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YOU WERE NOT BORN THAT WAY

THE FULL UNTOLD STORY BEHIND THE GAY GENE LIE

YOU WERE NOT BORN THAT WAY
THE FULL UNTOLD STORY BEHIND THE GAY GENE LIE.

Homosexual people believe they were born gay, and this belief is based on a lie that was told by a homosexual scientist, and this is its story.

INTRODUCTION In the first presented peer reviewed article titled “Male Homosexuality: Absence of Linkage to Microsatellite Markers at Xq28” it presents empirical evidence that proves the “gay gene” to be un-locatable and nonexistent. A Canadian group of Scientists attempted to recreate the same and similar results and discovered that the initial experimentation was false and incorrect. The second journal article is a rebuttal to the above denial; it comes from Dean Harmer, the scientist who first proposed the research. The response to this rebuttal that is highlighted in yellow is a complete disclosure on the impossibility of the “gay gene” existing in the aforementioned section of DNA. It provides further evidence that completely invalidates Harmers scientific method and dispels the possibility of the “gay genes” existence. Lastly there is a complete dissertation about the story of the “gay gene”, it provides the clearest account ever produced on this subject, and it clearly shows how the media and homosexual advocates (D. Harmer the researcher who presented the idea being one of them) took a scientific postulation (or theoretical probability) and made it into a cultural truth or truism without proper solid science based evidence to back it. This disclosure shows how the UK did not buy into the idea of the “gay gene” as did many in America, and it also reveals the aftermath and outcome of what happened to Harmer when the Canadian team proved that his methodology was wrong. The gay gene, if such a thing could ever exist, has never been found to actually exist. The belief in its reality is pure rhetoric.

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Genetics and Male Sexual Orientation
Sexual orientation is a complex trait that is
probably shaped by many different factors, including multiple genes, biological, environmental, and sociocultural influences. In a 1993 report, my group (1) provided initial evidence that a locus at the q28 region of the X chromosome was involved in male sexual orientation in some, but not all, individuals. The Xq28 hypothesis was based on both family pedigree analysis, which revealed that gay men had more homosexual male relatives through maternal than through paternal lineages, and linkage analysis of gay male siblings, which found significantly increased sharing of Xq28 DNA markers. Recently, George Rice et al. (2) challenged the Xq28 hypothesis on the basis of a new linkage study in Canada and have questioned the degree to which genes contribute to sexual orientation. It appears to us that (i) the family pedigree data from the Canadian study (2) actually support the Xq28 hypothesis; (ii) three other available Xq28 DNA studies did find linkage; and (iii) the heritability of sexual orientation is supported by substantial evidence independent of the X-chromosome linkage data. The original impetus for the Xq28 hypothesis was the finding that gay male probands had more gay male relatives through maternal than through paternal lineages (1); this is the expected pattern for a trait that is influenced by gene on the X chromosome, which males inherit only from their mothers. According to a poster presented at the International Academy of Sex Research meeting in 1995 (3, 4), the Canadian group found a similar pattern in their own family data. Specifically, they interviewed the probands from 182 families that were ascertained on the basis of having two or more gay brothers and found that 13.4% (35/261) of their maternal uncles were gay as compared to 6.9% (24/364) of their paternal uncles. This is a significant difference in favor of maternal transmission (chisquare value 7.1, p 0.008), as predicted by the Xq28 hypothesis. The difference could not be attributed to reporting bias because the same families showed a slight excess of lesbian aunts on the paternal side of the family (3, 4). This important family pedigree data was not included in the report by Rice et al. (2), which describes only the genotyping results for a subset of 48 families. DNA linkage analysis provides a more direct test of the Xq28 hypothesis. If male sexual orientation is influenced by a gene or genes at Xq28, then gay brothers should share more than 50% of their alleles at this region, whereas their heterosexual brothers should share less than 50% of their alleles. By contrast, if there is no such gene, then both types of brothers should display 50% allele sharing. To date, there have been four X-chromosome linkage studies of male sexual orientation (Fig. 1). Hamer et al. (1) analyzed 40 pairs of gay brothers and found that they shared 82% of their alleles in the Xq28 region; this was greater than the 50% allele sharing that would be expected by chance ( p 0.00001). In a follow-up study, Hu et al. (5) analyzed an independent series of 32 genetically informative pairs of gay brothers and found 67% allele sharing ( p 0.04). Hu et al. also found that the heterosexual brothers of Xq28-concordant gay sib-pairs had only a 22% likelihood of carrying the same Xq28 allele; this independent test of linkage was statistically significant ( p 0.05), giving an overall significance level of p 0.004 for their study. In 1998, the independent research group of Sanders et al. (6) reported the results of an X chromosome linkage analysis of 54 pairs of gay brothers. They found 66% Xq28 allele sharing ( p 0.04). The results of the study by Sanders et al. were indistinguishable from those in the study by Hu et al., both in terms of the degree of allele sharing (66% versus 67%) and the precise

Fig. 1. Comparison of four studies of linkage between alleles on the X chromosome and male homosexuality. Meta-analysis (combined data, last set of columns) shows overall estimated allele sharing of 64% ( p 0.0001). Sample size, n. Statistical significance, p.

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chromosomal location of maximum sharing (locus DXS1108). By contrast, Rice et al. (2) studied 52 pairs of gay brothers and found no evidence for linkage to Xq28; they reported approximately 46% allele sharing, a nonsignificant result. Given the modest sample sizes of these studies, the most accurate estimate of Xq28 linkage can be obtained by combining the data from each of the four datasets. This meta-analysis gives an estimated level of allele sharing of 64% ( p 0.0001) (Fig. 1). Basically, the same result is obtained if one discards the highest and lowest reported allele sharing values and uses only the Hu et al. (5) and Sanders et al. (6) data, which gives a figure for estimated allele sharing of 66% ( p 0.001). A 64% allele sharing level corresponds to a s value of 1.4, where s is the ratio for homosexual orientation in the brothers of a gay index subject, as compared with the population frequency, that is attributable to a gene in this region. This modest level of influence is typical for the effect of a single locus on a complex behavioral trait such as sexual orientation. Why did Rice et al. not find the Xq28 linkage that was observed in the three preceding studies? One possible explanation is derived from the fact that only 48 (26%) of the 182 families originally interviewed by Rice et al. were actually studied at the level of their DNA (2). According to data presented in 1995 (3), it appears that the genotyped families were not a representative subset of the starting population because they displayed an excess of paternal rather than ma-

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ternal gay relatives—exactly the opposite pattern found in the total dataset. One would not logically expect such a nonrepresentative subset of the families to display any X-chromosome linkage. It would be interesting in the future to examine genotypes for the remainder of the Canadian families, especially those with maternal loading. A second possible explanation for why Rice et al. did not observe linkage is the modest statistical power of their sample. A population of 52 sib-pairs has 65% power to detect 64% allele sharing at the 0.05 level of significance. Thus there was a 35% chance that Rice et al. would not detect linkage simply by chance. A third consideration is the lack of defined criteria for homosexuality in the study by Rice et al. Hamer et al. (1) and Hu et al. (5) assessed sexual orientation using the 6-point Kinsey scales of sexual attraction, fantasy, self-identification, and behavior. By contrast, Rice et al. (2) depended on the investigator’s judgment, in some cases based on a single question to the research subject (7). The validity and reliability of this method of phenotype classification are unknown. A final difference between the linkage studies is that Rice et al. (2) did not methodically exclude families inconsistent with the hypothesis of X chromosome linkage. The use of defined inclusion and exclusion criteria to select appropriate families for the study of a putative X-linked locus was a key feature of the studies by Hamer et al. (1) and Hu et al. (5). As noted by King (8), this is a valuable strategy to detect linkage for a complex trait, such as sexual orientation, for which one particular locus (Xq28) accounts for only a portion of the total variance. Hu et al. (5) found no Xq28 linkage in families who did not meet their inclusion criteria. Although Rice et al. (2) found that excluding two families that failed to meet such criteria did not change their linkage results, it appears unlikely that they collected sufficient data on their subjects or families to systematically apply this sort of selection. As noted by Rice et al. (2), there is substantial evidence from family and twin studies, such as those reported by Pillard, Bailey and colleagues (9), that sexual orientation is genetically influenced. Rice et al. also argued, however, that “there would be strong selective pressure against such a gene.” Linkage analysis of a single locus on a limited number of families can show no such thing. Moreover, there are many plausible evolutionary scenarios whereby a gene that predisposed some individuals toward homosexuality could survive or even increase in the population (10). In summary, a meta-analysis of all available DNA linkage data continues to support a modest but significant role of the Xq28 region in male sexual orientation. Although there is a 0.01% chance that the observed link represents a “false positive,” there is a greater than 10% chance that the conclusions in the report by Rice et al. represent a “false negative,” resulting from their use of a small, apparently nonrepresentative subset of families for genotyping. Moreover, their family pedigree data appear to actually support Xchromosome linkage. The search for sexual orientation genes will ultimately depend on the identification of functionally relevant polymorphisms in molecularly defined genes, rather than on the purely statistical evidence afforded by linkage analysis. In the meanwhile, the genetic analysis of sexual orientation, like any complex trait, should pay careful attention to all available family and molecular data. Dean H. Hamer Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA E-mail: deanh@helix.nih.gov
References
1. D. H. Hamer, S. Hu, V. L. Magnuson, N. Hu, A. M. Pattatucci, Science 261, 321 (1993). 2. G. Rice, C. Anderson, N. Risch, G. Ebers, ibid. 284, 665 (1999). 3. G. Rice, C. Anderson, G. Ebers, “Abstract for International Academy of Sex Research Annual Meeting,” Provincetown, MA (1995). 4. J. M. Bailey, Nature Genet. 11, 353 (1995). 5. S. Hu et al., ibid., p. 248. 6. A. R. Sanders et al., poster presentation 149, annual meeting of the American Psychiatric Association, Toronto, Ontario, Canada, 1998. 7. G. Rice, personal communication. 8. M.-C. King, Nature 364, 288 (1993). 9. R. C. Pillard and J. D. Weinrich, Arch. Gen. Psychiatry 43, 808 (1986); J. M. Bailey and R. C. Pillard, ibid. 48, 1089 (1991). 10. R. C. Pillard and J. M. Bailey, Hum. Biol. 70, 347 (1998). 12 May 1999; accepted 7 July 1999.

Response: In their initial X chromosome linkage study, Hamer et al. (1) stated, “As with all linkage studies, replication and confirmation of our results are essential.” We agree. To be convincing, such confirmation needs to be obtained by groups using similar methods but working independently of the initial investigators. Hamer presents a “meta-analysis” which appears statistically significant, but does not address the issue of nonreplicability by including his own data in the analysis. Considering only the two studies performed by independent investigators, ours (2) and the unpublished data of Sanders et al. (3), we obtain Xq28 allele sharing of 60/106 56.6%, which is not statistically greater than the null hypothesis value of 50% sharing ( p 0.05). In fact, the two independent replication studies combined deviate significantly from the results from Hamer’s group (1, 4) (chi-square 6.53, p .02). Thus, the con-

clusion remains that the original studies of Hamer and colleagues are not replicated. As stated in our report (2), our goal was to replicate the linkage at Xq28. We recruited sibships containing at least two gay brothers. Index subjects were only casually asked about second- and third-degree relatives (uncles and male cousins). The rate of maternal uncles reported as gay (35/261 13.4%) was higher than that for paternal uncles (24/346 6.9%; p 0.01). However, the total number of paternal uncles is even more significantly increased (maternal uncles 346 versus 261, p 0.001). A comparison of maternal to paternal relatives presupposes that the likelihood of ascertainment of this trait is the same for both, but this has not been established. Family history studies of more easily identified traits are known to be unreliable on distant relatives (5), and we place little confidence in such studies, our own included (2). Hamer considers our pedigree data to be important and appears to accept these findings unequivocally. Not all persons in the pedigree study by Hamer et al. were interviewed directly (1). Furthermore, a recent larger family history study (6) did not find an excess of maternal gay uncles or gay cousins through maternal aunts, inconsistent with an X-linkage hypothesis, and not replicating the original pedigree study by Hamer et al. (1). Of the original 182 families ascertained by us, 48 were genotyped because these families were willing to provide blood for DNA studies. These families did not deviate from the larger group in any significant way regarding family history. The subset of genotyped individuals was not different from the total sample in its constitution of paternal gay relatives from the total population from which it was sampled. In particular, only two of our 48 genotyped families had gay fathers. Therefore, the genotyped families were not “paternally” loaded (vide infra). Hamer questions the power of our sample to detect linkage. If Xq28 allele sharing in the gay brother pairs is actually 67%, as he states, our power to detect sharing at the 5% significance level, assuming 50 independent pairs, is 82%, a level which would be considered adequate under most statistical standards. The sharing in our sample, the largest published to date, was nowhere near the 67% figure. We can reject the hypothesis of 67% sharing with p 0.002 (exact binomial probability). The individuals in our linkage study were all self-identified as gay. On the basis of a more detailed questioning regarding sexual attractions, fantasies, and behaviors on a subset of these individuals, all subjects had Kinsey scores (7) of at least 5. We agree with Hamer that such individuals are unlikely to be incorrectly classified. “It seems unlikely, given the stigma of homosexuality, that a

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heterosexual would masquerade as gay” (8). Thus, our study population was unlikely to include heterosexual males, misclassified as being gay. Hamer criticizes our categorization of directly interviewed subjects, but appears not to find fault with the casual family history data which he states supports his conclusion. A major emphasis is placed by Hamer (1, 8) on “proper selection” of families on the basis of family history, but a coherent rationale for this selection procedure has not been given, to our knowledge. Presumably, the rationale for this selection procedure is based on the notion that only a subset of gay men carry an X-linked gene, and families need to be selected to enrich for such a gene. The best description of their selection process was given by Hamer and Copeland (8, p. 108). “First, the family should have exactly two gay brothers. If there were only one gay man there’d be no enrichment for the gene, and if there were more than two, we ran the risk of selecting rare and unusual genes. Second, there should be at most one lesbian in the family. This is because the family studies showed that male and female homosexuality were not commonly found together and we wanted to use typical (sic) families. Finally, we did not want families with gay fathers and gay sons, because this pattern would not be consistent with X-chromosome linkage.” Hamer et al. (1) and Hu et al. (4) did not exclude gay brother pairs with gay uncles or cousins on the paternal side, nor did we. According to these precise criteria, two of our families would be excluded because the fathers were gay, and two would be excluded because they contained three gay brothers. None of the siblings in our study had gay sons and none had more than one lesbian relative. One sib pair with a gay father shared Xq28 alleles, while the other pair with a gay father did not. One sib trio shared Xq28 alleles among the three sibs, while for the other trio, two were concordant and one discordant. Tallying the observed sharing in the remaining 44 sib pairs who met Hamer’s criteria, we obtain 19 of 44 ( 43%) chromosomes shared, which is less, but not significantly less, than the entire sample. Hamer argues that we collected insufficient data on our subjects or families to systematically apply this sort of selection. In fact, the opposite seems to be the case. We have good information on whether the father of the sibships is gay and whether the gay sibling pairs have gay sons and on the number of lesbian mothers or sisters. With the use of identical inclusion/exclusion criteria as employed by Hamer et al. (1) and Hu et al. (4), we obtained no evidence of excess allele sharing for Xq28 markers. On the other hand, the logic of these proposed exclusion criteria is not sound. Hamer and colleagues have not put forth a coherent genetic model on which such rules would be based. Presumably, an allele at Xq28 would account for a subset of gay male behavior, and sporadic influences might account for the rest (8 ). If this were the case, the probability that a gay brother pair shares an X-linked gene would not decrease if the father or any paternal relative is also gay or if there are lesbian relatives in the family. Furthermore, a sibship with three gay brothers would be even more likely to have inherited the causative X-linked allele than a simple sib pair. The exclusion of sibships with more than two gay brothers based on the “risk of selecting rare and unusual genes” is particularly paradoxical, because this is precisely the type of gene Hamer postulates. The logic of excluding families with lesbian relatives contradicts his own statement (1) that lesbians and gay men do not aggregate in families. If male and female homosexuality are genetically independent, the number of lesbian relatives in a family should be irrelevant. Given these considerations, it would be helpful to see the genotyping results of the families excluded from Hamer’s initial study. These data have not been reported, to our knowledge. One difference between our study and that of Hamer et al., not mentioned by Hamer, is that we used controls (brother pairs with multiple sclerosis) to allow blinded scoring of allele sharing. Apparently no such controls (blind or otherwise) were used by Hamer and, in fact, the initial genotyping was performed by Hamer himself (8). Different individuals in the laboratory should perform different steps: phenotypic characterizations and genotypic analyses. We still contend that an X-linked gay gene could not exist in the population with any sizeable frequency, due to the strong selection against it. Hamer reports that gay men in his study had one-tenth the number of offspring of their heterosexual brothers. This degree of selection is comparable to or greater than that for many X-linked genetic diseases such as hemophilia, which exist at low frequencies (approximately 1/10,000) in the population as a result of selection pressure. We agree with Hamer that our results do not exclude the possibility of genetic effects underlying male homosexuality. But with the use of similiar methods of family ascertainment, phenotyping, and genotyping, we were unable to confirm evidence for an Xq28linked locus underlying male homosexuality. Sanders et al. (3) came to the same conclusion with their linkage study. The basis of sexual orientation remains uncertain, but the pathways involved can be expected to be complex. The controversies and methodological difficulties notwithstanding, the study of sexual orientation contains fascinating riddles, and further careful systematic study has the potential to reveal important insights about who we are. George Rice Department of Clinical Neurological Sciences, University of Western Ontario, London, Ontario, Canada, N6A 5A5 Neil Risch Department of Genetics, Stanford Medical School, Stanford, CA 94305–5120, USA George Ebers Department of Neurological Sciences, University of Western Ontario
References
1. D. H. Hamer, S. Hu, V. L. Magnuson, N. Hu, A. M. Pattatucci, Science 261, 321 (1993). 2. G. Rice, C. Anderson, N. Risch, G. Ebers, Science 284, 665 (1999). 3. A. R. Sanders et al., poster presentation 149, annual meeting of the American Psychiatric Association, Toronto, Ontario, Canada, 1998. 4. S. Hu et al., Nature Genet. 11, 248 (1995). 5. W. D. Thompson et al., Arch. Gen. Psychiatry. 1, 53 (1982); N. C. Andreasen, ibid. 34, 1229 (1977). 6. J. M. Bailey et al., Behav. Genet. 29, 79 (1999). 7. A. C. Kinsey, W. B. Pomeroy, C. E. Martin, Sexual Behavior in the Human Male (Saunders, Philadelphia, PA, 1948). 8. D. H. Hamer and P. Copeland, The Science of Desire: The Search for the Gay Gene and the Biology of Behavior (Simon and Schuster; New York, 1994). 21 June 1999; accepted 7 July 1999

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Constructing the ‘gay gene’ in the news: optimism and skepticism in the US and British press
Peter Conrad & Susan Markens
Brandeis University & Temple University, USA

Health Copyright © 2001 SAGE Publications (London, Thousand Oaks and New Delhi) [1363–4593 (200107) 5:3] Vol 5(3): 373–400; 017577

In the 1990s the discovery of a ‘gay gene’ was widely reported in the news media, often as front-page stories. Focusing on the print media presentation of Dean Hamer’s 1993 and 1995 scientific papers reporting finding a genetic marker for homosexuality, we examine how these studies were framed in a selected sample of US and British newspapers and news magazines. We found disparate constructions of the ‘gay gene’ in each press culture. The US press reported Hamer’s study as good science and treated it with ‘cautious optimism’ while the British press reported the research as ‘the perils of the gay gene.’ We discuss how these studies received such widespread attention and the sources and implications of the variant images of the ‘gay gene’ in the news.
A B S T R AC T

gay gene; homosexuality; public understanding of genetics; science reporting; US and British press
KE YWO R D S

Peter Conrad, Department of Sociology (MS 071), Brandeis University, Waltham, MA 02454, USA. [Tel: +1 781 736 2635; fax: +1 781 736 2653; e-mail: conrad@brandeis.edu]
A D D R E SS

Thanks to Ben Davidson and Stephanie Hamer for their research assistance and to John Turney for sharing his clippings of the British press coverage of Dean Hamer’s 1993 study. This research was supported in part by grants from the section on Ethical, Legal and Social Implications of the Human Genome Project of the National Institutes of Health (1 R55 HGOO849–01A1) and the Brandeis University Mazer Fund (Conrad) and a Mellon Postdoctoral Fellowship (Markens).
AC K N O W L E D G E M E N T S

Introduction
For at least a century, scientists and physicians have offered theories about the hereditary predisposition or congenital nature of homosexuality. Scholars and activists in the latter 19th- and early 20th-centuries, including K.M. Benkart, Magnus Hirschfield, Richard von Krafft-Ebbing, and Henry Havelock Ellis, proposed hereditary or congenital theories of 373

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Health 5(3) homosexuality (Greenberg, 1988; Conrad and Schneider, 1992).1 More than anyone else, Franz Kallman, a German-born American psychiatrist, championed hereditary theories in the first half of the 20th century. In an early twin study Kallman (1952) reported that all sets of monozygotic and half of the dizigotic pairs of twins in his sample were homosexual, thus claiming the importance of genetic factors in homosexuality. Subsequent research cast doubt on genetic explanations for homosexual conduct. Research on the biology of homosexuality waned in the 1960s with the rise of the gay liberation movement, the demedicalization of homosexuality, and the emergence of open homosexual and lesbian ‘lifestyles’ (later called orientations) and there was little research or public discussion on the heritability of homosexuality in the 1970s and early 1980s. A few studies in the late 1980s suggested a possible genetic connection (e.g. Pillard and Weinrich, 1986), but it was not until the 1990s that a flurry of scientific papers were published and received widespread attention and news coverage. Between 1991 and 1993 five studies that implicated genetics in the development of homosexuality were published in scientific journals (Bailey and Pillard, 1991; LeVay, 1991; Allen and Gorski, 1992; Bailey et al., 1993), culminating with Dean Hamer’s paper reporting the identification of a genetic marker for homosexuality (Hamer et al., 1993). In 1995 Hamer published a second paper making essentially the same claims with a different sample (Hu et al., 1995). Variously, these studies reported distinct areas of the brain related to homosexuality or a high concordance of twins with homosexual orientations. Together these studies received widespread media attention and reopened the public discourse on the heritability of homosexuality. While a number of critiques have been published (Billings and Beckwith, 1993; Byne and Parsons, 1993; Hubbard and Wald, 1993; Byne, 1995), these studies received a significant amount of news coverage and have spurred new debates on the plausibility, validity, and implications of the connection between genes and homosexual orientation. For instance, magazines like Atlantic Monthly devoted a lengthy cover story to the biology of homosexuality (Burr, 1993), while in 1995 Scientific American published two opposing articles on the scientific status of the issue by the major protagonists in the debate (LeVay and Hamer, 1994; Byne, 1995). Additionally, LeVay (1993) and Hamer (Hamer and Copeland, 1994) both wrote popular books about their research and discoveries, a rather unusual medium of communication for scientists. Together these studies revived the nature–nurture debate about homosexuality and spurred a renewed interest in the biological contributions to sexual orientation. While all the studies were widely covered by the press, it was Hamer’s research that gave impetus for a public discussion of the ‘gay gene.’ This article examines how a systematic sampling of influential or national newspapers and newsmagazines in the USA and UK reported the findings and implications of Hamer’s two studies. Our goal in analyzing press accounts is to reveal the media’s role in the social construction of public 374

Conrad & Markens: Constructing the ‘Gay Gene’ in the News understandings of genetic knowledge in general, and the ‘gay gene’ in particular. We focus on Hamer’s research because his studies were the first to identify an actual genetic marker for homosexuality (as opposed to suggesting heritability), and because they also received the most media attention. We first review briefly scholarship on the social construction of the news, with a particular emphasis on science in the news. In particular, we draw on a framing analysis of news reporting that emphasizes the cultural and institutional processes that affect what and how news is reported. After describing the data examined and the methods employed for analysis, we provide a brief overview of the media presentation of the studies that preceded Hamer and a description of his first study. This is followed by a comparison of coverage of the two Hamer studies in the US and British press. Our analytic emphasis is on optimism and skepticism – of both the science of the research and the implications of it – in the media presentation of the ‘gay gene.’ We find that the predominant framing of US and British press stories on Hamer’s research differed enormously in terms of optimism and skepticism, and consequently the ‘story’ of the ‘gay gene’ was told quite differently in each nation. In our concluding section we speculate as to why these differences in press reporting occurred and the significance of such differences in news reporting.

Constructing the news: a framework
Sociologists have examined the social construction of news, describing how social factors have influenced the selection, shaping, and presentation of the news (e.g. Molotch and Lester, 1974; Tuchman, 1978; Gans, 1979; Gamson, 1992; Schudson, 1995). The assumption is that news is a cultural product, reflecting both what is deemed significant and the social organization of news work. As Tuchman notes, ‘newsworthiness is a negotiated phenomenon rather than an application of independently derived criteria to news events’ (1978: 46). Journalists do not simply report ‘the facts’ or ‘both sides of a story,’ but rather present the news in the context of a particular ‘frame.’ Journalists develop specific media frameworks that enable them to process, report, and present large amounts of information quickly and routinely:
Media frames are persistent patterns of cognition, interpretation, and presentation, of selection, emphasis, and exclusion, by which symbol handlers routinely organize discourse, whether visual or verbal. (Gitlin, 1980: 7)

Media frames often determine what becomes ‘news’ and how it is reported. Frames become the central organizing idea to selectively represent certain aspects of the stories (Gamson and Modigliani, 1989; Binder, 1993) and accentuate some information while excluding others. Through everyday news work – selecting what to report, locating and quoting expert 375

Health 5(3) commentary, and organizing and presenting the news – news organizations provide an important piece of the public discourse. When journalists construct a news story, they must decide how to frame the issue, choosing from a number of available frames to give meaning to their story. Thus reporters are more than messengers of information (Gans, 1979); their presentation adds something to the story. The process of placing the news in some type of context, developing a narrative line about an event, can be depicted as a type of story telling (Schudson, 1989). Different frames can lead to different stories. In the past few decades science, medicine, and health have become a more regular part of news reporting. Many newspapers and magazines have special science sections that regularly report and showcase medical and scientific findings. In a sense, science and medicine have become news beats for specialized reporters, much like the police station was a long-time reporting beat. Major scientific/medical journals and professional organizations, as well as university public relations offices, have contributed to the dissemination of scientific news. Scientific findings are often complex and ambiguous, yet reporters need to write non-technical, compelling, and readable stories. ‘Science writers, in effect, are brokers, framing social reality for their readers and shaping the public consciousness about science-related events’ (Nelkin, 1995 [1987]: 161). As Van Dijck (1998) suggests, the popularization of science is a process of translation and negotiation. For most people, the reality of science is what they know from the press (Nelkin, 1995 [1987]). Science reporting is often accused of distorting science through inaccurate, sensationalist, or unbalanced reporting (Durant and Hansen, 1995). On the other hand, the media is also criticized for presenting uncritical and overenthusiastic views of scientific discoveries (Nelkin, 1995 [1987]). Only a small amount of the research produced by scientists is covered by the media at all, and even a smaller portion of this receives enough attention to become national news. By offering ‘the public an item of news, [the media] confer upon it public legitimacy,’ amplifying its importance, and distributing it widely in its particular story frame. The news, then, becomes part of ‘public knowledge’ (Schudson, 1995: 19). For our analysis, it is useful to build on Schudson’s (1995) conception of journalism as a cultural system, replete with beliefs, values, and assumptions about the world as well as about their audience. He writes:
The news . . . is produced by people who operate, often unwittingly, with a cultural system, a reservoir of stored cultural meanings and patterns of discourse . . . News as a form of culture incorporates assumptions about what matters, what makes sense, what time and place we live in, what range of considerations we should take seriously. (Schudson, 1995: 14)

In this sense, we can see media cultures as systems of cultural meanings that influence what becomes news and how it is reported. These are fluid 376

Conrad & Markens: Constructing the ‘Gay Gene’ in the News cultures, of course, but contain some discernible assumptions and beliefs that influence how news is framed. Given that this research examines print media, our analytical framework focuses on comparing how different ‘press cultures’ reported scientific studies on genetics and homosexuality. Our unit of analysis, then, is not individual journalists or even for the most part particular newspapers or magazines, but rather two national press cultures: the mainstream US press and the mainstream British press.2 But in our comparison, the focus is even narrower, on what might be called ‘science reporting’ press cultures. The major emphasis of this article is to compare how two press cultures have covered the research of Dean Hamer and his colleagues and thus constructed a media discourse about the ‘gay gene.’

Methods and data
We developed two separate national media samples from the USA and the UK for this study. For each we attempted to be comprehensive, including all articles within the sample frame. In both samples we used newspapers that are widely recognized as among the national or regional leaders. While print media is not necessarily identical to broadcast or popular magazine coverage, it certainly can be seen as representative of news presentation (Adelman and Verbrugge, 2000). In the context of a larger study (Conrad, 1997), we developed a US sample that included six major newspapers and three news magazines reporting on six studies over a two-year period. The newspapers included New York Times (NYT), Boston Globe (BG), Washington Post (WP), Wall Street Journal (WSJ), Los Angeles Times (LAT), and San Francisco Chronicle (SFC). The initial time frame studied was from 30 August 1991, when LeVay’s study was first reported, to 30 August 1992, a month after Hamer’s first study was released, and for a month after the publication of Hamer’s second study (November 1995). For this article, we only use the articles reporting on Hamer’s first (N=15) and second (N=9) studies plus three additional articles from Newsweek, Time, and US News and World Report. Our sample includes news stories, features, editorials, and op-ed pieces. In 1993 all articles were written by science reporters for the individual newspapers. For the 1995 sample, three of the nine reports were from wire service stories, the remainder individually authored. All of the news magazine stories were individually authored as well. The second sample was comprised of clippings from the British press reporting Hamer’s two studies. The included articles from The Times, the Telegraph, the Guardian, the Independent, the Daily Mail, the Observer, and The Economist from 1993 and 1995, most of which were published within a short period of the studies’ release. The British sample included 48 articles. All of the British articles were authored by reporters for individual newspapers. We used a modified form of qualitative content analysis to analyze our 377

Health 5(3) data, emphasizing careful coding and inductive analysis in the grounded theory tradition (Glaser and Strauss, 1967). We examined how news stories were framed, how the studies were reported (e.g. findings, implications), the headlines used, where the story was placed, the number and types of ‘experts’ quoted, and the stance (if any) presented in the story.

Optimism and skepticism about a ‘gay gene’
Opening the media discourse: from LeVay to Hamer
Prior to the 1990s there were very few articles in the popular press on biology and homosexuality. Beginning at the end of August 1991 with articles on Simon LeVay’s findings of a smaller hypothalamus in brains of gay men who had died of AIDS, the US press gave significant attention to studies linking homosexuality to biology. Reports on LeVay’s study reopened the media discourse on biology and homosexuality; this was essentially the first national news coverage of a new biology of homosexuality. The US press covered LeVay’s findings widely: on 31 August the study was front-page news in virtually all the newspapers in our sample and was covered by all the news magazines in their 9 September issue. Other studies by Bailey and Pillard (1991), Allen and Gorski (1992), and Bailey et al. (1993) were also well covered by the newspapers, although receiving less attention than LeVay’s.3 The articles were briefer and each of the other three studies became a front-page story only in one newspaper (although many were placed in other prominent locations, such as page three). The news magazines, on the other hand, tended not to report these studies, except as part of longer articles. In one exceptional case, Newsweek featured the LeVay and Pillard studies in a nine-page cover story (24 February 1992). The striking cover showed a super close-up of a young child’s face with soft eyes, asking in bold letters ‘Is this child gay? Born or bred: The origins of homosexuality.’ All of this attention preceded the publication of the two Dean Hamer studies when we see the news media increasingly focusing its reports around existence of a ‘gay gene.’ Indeed, compared to Hamer’s study, these articles stimulated few op-ed pieces and no editorials. In the 16 July 1993 issue of the prestigious journal Science Dean Hamer and his associates at the National Institutes of Health (NIH) published ‘A linkage between DNA markers on the X chromosome and male sexual orientation’ (Hamer et al., 1993). This article reported the discovery of a genetic marker for homosexuality on the Xq28 region of the X chromosome. Beginning that day, headlines around the world announced the discovery of a new genetic link to homosexuality, which soon became termed by some as the ‘gay gene.’ As part of their regular procedure, Science produced a press release highlighting some of the more interesting research published in their current issue. The news release is sent a week early to journalists (so they may have time to prepare their story) and embargoed until the night before the 378

Conrad & Markens: Constructing the ‘Gay Gene’ in the News journal is officially published. At Hamer’s home institution, the National Cancer Institute, the public relations office also created a news release (National Cancer Institute, 1993). The first page and a half of the Science news release for the 16 July issue featured a summary of Hamer’s research. Hamer was concerned about the potential of media misinterpretation and thus helped write the release (Landau, 1995). Under ‘DNA markers link male homosexuality to X chromosome,’ the release began:
Researchers at the National Institutes of Health have used pedigree analysis and family DNA linkage studies to identify a region on the X chromosome that may be linked to sexual orientation in a select group of males. This analysis constitutes the first step toward mapping and isolating a genetic locus that may influence sexual orientation within a certain subset of male homosexuals. (American Association for the Advancement of Science, 1993)

The language was appropriately qualified: ‘region,’ ‘may be linked,’ ‘in a select group of males,’ ‘first step,’ and ‘which may influence.’ The next two paragraphs went on to describe briefly the methods and findings of the study, ending with:
They found 64% of the sibling pairs tested had a cluster of five identical markers within a discrete region on the tip of the long arm of the X chromosome. This region, called Xq28, is approximately 4 million base pairs long, and is large enough to contain several hundred genes. Identification of an individual gene that might predispose certain males toward homosexuality will require further linkage analysis to narrow the target chromosomal region or complete sequencing of the region. ‘Once a specific gene has been identified,’ say the authors, ‘we can find out where and when it is expressed, and how it ultimately contributes to development and function in both homosexuals and heterosexuals.’ (American Association for the Advancement of Science, 1993)

Here the language is more precise – ‘64% of sibling pairs tested,’ ‘five identical markers,’ ‘Xq28,’ ‘contain several hundred genes’ – and also circumspect – ‘requires more linkage analysis,’ ‘contributes,’ ‘development and function in both homosexuals and heterosexuals.’ The news release was tempered and replete with all the caveats noted in the study. In essence, the release described well what had been discovered: an association between a set of genetic markers on the X chromosome with sexual orientation in a select group of homosexual male sibling pairs. A contact telephone number for Hamer was included at the end. The NCI release was similar in content though not quite as detailed, and contained numerous cautious quotations from Hamer, including that no single gene had been identified. Nowhere in the news releases, or in the article itself, does it say that a ‘gay gene’ had been discovered or even that a specific gene had been identified. On 16 July, newspapers in the United States, Great Britain, and presumably elsewhere reported this study. In most of the US and British papers, the story was presented as front-page news. In the month that 379

Health 5(3) followed hundreds of news articles, columns, and editorials related to the research were published. We examined the total coverage of articles in our two samples, which yielded 27 US, and 48 British press articles. Due to somewhat different styles of newspaper reporting, the British articles tended to be shorter but more numerous than the US ones (e.g. two or three separate articles may appear in a UK paper, which might be combined into a single article in the USA). What was most striking about the coverage in the two samples was the varying frames used to report the study. While each press culture demonstrated certain amounts of optimism and skepticism about the study, these appeared in different doses and packaging. We suggest, therefore, that by framing the story rather differently, the press constructed rather different images of the ‘gay gene’ and its implications. That is, the ‘gay gene’ was refracted by the different press cultures reporting it, thereby potentially shaping different public understandings and responses to new genetic knowledge.

The US press: cautious optimism
Hamer’s study was reported widely in the mainstream US press; five of six papers in our sample treated it as front-page news and all three news magazines covered it. While the study was reported on the front page, the headlines tended to be descriptive and moderate in tone: ‘Report suggests homosexuality is linked to gene’ (NYT, 16 July 1993) or ‘Genes help explain the origin of homosexuality’ (BG, 16 July 1993). Two of the papers employed ‘gay gene’ in their headline: ‘Research points toward a “gay” gene’ (WSJ, 16 July 1993) and ‘New evidence of “gay gene” in some men’ (SFC, 16 July 1993). In all the US papers, the thrust of the headline focused on what the researchers purportedly discovered, a genetic link to homosexuality. The overall framing in the US press was one of ‘cautious optimism’ about the findings and their implications. The tenor of the reporting was optimistic, but was tempered by cautions that this was only a single study and needed to be replicated. This admonition reflected the journalists’ recent experience of seeing a number of other media-heralded behavioral genetic ‘discoveries’ quickly disconfirmed by further research (Conrad, 2001). The framing of the potential implications of Hamer’s study was also cautiously optimistic: ‘naturalizing’ homosexuality could reduce discrimination against gays but also could have more adverse results. The US press treated the study as a significant piece of scientific research. Depictions like ‘. . . strongest evidence yet . . .’ were common. The study was reported respectfully, often with great scientific detail. It was presented as an important scientific contribution in an on-going line of research (related to LeVay, Bailey, and Pillard, among others); as the Washington Post noted, the ‘findings add to a growing body of evidence . . .’ (16 July 1993). The study was deemed as one step toward future discoveries: 380

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. . . eventually, biologists hope, they will learn how the gene works. (Newsweek, 26 July 1993) . . . researchers . . . are racing to identify the specific gene from the 100 or more in the region. (LAT, 16 July 1993)

Most journalists recognized this was only one study that needed confirmation, but reported with confidence that genetics seems to predispose some men toward homosexuality. US News and World Report wrote that the research ‘suggest[ed] with 99% certainty that sexual orientation in men was genetically influenced’ (26 July 1993), while Time reflected the Science article claim that the study ‘. . . strongly suggests that at least one gene related to homosexuality is located in the region’ (26 July 1993). Their confidence was buoyed by scientists who praised the research as good science; for example, Eliot Gershon called it an ‘excellent study’ (WP, 16 July 1993) and ‘a major breakthrough in behavioral genetics’ (LAT, 16 July 1993), while others doubted that it could be totally disconfirmed. Many, including Hamer and LeVay, were optimistic about the potential impact of scientific evidence on the status of homosexuals and homosexuality. Gay rights activists suggested that if sexual orientation could be shown to be genetic, then it would be deemed ‘natural’ and ‘not chosen.’ Activists like Greg King and Richard Green were frequently quoted saying that the ‘evidence could be liberating,’ that this was a ‘landmark study . . . (for) civil rights’ and ‘immutability’ could lead ‘to an overturning of discrimination laws’ (quoted in US News and World Report (USNWR), Newsweek, and LAT). A Boston Globe editorial reflected the optimism of Hamer and the gay activists:
The discovery that male homosexuality may be caused in part by a certain gene or cluster of genetic material raises hopes that the debate over sexual orientation may soon move into a more rational, factual and appropriate sphere . . . If proven . . . [this evidence would] go far toward undermining the narrowly gauged argument that homosexual behavior is misconduct . . . [and] . . . could ease the struggle to secure equal protection. (20 July 1993)

Others voiced optimism that the findings could have a positive impact on relations between parents and their gay sons, in terms of reducing guilt and blame (Time, 26 July 1993). The US press showed general acceptance of Hamer’s findings, although with a few caveats. Several articles pointed to limits in the science: a gene was not yet isolated (WP, 16 July 1993) and it was not yet known how such a gene might work (BG, 26 July 1993; Billings in SFC). Newsweek and Ruth Hubbard (a well-known biologist and public commentator on science) in an op-ed piece in The Times (2 August 1993) pointed out methodological shortcomings: the researchers had not tested the DNA of heterosexuals, particularly checking for the genetic markers in heterosexual brothers. By far the most common admonition, mentioned in nearly all the articles, was the need for the findings to be replicated. As the New York Times (18 July 381

Health 5(3) 1993) noted, ‘the results have got to be confirmed by another laboratory’ and even if they hold up, this ‘is surely just a single chapter’ in understanding sexual orientation. Several of the articles noted that previous genetic findings for alcoholism, schizophrenia, and manic-depression were soon disconfirmed. As the Washington Post commented (16 July 1993), ‘claims of genes relating to behaviors have been notoriously difficult to prove.’ Although highly skeptical op-ed pieces by Hubbard (NYT) and geneticist Paul Billings (SFC) were published, the overall tenor in the press was that it seemed to be good science. There was, however, more skepticism about the interpretation of the data. Many of these cautions were articulated by Hamer when he was quoted in the press. Indeed, the news articles prefaced many of their points with ‘the researchers concede’ or ‘the researchers warned,’ highlighting that the scientists were aware of the limits of their study. These included comments indicating that Hamer had not found the gene for homosexuality and ‘. . . it was not the only cause of homosexuality’ (Newsweek, 26 July 1993), especially since ‘some gay men in the study did not fit the pattern, showing clearly that no single gene or set of genes can explain . . .’ sexual orientation (SFC, 16 July 1993). Several articles noted that a ‘gay gene’ had not been discovered: ‘the researchers warned against over-interpreting the work, or taking it to mean anything as simplistic as a “gay gene” had been found’ (SFC) and ‘the findings . . . do not prove there is a “gay gene” that invariably causes homosexuality or that all men have it’ (WP, 23 July 1993). Virtually all these caveats had been anticipated by Hamer, either in the Science article or in his quoted comments. A certain amount of concern and skepticism was voiced about the potential implications of this research. In contrast to the optimism of Greg King, a number of gay commentators were less sanguine about the enthusiasm in parts of the gay community for Hamer’s research and observed that ‘. . . science is unlikely to be much help in our search for rationality and justice’ (WP, 13 August 1993). Several articles noted that the genetic testing could lead to more employment and insurance discrimination. The San Francisco Chronicle wrote, ‘if a test for a “gay gene” were ever possible, regulations might be needed to prevent information from being used in hiring or other practices’ (16 July 1993). A few writers presented more dire concerns about prenatal testing, suggesting that ‘identification of a “gayness gene” [could] prompt efforts to tinker with the genetic code or test during pregnancy about potentially gay fetuses’ (Time, 26 July 1993). Several activists were quoted expressing eugenic concerns; for example, John DeCecco, editor of the Journal of Homosexuality warned there is ‘no guarantee that [genetic] information won’t be used for sterilization or to pressure others not to bear children’ (SFC, 16 July 1993). Both Time and Newsweek mentioned Jonathan Tolins play, ‘Twilight of the Golds,’ which provocatively and tragically depicts the dilemmas and pain a test for a ‘gay gene’ can have on a family. But it is important to note here that while testing and selective 382

Conrad & Markens: Constructing the ‘Gay Gene’ in the News abortion were mentioned in the mainstream US press, they were by no means the predominant concern. They were mentioned along with other potential implications, like employment, military, and insurance discrimination. However, for the most part, the US press was predominantly optimistic, and much of this optimism was framed around the high quality of the science involved in the research.

The British press: the perils of finding a ‘gay gene’
The British press reported Hamer’s finding widely but with a different framing. The tenor of the reporting was clearly less supportive of the science and more concerned about the dire potentials of such a discovery. The headlines announcing the research fell into two categories. Some paralleled the US newspaper headlines: ‘Homosexuality linked to genes’ (Independent, 16 July 1993) and ‘Genetic basis for homosexuality, scientists claim’ (Telegraph, 16 July 1993). But the tone of most of the headlines of a number of articles published over the next two days highlighted a different framing of the story:
‘Gay Gene’ raises screening fear (The Times, 17 July 1993) Genetic genies won’t go back in the bottle (The Times, 17 July 1993) The ‘gay gene’ raises a host of issues (Independent, 17 July 1993) The genetic tyranny (Independent, 18 July 1993, editorial) Your mother should know (Guardian, 18 July 1993) Born to be gay (Telegraph, 18 July 1993) The myth of the gay gene (Observer, 18 July 1993) Genes, gays and a moral minefield (Daily Mail, 17 July 1993)

The headlines presage a framing press highly critical of the implications of the study. The British press actually published relatively more articles on the first Hamer study. But the articles contained far less detail about the research (with the exception of the news magazine The Economist (17 July 1993)). While a US news story might include from three to eight paragraphs on the findings, often with a graphic about pedigree or DNA findings, most British articles took a more bare bones approach. Few articles included more information than noting it was a study of gay brothers, with perhaps a few numbers (e.g. 33 of 40 brothers had the same markers) or percentages, and that the marker was located on the Xq28 region, and most had less. Details about the findings, pedigrees or method were largely absent from even the initial reports. The British articles seldom included quotations from scientific ‘experts,’ other than Hamer. There was simply much less about the science in the stories. The overall framing of the story in the British press was that finding a 383

Health 5(3) ‘gay gene’ held within it many perils, especially the eugenic potentials for gays through ‘testing and termination.’ Although this frame dominated the British coverage of Hamer’s first study, some rays of optimism were visible. The British press displayed some optimism about the research, though it was often muted. While the Independent reported ‘Scientists have found the first hard evidence for a genetic basis for homosexuality’ (16 July 1993), The Times was more circumspect: ‘American scientists believe they have discovered . . .’ (16 July 1993, emphasis added). The Daily Mail called it the ‘firmest evidence yet of a biological basis for homosexuality’ (17 July 1993) but many articles said little about the science. A few articles (e.g. Guardian, 17 July 1993) presented moderate detail about the study itself, but most contained very limited or no specifics about the research and the findings. Several articles showed a general optimism about the accumulation of evidence in this line of research:
Evidence has been growing that there is an inherited component in homosexuality. (The Times, 16 July 1993) Piece by piece, evidence is mounting that genetic factors predispose people toward homosexuality. (Independent, 16 July 1993, editorial) . . . we might, by the end of the century, discover the identity of the gene, if it exists . . . (Observer, 18 July 1993)

Less attention was given to whether or not this study represented good science. However, the Telegraph (16 July 1993) quoted one scientist as saying it was ‘more significant’ than previous studies (Telegraph, 16 July 1993), and the well-known geneticist Steve Jones, in his article in the Daily Mail (17 July 1993), noted that the early studies of the gay gene were ‘rubbish’ and ‘this one almost certainly is not.’ It is difficult to find much genuine optimism in the British press about the potential implications of the study. A few articles and an editorial (The Times, 17 July 1993) mentioned in passing that if homosexuality were seen as inborn and in a more neutral light, it could possibly reduce discrimination. Several times journals would report ‘some hailed the report as sensible and helpful,’ but follow this with a barrage of quotations cataloguing the potential perils of the research. Indeed, British writers attributed optimism about the findings’ implications to Americans. As part of three articles filling an entire broadsheet page, a journalist wrote in the Sunday Telegraph:
Many Americans are predisposed to accept the idea that they are ‘born to be gay’ if it provides hard evidence that they are indeed ‘different’ and should no longer be victims of stigmatization or social penalty. They believe that with this proof they will be able to change the law. (18 July 1993)

But most of the quoted British activists in that article were more skeptical

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Conrad & Markens: Constructing the ‘Gay Gene’ in the News about the research and its implications. Even when potential social benefits were mentioned, British writers adopted a clear ‘yes, but’ frame, followed by a litany of liabilities. While it is possible to find optimistic statements in the British press, the dominant framing of the perils of the ‘gay gene’ influenced all the reporting, from the scientific findings, to the interpretations of the study, to its implications. The tone of reporting often intimated a sense of disbelief, as when The Times put ‘the first hard evidence’ in quotation marks (17 July 1993). Two articles pointed out that the record of science on homosexuality was mostly ‘rubbish’ (e.g. Daily Mail, 17 July 1993; Independent, 18 July 1993). The reports contained a few critiques of methodology by biologists like Ruth Hubbard and Steven Rose, but by and large the news reports did not present specific criticisms of the study. Several articles mentioned the previous disconfirmations of other behavioral genetic findings. In a sense, the British press followed Hamer’s lead in interpreting the findings. His cautious statements that homosexuality cannot be explained by a single or groups of genes, that it has a variety of causes, and that he had not discovered a gene for sexual orientation are well represented in the press. Writers in the Independent emphasized what has not been discovered. While they point out that a gene for sexual orientation had not been identified, they go on to say ‘we don’t yet know what this gene does, and until we do, its role is a matter of speculation.’ They continue: ‘It is a myth that just because something is “in your genes” your fate is immutably determined’ (18 July 1993). The Times quoted a scientist who doubts complex social behavior is controlled only by genes (18 July 1993) and the Guardian reminded us ‘genes have no monopoly on determining human behavior’ (22 July 1993). While Hamer and his associates articulated similar points as caveats to their study, they seem to be presented here as indications of flaws in the research. One issue raised by the British but not the US press was ‘the Darwinian puzzle;’ why, in evolutionary terms, had the homosexuality gene persisted and ‘not been wiped out by natural selection’ (Independent, 17 July 1993). Most of the explanations of potential evolutionary advantage or genetic persistence are totally speculative. Yet, asking the question about genetic survival assumed that there is a ‘gay gene,’ and that understanding ‘it’ in evolutionary terms is a sensible endeavor. While the evolutionary issue raised intriguing intellectual questions in its own right, it also reflected on the dangers of tinkering with nature’s way. This type of perilous frame dominated the discussion of the implications of the research. The perils of ‘testing and termination’ eclipsed all other issues in news coverage. From the tabloid Daily Mail’s headline ‘Abortion hopes after “gay gene” findings’ (17 July 1993) – which was quoted several times in other reports – to the repeated concerns in the broadsheet press, this issue became ‘the’ focus of the story. Several articles led with the issue:

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Evidence of a genetic component to homosexuality was published by an American team today, opening up the possibility of testing and eventually manipulating sexual orientation. (Telegraph, 16 July 1993) Scientists, medical ethicists, and gay activists yesterday warned of the dangers of using the discovery of a genetic basis for [homosexuality] to tinker with homosexual preferences . . . They were unanimous in their disgust . . . [about the] possibility of selective abortions. (Independent, 17 July 1993)

There was a repeated concern that with a test for the ‘gay gene’ would come a widespread demand for abortion. The Times devoted one-third of a lengthy article to selective abortion (17 July 1993). The Telegraph wrote of a fear that Hamer’s finding could be used ‘as a basis for blood test for homosexuality and attempts to eliminate it by selective abortion’ (16 July 1993) or ‘abortion of the foetus “at risk” ’ (17 July 1993). Several gay activists were quoted as fearing testing and selective abortions of gay sons; Peter Tatchell said ‘that would be tantamount to prenatal genocide’ (Daily Mail, 17 July 1993). Two newspapers printed lists of famous people who might have been ‘lost’ through selective abortion, including Benjamin Britton, Virgina Woolf, Tennessee Williams, Michaelangelo, W.H. Auden, and Martina Navratalova. The Guardian wrote that the findings ‘set alarm bells ringing . . .’ (17 July 1993) perhaps most specifically in David Alton, a liberal member of Parliament, who called for a ‘gene charter’ to protect homosexuals and others from testing. Virtually all the papers quoted medical ethicists declaring that it was wrong to abort for social reasons. An Independent editorial suggested there was reason for alarm: ‘Scientists have implied their work is wholly beneficial, designed purely to eliminate “defective genes”. This is why gays have reacted with alarm to last weekend’s news . . .’ (18 July 1993). One response to Hamer’s research did create a reaction of its own. Rabbi Jakobovits, the former chief rabbi in the UK, wrote in a letter to The Times (17 July 1993) that homosexuality was ‘a grave departure from the natural norm which we are charged to overcome like any other affliction, genetic or not.’ In the letter and later elaborations, he suggested if medicine discovered a way to ‘cure’ the genetic ‘disability,’ there was no reason not to pursue some forms of genetic engineering to eliminate the trait. Lord Jakobovits specifically did not counsel for abortion, but his statements brought a loud response of protest, mostly in letters to the editor (seven were published in the Guardian alone). While Jakobovits’ statements did not receive inordinate press attention, they reinforced concerns about genetic interventions to eliminate gays. The eugenic concerns of ‘testing and termination’ were paramount and dwarfed all other potential implications. There was some mention of the potentials of discrimination and notice that ‘moral questions are too complicated to be settled by scientific discoveries’ (The Times, 17 July 1993), but as the openly gay actor Ian McKellan wrote in the Guardian, the 386

Conrad & Markens: Constructing the ‘Gay Gene’ in the News over-riding issue in the press was whether a mother should have the right to abort her gay fetus. Yet despite their skeptical viewpoint, the British press tended to report the story as if there were a ‘gay gene.’ They use the term more freely than the US press, both in headlines and stories, and often tended to report as if they are writing against the ‘gay gene’ finding. They raised the ‘Darwinian puzzle,’ which assumed there was such a surviving gene. There is an irony here: the British press presented Hamer’s study with skepticism and fraught with peril, yet at the same time their reporting of the research amplified the idea that there actually is a ‘gay gene’ which could create such apprehension.

Hamer refraire
In the November 1995 issue of Nature Genetics Hamer and his colleagues published their second article on the Xq28 chromosome and homosexual orientation. The National Cancer Institute press release announced that a collaborative study ‘reported new results that support and extend the previous finding of a genetic link for sexual orientation in some men’ (National Cancer Institute, 1995: 1). The release contained a general statement about the conclusions, but few details about the study. Included was a cautious quotation from Hamer:
Sexual orientation is a complex characteristic that is influenced by many different factors. Although there is a reproducible statistical relationship, the Xq28 region is neither necessary nor sufficient for a homosexual orientation in men, nor can it rigorously be excluded from playing a subtle role in women. (National Cancer Institute, 1995: 1)

The release briefly noted some related studies, but did not use the term ‘gay gene.’ The press reported Hamer’s new study, but with considerably less attention than the first study. While we included all articles relating genetic research and homosexuality in our 1995 sample, there were considerably fewer than in 1993, perhaps because it could no longer be deemed a ‘breakthrough.’ The US press sample had nine and the British press 12 articles. We examined each press sample to gauge the continuities and divergences with their previous framing of the genetics and homosexuality story. Until the publication of Hamer’s article, it had been a quiet year for stories on genetics and homosexuality in the US press; the only exception was a rather detailed story in Time magazine in June reporting on the genetics of ‘homosexual’ fruit flies. This is interesting in light of the potential news about Hamer and the research. On 25 June, John Crewdson, a Pulitizer Prize winning journalist, wrote an article in the Chicago Tribune that reported allegations by a former postdoctoral colleague that Hamer selectively reported his data in ways that supported his conclusion. These allegations were being investigated by the Office of Research Integrity (ORI) 387

Health 5(3) at NIH. In addition, Crewdson reported that a Canadian geneticist, George Ebers, had failed to replicate Hamer’s findings on Xq28. Ebers, in an unpublished study, had found no significant differences in the markers among homosexual brothers. Science magazine reported the Crewdson article in the news section of its 30 June issue as ‘NIH’s “gay gene” study questioned’ (Marshall, 1995). This story was ignored by all the major US newspapers and magazines in our sample, although it was picked up via the wire services in a few other newspapers (York, 1996), and was reported in two articles in the British press sample. Only when Hamer’s second study was published did the allegations or Ebers’ study get any mention at all in our mainstream US press sample.4 The American Press II The media coverage of Hamer’s second article was variable. For example, the Washington Post highlighted it with a lengthy front-page article ‘above the fold,’ the Boston Globe reported only with a one-paragraph wire service story, the New York Times featured an article on genetics and schizophrenia from the same Nature Genetics issue and discussed Hamer only in the last three paragraphs of a 20-paragraph story, and the Wall Street Journal did not cover it at all. In some journalists’ eyes it was an important replication (WP) while in others it did not qualify as new news. By 1995, it was common to use the term ‘gay gene’ in news stories, as was evident in headlines like ‘Study provides new evidence of “gay gene” ’ (WP, 31 October 1995) and ‘Search for the gay gene’ (Time, 12 June 1995). Most of the media reported the Hamer study as ‘bolstering’ (Associated Press story in BG and LAT) or ‘confirming and extending’ (NYT; WP) the earlier study. Some saw it as ‘stronger evidence’ while noting the usual caveats. As the almost breathless Washington Post story pointed out, however, the ‘gay gene’ was gaining acceptance at a rapid pace.
A few years ago, the notion of a ‘gay gene’ was regarded as speculative, if not outlandish. But now numerous labs across the country are investigating whether and how genetic variation may affect sexuality, and the next few years will produce an explosion of data in this highly volatile field. (31 October 1995)

Time was a bit more restrained regarding the genetic origins of homosexuality: ‘It seems now that the answer is a definite, maybe’ (12 June 1995). It is notable that in this set of articles, we see virtually no discussion of the potentially beneficial implications of finding a ‘gay gene’ for gays and lesbians. There were a few passing lines about a split in the gay community over whether finding a gene linked to homosexuality would be advantageous or harmful to gays, but nothing about the benefits of the ‘naturalization’ of homosexuality or its impact on gay rights. This may be due in part to shorter stories or that this had already been presented in the 1993 stories. The continuing optimism was based mostly on that the research was seen for the most part as good science. 388

Conrad & Markens: Constructing the ‘Gay Gene’ in the News The New York Times (31 October 1995) story was unusually skeptical of the science of behavioral genetics: ‘the only thing they are sure of in their various hunts is that no single gene can explain any behaviors they studied,’ particularly in the light of previous disconfirmations and, in Hamer’s case, lack of verification by an independent lab. Science reporter, Natalie Angier, wrote that: ‘For now, the putative “gay gene,” like the unicorn, remains a tantalizing quarry well beyond the hunter’s grasp’ (NYT, 31 October 1995). Most articles point out that even if this bolsters the earlier findings, a specific gene had not yet been identified. Overall, they were a bit more circumspect about the study, noting for example: ‘Even a “gay gene” might not mean that homosexuality is predestined’ (Newsweek, 13 November 1995) or quoting Bailey, ‘I wouldn’t say the findings are definitive’ (USNWR, 13 November 1995). Perhaps the press expected more than Hamer replicating his own findings, albeit with a different sample. The mainstream press sample had not covered the allegations made against Hamer nor Ebers’ research in June and only a few gave it much attention when reporting Hamer’s second study. Two of the news magazines noted it in one or two sentences at the end of their articles. The Washington Post did discuss Ebers’ inability to confirm Hamer’s results, but spent much of the space neutralizing Ebers’ findings, by saying that even if it were true, they would not automatically invalidate Hamer’s findings and that this happens often in the early stages of pioneering science. The New York Times mentioned that an Ontario team had failed to replicate, but did not identify Ebers by name. Overall, then, the tenor of the reporting in the US mainstream press remained cautiously optimistic about a ‘gay gene,’ although the reporters’ optimism did not seem to have increased in the two years between the studies. The British Press II All newspapers in our British sample reported Hamer’s second study, but also with less vigor and attention (e.g. shorter stories and no front-page placements). By this time virtually all the papers readily used ‘gay gene’ in their headlines, despite highlighting different issues. But the British press was less reticent about reporting Crewdson’s story. On 9 July the Sunday Mail headlined a story: ‘Exposed: Suspect science – flawed work of gay scientist who misled the world.’ In a vituperative story, Mark Almond criticized Hamer, the research, and the ‘vocal homosexual lobby.’ He said rather little about the actual allegations, only alluded to Ebers’ study, and briefly mentioned the ORI investigation, but used this as an occasion to attack Hamer and his study. Almond wrote, ‘I read his findings with distaste and skepticism. To me he was a scientist playing God . . .’ He accused Hamer of having a ‘hidden agenda’ and felt vindicated because other scientists (presumably Ebers) were unable to verify the genes. He identified Hamer as gay (only one US newspaper had done this in a 1993 389

Health 5(3) editorial) and charged him with having a ‘sociopolitical agenda.’ He continued his ad homonym critique by contending that Hamer’s ‘much publicized private life has raised questions of his objectivity.’ One could dismiss such an attack as the opinions of one journalist with an axe to grind, but it also represents a press that all along had been deeply skeptical of Hamer and his research. A day later the more up-market The Times also reported the Crewdson story (10 July 1995), perhaps with less nastiness but no less skepticism. Noting Hamer was under investigation for possible misconduct, The Times wrote:
Now, however, Dr Hamer’s findings are thrown into doubt by the disclosure he is a subject of an inquiry by the US Office of Research Integrity. The agency is investigating allegations by one of Hamer’s colleagues that he selectively reported data in ways that biased his conclusion.

When Hamer’s second article was published in November, the British press would include these issues as a significant part of their stories. The articles reporting the second study consistently deemed it as ‘confirming’ (The Times, Independent, Telegraph, Guardian) Hamer’s previous findings, although perhaps ‘only up to a point’ (The Economist, 4 November 1995). Most of the articles again were rather sparse in presenting the scientific findings, although the Independent (31 October 1995) reviewed the 1993 findings in rich detail while presenting a sketchy picture of the current findings. In both Independent articles, Hamer was quoted enthusiastically as saying: ‘. . . we’re twice as sure as before,’ while noting once again ‘that does not mean we have found a gay gene’ (1 November 1995). The leads of stories set the tone for what follows and often reflect the framing of the stories:
When the ‘gay gene’ was discovered in 1993, the announcement was greeted with horror. (The Times, 3 July 1995) Fresh controversy has flared up over the alleged ‘gay gene’ after the homosexual scientist who says he discovered it said his latest research further supports the claims. (Daily Mail, 1 November 1995) [genes] . . . influenced the sexuality only of men and has not been linked to lesbian behavior. (Telegraph, 1 November 1995)

Whether the lead overplayed public response (‘horror’), highlighted a ‘fresh controversy,’ or emphasized what had not been found, each placed the research squarely within a skeptical frame. Several articles in the sample included mention of the ORI investigation and Ebers’ non-confirming findings as an important part of the story (The Times, Independent, Daily Mail, The Economist). These were seen as further caveats on Hamer’s research. The Times suggested because of the investigation Hamer’s ‘findings [are] thrown into doubt,’ adding ‘Ebers says there is no support for the idea that anything on the X chromosome is predisposing to homosexuality’ (1 November 1995). Overall, half the articles 390

Conrad & Markens: Constructing the ‘Gay Gene’ in the News (seven out of 12) mentioned the misconduct allegations or the ORI investigation while three mentioned Ebers’ non-confirmation. The Crewdson story provided a new type of skepticism that was easily incorporated in the British press’ framing of the story. Similar to 1993, the British press followed Hamer’s lead in articulating the limitations of this study, including the now familiar caveats. But these were presented in ways that could dismiss the story. As the Guardian (1 November 1995) noted, despite the apparent confirmation, ‘. . . the discovery of the “gay gene” seems as far away as ever, and why some people are gay and others are not, just as confused.’ The Times (1 November 1995) stated bluntly: ‘So far the research for what the gene in Xq28 is actually has drawn a blank.’ While the British press recognized that a number of gay groups welcome the research, especially in the USA (The Times, 13 March 1995), they continued to emphasize the ‘outcry’ from gay activists, especially in Britain. The over-riding concern, as two years earlier, was the development of a prenatal test and possible abortion of the fetus carrying the gene (e.g. Telegraph; Independent). The perils of testing and termination were mentioned regularly, although with fewer alarmist statements than in 1993. There was considerable continuity with the British press’ framing of the ‘gay gene’ story over the two years. Although clearly less news attention was devoted to the second story, the skepticism remained, this time demonstrated by reporting of the ORI investigation and Ebers’ unpublished disconfirmation. Two years did not make the British press any warmer to Hamer’s findings.

Framing of the ‘gay gene’ in the 1990s
Numerous critics, including some journalists and gay activists, have accused the media of sensationalizing the ‘gay gene’ story (e.g. York, 1996). While there are certainly a few examples of this, especially in several alarmist stories in the British press, most of the print media reporting of the content of Hamer’s studies were generally accurate and straightforward. What is true, however, is that in both the British and US press Hamer’s research was published as front-page news and thus received wide public exposure. For a few days, reports of Hamer’s first study received worldwide attention. After a short period in the spotlight, the genetics and homosexuality story quickly faded from the news. How is it that this piece of research received such widespread media attention? Probably a number of factors contributed to this. First, the article was published in the prestigious journal Science, which is one of the few journals that all science reporters regularly monitor. Journalists have great confidence in the research reported here, although there are thousands of other peer-reviewed journals. The Hamer study was featured as an important new discovery in press releases by the journal and NIH. Additionally, 391

Health 5(3) genetics as a genre has been widely covered by the press in the last decade (Nelkin and Lindee, 1995; Conrad, 1997; Condit, 1999) and the genetics of homosexuality was an especially ‘sexy’ story for the media. The four studies that preceded Hamer’s had already rekindled a new public discourse on the biology of homosexuality and in a sense prepared the press and public for a study that identified a genetic marker. Thus Hamer’s findings fit into a line of science stories written in the previous two years. The social context probably affected the media coverage as well. The AIDS epidemic has been widely covered in the press (Kinsella, 1989; Colby and Cook, 1991) and allowed journalists to develop ready ‘sources’ in the gay community. Interest in writing stories about homosexuality, at least in the United States, was heightened in the 1990s due to several gay rights referenda (e.g. Colorado, Oregon) and after November 1992 by President Clinton’s campaign for gays in the military. Moreover, Dean Hamer acted as a publicist for his own research. He was easily available for quotations and made numerous television appearances, including on the popular news show ‘Nightline.’ Hamer attempted to exert some control over how the story was presented in the news, first by aiding in writing the press releases and then by his ubiquitous quotations in the news stories. Hamer’s quoted comments might be characterized as presenting a very optimistic but cautious stance to his study. His optimism about the genetics of homosexuality is apparent in quotations like ‘this is the strongest evidence to date that there is a genetics component to sexual orientation’, ‘we’re 99% sure that specific genes increase the chances of being gay,’ and ‘all scientists already agree there is little element of choice in sexual orientation.’ But at the same time, he remained a cautious scientist when he said ‘genes are only part of the story . . . not all the story,’ ‘it does not mean we discovered a gay gene,’ and ‘sexual orientation is too complicated to be determined by a single gene.’ When he published his second study, he announced ‘we’re now twice as sure’ about the findings. Hamer also readily acknowledged that he has only discovered a marker, representing a genetic linkage, and not identified a specific gene or genes associated with homosexuality. While Hamer certainly recognized the limits of his study, he actively promoted the genetics of homosexuality and freely used the term ‘the gay gene’ although no gene has yet been discovered.5 However, neither the scientist nor the science can control how the research is framed in the news. As we have shown, the US and British press each framed the ‘gay gene’ story in somewhat different fashion. The US press shows more appreciation for the science of the study and takes a more optimistic stance toward its implications. The British press paints a much darker picture of the ‘gay gene,’ emphasizing the potential perils of ‘testing and termination.’ What do we make of these differences in news coverage and what might influence the different framing of the stories? At this point, our interpretations can only be speculative. Broad cultural factors may affect 392

Conrad & Markens: Constructing the ‘Gay Gene’ in the News indigenous press cultures (Schudson, 1995). For instance, it would be simple to say that Americans are optimistic and British more pessimistic, but even if true (and we cannot gauge this) it would tell us little. The US press has been generally optimistic about genetic studies (Nelkin and Lindee, 1995) and perhaps especially molecular genetic research. This aura may well include genetic studies of behavior, although the press is cautious to note that studies needed replication (this is in part a result of a number of previous studies, widely reported in the press, that were later disconfirmed). Our findings are generally consistent with other recent studies of genetic reporting in the British press. The reporting of Hamer’s study in the UK was clearly dominated by what Durant and Hansen (1995) term a ‘rhetoric of concern’ with little room for a companion ‘rhetoric of great promise.’ David Miller (1995) examined the British coverage of Hamer’s first study. He found a lack of homophobia in the press coverage and contends that the emphasis on the ethical issues around the ‘gay gene’ largely results from the liberal perspectives of science journalists and their sources. He argues ‘the major media response to the “gay gene” was a liberal opposition to the use of the “findings” to further discriminate against lesbians and gay men’ (Miller, 1995: 269). While this may have some validity, it does not explain why the dominant framing of the story was the ‘perils of the “gay gene” ’ and why ‘testing and termination’ eclipsed all other issues. It could be argued that the mainstream US press is at least as liberal as the British press, yet they adopted different framing to the story. The reasons for the dominance of a ‘rhetoric of concern’ in the UK, the overwhelming attention given to dire potential implications of the research, are not clear. The over-riding concern with testing and termination may reflect greater public consensus of the availability of abortion on demand in Britain. While abortion remains a divisive and contentious issue in the USA, in the UK there is a wide public acceptance that abortions should be readily available. Thus, if there were a ‘gay gene,’ it would be easy enough for people, should they so wish, to abort the ‘potentially gay fetus.’ This may also perhaps be true in practice in the USA, but the public perception of abortion availability is not the same. A dominant academic perspective for examining the media is the transmission model that assumes the news is a vehicle for transmitting ideas, information, and knowledge from the sender to the receiver. In contrast, James W. Carey suggests that the media also be seen as performing a ‘ritual’ function of building social solidarity by reaffirming shared cultural understandings and values (Carey, 1989). In this view, news can be seen as reenacting beliefs for a community in addition to transmitting a message. Thus taking an optimistic frame about the ‘gay gene’ perhaps reasserts the US belief in the positive power of science, while the British framing reflects a deeper cultural distrust in science or a ‘rhetoric of concern’ (Durant and Hansen, 1995). Thus the news framing is less about social views of genetics and homosexuality than it is about what each culture values. 393

Health 5(3) In addition to cultural influences, structural and institutional factors more directly connected to journalism may have influenced the differences in press framing and reporting. First, there are differences in science reporting. Science reporting is more developed in the USA than the UK, with major newspapers having more science and medicine stories and even special science sections (see Hansen, 1994). The US news stories are longer, perhaps allowing for more scientific detail to be presented. Most British papers have one or two science reporters, while papers like the New York Times, Washington Post, and Boston Globe have six or more reporters specializing in science and medicine. The small and largely London-based science writing culture allows most reporters to know each other and facilitates exchange of ideas and perspectives (Wilkie, 1996). Since British newspapers are more closely aligned with particular political parties, much of British reporting (including some science reporting) strikes a US reader as more opinionated that one might expect in daily press stories. It is also important to recognize that US and British papers are in fundamentally different situations regarding their relation to their readership. In Britain there are five broadsheets and half a dozen tabloids that compete as ‘national’ newspapers for the same readership; the US papers are segmented geographically and have their own home readers. The direct competition in the British press may cause editors to be more attuned to ‘readers’ interests’ and thus encourage reporting of the human implications of the stories. Emphasizing the ‘perils’ is clearly one of those implications. A piece of the answer might reside in the vicissitudes of the media’s relations with the scientist. It is plausible the British press might have experienced fewer ‘familiarity’ constraints in the story, since Hamer was American and across the ocean, and thus they could more readily criticize Hamer the scientist, the implications of his findings, and publish the alleged allegations of misconduct in some detail. In contrast, the US press may be more sympathetic to the work of an American scientist, and more reluctant to report (unproven) scientific misconduct allegations, since they know him and may want to keep good relations with his lab.6 Finally, gay activists and organizations could affect journalistic perceptions. In Britain a small number of gay activists – Peter Tatchell and a couple of others – were quoted in most of the stories while in the US a wide range activists and organizations were represented in the press. The views of a few activists in the UK could exert influence on the perception and coverage of the ‘gay gene,’ which would be more difficult given the more diffuse gay and lesbian representation in the USA (see Conrad, 1999). In fact, the diversity of voices from the US gay community can be gauged by examining the response of the gay press to Hamer’s research.7 The US gay press was more ambivalent about the research than the mainstream press and surprisingly devoted relatively less attention to it than did the mainstream press. The gay press gave much more space to articles about gay discrimination, AIDS, and gays in the military, perhaps deemed of 394

Conrad & Markens: Constructing the ‘Gay Gene’ in the News greater concern to the gay community. The length and content of the articles varied considerably, especially the details of the research. With one exception, the articles reported the study with moderate detail and cast it in the context of the previous twin and brain studies. The articles tended to recognize the limits of Hamer’s research, while presenting it in a positive manner. In these articles, however, there was an equivocal stance about the potential implications. Quoted gay activists were both optimistic and skeptical about the potentials. Some groups were ‘excited’ by the prospect of the evidence for ‘naturalness’ of sexual orientation, both because it could be a key to gay rights and because it reinforces what they always believed (Washington Blade, 16 July 1993). Yet, the gay press saw the study as a ‘doubleedged sword.’ As noted, there was general respect for the study and some clear optimism among gay activists, but there was also genuine skepticism that the implications were not necessarily beneficial to gays (see Conrad, 1997). The optimism of the study was tempered by the reality that it could have negative impacts. Although concerns about ‘testing and termination’ were often mentioned, they were just one set of concerns among many. Despite some real optimism, the gay press seemed to recognize that scientific findings by themselves would not transform people’s opinion of homosexuality (Bay Areas Reporter, 1 July 1993; San Francisco Sentinel, 21 July 1993; Bay Windows, 22 July 1993). What remains clear is that the ‘gay gene’ as yet is more a social construction than a biological reality. It is not, however, merely a media construction; scientists and gay activists have readily adopted and promoted the conception, but the media has brought it into common currency. The two press cultures, by their different framing of the research, presented disparate pictures of the ‘gay gene.’ The US and British press constructed popular images of a ‘gay gene’ by their framing of Hamer’s (and others’) research in the news. As Van Dijck notes, ‘the shaping of knowledge occurs in science and journalism as well as popular culture’ (1998: 11). Rather than by persuasive factual presentation or logical arguments, it is through ‘images and imaginations’ (mental pictures or compelling stories) that genetics is interpreted in popular culture. While the scientists and some journalists have been cautious about the limits of the research, notions like the ‘gay gene’ subsume all the scientific caveats and easily slip beyond current scientific knowledge. As Kitcher (1996) notes, we are all too cavalier with our genetalk; we leap from a genetic association to assume quickly there is a gene ‘for’ a particular trait, moving easily and misleadingly to attributions of genetic causation. The very use of the term ‘gay gene’ gives wider dissemination to the image of homosexuality as a genetically driven phenomenon – regardless of the framing that is used. At the very least, such conceptions overemphasize the importance of genetics in human behavior, and their ready employment by the media amplifies these ideas far beyond their scientific source. At the 395

Health 5(3) same time, media constructions influence the public image of homosexuality, how we think about homosexual orientation, and how we treat people who are gay. It is not just the use of the term, but how the ‘gay gene’ is constructed that is consequent.

Notes
1. In general, when we refer to homosexuality in this article we mean male samesex conduct. Historically most research assumed homosexuality was male and very little research was conducted about lesbianism. 2. In Britain where there are clear distinctions between the broadsheet and tabloid press, there may be variations to the press culture. In this case we focus largely on the broadsheet or ‘quality papers’ press culture, which is more comparable to the American mainstream press. 3. In August 1991 Simon LeVay (1991), a neuroanatomist, published ‘A difference in hypothalamic structure between heterosexual and homosexual men’ in the prestigious journal Science. He compared the hypothalamus (a small part of the brain that has been identified with the sex drive) of gay men, (presumably) heterosexual men, and (presumably) heterosexual women. He found part of the hypothalamus, the interstitial nuclei of the third anterior (INAH-3) region, was two or three times smaller in gay men than in heterosexual men, or about the same size on average as heterosexual women. LeVay concluded: ‘This finding . . . suggests that sexual orientation has a biological substrate’ (1991: 1037). J. Michael Bailey and Richard C. Pillard, a psychologist and a psychiatrist, building on their previous research, in December 1991 published ‘A genetic study of male sexual orientation’ in the Archives of General Psychiatry (Bailey and Pillard, 1991). They reported the results of a study of 56 pairs of identical and 54 pairs of fraternal twins; they knew one twin in each pair was gay and used a questionnaire (when possible) to determine the sexual orientation of the other twin. They found in identical (monozygotic) twins, 52 per cent of the cotwin brothers were gay; for fraternal (dizygotic) twins it was 22 per cent; for adoptive brothers, 11 per cent; and for non-twin biological brothers, 9.2 per cent. Bailey and Pillard interpreted the data as supporting an approximately 50 per cent genetic influence for homosexuality; they estimated that 30–70 per cent of male sexual orientation was linked to genetics. Two years later they published another article with two colleagues, ‘Heritable factors influence sexual orientation in women,’ in the same journal (Bailey et al., 1993). Using a similar methodology, they studied lesbian twins. They found 48 per cent of the identical co-twins, 16 per cent of the fraternal co-twins, 6 per cent of the adoptive sisters, and 14 per cent of the non-twin biological sisters were lesbians. Again, they concluded their twin studies suggested a strong association between genetics and homosexuality. In between the two twin studies, Laura S. Allen and Roger A. Gorski (1992) published ‘Sexual orientation and the size of the anterior commissure in the human brain’ in Proceedings of the National Academy of Sciences. They measured differences in the sizes of the midsagittal plane of the anterior commissure in the postmortem brains of 90 documented homosexual men and presumed heterosexual men and women. They found the region in homosexual

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men to be 18 per cent larger than in heterosexual women and to be 34 per cent larger than in heterosexual men. Although this structure is not known to have any role in sexuality, it added to the evidence of biological differences between homosexual and heterosexual men. A year later the Office of Research Integrity reported finding no evidence of wrongdoing by Hamer and his associates. Ebers’ study remained unpublished for several years and finally appeared in Science (Rice et al., 1999). This is very apparent in his book, The science of sexual desire: The search for the gay gene and the biology of behavior, co-authored with journalist Peter Copeland (Hamer and Copeland, 1994) but written in the first person ‘I.’ It is very unusual for scientists to write books about their research for a popular audience, and perhaps even more unusual to write a book that is essentially based on a single scientific article, which has as yet to be replicated. Hamer freely uses ‘the gay gene’ all through the book, something he eschewed in his earlier newspaper comments. He uses language that reifies ‘the gay gene,’ such as ‘Figure B shows what happens when “the gay gene” is passed down from the maternal grandmother’ (Hamer and Copeland, 1994: 81). While clearly Hamer the scientist must recognize that there is no ‘gay gene,’ Hamer the publicist regularly refers to it. Hamer wants to be protective of the uses to which his finding could be put. In numerous public statements he has declared: ‘There will never be a test to tell if someone is gay and we know that for a scientific fact’ (WP, 22 February 1994) and such a test ‘would be wrong, unethical and an abuse of the research’ (quoted in Holmes, 1994). Hamer has promised he would act through patent rights to block any commercialization of a genetic test for homosexuality and has spoken out against genetic testing and manipulation, genetic discrimination, and of his own obligation to protect his scientific finding from misuse or appropriation (Hamer and Copeland, 1994: 216–17). He believes (perhaps naïvely) that the lab that discovers a ‘gay gene’ will be able to control the use of technology through intellectual property rights. Whatever the quality of his scientific research, and the tenacity of his ethical stance, all this has made Hamer something of a minor celebrity. York (1996) queried science reporters at the New York Times and Washington Post about why they did not include much about the allegations or the ORI investigation in their reporting of Hamer’s 1995 study. Curt Suplee of the Post felt he could not get sufficient solid information, the charges were too vague. Natalie Angier of the New York Times felt anonymous allegations were not fair, the person should have the ‘courage to put their name on it.’ Since it was an ongoing investigation and Hamer could not talk about it, ‘it’s like tacking a big “guilty” sign to his forehead, and I don’t think that’s fair.’ We collected a small sample of clippings from the US gay press reporting both of Hamer’s studies. Our ‘gay press’ sample included articles in gay publications from the same locales as the US mainstream newspapers: New York Native (NYN), Bay Windows (NW) (Boston), Washington Blade (WB), Bay Area Reporter (BAR), San Francisco Sentinel (SFS) and The Advocate. We examined these papers for one month after the studies were published, although we included a couple of articles that appeared a short time later. The gay sample consisted of 11 articles.

4.

5.

6.

7.

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Author biographies
PETER CONRAD is the Harry Coplan Professor of Social Sciences and Chair of the Department of Sociology at Brandeis University. He has published nine books, including the award-winning Deviance and medicalization: From badness to sickness (with Joseph W. Schneider), and dozens of journal articles and chapters. He has recently published a series of papers examining genetics and behavior in the news. His current research focuses on the structures and meanings of human enhancement.

is an assistant professor of sociology at Temple University. She has published articles on PMS, the medicalization of pregnancy and prenatal testing. Her current research concerns the rise of new genetic and reproductive technologies, with a particular focus on the impact of prenatal genetic screening on women’s reproductive autonomy.
SUSAN MARKENS

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