Any idea in which trimester the pathogen would be most likely to have an impact on fetal brain development? I did some browsing over at the GSS and found that gay men were particularly likely to have been born in the month of June, which would put them in the first trimester of fetal development at the height of flu season.
Infectious Causation of Disease: An Evolutionary Perspective
GM Cochran, PW Ewald, KD Cochran – PERSPECTIVES IN BIOLOGY AND MEDICINE, 2000
Here we talk about it a bit, as one example of a common, unexplained fitness-reducing syndrome.
Peer-reviewed. Like that means a lot. I’ve had reviewers argue history from what they saw in a movie (Fiddler on the Roof as a guide to Jewish occupations in the Middle Ages). I’ve also had reviewers who don’t believe that there _is_ such a thing as positive selection.
Over and over, people keep assuming that this hypothetical pathogen must act before birth. It might, but there is no reason that it would have to, and I’d say that the odds were against it: we’re subject to a lot more infectious diseases after birth than before birth.
We know of examples in which post-birth infections ruin a particular subpopulation of neurons (Von Economo’s encephalitis and dopaminergic neurons, also possibly narcolepsy) and that is all that would be required.
Origins of male homosexuality – The Vitamin D theorypeople with MS are more likely to be born in MayStudies of infectious disease have been unable to find a bacterium or virus that might cause MS, and diet has been ruled out as a factor in the disease. But a study of 40,000 MS patients from Canada, Great Britain, Denmark and Sweden have shown that people with MS are more likely to be born in May. Babies born at this time have gone through a period of rapid growth in the womb at the end of winter when the mother’s vitamin D levels are at their lowest. On the other hand there are fewest births of people with MS in November when sunny summer holidays ensure that rapid growth in the womb is supported by plenty of vitamin D.[...]investigations by the Oxford team in collaboration with Canadian scientists have shown that MS is inherited preferentially through the female line as an “imprinted” gene. This explains why MS affects three or four women to every man.[...]It now seems likely that insufficient vitamin D is the crucial environmental factor that modifies the DRB1 gene into the imprinted form that causes MS and transmits it from one generation to the next. DRB1 is one of a family of HLA genes that code for structures on the surface of human white blood cells. And it is white blood cells that are involved in the “autoimmune” reaction that destroys the nervous system of MS sufferers.
The Oxford team believe that people with MS have white cells that are incorrectly programmed early in life. There are millions of different T-cells, a particular type of white cell produced in the thymus gland, each programmed to recognise and attack different types of invading bacteria and viruses. Ordinarily the T cells that might attack the body itself are deleted early in life in a stock-taking process. But this process can go wrong when certain genes that are normally masked by the imprinting process are mistakenly unmasked.
When a certain stage of pregnancy occurs during the winter a lack of available Vitamin D may “ruin a particular subpopulation of neurons” and produce homosexuality.
Evolution has stored vitamin D for getting through winter in the bodyfat, the breakdown and metabolism of adipose tissue in results in the stored vitamin D being released to supply the bodies requirements.
In the modern world there is no winter period of food scarcity and hence adipose tissue fails to release its stores of vitamin D.
A calorific deficit in the winter to induce the metabolism of fat stores is lacking for the first time.
Prevalence of vitamin D insufficiency in obese children and adolescents.“Tayside, where just over 20% of primary one pupils (5 year olds) are overweight”
On Tayside one in 300 people suffer from MS.
There is no consensus yet on the timing of prenatal effects on human behavioral development. Below is a paragraph from C.C.C. Cohen-Bendahana,C. van de Beeka, & S.A. Berenbaum (2005). Prenatal sex hormone effects on child and adult sex-typed behavior: methods and findings. Neuroscience and Biobehavioral Reviews, 29, 353–384.
"Sensitive periods for organizational effects. It is widely accepted that organizational effects are maximal during circumscribed sensitive periods when the brain is developing, but the exact sensitive periods for human behavioral effects of sex hormones are not known. Weeks 8–24 of gestation have long been considered the key period [e.g., 21,22], given data showing a testosterone surge in male fetuses then . Nevertheless, there is increasing recognition that there may be multiple sensitive periods, and that different brain regions (and thus different behaviors) may be affected by hormones at different times. There are only limited data on this issue in human beings [24,25], but ample data from other species, including primates, illustrate this point . For example, as mentioned above, data from rhesus macaques show that androgen exposure early in gestation masculinizes different behaviors than exposure late in gestation .
There may be another sensitive period shortly after birth, associated with another peak in testosterone in male infants during postnatal months 1–5. Its significance for human behavior is not well studied, but some information can be gleaned from studies in infant male monkeys who exhibit the same early postnatal peak. Those studies show that neonatal testosterone is important for genital development [26,27], but there is not clear evidence for its role in behavioral development: neonatal testosterone has been found to affect mother-offspring interaction in one study of juveniles , but not in another study of infants , and not to affect sex-dimorphic play or sexual behavior [28–30]. Given continuing postnatal brain development, it would not be surprising to find that sex hormones continue to affect thebrain and behavior after birth."
Your 2000 article does not do justice to the 'gay germ' theory (I've added a link to it in my post). It provides only a brief summary that leaves out many elements. When people ask me for a good description of this theory, I refer them to other documents available at The World of Greg Cochran.
Yes, peer review is the worst possible system — except for the others. All of my published articles have benefited from peer review, often considerably so. Even when I disagree with a reviewer, I know there's a problem that has to be addressed somehow.
I agree that this pathogen could act after birth, but some male homosexuality must be due to pre-natal events. How else would you explain the correlation between male homosexuality and digit ratio (a marker of prenatal androgenization)?
I've heard of the vitamin D theory of male homosexuality, but this is the first time I've seen the primary literature on this topic. I agree with the main point: until recently, we evolved in an environment where body fat was normally burned off in early spring, thus releasing significant amounts of vitamin D and other nutrients. I suspect a lot of vitamin D deficiency is due to the permanent maintenance of excess body fat.
The idea that genetic disease affect only 1 in 10,000 does not make sense considering that the birth defect rate is around 3% of births. The 2-3% homosexual rate is similar to the 3% birth defect rate, which suggests that homosexuality could be genetic in origin.
I agree that this pathogen could act after birth, but some male homosexuality must be due to pre-natal events. How else would you explain the correlation between male homosexuality and digit ratio (a marker of prenatal androgenization)?It is possible that the stronger immune system of men with a high digit ratio is more likely to destroy their sexual ‘search image’ in over-reacting to an infection which leaves them with the ‘default setting’. (Vitamin D is a potent inhibitor of the proinflammatory response)Shape regression on 2D : 4D ratio
Greg cites Henry Harpending as saying Bushmen aren’t homosexual. I wonder about how honest Bushmen are about something like that. Especially as “daily life is pervaded with put-downs” in that society according to Cultural Diversity
Bushmen and Amerindians may have some reported cases of homosexuality, but am I wrong by thinking that it is not of the same magnitude that in the occidental societies? Everybody, scientist or not, seem to agree that true cases of genetic transgender are extremely rare, and that most of the homosexuality we see today is environmental and cultural in origin, even if this is denied.Cultural, which goes with political correctness, TV, education and sedentary lifestyle and environnmental, which goes with pesticides, antibiotics and hormones introduced in the food chain.
The authors noted one inconsistent result, with respect to non-twin brothers (not part of the data reported above). The rate of homosexuality was on 9.2% (13/142), significantly lower than the expected rate. (In the absence of environmental factors, the rate for non-twin brothers should be the same as for dizygotic twins.) Comparisons between MZ and DZ are ignoring this anomaly.
Schizophrenia in DZ twins?Greater occurrence of schizophrenia in dizygotic but not monozygotic twins. Register-based study
A possible association between the genetic predisposition for dizygotic twinning and schizophrenia————
This is an silly argument, based on a total unwillingness to look at how culture shapes behavior. Romantic attraction is highly complex and culturally specific. There are numerous reasons having to do with the complexity of romantic attraction that characteristics conducive to homosexuality could be selected for. (It's actually pretty amazing that none of the solemn pseudo-scientists discussing these questions notice how attracted women tend to be to homosexual men). Depending on the cultural setting, those characteristics will be more or less expressed in actual homosexuality.
By the way, use Wifi jammer to block all secret devices in your room or at work.
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"If Greg Cochran is right, a gay man is a vehicle that a pathogen has constructed for its own survival and reproduction" – not necessarily true. If the pathogen is (for example) chickenpox, then the gay man does not have lifelong infectivity. The neurological damage is merely a permanent byproduct of a temporary infection. Likewise, narcoleptics are not a reservoir of the pathogen that destroyed a small part of their hypothalamus.
The trim lever http://easyslimgb.com is on the left side behind and http://dropweightgb.com below the throttle (not visible in this picture). It's a http://thinningquick.com full-resolution picture, so click on it if you're interested.
Given that we are sure that same sex preference is not genetic (ie no gene) and no one is 100% sure what environ octal factor or factors cause same sex preference. This is as good a guess as any and every good theory starts with a good guess that can be tested scientifically.
[…] never does what you expect from biology? Do you expect half the geese to fly north for the winter? http://www.unz.com/pfrost/origins-of-male-homosexuality-germ/ “Homosexual men are nature’s Petri dishes” […]
The hereditability of homosexuality is only about .20 to .25 (based on analysis of all identical twin studies).