As it has happened many times in the early studies in biochemistry, it has been the study of the abnormal (the word “abnormal” from here onwards, is used in the context of that of the minority of the human population, that is the 1 in 10) that has provided the first insights into the normal biochemical situation. Thus early studies on the family tree of homosexual males pointed to the fact the genetic trait of homosexuality carried by these individuals was inherited from their heterosexual mothers and later researchers concentrated their studies on the X chromosome. A heterosexual grandmother has a 1 in 2 chance of passing this trait to her children by way of one of her two X chromosomes), whether they be sons or daughters. The sons will have a 1 in 2 chance of inheriting the trait and those that do will be genetically homosexual (the “gay” uncle). The daughters will have a 1 in 2 chance of inheriting the trait and their sons (the grandsons) will in turn have a 1 in 2 chance of inheriting the trait.

If the gene coding for “sexual attraction” is carried on the X chromosome in the gay male, is it not reasonable to conclude that the gene for determining sexual attraction in the remainder of the human population is also carried on the X chromosome? This is my starting hypothesis. The gay male has the same genetic coding as the heterosexual female – there is no mutation and no “gay gene” – just an inheritance by the male of a normal female gene. So in this 90% of the population, the two sequences of the genes on the X chromosomes (XX in the female) produce enough “product protein” to confer on the individual, an attraction to the male whilst with only one sequence there is only enough product protein to make the individual attracted to the female. The genetically gay male then would behave as if he had an XX and the lesbian would behave as a single X (in so far as this particular gene sequence is concerned and not the whole X chromosome). This could have come about in our ancestral past if there were a defect in the replication of that part of the X chromosome that produced a situation whereby the gene in question migrated from a normal sequence in the X chromosome (leaving that X chromosome deficient for that gene) and attaching itself to another normal sequenced X chromosome making it surplus by one for that gene). This postulates that there are three variants (with respect to coding for sexual orientation) of the X chromosome in the human population, one producing no product for sexual orientation because the gene sequence is missing, one producing a normal amount of product and one producing a double amount of product. I have called these X-, X and X+. As the X- and the X+ are postulated to have arisen from the same single event, it would not be surprising that they would be found (or seen to be expressed) in the population to the same extent (now believed to be about 10%).

From this, it is hypothesised that most lesbians would be XX- ; a heterosexual female would be XX or X-X+; and a nymphomaniac would be a XX+ or X+X+. Similarly for the male population, the gay male would be X+Y, the heterosexual male would be XY and the womaniser may be X-Y. As stated above and elsewhere, actual sexual behaviour of an individual will be the result of many factors, both genetic and non-genetic such as social, peer and religious pressures and could vary during the lifetime of that individual. It will be up to others, if thought worthwhile, to examine the detailed analytical genetic work of others such as Dean Hamer to determine whether it either supports or argues against (or are not capable of either) this hypothesis. I am unsure whether sequencing or other techniques are capable of determining whether a particular gene sequence does occur twice in the same chromosome or not.

Thanks for your response. This is why I assumed the Autism study pointed towards environment.

“However, only a small percentage — less than 10 percent — of the affected genes were affected by DNA mutations.”

If less than 10 percent of the difference in genetic expression was the result of heredity doesn’t that strongly argue for environment? I understand that Autism might get rolling because of a problem in the >10%. But all things being equal wouldn’t the smart money bet that the trigger resides in the <90%?

And to your second point, I wholeheartedly agree – as with many other psychiatric disorders, even ones with fairly late onset like schizophrenia, all the evidence suggests the initial insults are in early (prenatal) neurodevelopment

Greg Cochran is of course correct. Since Autism was mentioned the latest evidence strongly suggests an environmental trigger. For anyone who has at least some faith in natural selection this doesn’t come as a surprise.

http://www.sciencedaily.com/releases/2011/11/111107162734.htm

“The study searched, on a genome-wide scale, for genes that show an abnormal epigenetic signature — specifically histone methylation. Histones are small proteins attached to the DNA that control gene expression and activity. While genetic information is encoded by the (genome’s) DNA sequence, methylation and other types of histone modifications regulate genome organization and gene expression. The study found hundreds of loci (the places genes occupy on chromosomes) across the genome affected by altered histone methylation in the brains of autistic individuals. However, only a small percentage — less than 10 percent — of the affected genes were affected by DNA mutations.”

In related news it’s likely that Autism begins in the womb.
http://www.sciencedaily.com/releases/2011/11/111108200720.htm

“The researchers found that children with autism had 67 percent more neurons in the prefrontal cortex and heavier brains for their age compared to typically developing children. Since these neurons are produced before birth, the study’s findings suggest that faulty prenatal cell birth or maintenance may be involved in the development of autism. Another possible factor that may contribute to the neuronal excess is a reduction in apoptosis, or programmed cell death, which normally occurs during the third trimester and early postnatal life.”

Remember, genes are NOT blueprints. This means you can’t, for example, insert “the genes for an elephant’s trunk” into a giraffe and get a giraffe with a trunk. There are no genes for trunks. What you CAN do with genes is chemistry, since DNA codes for chemicals. For instance, we can in theory splice the native plants’ talent for nitrogen fixation into a terran plant.

Academician Prokhor Zakharov, “Nonlinear Genetics”

Sid Meier’s Alpha Centauri

One of the points you bring up is that most of these are defects in a gene, so a lede that starts with “Scientists have discovered a genetic defect that leads to X” might be a good start. Or possibly “implicated in X.”

It is safe to say that it is intentional on Richard Dawkins part when he makes use of “a gene for” language as he explicitly defended doing so in The Selfish Gene. His point was that it entirely proper to speak of a a gene for something as long as that gene made such a phenotypic effect more probable, all other things being equal. So when Dawkins is talking about a gene for something, he is talking more about what it does, rather than why it was selected.