Excess body fat or body mass relative to height aggregates in families. It is commonly recognized that this familial aggregation of human obesity is accounted for in part by a significant genetic component. Thus the genetic heritability of the obesity phenotypes accounts for approximately 25-40% of the age- and gender-adjusted phenotypic variances. There is also growing evidence that single-gene effects can be detected under appropriate conditions. The focus of research has now shifted to candidate genes and DNA markers of various obesity phenotypes. To date, linkage results have been published from the Pima Indian Study, the San Antonio Family Heart or Diabetes Studies, the Paris Cohort of Obese Siblings, the University of Pennsylvania Family Obesity Study and the Quebec Family Study. The only genomic scan (with approximately 600 markers) reported to date is that from the Pima Indian sibling study. In that study, the strongest evidence for linkage with body fat was with markers on chromosome 11q, 6p and 3p. Evidence for linkage with markers on 7q was obtained in all family studies with the only apparent exception being the Pima Indians. Our own results from the Quebec Family Study suggest that there are linkages between body fat, as assessed from hydrodensitometry, and markers on 1p32-p22. Other linkages have been reported in the past but they are generally based on smaller sample size and weaker evidence.