The genetic basis of fitness traits has been studied widely in animals, yet the contribution of genetic variation to these traits in humans is controversial. In particular, it is difficult to disentangle genetic versus environmental effects on fertility, because of within-family correlations of sociocultural, economic, and other nongenetic factors that influence family sizes. In this study, we investigated the genetic architecture of reproductive fitness traits in a fertile human population whose communal lifestyle assures uniform and equal access to resources. Our study revealed significant heritabilities for reproductive traits in both men and women, after accounting for common household effects shared among siblings and demographic changes in reproductive practices. Furthermore, our results indicate that both autosomal and X-linked additive and dominance variances contribute to these traits. We therefore propose that reproductive traits should be amenable to genetic mapping studies, and the results we present here will facilitate the search for the novel genes influencing natural fertility in humans.life history traits | human fertility R eproductive fitness reflects the ability of individuals to pass on their genes to subsequent generations. Fitness traits, also referred to as life-history traits, include measures of fertility and mortality and are complex phenotypes that are direct targets of Darwinian selection. Understanding the genetic basis of variation in these traits and inheritance in animals has long been a central theme in evolutionary biology (1). However, partitioning the observed variation into the genetic and environmental sources, and therefore determining the heritability of these traits, remains challenging in humans. As a result, current theories on the evolution and heritability of fitness, and the empirical data, come largely from animal studies (for examples, see refs. 2-8). However, studies of model organisms suggest that hundreds of genes influence fertility in mammals (9). Standing variation in any of those genes could contribute to interindividual differences in fitness in natural populations.The difficulty in assessing genetic contributions to human fertility is caused in part by the fact that human family sizes are often deliberately limited, with few populations reaching their true reproductive potential, and because the many nongenetic factors that influence human family size are often shared within families. As a result, disentangling the effects of shared genes from shared environment is often impossible. For example, parent-child correlations in family sizes have been reported for a number of human populations (10-16). However, in nearly all of these studies, the investigators concluded that social or cultural transmission, such as patterns of emigration (10), polygyny and higher male mortality (11), education or marital age (12), or differential access to resources and ability to acquire a mate (15), but not genetic factors, accounted for the observed intergenerational correl...