December 15, 2009
Olivier C. Martin
Université Paris-Sud
Laboratoire de Physique Théorique et Modès Statistiques
F-91405 Orsay

Dear Olivier Martin:
It is most humbling to read your article (Effects of Recombination on Complex Regulatory Circuits, Olivier C. Martin and Andreas Wagner, GENTICS vol. 183 no. 2 October 2009 page 673).  You have produced and investigated a model for populations in which you compare the effects of mutations and recombination on the fitness of the population.  This is something I have grappled with for several years.  One difference is that I also consider the effect of varying population size.  This turns out to have an effect on fertility in the presence of mutation pressure. 

I have enclosed a DVD which sketches out my results and supporting data in about 10 minutes (or about one minute per year of work).  I also enclose a CD with a couple versions of my program.  Linton 2 is the version I most use.  You can get more details from my website (where I also post open letters such as this) looking at the posting I did on October 26 of this year. 

As the DVD will show, when you take certain parameters of mutation as constant and then increase population size (in different runs) fertility rises rapidly as inbreeding is escaped, falls rapidly and levels off below zero.  My approach is most crude and the only thing I can say in my own defense is that it does account for a great deal of data that is otherwise unexplained.

Let me point out three other things.  One is that infertility is a serious problem in the modern developed world.

A second thing is that the ethnic and national distinctions we as humans make are of no biological significance, at least according to my model.  Long before kinship has decreased to the level of a different nationality, the fertility curve has fallen below replacement and is essentially horizontal. 

A third thing is that my model seems unattractive from an intuitive standpoint.  If I try to structure my genes so that a locus on one chromosome is fine tuned to another locus on the same chromosome and its homologue, what I get does not reflect reality.  When I fine tune each locus to its own homologue and degrade that with mutations, that is when it works.  Perhaps the fine tuning in question is between nucleus and mitochondrion; that would follow the same mathematics.  I have requested information as to whether that is plausible considering mitochondrial DNA mutation rates, but I expect I shall wait for a reply in vain.

I think the world would be better off if you had considered the effect of population size and I had gone on taking care of sick people.  Still, it is not too late to pass the torch.  Let me know if you are interested or there is anything I can do to explain further of help.


M. Linton Herbert MD 

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