Scientific Consensus: Is Homosexuality a Biological Reality?
After extensive research, I could not find one single peer reviewed study in the last decade that found homosexuality to be nonbiological. There is a firm consensus among scientists that there is a clear correlation between homosexuality and biology with twin studies being the strongest evidence (Barash 2013; Blanchard 2006; Langstrom et al. 2010; Rice et al. 2006, 2012; Jain et al. 2009). In fact, one critique of these twin studies was a possible participatory bias where more gay twins would be attracted to volunteer for these homosexuality studies. Langstrom et al. controlled for this bias by conducting a study of every adult twin in Sweden, this was by far the most massive and comprehensive twin study on homosexuality. The results were consistent with the consensus that homosexuality is more highly represented among twins with genetic factors accounting for a large portion of the population (Langstrom et al. 76). However, Barash takes the conversation a step further, reaffirming that "Homosexuality does have biological roots, and the question is how the biological mechanism developed over evolutionary time." This is precisely what I found throughout the scientific body of literature on homosexuality: not a question of if but a question of how to understand the biological workings of homosexuality.
Homosexuality: Profoundly Overdetermined
"Most researchers who study the origins of sexual orientation believe that
homosexuality in human males has multiple causes. Some researchers also
acknowledge the possibility that the various etiologic factors that contribute
to homosexuality may interact with each other (e.g., Mustanski et al.,
2002b)—that the effect of two or more factors together may be quite different
from the sum of their effects in isolation." (Blanchard et al. 2005).
This is a quote from a study that Blanchard et al. conducted combining two established variables associated with homosexuality: Fraternal Birth Order (FBO) and Handedness (note that these are not causes, but merely variables that correlate with homosexuality). The former is the effect of the order and number of male siblings that has a positive correlation with homosexuality: "A meta-analysis of aggregate data from 14 samples representing 10,143 male subjects has shown that homosexuality in human males is predicted by higher numbers of older brothers, but not by higher numbers of older sisters, younger brothers, or younger sisters" (Blanchard 405). The aggregate data means that the conclusion about the FBO effect comes from an immense body of literature and is almost unanimously agreed upon among scientists as influencing homosexuality in some way yet to be understood. Blanchard, Cantor, and Bogaert combine the understanding of Fraternal Birth Order with another odd variable that is Handedness. They cite a previous study which found that "the odds of non-righthandedness were 34% higher for homosexual than for heterosexual men" (406). The fact that this study combined these two variables--Fraternal Birth Order and Handedness--shows a laying of variables and factors that contribute to homosexuality that to many scientists appear almost silly in their obscure correlations (in this CBS highlight, Blanchard's research findings are presented in this way described). This layering of variables is seen even in the title of this study--"Interaction of Fraternal Birth Order and Handedness in the Development of Male Homosexuality"--the key word there for me being "Interaction." I call the science of homosexuality overdetermined because there is not a great deal of debate about differing theories, not displacement of theories due to new ones; but instead, there is a layering of theories attempting to understand homosexuality.
A "Debate:" The interaction Between Theories, Models, and Overall Understandings of Homosexuality
The "interaction" in these studies is crucial to understanding the positions of scientists on homosexuality and biology. While reading this body of literature, the only thing that appears definite is that almost nothing is ruled out. The only real shift I noticed occurred in the past year. In their newly published article, "Homosexuality as a Consequence of Epigenetically Canalized Sexual Development" Rice, Urban, and Gavrilets attempt to reconsider the genetic/biological models that have attempted to explain and understand homosexuality. They list two dominant models that attempt to explain homosexuality: kin selection and the sexual antagonism model, both of which rely on a "genetic loci" meaning a genetic location(s) that mark the phenotype of homosexuality. These two dominant theories, as framed in the past, are similar to what popular culture would call "the gay gene" quest. However, Rice and his research team argue that, "despite numerous studies over the last decade searching for polymorphisms associated with homosexuality, no convincing molecular genetic evidence has been found despite the fact that pedigree and twin studies clearly show that homosexuality is familial" (Rice et al. 344). Rice and his team are claiming that the past emphasis on "molecular genetic evidence" (the gay gene)has come up short. This is the most clear "debate" (if I could call it that) I have found in my research, where Rice is departing from the dominant paradigm of homosexual genetic studies.
He offers instead an epigenetic causality for homosexuality. Epigenetics or "nongenetic changes in DNA packaging" (343) explains the
expression of phenotypes that are not dependent upon the sequencing of DNA but via biological structures outside/above (epi) DNA that impacts how the genotype is expressed. The resulting phenotype (in this case homosexuality) is therefore not traceable to a genetic loci, yet there is also evidence that these epigenetic markers can still be inherited. The theory puts forth that the elusive genetic understanding of homosexuality can more adequately be described via epigenetic markers as opposed to the old genetic loci model. However, they still utilize (i.e. layer) research and theories from the past, sexual antagonism in particular, in an attempt to understand and explain the somewhat biologically meaningless data on homosexuality (344). Sexual antagonism is traditionally associated with specific, identifiable, alleles that when present in a particular sex have either positive or deleterious effects on fitness of the population. Rice et al. have expanded this traditional notion of sexual antagonism to the realm of epigenetics in the hopes of developing a more accurate model for understanding genetic homosexuality.
homosexuality in human males has multiple causes. Some researchers also
acknowledge the possibility that the various etiologic factors that contribute
to homosexuality may interact with each other (e.g., Mustanski et al.,
2002b)—that the effect of two or more factors together may be quite different
from the sum of their effects in isolation." (Blanchard et al. 2005).
This is a quote from a study that Blanchard et al. conducted combining two established variables associated with homosexuality: Fraternal Birth Order (FBO) and Handedness (note that these are not causes, but merely variables that correlate with homosexuality). The former is the effect of the order and number of male siblings that has a positive correlation with homosexuality: "A meta-analysis of aggregate data from 14 samples representing 10,143 male subjects has shown that homosexuality in human males is predicted by higher numbers of older brothers, but not by higher numbers of older sisters, younger brothers, or younger sisters" (Blanchard 405). The aggregate data means that the conclusion about the FBO effect comes from an immense body of literature and is almost unanimously agreed upon among scientists as influencing homosexuality in some way yet to be understood. Blanchard, Cantor, and Bogaert combine the understanding of Fraternal Birth Order with another odd variable that is Handedness. They cite a previous study which found that "the odds of non-righthandedness were 34% higher for homosexual than for heterosexual men" (406). The fact that this study combined these two variables--Fraternal Birth Order and Handedness--shows a laying of variables and factors that contribute to homosexuality that to many scientists appear almost silly in their obscure correlations (in this CBS highlight, Blanchard's research findings are presented in this way described). This layering of variables is seen even in the title of this study--"Interaction of Fraternal Birth Order and Handedness in the Development of Male Homosexuality"--the key word there for me being "Interaction." I call the science of homosexuality overdetermined because there is not a great deal of debate about differing theories, not displacement of theories due to new ones; but instead, there is a layering of theories attempting to understand homosexuality.
A "Debate:" The interaction Between Theories, Models, and Overall Understandings of Homosexuality
The "interaction" in these studies is crucial to understanding the positions of scientists on homosexuality and biology. While reading this body of literature, the only thing that appears definite is that almost nothing is ruled out. The only real shift I noticed occurred in the past year. In their newly published article, "Homosexuality as a Consequence of Epigenetically Canalized Sexual Development" Rice, Urban, and Gavrilets attempt to reconsider the genetic/biological models that have attempted to explain and understand homosexuality. They list two dominant models that attempt to explain homosexuality: kin selection and the sexual antagonism model, both of which rely on a "genetic loci" meaning a genetic location(s) that mark the phenotype of homosexuality. These two dominant theories, as framed in the past, are similar to what popular culture would call "the gay gene" quest. However, Rice and his research team argue that, "despite numerous studies over the last decade searching for polymorphisms associated with homosexuality, no convincing molecular genetic evidence has been found despite the fact that pedigree and twin studies clearly show that homosexuality is familial" (Rice et al. 344). Rice and his team are claiming that the past emphasis on "molecular genetic evidence" (the gay gene)has come up short. This is the most clear "debate" (if I could call it that) I have found in my research, where Rice is departing from the dominant paradigm of homosexual genetic studies.
He offers instead an epigenetic causality for homosexuality. Epigenetics or "nongenetic changes in DNA packaging" (343) explains the
expression of phenotypes that are not dependent upon the sequencing of DNA but via biological structures outside/above (epi) DNA that impacts how the genotype is expressed. The resulting phenotype (in this case homosexuality) is therefore not traceable to a genetic loci, yet there is also evidence that these epigenetic markers can still be inherited. The theory puts forth that the elusive genetic understanding of homosexuality can more adequately be described via epigenetic markers as opposed to the old genetic loci model. However, they still utilize (i.e. layer) research and theories from the past, sexual antagonism in particular, in an attempt to understand and explain the somewhat biologically meaningless data on homosexuality (344). Sexual antagonism is traditionally associated with specific, identifiable, alleles that when present in a particular sex have either positive or deleterious effects on fitness of the population. Rice et al. have expanded this traditional notion of sexual antagonism to the realm of epigenetics in the hopes of developing a more accurate model for understanding genetic homosexuality.
A Need to (Re)Develop the Models: Both Theoretical and Mathematical
The current state of the genetic understandings/explanations of homosexuality is highly dependent upon the development of theoretical and mathematical models that will aid future studies in analyzing empirical patterns of the occurrence of homosexuality (Gavrilets and Rice 2006; Jain, Sharmaa, Sharmaa 2009). There is a theoretical emphasis to the scientific study of homosexuality that scientists admit is crucial to the field; in other words, meaning that current models are not sufficiently able to adequately explain and predict homosexuality, despite the fact that they are sure of the biological correlation via twin studies and homosexual representation within populations all over the globe. Even the epigenetic model proposed by Rice et al. is so new that it hasn't had an opportunity to play out in the field, and even so epigenetics is a very young study anyways leaving the study of homosexuality still shrouded in obscurity.