A model-integrated multipoint Bayesian analysis of hypertension in the Framingham Heart Study data finds little evidence of linkage.

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Abstract

This Genetic Analysis Workshop 13 contribution presents a linkage analysis of hypertension in the Framingham data based on the posterior probability of linkage, or PPL. We dichotomized the phenotype, coding individuals who had been treated for hypertension at any time, as well as those with repeated high blood pressure measurements, as affected. Here we use a new variation on the multipoint PPL that incorporates integration over the genetic model. PPLs were computed for chromosomes 1 through 5, 11, 14, and 17 and remained below the 2% assumed prior probability of linkage for 73% of the locations examined. The maximum PPL of 4.5% was obtained on chromosome 1 at 178 cM. Although this is more than twice the assumed prior probability of linkage, it is well below a level at which we would recommend committing substantial additional resources to molecular follow-up. While the PPL analysis of this data remains inconclusive, Bayesian methodology gives us a clear mechanism for using the information gained here in further studies.

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Logue, M. W., Goedken, R. J., Vieland, V. J., & Framingham Heart Study. (2003). A model-integrated multipoint Bayesian analysis of hypertension in the Framingham Heart Study data finds little evidence of linkage. BMC Genetics, 4 Suppl 1. https://doi.org/10.1186/1471-2156-4-s1-s75

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