Originally posted by lord of the mark
Why would a recessive gene thats not evolutionarily disadvantageous be "drowned out"? Clearly the phenotype would show up less frequently then the gene, but sheer chance would mean that the phenotype would be expressed, depending on the frequency of the gene.
Why would a recessive gene thats not evolutionarily disadvantageous be "drowned out"? Clearly the phenotype would show up less frequently then the gene, but sheer chance would mean that the phenotype would be expressed, depending on the frequency of the gene.
Originally posted by lord of the mark
Whats much more interesting is how clearly disadvantgeous recessive genes, ones that cause fatal diseases, survive. The candidates, IIUC, are genetic drift (sheer chance from a small founder population) versus heterozygote advantage (its good to be a carrier - the classic example is Sickle Cell Anemia and its relation to malaria - a more controversial theory (not widely accepted) is Cochrans views on Tay Sachs and other lipid/neurological conditions and Ashkenazi intelligence)
Whats much more interesting is how clearly disadvantgeous recessive genes, ones that cause fatal diseases, survive. The candidates, IIUC, are genetic drift (sheer chance from a small founder population) versus heterozygote advantage (its good to be a carrier - the classic example is Sickle Cell Anemia and its relation to malaria - a more controversial theory (not widely accepted) is Cochrans views on Tay Sachs and other lipid/neurological conditions and Ashkenazi intelligence)
Is there any science behind Cochran's theories, or are they just pure conjecture, i.e. trying to draw a parallel between Tay-Sachs (et.al.) and malaria resistance in Sickle cell? Slippery slope IMO.
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