Genome-wide linkage studies are hypothesis generating and, through surveying the whole genome, aim to identify new, unanticipated genetic variants associated with a disease or trait of interest. Genome-wide linkage studies rely on the relatedness of study participants and test whether certain chromosomal regions cosegregate with a disease or trait across generations [17]. A whole-genome linkage survey requires 400–600 highly polymorphic markers, genotyped at 10 cM intervals. Thus, genome-wide linkage studies have a rather coarse resolution and typically identify broad intervals that require follow-up genotyping to pinpoint the genes that underlie the linkage signal. Since the first genome-wide linkage study was published in 1997 [34], the number of chromosomal loci linked to obesity-related traits has grown exponentially. The latest Human Obesity Gene Map update reported 253 loci from 61 genome-wide linkage scans, of which 15 loci have been replicated in at least three studies [29]. Yet, none of these replicated loci could be narrowed down sufficiently to pinpoint the genes or variants that underlie the linkage signal. Despite substantial power, a meta-analysis of 37 genome-wide linkage studies with data on >31,000
