Simon LeVay The anterior hypothalmus of the brain participates in the regulation of male-typical sexual behavior. The volumes of four cell groups in this region [interstitial nuclei of the anterior hypothalmus (INAH) 1, 2, 3, and 4] were measured in postmortem tissue from three subject groups: women, men who were presumed to be heterosexual, and homosexual men. No differences were found between the groups in the volumes of INAH 1, 2, or 4. As has been reported previously, INAH 3 was more than twice as large in the heterosexual men as in the women. It was also, however, more than twice as large in the heterosexual men as in the homosexual men. This finding indicates that INAH is dimorphic with sexual orientation, at least in men, and suggests that sexual orientation has a biological substrate.
Sexual orientation -- specifically, the direction of sexual feelings or behavior towards members of one's own or the opposite sex -- has traditionally been studied at the level of psychology, anthropology, or ethics (1). Although efforts have been made to establish the biological basis of sexual orientation, for example, by the application of cytogenetic, endocrinological, or neuroanatomical methods, these efforts have largely failed to establish differences between homosexual and heterosexual individuals (2, 3).
A likely biological substrate for sexual orientation is the brain region involved in the regulation of sexual behavior. In nonhuman primates, the medial zone pf the anterior hypothalmus has been implicated in the generation of male-typical sexual behavior (4). Lesions in this region in male monkeys impair heterosexual behavior without eliminating sexual drive (5). In a morphometric study of the comparable region of the human hypothalmus (from men and women of unknown sexual orientation), two small groups of neurons (INAH 2 and 3) were reported to be significantly larger in men than women (6). Thus, these two nuclei could be involved in the generation of male-typical sexual behavior.
I tested the idea that one or both of these nuclei exhibit a size dimorphism, not with sex, but with sexual orientation. Specifically, I hypothesized that INAH 2 or INAH 3 is large in individuals sexually oriented toward women (heterosexual men and homosexual women) and small in individuals sexually oriented toward men (heterosexual women and homosexual men). Because tissue from homosexual women could not be obtained, however, only that part of the hypothesis relating to sexual orientation in men could be tested.
Brain tissue was obtained from 41 subjects
at routine autopsies of persons who died at seven metropolitan hospitals in
The brains were fixed by immersion for 1 to 2 weeks in 10 or 20% buffered formalin. Tissue blocks containing the anterior hypothalmus were dissected from these slices and stored for 1 to 8 weeks in 10% buffered formalin. These blocks were then given code numbers; all subsequent processing and morphometric analysis was done without knowledge of the subject group to which each block belonged. The blocks were infiltrated with 30% sucrose and frozen-sectioned at a thickness of 52 micrometers in planes parallel to the original slices. The sections were mounted serially on slides, dried, defatted in xylene, stained with 1% thionin in acetate buffer (15 to 30 min), and differentiated with 5% rosin in 95% alcohol (4 to 10 min). With the aid of a compound microscope equipped with a camera lucida attachment, the outlines of the four nuclei (INAH 1, 2, 3, and 4) were traced in every section at a linear magnification of x83. These four nuclei included the two nuclei reported by Allen et al. (6) to be sexually dimorphic and two other nuclei (INAH 1 and 4) for which no sex differences were found (6). The criteria described in (6) were followed in identifying and delineating the nuclei (Fig. 1). The outline of each nucleus was drawn as the shortest line that included every cell of the type characteristic for that nucleus, regardless of cell density. In 15 cases the nuclei in both left and right hypothalmus were traced. In 12 cases only the left hypothalmus was studied, and in 14 cases only the right. The areas of the traced outlines were determined with a digitizing tablet, and the volume of each nucleus was calculated as the summed area of the serial outlines multiplied by the section thickness.
In the 15 cases where both left and right sides were studied, no significant interhemispheric differences were found for any of the four nuclei. Therefore, in furthur analysis, the mean of the two sides was used, and the cases where only one side was available were analysed without regard to the side of origin.
One-way analysis of variance (ANOVA) was used to look for significant differences between subject groups (Fig. 2). No differences were found for INAH 1, 2, or 4. The results from INAH 1 and 4 are consistent with those of Allen et al. (6, 10). However, INAH 2 was reported to be about twofold larger in men than women (6). The failure to replicate that finding may have to do with the relatively young age of the subjects in the present study; as noted in (6), no sex difference was apparent when women of repropductive age were compared with men of similar ages. Thus INAH 2 is not dimorphic with either sex or with sexual orientation, at least within the age range studied.
INAH 3 did exhibit dimorphism. One-way
ANOVA showed that the three sample groups (from women, heterosexual men, and
homosexual men) were unlikely to have come from the same population (P =
0.0014). Consistent with the hypothesis outlined above, the volume of this
nucleus was more than twice as large in the heterosexual men (0.12 +/- 0.01
mm^3, mean +/- SEM) as in the homosexual men (0.051
+/- 0.01 mm^3). Because of uncertainty about the nature of the underlying
distribution, the dignificance of this difference was
evaluated by a
INAH 3 is situated about 1 mm lateral to the wall of the third ventricle, and about 1 to 2 mm dorsal to the anterior tip of the paraventricular nucleus. It is spherical or ellipsoidal and contains relatively large, densely staining, polygonal neurons (Fig. 1B). The borders of the nucleus are not well demarcated; hence a blind procedure was used to reduce bias effects. In most of the homosexual men (and most of the women) the nucleus was represented by only scattered cells (Fig. 1C). Because of the difficulty in precisely defining the neurons belonging to INAH 3, however, no attempt was made to measure cell number or density.
Brain tissue from individuals known to be homosexual has only become available as a result of the AIDS epidemic. Nevertheless, the use of this tissue source raises several problems. First, it does not provide tissue from homosexual women because this group has not been affected by the epidemic to any great extent. Thus, the prediction that INAH 3 is larger in homosexual than in heterosexual women remains untested. Second, there is the possibility that the small size of INAH 3 in the homosexual men is the result of AIDS or its complications and is not related to the men's sexual orientation. This does not seem to be the case because (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. Nevertheless, until tissue from homosexual men dying of other causes becomes available, the possibility that the small size of INAH 3 in these men reflects a disease effect that is peculiar to homosexual AIDS patients cannot be rigorously excluded.
A third problem is that possibility that AIDS patients constitute an unrepresentative subset of gay men, characterized, for example, by a tendency to engage in sexual relations with large numbers of different partners or by a strong preference for the receptive role in anal intercourse [both of which are major risk factors for acquiring human immunodeficiency virus (HIV) infection (13)]. Sexual activity with large numbers of partners is (or was until recently) common among gay men, however, and therefore does not define an unrepresentative minority (14). In addition, the majority of homosexual men who acquired HIV infection during the Multicenter AIDS Cohort Study (15) reported that they took both the insertive and the receptive role in anal intercourse, and the same is likely to be true of the homosexual subjects in my study. Nevertheless, the use of postmortem material, with the consequent impossibility of obtaining detailed information about the sexuality of the subjects, limits the ability to make correlations between brain structure and the diversity of sexual behavior that undoubtedly exists within the homosexual and the heterosexual populations.
The existence of "exceptions" in the present sample (that is, presumed heterosexual men with small INAH 3 nuclei, and homosexual men with large ones) hints at the possibility that sexual orientation, although an important variable, may not be the sole determinant of INAH 3 size. It is also possible, however, that these exceptions are due to technical shortcomings or to misassignment of subjects to their subject groups.
The discovery that the nucleus differs in size between heterosexual and homosexual men illustrates that sexual orientation in humans is amenable to study at the biological level, and this discovery opens the door to studies of neurotransmitters or receptors that might be involved in regulating this aspect of personality. Further interpretation of the results of this study must be considered speculative. In particular, the results do not allow one to decide if the size of INAH 3 in an individual is the cause or consequence of that individual's sexual orientation, or if the size of INAH 3 and sexual orientation covary under the influence of some third, unidentified variable. In rats, however, that sexual dimorphism of the apparently comparable hypothalmic nucleus, the sexually dimorphic nucleus of the preoptic area, (SDN-POA) (16), arises as a consequence of the dependence of its constituent neurons on circulating androgen during a perinatal sensitive period (17). After this period, even extreme interventions, such as castration, have little effect on the size of the nucleus. Furthermore, even among normal male rats there is a variablity in the size of SDN-POA that is strongly correlated with the amount of male-typical sexual behavior shown by the animals (18). Although the validity of the comparison between species is uncertain, it seems more likely that in humans, too, the size of INAH 3 is established early in life and later influences sexual behavior than that the reverse is true. In this connection it would be of interest to establish when the neurons composing INAH 3 are generated and when they differentiate into a dimorphic nucleus.
References and Notes:
1. For examples of the variety of approaches to the topic, see S. Freud [_Three Essays on the Theory of Sexuality_, in _Collected Works of Freud_, J. Strachey, Ed. and Transl. (Hogarth, London, 1959), pp. 125-243], C. S. Ford and F. A. Beach [_Patterns of Sexual Behavior_ (Ace, New York, 1951)], Vatican Council II [_Declaration on Certain Problems of Sexual Ethics_, in _Vatican Collection_, A. Flannery, Ed. and Transl. (Eerdmans, Grand Rapids, MI, 1982), vol. 2, pp. 486-499], M. Ruse, _J. Homosex._ 6, 5 (1981)], and R. C. Friedman [_Male Homosexuality: A Contemporary Psychoanalytic Perspective_ (Yale Univ. Press, New Haven, CT, 1988)].
2. [I'm going to omit detailed references -- if you're going to go to a science library to get the referenced journal, you can get Science as well. I'll just include notes. -- Chris]
3. The suprachiasmatic nucleus (SCN) of the hypothalmus has been reported to be larger in homosexual than in heterosexual men. [ref omitted]. There is little evidence, however, to suggest that SCN is involved in regulation of sexual behavior aside from its circadian rhythmicity [ref omitted].
4, 5, 6 [refs omitted]
7. Two of these subjects (both AIDS patients) had denied homosexual activity. The records of the remaining 14 patients contained no information about their sexual orientation; they are assumed to be heterosexual on the basis of the numerical preponderance of heterosexual men in the population [ref to Kinsey omitted].
8. The causes of death for the ten male subjects who did not die of AIDS were lung carcinoma (two cases), renal failure (two cases), coronary thrombosis, acute lymphocyte leukemia, amytropic lateral sclerosis, pancreatic carcinoma, pulmonary embolism, and aspiration pneumonia. For the five female subjects who did not die of AIDS, the causes of death were systemic lupus erythematosus, pancreatic carcinoma, liver failure (two cases), and abdominal sepsis secondary to renal transplantation. All six of the heterosexual male AIDS patients and three of the homosexual men had history of intravenous drug abuse. Three of the women, two heterosexual men who did not have AIDS, and one homosexual man had histories of chronic alcohol abuse.
9. Criteria for inclusion of subjects in the study were as follows: (i) age 18 to 60, (ii) availability of medical records, (iii) in AIDS patients, statement in the records of at least one AIDS risk group to which the patient belonged (homosexual, intravenous drug abuser, or recipient of blood transfusions), (iv) no evidence of pathalogical changes in the hypothalmus, and (v) no damage to the INAH nuclei during removal of the brain or transection of these nuclei in the initial slicing of the brain. Fourteen specimens (over and above the 41 used in the study) were rejected for one of these reasons; in all cases the decision to reject was made before decoding.
10. INAH 1 is the same as the nucleus named the "sexually dimorphic nucleus" and reported to be larger in men than women [ref omitted]. My results support the contention by Allen et al. (6) that this nucleus is not dimorphic.
11. The ratio of the mean INAH 3 volumes for the heterosexual and homosexual male groups was calculated. The INAH 3 volume values were then randomly reassigned to the subjects, and the ratio of means was recalculated. The procedure was repeated 1000 times, and the ordinal position of the actual ratio in the set of shuffled ratios was used as a measure of the probability that the actual difference between groups arose by chance. Only one of the shuffled ratios was larger than the actual ratio, giving a probability of 0.001.
12. Application of ANOVA or correlation measures failed to identify any confounding effects of age, race, brain weight, hospital of origin, length of time between death and autopsy, nature of fixative (10 or 20% formalin), duration of fixation, or, in the AIDS patients, duration of survival after diagnosis, occurrence of particular complications, or the nature of the complication or complications that caused death. There were no significant positive or negative correlations between the volumes of the four individual nuclei across the entire sample, suggesting that there were no unidentified common-mode effects such as might be caused by variations in tissue shrinkage. The mean brain weight for the women (1256 +/- 41 g) was smaller than for either the heterosexual (1364 +/- 46 g) or the homosexual (1392 +/- 32 g), but normalizing the data for brain weight had no effect on the results. There was no correlation between subject age and the volume of any of the four nuclei, whether for the whole sample or for any subject groups; this finding does not necessarily conflict with the report in (6) of age effects in INAH 1, and possibly INAH 2, because in (6) a much wider range of ages was examined than was used in the present study.
13. [ref omitted]
14. In the largest relevant study [ref omitted, 1978], nearly half the homosexual male respondents reported having had over 500 sexual partners.
15, 16, 17, 18 [refs omitted]
19. I thank the pathologists who made this study possible by providing access to autopsy tissue; [various other acknowledgements omitted]
29 January 1991; accepted 24 June 1991.
Gay Genes, Revisited; November 1995; Scientific American Magazine; by Horgan; 1 Page(s)
In recent years,
two studies published in Science seemed to provide dramatic evidence that
male homosexuality has biological underpinnings. In 1991 Simon LeVay, then at
the Salk Institute for Biological Studies in
Both announcements made headlines worldwide. LeVay and Hamer appeared on talk shows and wrote books. They also co-authored an article published in this magazine in May 1994. But LeVay's finding has yet to be fully replicated by another researcher. As for Hamer, one study has contradicted his results. More disturbingly, he has been charged with research improprieties and is now under investigation by the Federal Office of Research Integrity.
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CRITIQUE NUMBER 2
This three-part series will address the pro-gay theology by dividing its arguments--or tenets--into three categories: social justice arguments, general religious arguments, and scriptural arguments. A brief description of these arguments will be provided, followed by a response/rebuttal to each.
We have created a table of contents for easier navigation through this document. Start at the beginning of the article, or just click on any issue that interests you.
Social Justice Arguments
Social Justice Argument #1: "Homosexuality Is Inborn."
Argument #1-A: Simon LeVay And the Hypothalamus
Argument #1-B: Twins
Argument #1-C: Genes
Social Justice Argument #2: "Homosexuality Cannot Be Changed."
Social Justice Argument #3: "10% of the Population Is Gay. Could So Many
People Be Wrong?"
General Religious Arguments
Religious Argument #1: "Jesus Said Nothing About Homosexuality."
Religious Argument #2: "I'm a Born-Again Believer and I'm Gay. How Can
That Be, If Homosexuality Is Wrong?"
Religious Argument #3: "I Attend a Gay Church Where the Gifts of the
Spirit and the Presence of God Are Manifest. How Can That Be, If
Homosexuality Is Wrong?"
Religious Argument #4: "My Lover and I Are in a Monogamous Relationship,
and We Truly Love Each Other. That Can't Be Wrong!"
Creation/Created Intent: Genesis 1:27-28; 2:18, 23-24
The Destruction of Sodom: Genesis 19:4-9
The Levitical Law: (Leviticus 18:22; 20:13)
Paul on "Natural" and "Unnatural": Romans 1:26-27
Paul and 'Arsenokoite': 1 Corinthians 6:9-10; 1 Timothy 1:9-10
ARGUMENT #1-A: Simon LeVay And the Hypothalamus
1991 Dr. LeVay, a neuro-scientist at the Salk
He reported this region of the brain to be larger in heterosexual men than in homosexuals; likewise, he found it to be larger in heterosexual men than in the women he studied. For that reason, he postulated homosexuality to be inborn, the result of size variations in the INAH3, and his findings were published in Science in August of 1991.(1) This is the study most often quoted when people insist homosexuality has been "proven" to be inborn.
Response: This argument is exaggerated and misleading for six reasons:
First, LeVay did not prove homosexuality to be inborn; his results were not uniformly consistent. On the surface it appears all of LeVay's homosexual subjects had smaller INAH3's than his heterosexual ones; in fact, three of the homosexual subjects actually had larger INAH3's than the heterosexuals. Additionally, three of the heterosexual subjects had smaller INAH3's than the average homosexual subject. Thus, six of LeVay's 35 male subjects (17% of his total study group) contradicted his own theory.(2)
Second, LeVay did not necessarily measure the INAH3 properly. The area LeVay was measuring is quite small--smaller than snowflakes, according to scientists interviewed when his study was released. His peers in the neuroscientific community cannot agree on whether the INAH3 should be measured by its size/volume or by its number of neurons.(3)
Third, it's unclear whether brain structure affects behavior or behavior affects brain structure. Dr. Kenneth Klivington, also of SALK Institute, points out that neurons can change in response to experience. "You could postulate," he says, "that brain change occurs throughout life, as a consequence of experience."(4) In other words, even if there is a significant difference between the brain structures of heterosexual and homosexual men, it is unclear whether the brain structure caused their homosexuality, or if their homosexuality affected their brain structure.
In fact, one year after LeVay's study was released, Dr. Lewis Baxter of UCLA obtained evidence that behavioral therapy can produce changes in brain circuitry, reinforcing the idea that behavior can and does affect brain structure.(5) Therefore, even if differences do exist between the INAH3's of homosexual and heterosexual men, it is possible that the diminished size of the homosexual's is caused by his behavior, rather than his behavior being caused by the INAH3's size.
Fourth, LeVay was not certain which of his subjects were homosexual and which were heterosexual. Dr. LeVay admits this represents a "distinct shortcoming" in his study. Having only case histories on his subjects to go by (which were by no means guaranteed to provide accurate information about the patient's sexual orientation), he could only assume that, if a patient's records did not indicate he was gay, he must have been heterosexual.
Yet 6 of the 16 reportedly heterosexual men studied had died of AIDS, increasing the chances their sexual histories may have been incompletely recorded.(6) If it is uncertain which of LeVay's subjects were heterosexual and which were homosexual, how useful can his conclusions about "differences" between them really be?
Fifth, LeVay did not approach the subject objectively. Dr. LeVay, who is openly homosexual, told Newsweek that, after the death of his lover, he was determined to find a genetic cause for homosexuality or he would abandon science altogether. Furthermore, he admitted, he hoped to educate society about homosexuality, affecting legal and religious attitudes towards it.(7) None of which diminishes his credentials as a neuroscientist. But his research can hardly be said to have been unbiased.
the scientific community did not by any means unanimously accept Dr. LeVay's
study. Comments from other scientists in response to
LeVay's work are noteworthy. Dr. Richard Nakamura of the National Institute of
Mental Health says it will take a "larger effort to be convinced there is
a link between this structure and homosexuality."(8) Dr. Anne-Fausto Sterling of
My freshman biology students know enough to sink this study.(9)
Dr. Rochelle Klinger, at Psychiatrist at Medical College of Virginia, doubts we will "ever find a single cause of homosexuality."(10) And Scientific American sums up the reason many professionals approach the INAH3 theory with caution:
LeVay's study has yet to be fully replicated by another researcher.(11)
CRITIQUE NUMBER 3
Does prenatal (or neonatal) exposure to particular steroid hormones impose permanent sex-specific changes on the central nervous system? Such sex-specific neural changes have been shown in regions of the brain that regulate "involuntary" sexual physiology. The cyclic secretion of luteinizing hormone by the adult female rat pituitary, for example, is dependent on the lack of testosterone during the first week of the animal's life. The luteinizing hormone secretion of female rats can be made noncyclic by giving them testosterone 4 days after birth; conversely, the luteinizing hormone secretion of males can be made cyclical by removing their testes within a day of birth (Barraclough and Gorski 1962). It is thought that sex hormones may act during the fetal or neonatal stage of a mammal's life to organize the nervous system in a sex-specific manner, and that during adult life, the same hormones may have transitory, activational effects. This idea is called the organization/activation hypothesis.
Interestingly, the hormone chiefly responsible for determining the male brain pattern is estradiol, a type of estrogen.* Testosterone in fetal or neonatal blood can be converted into estradiol by the enzyme P450 aromatase, and this conversion occurs in the hypothalamus and limbic systemtwo areas of the brain known to regulate hormone secretion and reproductive behavior (Reddy et al. 1974; McEwen et al. 1977). Thus, testosterone exerts its effects on the nervous system by being converted into estradiol. But the fetal environment is rich in estrogens from the gonads and placenta. What stops these estrogens from masculinizing the nervous system of a female fetus? Fetal estrogen (in both males and females) is bound by a-fetoprotein. This protein is made in the fetal liver and becomes a major component of the fetal blood and cerebrospinal fluid. It will bind and inactivate estrogen, but not testosterone.
Attempts to extend the organization/activation hypothesis to "voluntary" sexual behaviors are more controversial because there is no truly sex-specific behavior that distinguishes the two sexes of many mammals, and because hormonal treatment has multiple effects on the developing mammal. For instance, injecting testosterone into a week-old female rat will increase pelvic thrusting behavior and diminish lordosisa posture that stimulates mounting behavior in the malewhen she reaches adulthood (Phoenix et al. 1959; Kandel et al. 1995). These behavioral changes can be ascribed to testosterone-mediated changes in the central nervous system, but they could also be due to hormonal effects on other tissues. Testosterone enables the growth of the muscles that allow pelvic thrusting. And since testosterone causes females to grow larger and to close their vaginal orifices, one cannot conclude that the lack of lordosis is due solely to testosterone-mediated changes in the neural circuitry (Harris and Levine 1965; De Jonge et al. 1988; Moore 1990; Moore et al. 1992; Fausto-Sterling 1995).
In addition, the effects of sex steroids on the brain are very complicated, and the steroids may be metabolized differently in different regions of the brain. Male mice lacking the testosterone receptor still retain a male-specific preoptic morphology in the brain, and male mice lacking the aromatase enzyme are capable of breeding (Breedlove 1992; Fisher et al. 1998). These studies show that there is more to sex-specific morphology and behavior than steroid hormones. Despite best-selling books that pretend to know the answers, we have much more to learn regarding the relationship between development, steroids, and behavior. Moreover, extrapolating from rats to humans is a very risky business, as no sex-specific behavior has yet been identified in humans, and what is "masculine" in one culture may be considered "feminine" in another (see Jacklin 1981; Bleier 1984; Fausto-Sterling 1992). As one review (Kandel et al. 1995) concludes:
There is ample evidence that the neural organization of reproductive behaviors, while importantly influenced by hormonal events during a critical prenatal period, does not exert an immutable influence over adult sexual behavior or even over an individual's sexual orientation. Within the life of an individual, religious, social, or psychological motives can prompt biologically similar persons to diverge widely in their sexual activities.
Certain behaviors are often said to be part of the "complete" male or female phenotype. The brain of a mature man is said to be formed such that it causes him to desire mating with a mature woman, and the brain of a mature woman causes her to desire to mate with a mature man. However, as important as desires are in our lives, they cannot be detected by in situ hybridization or isolated by monoclonal antibodies. We do not yet know if sexual desires are primarily instilled in us by our social education or are fundamentally "hardwired" into our brains by genes or hormones during our intrauterine development or by other means.
In 1991, Simon LeVay proposed that part of the anterior hypothalamus of homosexual men has the anatomical form typical of women rather than of heterosexual men. The hypothalamus is thought to be the source of our sexual urges, and rats have a sexually dimorphic area in their anterior hypothalamus that appears to regulate their sexual behavior. Thus, this study generated a great deal of publicity and discussion. The major results are shown in Figure 17.14. The interstitial nuclei (neuron clusters) of the anterior hypothalamus (INAH) were divided into four regions. Three of them showed no signs of sexual dimorphism. However, one of them, INAH3, showed a statistically significant difference in volume between males and females; it was claimed that the male INAH3 is, on average, more than twice as large as the female INAH3. Moreover, LeVay's data suggested that the INAH3 of homosexual men was similar in volume to that of women and less than half the size of heterosexual men's INAH3. This finding, LeVay claimed, "suggests that sexual orientation has a biological substrate."
There have been several criticisms of LeVay's interpretation of the data. First, the data are from populations, not individuals. One can also say that there is a statistical range and that men and women have the same general range. Indeed, one of the INAH3 from a homosexual male was larger than all but one of those from the 16 "heterosexual males" in the study. Second, the "heterosexual men" were not necessarily heterosexual, nor were the "homosexual men" necessarily homosexual; the brains came from corpses of people whose sexual preferences were not known. This brings up another issue: homosexuality has many forms, and is probably not a single phenotype. Third, the brains of the "homosexual men" were taken from patients who had died of AIDS. AIDS affects the brain, and its effect on the hypothalamic neurons is not known.
Fourth, because the study was done on the brains of dead subjects, one cannot infer cause and effect. Such data show only correlations, not causation. It is as likely that behaviors can affect regional neuronal density as it is that regional neuronal density can affect behaviors. If one interprets the data as indicating that the INAH3 of male homosexuals is smaller than that of male heterosexuals, one still does not know whether that is a cause of homosexuality or a result of it. Indeed, Breedlove (1997) has shown that the density and size of certain neurons in rat spinal ganglia depend on the frequency of sexual intercourse. In this case, the behavior was affecting the neurons. Fifth, even if a difference in INAH3 does exist, there is no evidence that the difference has anything to do with sexuality. Sixth, these studies do not indicate when such differences (if they exist) emerge. The question of whether differences among the heterosexual male, female, and homosexual male INAH3 occur during embryonic development, shortly after birth, during the first few years of life, during adolescence, or at some other time was not addressed.
In 1993, a correlation was made between a particular DNA sequence on the X chromosome and a particular subgroup of male homosexuals: homosexual men who had a homosexual brother. Out of 40 pairs of homosexual brothers wherein one brother had inherited a particular region of the X chromosome from his mother, the other brother had also inherited this region in 33 cases (Hamer et al. 1993). One would have expected both brothers to have done so in only 20 cases, on average. Again, this is only a statistical concordance, and one that could be coincidental. Moreover, the control (the incidence of the same marker in the "nonhomosexual" males of these families) was not reported, and the statistical bias of the observations has been called into question, especially since other laboratories have not been able to repeat the result (Risch et al. 1993; Marshall 1995). More recent studies (Hu et al. 1995; Rice et al. 1999) found little or no increase in the incidence of this DNA sequence when homosexual men were compared to their nonhomosexual brothers. Hu and colleagues concluded that this sequence is "neither necessary nor sufficient for a homosexual orientation." Thus, despite the reports of these studies in the public media, no "gay gene" has been found.
Genes encode RNAs and proteins, not behaviors. While genes may bias behavioral outcomes, we have no evidence for their "controlling" them. The observance of people with schizophrenia, or people whose personalities change radically after a religious conversion or a traumatic experience, indicates that a single genotype can support a wide range of personalities. This is certainly a problem with any definition of a "homosexual phenotype," since people can alternate between homosexual and heterosexual behavior, and the definition of what is homosexual behavior differs between cultures (see Carroll and Wolpe 1996). Thus, whether homosexual desires are formed by genes within the nucleus, by sex hormones during fetal development, or by experiences after birth is still an open question.
*The terms estrogen and estradiol are often used interchangeably. However, estrogen refers to a class of steroid hormones responsible for establishing and maintaining specific female characteristics. Estradiol is one of these hormones, and in most mammals (including humans), it is the most potent of the estrogens.