Thursday, August 18, 2016

Genetics, Homosexuality, and Autism

"Being queer/transgender is a choice."

"Being autistic is as a result of vaccinations, genetically-modified organisms, lack of [insert vitamin or other vital nutrient here] during pregnancy, or simply not enough discipline."

It is common now that I find that it to be routinely accepted that being queer has powerful neurogenetic ties.  One of the earliest pieces of literature to promote this notion that I have found is from an article initially published in The Atlantic magazine in March of 1993 (which was published digitally in June of 1997).  Given America's coming to terms with the AIDS epidemic of the 1980's and the stigma that was heavily and undoubtedly faced by gay and bisexual men at the time, such a publication was, through my lens, something that likely penetrated through that web of fretful lies about queer men and about "the homosexual lifestyle," and not solely the fact that many heterosexual couples also fell victim to the devastating disease that AIDS can prove itself to be if left untreated.  This particular article also discusses many of the hormonal influences that can determine an individual's sexual orientation, which, again, is quite something in consideration of the time period in which it was initially published.

This fairly-recent November 2014 article cites a publication from Cambridge University that notes a mutation found in gay men on chromosome site Xq28.  Said chromosome has been found to be linked to Rett's syndrome, which in the DSM-4 as well as the DSM-4-TR as a pervasive developmental disorder that possesses characteristics of autism as well as a host of other physical disabilities in the likes of Parkinson's disease.  Yet, here's the catch: Rett's is not autism itself, and it occurs almost exclusively in females (most males with Rett's syndrome, reportedly, have died before the age of two years, with some notable exceptions).  Is it purely coincidental that the same site on the X chromosome has been linked to male homosexuality as well as to a developmental disability with some autistic traits, yet is genetically and physically distinct from autism?  I would contend that is so, yet at the same time, it is something that stirs my curiosity.  I cannot propose any hypotheses as a result of not being a geneticist, so my curiosity, in this case, is moot.

An overwhelming amount of the research out there that deals with homosexuality places an emphasis on gay men as test subjects, such as the one aforementioned and this more recent article published in Science magazine in October of 2015 .  I find it to be of excruciating difficulty to find anything other than this June 2012 Huffington Post article that cited a 2011 study conducted in the UK that found at least a twenty-five-percent inheritance rate between sets of identical and fraternal lesbian twins.  This study, while one that certainly contributes to the study of genetics as a determinant of sexual orientation, is merely not enough.

The genetics of autism are complex, perhaps just as complex as the genes that determine one's sexual orientation. This 2008 research paper documents how the C4B gene null allele is commonly found to be either missing or mutated in autistic individuals; however, said missing or mutated gene was also found in a comparable population of neurotypical test subjects.  Earlier this year-- February, to be exact-- this gene was believed by researchers to be the gene that will "open the black box" into studying schizophrenia, the psychiatric disability that at one point, its childhood form was believed to be autism (there was in fact an "epidemic" of childhood schizophrenia, much as there is now an "epidemic" of autism).  As it turns out, in 2009, as this paper unveils, a genetic overlap was discovered between autism, schizophrenia, and bipolar disorder.

However, as the phrase goes, "when you meet one autistic person, you meet one autistic person."  This is true even at a molecular biological level.  In 2007, a paper was published based upon a study of children with diagnoses all over the autism spectrum and of varying degrees of ability and care requirements.  This paper discovered that many of these children possessed a mutation on the SHANK3 protein, as well as a deletion of the 22q13 gene.  Autism is fairly-common in those with Phelan-McDermid syndrome, a rare genetic disorder marked by the absence of the 22q13 gene. 

Many people on the autism spectrum have proven time-and-time again to possess a number of de novo copy number variations, as this article published on Medscape, which cites a September 2015 study, demonstrates. According to said study, sixty-five candidate genes for autism have been identified, twenty-eight of those genes contribute, quoting the article, a "high risk" for the development of autism.  There have been numerous studies in the past that have brought to light the contribution of de novo copy number variations in the development of autism, yet this is perhaps the most-recent of such studies.  

Both sexual orientation and autism not only have strong genetic origins, but also those epigenetic in nature.  This December 2012 article cites a research paper published in The Quarterly Review of Biology of which states that "sexually-antagonistic" epimarkers can be passed on to opposite-sex offspring  and render them as being "sexually-disadvantaged."  In essence, this study makes the claim that sexual orientation is primarily if not exclusively epigenetic, and that homosexuality "runs in families, but is not genetic."  I would contend that evidence exists to digress against such a statement, but it is still an effort to foray into the study of epigenetics and their contributing factors to sexual orientation.

In regards to autism, this 2013 paper cites various epigenetic factors that could plausibly contribute to the expression of autism phenotypes.  In its conclusion, it admits that the study of epigenetic factors in regards to autism is "in its infancy--" signaling that much work is to be done in regards to the study of epigenetic factors contributing to autism.

I am adamantly in support of genetic research in regards to sexual orientation solely to, once and for all, silence those whom claim that us members of the LGBT community are queer and/or transgender by virtue of selection.  I feel that many would contend such an undertaking is reasonable (especially since being queer is not immune to the linking of vaccines to things deemed as "unnatural").

However, my support for genetic research in regards to autism is far-more cautious.  On one hand, researching how certain genes interact with one another can possibly alleviate some co-morbid conditions that can arrive with autism that many who have such conditions are not beneficial, such as epilepsy or gastrointestinal issues.  It is also a great manner in which to silence those who oppose vaccination because they fear having a child much like myself or one of my cousins.  At the same time, I do not wish for autism-related genetic researchers to fall into the unscrupulous hands whose sole motive is to eradicate autism from the gene pool.  My position on finding a "cure" for autism is quite clear, as it is of so many in support of the neurodiversity paradigm: it would be highly-unethical for a myriad of reasons, notwithstanding the fact that disability is an organic aspect of human reality.  For certain, do I know that I do not wish to live in an overly-sanitized humankind where which diversity of any sort, inclusive of disability, is nonexistent.

Acceptance of both queerness and of autism as simply just being should be the end-goal of our society.  Genetic research may answer the thousands of questions that we ask pertaining to how such things as queerness and as autism come about in the human species; but, what ethical costs, particularly in regards to autism, might we be paying as a result?  It was only scant over forty years ago that it was made cognizant that homosexuality was merely a variant of human expression.  How much longer shall it be until autism is regarded in the same light: as a variant in the expression of human neurology?