March 7, 2014

Dean Hamer Please forward to Dean Hamer; he’ll like it.

Dear Professor Hamer:

Your name came up in a recent article (Michael Balter Science Misused to Justify Ugandan Antigay Law SCIENCE vol. 343 no. 6174 February 28, 2014 page 956), and I learn that you have taken an intereste in a genetic background to homosexuality.  That is not my field of interest, but perhaps this will be useful to you.  (Probably not; I see that as a Scientist Emeritus at the NIH you cannot be involved with biomedical research, but I only offer and ask nothing.)

My field of interest is in normal variation in human fertility.  That means fertility excluding any medical illness of either the male or female of a couple trying to have a baby.  Pretty much if the male is ok and the female ok, then everything is taken to be ok.  But there is a lot of normal variation, say from 9.2 children per woman in Yemen in 1983 to 1.4 in Denmark that same year.  I don’t think anyone believes that diagnosable infertility could have so much effect, much less than that people are healthier in Yemen than in Denmark.

Excluding communicable disease, there is no biological consequence of homosexual activity.  However if such interest diverts a person from heterosexual activity, then there is a consequence, which from my standpoint is simply another form of normal variation in fertility.

And normal variation follows a couple of very strict rules.  Here is a link:
It has all I have to say along with references.

Infertility, whether abnormal or normal, can be classed as pre-zygotic or post-zygotic, depending on whether the mechanism is activated before or after the zygote forms.  According to a paper I contributed to, which I attach, it appears that in fruit flies there is only a post-zygotic mechanism while in mice and humans there are at least two, one pre and one post.  Both rules demand that the number of offspring depends on the kinship of the couple and of their ancestors.

I digress on the matter or race, which is not my interest either.  It seems that an aversion to other races is instinctive.  So is the fear of snakes.  I was once alarmed by a glass snake.  My brother said it was only a legless lizard.  “What’s the difference?”  “It has eyelids.”  Sure enough, it blinked and I could feel the tension easing out of me.  So asking a person to ignore race is like asking him or her to ignore a snake or a danger of falling; don’t expect much.  But I’m asking you.  Race is irrelevant here.  Everything important happens within about 10 generations; after that all are equal.

The rule, roughly speaking, is that the closer kin the more children until a state in inbreeding occurs.  Look at the Iceland data on the link.  In the first generation the number of children falls very swiftly as consanguinity falls and then levels off at about 9th cousin.  This appears to be a pre-zygotic effect.  The number of grandchildren rises as kinship falls but then falls in parallel with the first generation.  This is totally a post-zygotic mechanism.  It is here that one sees an inbreeding effect.

Dismiss from your mind the hope that this is a matter of choice.  The Danish study I cite specifically addresses that, and it finds that once issues of consanguinity are controlled for, there is no effect of education or income on fertility – none at all.  The choice is made at the altar, not in bed, and this is as true for heterosexual partners as it is for homosexual partners.  The tight error bars in the Icelandic data confirm this.

The effect accumulates over at least two generations in the Icelandic study, over at least three in a Swedish study I cite in the link and for an indeterminate number in the Danish study.

I am sure you are thinking, “Balderdash.  Why would evolution produce a mechanism that reduces fertility?”  You have met the same question in response to your own work.  Briefly summarizing part of that link, if evolution is a race, then speciation is a race.  Alfred Russel Wallace pointed that out.  My best ballpark guess is that speciation requires about two thousand generations of separation, and almost certainly depends on DNA mutations.  Now if all the relevant genes for a particular speciation event lie on the same chromosome – obviously an oversimplification – and if they are separated for two thousand generations to produce infertility, then a population of random mating animals of over a thousand will have a population crash since there are two thousand copies of the chromosome in the population and on average it will take them that many generations to get together after they separate to different siblings. 

So there is a mechanism that queries the two genomes of a couple to see if they are as related as they should be in a population of a thousand, that is within the past 10 generations, two to the tenth being about a thousand.  If they do not make the grade their fertility is penalized, and this accumulates over generations. 

As I point out in the paper, the mechanism has to be epigenetic.  That’s why it’s hard to demonstrate by looking at genes.  It’s in the epigenetic markers, which are inherited to a degree from one generation to the next.  Not enough match of the methylation pattern?  Pay the price.

The “purpose,” the effect, of this is to exterminate any population that gets too big; otherwise over thousands of generations it will interbreed with other populations of the same species and the whole species will be lost.  So it makes sense that a population that is on the way out will have a number of problems: poor male development, falling sperm counts, less interest in children, and quite possibly a horror of marrying kin (which might rectify matters, but nature has “made up her mind”) and at a stretch homosexuality to the exclusion of heterosexuality. 

On principle, I don’t blame people for things.  You just don’t know enough of what they have been through.  Of course I sometimes fail to live up to my own principles.  But if one were to place blame for homosexuality – assuming everything I have said is true – it should be the parents and their choice of mate. 

So now we have a testable hypothesis.  There might be a correlation with tendency toward homosexuality and a tendency to regard marrying kin with disgust.  If it is important, it should be a very strong correlation.  I’m sure you have, or know somebody that has, lists of helpful people sorted by sexual inclination and matched for age, income and whatever.  Come up with a few questions about attitude toward marrying kin.  A dozen phone calls on each list and a few moments’ interview and you will know.

I have written any number of people who have had business to take an interest in this vital matter.  Usually I beg for, and receive not, a reply.  In your case I make no such request.  This is a troubling field and I am sure you have had your share of criticism.  Nothing comes to mind that you could do for me anyway.  But I do suggest that when thinking about homosexuality and heredity you think epigenetic rather than genetic.


M. Linton Herbert MD

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