Literature DB >> 9076695

A genetic basis for the sudden infant death syndrome sex ratio.

D T Mage1, M Donner.   

Abstract

Sudden infant death syndrome, in 36 global data sets comprising 67378 postneonatal autopsied cases, has a male fraction of 0.612 which is significantly greater than the male birth fraction of 0.5122. Each of the sex ratios in the 36 data sets cannot be rejected as a random sample from a P = 0.612 binomial distribution. We hypothesize that an X-linked two-allele (a,A) single gene may be responsible for this consistent behavior. The Hardy-Weinberg principle predicts, given a 5% excess male birth rate, that a recessive allele (a) associated with sudden infant death syndrome, having a frequency of q = 2/3, could be responsible for the male fraction of 0.612. The absence of the A allele would be a necessary precondition for sudden infant death syndrome. We hypothesize that the syndrome occurs only with additional rare environmental conditions and rare physiological factors leading to extreme hypoxic stress, which reduces the sudden infant death syndrome rate to the order of 1 per 1000 live births.

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Year:  1997        PMID: 9076695     DOI: 10.1016/s0306-9877(97)90280-2

Source DB:  PubMed          Journal:  Med Hypotheses        ISSN: 0306-9877            Impact factor:   1.538


  9 in total

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6.  Association between monoamine oxidase A promoter polymorphism and the risk of sudden infant death syndrome: a meta-analysis.

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Review 7.  The genomic load of deleterious mutations: relevance to death in infancy and childhood.

Authors:  James Alfred Morris
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8.  An Acute Respiratory Infection of a Physiologically Anemic Infant is a More Likely Cause of SIDS than Neurological Prematurity.

Authors:  David T Mage; Maria Luisa Latorre; Alejandro G Jenik; E Maria Donner
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9.  A Unifying Theory for SIDS.

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  9 in total

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