer and Paul R. McHugh, “Sexuality and Gender: Findings from the Biological, Psychological, and Social Sciences,” The New Atlantis: A Journal of Technology and Society,” (Fall 2016): 27.

[66] J. Michael Bailey, Michael P. Dunne, and Nicholas G. Martin, “Genetic and Environmental Influences on Sexual Orientation and Its Correlates in an Australian Twin Sample” Journal of Personalilty and Social Psychology 78, no. 3 (2000): 525.

[67] Neil Whitehead and Briar Whitehead, My Genes Made Me Do It!: A Scientific Look at Sexual Orientation, 191-192.

[68] Ibid., 174.

[69] Ibid., 193.

[70] Bailey, Dunne, and Martin, “Genetic and Environmental Influences on Sexual Orientation and Its Correlates in an Australian Twin Sample,” 526.

[71] Ibid., 530.

[72] Ibid.

[73] Bailey, “Genetic and Environmental Influences on Sexual Orientation and Its Correlates in an Australian Twin Sample,” 531.

[74] Mayer and McHugh, “Sexuality and Gender: Findings from the Biological, Psychological, and Social Sciences,” 27.

[75] Bailey, “Genetic and Environmental Influences on Sexual Orientation and Its Correlates in an Australian Twin Sample,” 531.

[76] Ibid.

[77] Ibid.

[78] Jones and Yarhouse, Ex Gays: A Longitudinal Study of Religiously Mediated Change in Sexual Orientation, 3058, Kindle.; Mayer and McHugh, “Sexuality and Gender: Findings from the Biological, Psychological, and Social Sciences,” 27.

[79] Bailey, “Genetic and Environmental Influences on Sexual Orientation and Its Correlates in an Australian Twin Sample,” 534.

[80] Mayer and McHugh, “Sexuality and Gender: Findings from the Biological, Psychological, and Social Sciences,” 28.

[81] Ibid.

[82] Whitehead and Whitehead, My Genes Made Me Do It!: A Scientific Look at Sexual Orientation, 170.

[83] Ibid., 174.

[84] Elke D. Eckert, Thomas J. Bouchard, Joseph Bohlen, and Leonard L. Heston, “Homosexuality in Monozygotic Twins Raised Apart,” British Journal of Psychiatry 148 (1986): 421-422.

[85] Ibid., 421.

[86] Scott L. Hershberger, “A Twin Registry of Male and Female Sexual Orientation,” The Journal of Sex Research 34, no. 2 (1997): 213.

[87] Ibid., 220.

[88] Ibid., 221.

[89] Niklas Langstrom, Qazi Rahman, Eva Carlstrom, and Paul Lichtenstein, “Genetic and Environmental Effects on Same-sex Sexual Behavior: A Population Study of Twins in Sweden,” Archives of Sexual Behavior 39 (2010): 75.

[90] Ibid., 77.

[91] Ibid., 75.

[92] Peter S. Bearman and Hannah Bruckner, “Opposite-Sex Twins and Same-Sex Attraction,” American Journal of Sociology 107, no. 5 (March 2002): 1179, 1199.

[93] Ibid., 1181.

[94] Elaine N. Marieb and Katja Hoehn, Human Anatomy and Physiology, 7th ed., (San Francisco, CA: Pearson Benjamin Cummings, 2007), 630.

[95] Saul Rozenzweig and R. G. Hoskins, “A Note on the Ineffectualness of Sex-Hormone Medication in a Case of Pronounced Homosexuality,” Psychosomatic Medicine 3, no. 1 (1941): 87.

[96] Balthazart, The Biology of Homosexuality, (New York: Oxford University Press, 2012), 48-56.

[97] Saul Rozenzweig and R. G. Hoskins, “A Note on the Ineffectualness of Sex-Hormone Medication in a Case of Pronounced Homosexuality,” Psychosomatic Medicine, 87.

[98] Ibid., 87-89.

[99] Jennifer Downey, Anke A. Ehrhardt, Mindy Shiffman, Inge Dyrenfurth, and J. Becker, “Sex Hormones in Lesbian and Heterosexual Women,” Hormones and Behavior 21 (1987): 347, 352-353.

[100] Ibid., 355.

[101] Ibid., 354.

[102] Jacques Balthazart, The Biology of Homosexuality, (New York: Oxford University Press, 2012), 102.

[103] William Byne and Bruce Parsons, “Human Sexual Orientation: The Biologic Theories Reappraised,” Archives of General Psychiatry 50 (March 1993): 231.

[104] Balthazart, The Biology of Homosexuality, 52, 55-56.

[105] Meyer-Bahlburg HFL, “Sex Hormones and male homosexuality in comparative perspective,” Archive of Sexual Behavior 6 (1977): 315.

[106] William Byne and Bruce Parsons, “Human Sexual Orientation: The Biologic Theories Reappraised,” Archives of General Psychiatry, 231.

[107] Karori Mbugua, “Reasons to Suggest that the Endocrine Research on Sexual Preference is a Degenerating Research Program,” History and Philosophy of the Life Sciences 28, no. 3 (2006): 344.

[108] Raymond M Berger, “What is a Homosexual? A Definitional Model,” Social Work 28, no. 2 (March-April 1983): 133.

[109] Balthazart, The Biology of Homosexuality, 102.

[110] Gunter Dorner, Wolfgang Rohde, Fritz Stahl, Lothar Krell, and Wolf-Gunther Masius, “A Neuroendocrine Predisposition for Homosexuality in Men,” Archives of Sexual Behavior 4, no. 1 (1975): 1-3.

[111] Ibid., 3.

[112] Ibid., 4-5.

[113] Ibid., 7.

[114] Ibid., 7.

[115] B.A. Gladue, R. Green, R.E. Hellman, “Neuroendocrine Response to Estrogen and Sexual Orientation,” Science 225, no. 4669 (September 28, 1984): 1496.

[116] F.J. Karsch., D.J. Dierschke, E.  Knobil, ‘Sexual Differentiation of Pituitary Function: Apparent Differences between Primates and Rodents’, Science 179 (1973): 484-486.

[117] Mbugua, “Reasons to Suggest that the Endocrine Research on Sexual Preference is a Degenerating Research Program,” History and Philosophy of the Life Sciences, 348.

[118] Ibid., 348-349.

[119] Louis Gooren, “The Neuroendocrine Response of Luteinizing Hormone to Estrogen Administration in Heterosexual, Homosexual, and Transsexual Subjects,” Journal of Clinical Endocrinology and Metabolism 63 (1986): 587.

[120] Ibid., 588.

[121] Ibid.

[122] Heino F. L. Meyer-Bahlburg, Anke A. Ehrhardt, Laura R. Rosen, and Rhoda S. Gruen, Norma P. Veridiano, Felix H. Vann, and Herbert F. Neuwalder “Prenatal Estrogens and the Development of Homosexual Orientation,” Developmental Psychology 31, no. 1 (1995): 12-13.

[123] Ibid., 14.

[124] Ibid., 14.

[125] Ibid., 14.

[126] Ibid., 14.

[127] Ibid., 14.

[128] Ibid., 16, 18.

[129] Ibid., 17.

[130] Ibid., 20.

[131] Ibid.

[132] May Clinic, “Congenital Adrenal Hyperplasia,” Mayo Clinic, http://www.mayoclinic.org/diseases-conditions/congenital-adrenal-hyperplasia/basics/causes/con-20030910 (accessed March 20, 2017).

[133] Ibid.

[134] Ralf W. Dittmann, Marianne E. Kappes and Michael H Kappes, “Sexual Behavior in Adolescent and Adult Females With Congenital Adrenal Hyperplasia,” Psychoneuroendocrinology 17 (1992): 153.

[135] Ibid., 162-163.

[136] Ibid., 163.

[137] Ibid., 164.

[138] Anglea M.L. Pattatucci, “Biopsychosoical Interactions and the Development of Sexual Orientation,” Lesbian, Gay, and Bisexual Identities in Families: Psychological Perspectives, (New York, NY: Oxford University Press, 1998), 27.

[139] Genetics Home Reference, “Androgen Insensitivity Syndrom,” U.S. National Library of Medicine, https://ghr.nlm.nih.gov/condition/androgen-insensitivity-syndrome (accessed March 20, 2017).

[140] Mbugua, “Reasons to Suggest that the Endocrine Research on Sexual Preference is a Degenerating Research Program,” History and Philosophy of the Life Sciences, 351.

[141] Toshihiro Aono, Akira Miyake, Takayuki Kinugasa, Keiichi Kurachi, and Keishi Matsumoto, “Absence of Positive Feedback Effect of Oestrogren on LH Release in Patients with Testicular Feminization Syndrome,” Acta Endocrinologica, 87 (1978): 262.

[142] Ibid., 259, 262.

[143] Mbugua, “Reasons to Suggest that the Endocrine Research on Sexual Preference is a Degenerating Research Program,” History and Philosophy of the Life Sciences, 351.

[144] Ibid., 351-352.

[145] Ibid., 352.

[146] Julianne Imperato-McGinley, Luis Guerrero, Teofilo Gautier, and Ralph E. Peterson, “Steroid 5-alpha-Reductase Deficiency in Man: An Inherited Form of Male Pseudohermaphroditism,” Science 186 (December 27, 1974): 1213.

[147] Mbugua, “Reasons to Suggest that the Endocrine Research on Sexual Preference is a Degenerating Research Program,” History and Philosophy of the Life Sciences, 352.

[148] Ibid., 351.

[149] Lawrance S. Mayer, M.B., M.S., Ph.D. and Paul R. McHugh, M.D., “Sexuality and Gender: Findings from the Biological, Psychological and Social Sciences” New Atlantis: A Journal of Technology and Society, (Fall 2016): 39-40.

[150] Simon LeVay, “A Difference in Hypothalamic Structure Between Heterosexual and Homosexual Men,” Science 253.5023 (August 1991): 1034+.

[151] Ibid.

[152] Ibid.

[153] Ibid.

[154] Ibid.

[155] Peter Sprigg and Timothy Dailey, ed. Getting it Straight: “What Causes Homosexuality?.” What the Research Shows about Homosexuality, (Washington, DC: Family Research Council, 2004), 2-3.

[156] LeVay, “A Difference in Hypothalamic Structure Between Heterosexual and Homosexual Men,” Science, 1034+.

[157] Mayer and McHugh, “Sexuality and Gender: Findings from the Biological, Psychological and Social Sciences” New Atlantis: A Journal of Technology and Society, 41.

[158] LeVay, “A Difference in Hypothalamic Structure Between Heterosexual and Homosexual Men,” Science, 1034+.

[159] William Byne and Bruce Parsons, “Human Sexual Orientation: The Biologic Theories Reappraised,” Archives of General Psychiatry 50 (March 1993): 231.

[160] Laura S. Allen and Roger A. Gorski, “Sexual Orientation and the size of the Anterior Commissure in the Human Brain,” Proceedings of the National Academy of Sciences USA 89 (August 1992): 7199.

[161] Ibid., 7199.

[162] Ibid., 7200.

[163] Ibid., 7200.

[164] Ibid., 7200.

[165] Ibid., 7199.

[166] Mitchell S. Lasco, Theresa J Jordan, Mark A Edgar, Carol K. Petito, and William Byne, “A Lack of Dimorphism of Sex or Sexual Orientation in the Human Anterior Commissure,” Brain Research 936 (2002): 96.

[167] Ibid.

[168] Ibid., 97.

[169] Mayer, and McHugh, “Sexuality and Gender: Findings from the Biological, Psychological and Social Sciences” New Atlantis: A Journal of Technology and Society, 39-40.

[170] Biointeractive, “The Human Suprachiasmatic Nucleus,” Howard Hughes Medical Institute, http://www.hhmi.org/biointeractive/human-suprachiasmatic-nucleus (accessed March 20, 2017).

[171] D. F. Swaab and M.A. Hofman, “An Enlarged Suprachiasmatic Nucleus in Homosexual Men,” Brain Research 537 (1990): 145.

[172] Ibid., 146.

[173] Ibid.

[174] American Psyciatric Association. “Position Statement on Psyciatric Treatment and Sexual Orientation, 2000.” https://www.camft.org/ias/images/PDFs/SOCE/APA_Position_Statement.pdf (accessed March 4, 2017).

[175] Stanton L. Jones and Mark A. Yarhouse, Ex Gays: A Longitudinal Study of Religiously Mediated Change in Sexual Orientation, (Downer’s Grove, IL: InterVarsity Press, 2007), 885, Kindle.

[176] Ibid., 924-937, Kindle.

[177] Ibid., 1254-1260, Kindle.

[178] Ibid., 1120, Kindle.

[179] Ibid., 1120, Kindle.

[180] Ibid., 1723, Kindle.

[181] Ibid., 3158-3160, Kindle.

[182] Ibid., 2785, 3205-3206, Kindle.

[183] Ibid., 3391, Kindle.

[184] Ibid., 3391, Kindle.

[185] Patrick M. Chapman, “A Critique of Jones And Yarhouse’s ‘Ex-gays?’ – Part 1,” Ex-Gay Watch, https://exgaywatch.com/2007/11/a-critique-of-jones-and-yarhouses-ex-gays-part-1/ (accessed on 4.19.2017).

[186] Stanton L. Jones, “Dr. Stanton Jones Replies,” Box Turtle Bulletin, http://www.boxturtlebulletin.com/2007/09/18/792 (accessed on 4.19.2017).

[187] Patrick M. Chapman, “A Critique of Jones And Yarhouse’s ‘Ex-gays?’ – Part 3,” Ex-Gay Watch, https://exgaywatch.com/2007/11/a-critique-of-jones-and-yarhouses-ex-gays-part-3/ (accessed on 4.19.2017).

[188] Jones and Yarhouse, Ex Gays: A Longitudinal Study of Religiously Mediated Change in Sexual Orientation, 4019-4023, Kindle.