Genotype by smoking interaction for leptin levels in the San Antonio family heart study

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Abstract
Recent studies reported a marked inverse effect of smoking on serum levels of leptin (an adipocyte derived protein), offering a possible explanation for variation in body weight between smokers and non‐smokers. The goal of this study was to examine the genetic architecture of the response to smoking in leptin levels using data from the San Antonio Family Heart Study. We employed a variance decomposition analysis using maximum likelihood methods to model genotype by smoking interactions for leptin levels, examined the impact of the exclusion of smokers in a subsequent linkage analysis, and incorporated the QTL identified in the linkage analysis in a model of genotype by smoking interaction. We found significant evidence (P = 0.001) for a genotype by smoking status interaction for serum leptin levels. In the subsequent linkage analysis with smokers excluded, we obtained a maximum LOD score of 3.1 (P = 0.00008) near D8S1102. Using this QTL in a model of genotype by smoking status interaction, we identified significant evidence for an interaction at this specific locus (P = 0.04). Given these results, we hypothesize that a quantitative trait locus in this vicinity of chromosome 8 may have a differential effect on the expression of leptin in smokers versus non‐smokers. Genet. Epidemiol. 22:105–115, 2002.