Аннотация:The male excess of infant mortality is well known but without causal explanation. We have inadvertently discovered while investigating sudden infant death syndrome (SIDS) that many causes of infant respiratory death have virtually the same male fraction as SIDS of about 0.61 male, subject to slight sampling variation. The only possible explanation for this consistency is that a recessive X-linkage is involved. We review the literature on infant mortality and propose that there exists a presently unidentified responsible X-linked gene that has a dominant allele with frequency p ≈ 1/3 and a corresponding recessive allele with frequency q ≈ 2/3, such that p+q=1. Either the dominant allele codes for an enzyme allowing anaerobic oxidation in respiratory control neurons or the recessive allele codes for a protein blocking anaerobic oxidation process in them. The gene and its alleles would only penetrate if, and only if, a susceptible infant attains an acute anoxic encephalopathy leading to critical respiratory control neuron death in the brainstem where the blood oxygen tension is the minimum in the entire body. Should the genetically susceptible infant dodge the potentially fatal anoxic condition, the gene may still penetrate later in childhood or adult life. Given an approximate 5% male birth excess, ~2/3 of the XY males will be at risk of having the recessive allele and q 2 ≈ 4/9 of XX females will be at similar risk. Therefore for ~1050 males born per 1000 females, ~700 males and ~444 females will be at risk with male fraction x ≈ 700/(700+444) ≈ 0.612. We show for 11 respiratory causes of death with over one half million cases, that the male fraction is ~0.604. It has not escaped our notice that a possible mode of prevention of SIDS may be possible.
