Annotated Bibliography
Barash, David P. "The Evolutionary Mystery of Homosexuality." The Chronicle of Higher Education 59.13 (2012). General OneFile. Web. 23 Oct. 2013.
David P. Barash puts forth debates within the sciences regarding whether or not homosexuality is biologically determined. He argues that "Homosexuality does have biological roots, and the question is how the biological mechanism developed over evolutionary time." This is consistent with every single peer reviewed source I came upon in my research of the science of homosexuality. This scientific consensus is a great place to start this conversation: homosexuality has a biological reality; how science goes about uncovering that reality is the question as Barash points out, in accordance to the research out today and eve the last few decades.
Blanchard, Ray, James M Cantor, Anthony F Bogaert, S. Marc Breedlove, and Lee Ellis. "Interaction of Fraternal Birth Order and Handedness in the Development of Male Homosexuality."Hormones and Behavior, 49.3 (2006): 405-414.
This study is cited quite often because of the attempt at rectifying these two odd variables statistically associated with (male) homosexuality: Fraternal Birth Order and Handedness. 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" (405). The aggregate data means that this conclusion 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). They use different models and theories to explain their study which combined these two variables: Fraternal Birth Order and Handedness.
Blanchard, Ray. "A Possible Second Type of Maternal–Fetal Immune Interaction Involved in Both Male and Female Homosexuality." Archives of Sexual Behavior, 41.6 (2012): 1507-1511.
Because of the complexities of this theory here is the framework in Blanchard's words:
"(according to a recent study) the mothers of firstborn homosexual sons produce fewer subsequent offspring than do the mothers of firstborn heterosexual sons. I hypothesized that a subset of mothers of firstborn homosexuals may be responsible for this finding. These mothers develop an immune response to one or more fetal products sometime during their first pregnancy. This response merely produces homosexuality in the first fetus but it kills later fetuses outright, perhaps because the immune response is augmented at the first delivery, when the tearing of maternal tissue allows larger quantities of fetal material to enter the mother’s circulation" (1507).
This is a development of a very popular theory explaining the Fraternal Birth Order effect that influences homosexuality. The Maternal-Fetal Immune theory posits that the mother can build an immunity to androgens responsible for sexual development, subsequently effecting sexuality. Previously, this theory was applied only to males, however, according to Blanchard these findings also correlate with lesbian women as well as gay men in comparison with a control study.
Jain, Madhu, Sudheer Kumar Sharma, and G.C Sharma. "A Mathematical Model of a Population Genetics: Effects of Genetic Variation on Homosexuality." Journal of the Korean Statistical Society, 38.3 (2009): 267-276.
This main aim of this source is to essentially help lead the way to an already paved road. There is no "new" research or theories here per se. However, there is a ton of sifting through the research and models already in circulation and recombining many of the theories into mathematical approaches to research. Jain, Sharma, and Sharma state their goal in this article: “Our goal is to develop different mathematical models for the purpose of predicting patterns to guide future genetics of homosexuality” (268). Although not explicitly stated, I can see after reading so many studies that there is a need for this. There is a ton of empirical data--studies on homosexuality--but there are little to no significant conclusions to be made other than: homosexuality has a strong biological root. This article and the new epigenetic model composed by Rice et al. are necessary because it is quite clear that many of the current research methods are far too inconclusive (Rice et al. "Homosexuality as a Consequence of Epigenetically Canalized Sexual Development" 344).
Rice, William R, Urban Friberg, and Sergey Gavrilets. "Homosexuality as a Consequence of Epigenetically Canalized Sexual Development." The Quarterly Review of Biology, 87.4 (2012): 343-368.
In this newly published article 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. They 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). Their new model is dependent upon epigenetics, or "nongenetic changes in DNA packaging" (343). Epigenetics explains the expression of phenotypes that are not dependent upon the sequencing of DNA but via biological structures outside/above (epi) DNA that impact how the genotype is expressed and which can also 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 research and theories from the past, sexual antagonism in particular (344).
David P. Barash puts forth debates within the sciences regarding whether or not homosexuality is biologically determined. He argues that "Homosexuality does have biological roots, and the question is how the biological mechanism developed over evolutionary time." This is consistent with every single peer reviewed source I came upon in my research of the science of homosexuality. This scientific consensus is a great place to start this conversation: homosexuality has a biological reality; how science goes about uncovering that reality is the question as Barash points out, in accordance to the research out today and eve the last few decades.
Blanchard, Ray, James M Cantor, Anthony F Bogaert, S. Marc Breedlove, and Lee Ellis. "Interaction of Fraternal Birth Order and Handedness in the Development of Male Homosexuality."Hormones and Behavior, 49.3 (2006): 405-414.
This study is cited quite often because of the attempt at rectifying these two odd variables statistically associated with (male) homosexuality: Fraternal Birth Order and Handedness. 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" (405). The aggregate data means that this conclusion 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). They use different models and theories to explain their study which combined these two variables: Fraternal Birth Order and Handedness.
Blanchard, Ray. "A Possible Second Type of Maternal–Fetal Immune Interaction Involved in Both Male and Female Homosexuality." Archives of Sexual Behavior, 41.6 (2012): 1507-1511.
Because of the complexities of this theory here is the framework in Blanchard's words:
"(according to a recent study) the mothers of firstborn homosexual sons produce fewer subsequent offspring than do the mothers of firstborn heterosexual sons. I hypothesized that a subset of mothers of firstborn homosexuals may be responsible for this finding. These mothers develop an immune response to one or more fetal products sometime during their first pregnancy. This response merely produces homosexuality in the first fetus but it kills later fetuses outright, perhaps because the immune response is augmented at the first delivery, when the tearing of maternal tissue allows larger quantities of fetal material to enter the mother’s circulation" (1507).
This is a development of a very popular theory explaining the Fraternal Birth Order effect that influences homosexuality. The Maternal-Fetal Immune theory posits that the mother can build an immunity to androgens responsible for sexual development, subsequently effecting sexuality. Previously, this theory was applied only to males, however, according to Blanchard these findings also correlate with lesbian women as well as gay men in comparison with a control study.
Jain, Madhu, Sudheer Kumar Sharma, and G.C Sharma. "A Mathematical Model of a Population Genetics: Effects of Genetic Variation on Homosexuality." Journal of the Korean Statistical Society, 38.3 (2009): 267-276.
This main aim of this source is to essentially help lead the way to an already paved road. There is no "new" research or theories here per se. However, there is a ton of sifting through the research and models already in circulation and recombining many of the theories into mathematical approaches to research. Jain, Sharma, and Sharma state their goal in this article: “Our goal is to develop different mathematical models for the purpose of predicting patterns to guide future genetics of homosexuality” (268). Although not explicitly stated, I can see after reading so many studies that there is a need for this. There is a ton of empirical data--studies on homosexuality--but there are little to no significant conclusions to be made other than: homosexuality has a strong biological root. This article and the new epigenetic model composed by Rice et al. are necessary because it is quite clear that many of the current research methods are far too inconclusive (Rice et al. "Homosexuality as a Consequence of Epigenetically Canalized Sexual Development" 344).
Rice, William R, Urban Friberg, and Sergey Gavrilets. "Homosexuality as a Consequence of Epigenetically Canalized Sexual Development." The Quarterly Review of Biology, 87.4 (2012): 343-368.
In this newly published article 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. They 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). Their new model is dependent upon epigenetics, or "nongenetic changes in DNA packaging" (343). Epigenetics explains the expression of phenotypes that are not dependent upon the sequencing of DNA but via biological structures outside/above (epi) DNA that impact how the genotype is expressed and which can also 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 research and theories from the past, sexual antagonism in particular (344).
Additional Works Cited
Gavrilets, Sergey, and William R Rice. "Genetic Models of Homosexuality: Generating Testable Predictions." Proceedings. Biological Sciences / the Royal Society, 273.1605 (2006): 3031-3038.
Långström, Niklas, Qazi Rahman, Eva Carlström, and Paul Lichtenstein. "Genetic and Environmental Effects on Same-sex Sexual Behavior: A Population Study of Twins in Sweden." Archives of Sexual Behavior, 39.1 (2010): 75-80
Rahman, Qazi, Anthony Collins, Martine Morrison, Jennifer Claire Orrells, Khatija Cadinouche, Sherene Greenfield, and Sabina Begum. "Maternal Inheritance and Familial Fecundity Factors in Male Homosexuality." Archives of Sexual Behavior, 37.6 (2008): 962-969.
Rice, William R, Urban Friberg, and Sergey Gavrilets. "Homosexuality Via Canalized Sexual Development: A Testing Protocol for a New Epigenetic Model." BioEssays, 35.9 (2013): 764-770.
Långström, Niklas, Qazi Rahman, Eva Carlström, and Paul Lichtenstein. "Genetic and Environmental Effects on Same-sex Sexual Behavior: A Population Study of Twins in Sweden." Archives of Sexual Behavior, 39.1 (2010): 75-80
Rahman, Qazi, Anthony Collins, Martine Morrison, Jennifer Claire Orrells, Khatija Cadinouche, Sherene Greenfield, and Sabina Begum. "Maternal Inheritance and Familial Fecundity Factors in Male Homosexuality." Archives of Sexual Behavior, 37.6 (2008): 962-969.
Rice, William R, Urban Friberg, and Sergey Gavrilets. "Homosexuality Via Canalized Sexual Development: A Testing Protocol for a New Epigenetic Model." BioEssays, 35.9 (2013): 764-770.