Why we’re not all hot?

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Why some people are more attractive than others:

Professor Petrie theorised that since genetic mutations can occur anywhere in the genome, some will affect the ‘DNA repair kit’ possessed by all cells. As a result, some individuals have less efficient repair kits, resulting in greater variation in their DNA as damage does unrepaired.

Although unrepaired DNA is generally harmful – causing tissue to degenerate or develop cancers – it is useful in some parts of the genome, such as those parts resposible for disease defence where variation can help in the resistance to disease. It has long been known that greater variation of DNA in the disease defending regions makes it more likely that an individual can resist attacks by bacteria and viruses.

Using a computer model to map the spread of genes in a population, Professor Petrie demonstrated that the tendency towards reduction in genetic diversity caused by sexual selection is outweighed by the maintenance in greater genetic diversity generated by mutations affecting DNA repair.

I haven’t read the paper…and the press release sounds kind of garbled. I guess the results here are suggesting that polymorphism at the disease resistence loci (e.g., MHC) is so important that DNA repair mechanisms can’t get too good. A byproduct of this is variance in the mutational load across the population. I suppose this sort of answer to “why we’re not all hot” is like the answer to why we’re not all parthenogenetic.

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6 Comments

  1. I don’t understand the lek paradox. In any population, some individuals will have “hotter” physical features than other individuals. We have a cognitive module (a “hotness detector”) that is exquisitely tuned to detect very slight differences in physical features. What’s the mystery?

  2. Paradox of evolutionary theory, often cited by creationists, is explained at last 
     
    This is a within-species puzzle. Given the common excuse from creationists that they don’t deny genetic variation or “micro-evolution”, only that “amoeba turn into elephants” and some such, that’s an amusing card to play: We believe in ‘micro-evolution’, except, of course, when we don’t.

  3. But wouldn’t we be selecting for mutations only in the MHC regions, not all through the genome? I don’t see why this would explain mutations that make for asymmetries in face or bad teeth or whatever? Is the idea that too-effective mechanisms to prevent any mutation would also prevent mutations to the genes used to do the randomized construction of antibodies and TCRs and variations in the shape of MHC1/2 molecules?  
     
    Isn’t a lot of the asymmetry based on developmental noise, disease, parasites, malnutrition, etc.? That doesn’t tell a mate how good your genes are (not directly), but may tell you whether you’re likely to crap out on them when they’re pregnant and chasing your 3-year-old son around the rainforest.

  4. One reason that seems obvious to me is that genes that affect attractiveness also affect behavior; behavior that may not be optimal or stable in certain ecological circumstances. So for instance male facial attractiveness also increases number of sex partners and reduces his liklihood of engaging in a paternal investment mating strategy. 
     
    An ESS keeps a broad attractiveness/behavior spectrum in the population.

  5. Related: 
     
    Geoffrey Miller on “Resolving the paradox of common, harmful, heritable mental disorders”. 
     
    http://www.matthewckeller.com/Keller_Miller_BBSPreprint_RevWTables.pdf 
     
    John Hawks on the puzzle of female orgasm variation. 
     
    http://www.johnhawks.net/weblog/reviews/evolution/dunn_female_orgasm_heritability_2005.html 
     
    Itzkoff on the puzzle of intelligence variation. 
     
    http://www.amazon.com/Humans-Vary-Intelligence-Evolution-Human/dp/0913993093/

  6. Miller’s paper would seem to undermine the case for Cochran’s pathogenic theory for traits with high fitness costs, 1% or greater frequency and no evidence of movement toward fixation.

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