Collective intelligence challenges are often entangled with collective action problems. For example, voting, rating, and social innovation are collective intelligence tasks that require costly individual contributions. As a result, members of a group often free ride on the information contributed by intrinsically motivated people. Are intrinsically motivated agents the best participants in collective decisions? We embedded a collective intelligence task in a large-scale, virtual world public good game and found that participants who joined the information system but were reluctant to contribute to the public good (free riders) provided more accurate evaluations, whereas participants who rated frequently underperformed. Testing the underlying mechanism revealed that a negative rating bias in free riders is associated with higher accuracy. Importantly, incentivizing evaluations amplifies the relative influence of participants who tend to free ride without altering the (higher) quality of their evaluations, thereby improving collective intelligence. These results suggest that many of the currently available information systems, which strongly select for intrinsically motivated participants, underperform and that collective intelligence can benefit from incentivizing free riding members to engage. More generally, enhancing the diversity of contributor motivations can improve collective intelligence in settings that are entangled with collective action problems.

The broad determinants of fertility are thought to be reasonably well identified by demographers, though the detailed quantitative drivers of fertility levels and changes are less well understood. This paper uses a novel ecological index of malaria transmission to study the effect of child mortality on fertility. We find that temporal variation in the ecology of the disease is well-correlated to mortality, and pernicious malaria conditions lead to higher fertility rates. We then argue that most of this effect occurs through child mortality, and estimate the effect of child mortality changes on fertility. Our findings add to the literature on disease and fertility, and contribute to the suggestive evidence that child mortality reductions have a causal effect on fertility changes.

We conduct a genome-wide association study (GWAS) of educational attainment (EA) in a sample of ~3 million individuals and identify 3,952 approximately uncorrelated genome-wide-significant single-nucleotide polymorphisms (SNPs). A genome-wide polygenic predictor, or polygenic index (PGI), explains 12-16% of EA variance and contributes to risk prediction for ten diseases. Direct effects (i.e., controlling for parental PGIs) explain roughly half the PGI's magnitude of association with EA and other phenotypes. The correlation between mate-pair PGIs is far too large to be consistent with phenotypic assortment alone, implying additional assortment on PGI-associated factors. In an additional GWAS of dominance deviations from the additive model, we identify no genome-wide-significant SNPs, and a separate X-chromosome additive GWAS identifies 57.

Educational attainment is strongly influenced by social and other environmental factors, but genetic factors are estimated to account for at least 20% of the variation across individuals. Here we report the results of a genome-wide association study (GWAS) for educational attainment that extends our earlier discovery sample of 101,069 individuals to 293,723 individuals, and a replication study in an independent sample of 111,349 individuals from the UK Biobank. We identify 74 genome-wide significant loci associated with the number of years of schooling completed. Single-nucleotide polymorphisms associated with educational attainment are disproportionately found in genomic regions regulating gene expression in the fetal brain. Candidate genes are preferentially expressed in neural tissue, especially during the prenatal period, and enriched for biological pathways involved in neural development. Our findings demonstrate that, even for a behavioural phenotype that is mostly environmentally determined, a well-powered GWAS identifies replicable associated genetic variants that suggest biologically relevant pathways. Because educational attainment is measured in large numbers of individuals, it will continue to be useful as a proxy phenotype in efforts to characterize the genetic influences of related phenotypes, including cognition and neuropsychiatric diseases.

Very few genetic variants have been associated with depression and neuroticism, likely because of limitations on sample size in previous studies. Subjective well-being, a phenotype that is genetically correlated with both of these traits, has not yet been studied with genome-wide data. We conducted genome-wide association studies of three phenotypes: subjective well-being (n = 298,420), depressive symptoms (n = 161,460), and neuroticism (n = 170,911). We identify 3 variants associated with subjective well-being, 2 variants associated with depressive symptoms, and 11 variants associated with neuroticism, including 2 inversion polymorphisms. The two loci associated with depressive symptoms replicate in an independent depression sample. Joint analyses that exploit the high genetic correlations between the phenotypes (|ρ^| ≈ 0.8) strengthen the overall credibility of the findings and allow us to identify additional variants. Across our phenotypes, loci regulating expression in central nervous system and adrenal or pancreas tissues are strongly enriched for association.