By Kenji Ikehara
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01 corresponded to an increase of approximately 3 mm Hg in systolic and 2 mm Hg in diastolic BP, and 10-15 % of the total variation in BP in those populations could be explained by recessive or partially recessive quantitative trait locus (QTL) alleles. It was estimated that several hundred (300-600) recessive QTLs could contribute to BP variation. Moreover, it was inferred that inbreeding accounts for 36 % of all hypertension in those populations. , 2003a). The study was carried out in 14 isolate villages on three neighboring islands in middle Dalmatia which present a wide range of levels of inbreeding and endogamy, and relative uniformity of environment so that the potential effects of inbreeding on those complex diseases may be detected.
This result suggests that inbred individuals are more common among the infected cases for both hepatitis and TB and, therefore, consanguinity appears significantly to increase the risk of these two major infectious causes of death in humans. Significant differences in r2 values between affected and unaffected individuals were not found for persistent hepatitis in the Italian genome scan, probably due to the low levels of inbreeding in that population. Correlations in heterozygosity among markers were not different between affected and unaffected individuals for leprosy in India, where the frequency of consanguineous marriages is high, suggesting no effect of inbreeding on this infectious disease.
The inbreeding coefficients computed from the Darwin/Wedgwood pedigree shows that some individuals of the dynasty presented rather high levels of inbreeding. 1255) because their parents were double first cousins. 0625. 0039). All the remaining individuals in the pedigree depicted in Figure 1 had F = 0, as did Charles Darwin and his father, Robert Darwin. , 2010). Child mortality was clearly higher for those families whose progeny had high inbreeding coefficient (Figure 4). 1255. 0%) among the 25 Darwin/Wedgwood families investigated.