A letter from a friend:
A friendly reader has written what I regard as a thoughtful and interesting letter.  And he has given me permission to discuss it and even to mention his name.  So my warmest regards to Chris Davies.  Here are some of his thoughts.

He says that the evidence is compelling and hopes that society will take notice but he doubts that will ever happen.  We are in agreement.  The limited results after so long a campaign do not bode well.  The reason is difficult to be sure of.  My speculations include the possibility that my communication skills are inadequate, that people are just too resistant to thinking something new, that it is so advantageous to the rich of the world that loyalties among extended families be eliminated that the idea can never be heard widely and that there is some biological signal that nature has implanted in us tha emerges when we have trod too close to demographic disaster that prevents us from seeing it.  I am clueless.  Any other ideas would be welcome. 

A second response is that unless it is my own failure to communicate then it’s not my fault.  This spares me what might otherwise be a massive guilt trip. 

Davies has in interest in using Human Leukocyte Antigen haplotypes as a means of tracking human population migrations.  I do wonder how such sophisticated measures might be impacted by warfare that annihilates sub populations as well as by the infertility with which I am concerned.  He goes on to ask whether the Major Histocompatibility Complex, genes critical in bone marrow transplant, may lead to infertility if they are not sufficiently similar.  This is quite plausible. 

From a simplistic standpoint one might take the position that maximum genetic heterozygosity is reached when two populations of greatest genetic distance are crossed.  Any effect should turn up in the first generation.   Yet we are looking at a process that plays out over about six or ten generations depending on the conditions.  But things are not so simple.  There are many histocompatibility alleles, versions of the genes, and for all I know they are all lined up together.

Take for example eye color.  If you cross a true blue eyed person with all blue alleles with a true brown eyed person with all brown alleles, the children should all be brown eyed.  Then if you have such a person marry another who is also a cross, then you should get three brown eyed children and one blue eyed.  That would be the case if the eye color allele were a single locus, place for a gene to sit.  But instead there is a line of loci.  Usually all the alleles on one chromosome will be inherited by an offspring or else none will be.  But because of chromosomal recombination, what we used to call “crossing over,” chromosomes can break and rejoin.  So a chromosome in an offspring might contain some but not all of the alleles from one grandparent.  That is the reason we get hazel eyes.  Make the cross, allow the population to survive a few generations and there will be people with some but less than half of their loci containing the brown allele.  These people will be hazel eyed.

My impression is that hazel eyes are not as common as they used to be.  They may have gotten a boost early in American history when brown and blue eyes mixed but then found their way into a small community where long term survival was possible.  The result would have been some hazel, so that when I see a hazel eyed person I now wonder if that person is from an old American family.  It’s not necessarily true or course; Shakespeare has Mercutio mention hazel eyes, and I have a good friend with Norwegian and English parents who has hazel eyes. 

At all events some such process might be going on with the histocompatibility genes such that one has the equivalent of hazel, which would accumulate over generations.  So I cannot reject the histocompatibility theory out of hand.  My first guess, however, remains an epigenetic process, mostly because this seems to be something that evolved in our distant past and not be a result of recent accidental combinations.  That is just a hunch. 

In parting, he offers a link:


When I follow the link it describes a condition called “enlarged parietal foramen” in a skull that belonged to an ancestral population 100,000 years ago.  The condition as they describe it is said to occur mostly in inbred populations, thus adding to the evidence that our ancient ancestors really were inbred.  It’s nice to notice.  The one thing we can be sure of is that our ancestors did reproduce successfully.  If people are noticing that, then maybe there is hope that the connection will be made.

I do notice one thing.  The parietal foramen, when there is one in humans, occurs near the saggital suture between the parietal bones.  The article shows a picture, and in the picture the hole is not near the suture but in it, rather like a persistent part of a fontanel.  That’s just a quibble. Maybe the genetic condition was simply named after an anatomical variant but was not exactly the same.  At all events there is other evidence.

So again my best thanks to Chris Davies.  His contribution is much appreciated.

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