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Dive into the research topics where Daniel J. Benjamin is active.

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Featured researches published by Daniel J. Benjamin.


Journal of the European Economic Association | 2006

Who is “Behavioral”? Cognitive Ability and Anomalous Preferences

Daniel J. Benjamin; Sebastian A. Brown; Jesse M. Shapiro

In this paper, we ask whether variation in preference anomalies is related to variation in cognitive ability. Evidence from a new laboratory study of Chilean high school students shows that small-stakes risk aversion and short-run discounting are less common among those with higher standardized test scores, although anomalies persist even among the highest-scoring individuals. The relationship with test scores does not appear to result from differences in parental education or wealth. A laboratory experiment shows that reducing cognitive resources using a cognitive load manipulation tends to exacerbate small-stakes risk aversion, with similar but statistically weaker effects on short-run impatience. Explicit reasoning about choice seems to reduce the prevalence of these anomalies, especially among the less skilled. Survey evidence suggests that the role of cognitive ability may extend to adult behaviors that are related to small-stakes risk preference and short-run time preference.


Psychological Science | 2012

Most Reported Genetic Associations With General Intelligence Are Probably False Positives

Christopher F. Chabris; Benjamin Hebert; Daniel J. Benjamin; Jonathan P. Beauchamp; David Cesarini; Matthijs J. H. M. van der Loos; Magnus Johannesson; Patrik K. E. Magnusson; Paul Lichtenstein; Craig S. Atwood; Jeremy Freese; Taissa S. Hauser; Robert M. Hauser; Nicholas A. Christakis; David Laibson

General intelligence (g) and virtually all other behavioral traits are heritable. Associations between g and specific single-nucleotide polymorphisms (SNPs) in several candidate genes involved in brain function have been reported. We sought to replicate published associations between g and 12 specific genetic variants (in the genes DTNBP1, CTSD, DRD2, ANKK1, CHRM2, SSADH, COMT, BDNF, CHRNA4, DISC1, APOE, and SNAP25) using data sets from three independent, well-characterized longitudinal studies with samples of 5,571, 1,759, and 2,441 individuals. Of 32 independent tests across all three data sets, only 1 was nominally significant. By contrast, power analyses showed that we should have expected 10 to 15 significant associations, given reasonable assumptions for genotype effect sizes. For positive controls, we confirmed accepted genetic associations for Alzheimer’s disease and body mass index, and we used SNP-based calculations of genetic relatedness to replicate previous estimates that about half of the variance in g is accounted for by common genetic variation among individuals. We conclude that the molecular genetics of psychology and social science requires approaches that go beyond the examination of candidate genes.


Nature Human Behaviour | 2018

Redefine Statistical Significance

Daniel J. Benjamin; James O. Berger; Magnus Johannesson; Brian A. Nosek; Eric-Jan Wagenmakers; Richard A. Berk; Kenneth A. Bollen; Björn Brembs; Lawrence D. Brown; Colin F. Camerer; David Cesarini; Christopher D. Chambers; Merlise A. Clyde; Thomas D. Cook; Paul De Boeck; Zoltan Dienes; Anna Dreber; Kenny Easwaran; Charles Efferson; Ernst Fehr; Fiona Fidler; Andy P. Field; Malcolm R. Forster; Edward I. George; Richard Gonzalez; Steven N. Goodman; Edwin J. Green; Donald P. Green; Anthony G. Greenwald; Jarrod D. Hadfield

We propose to change the default P-value threshold for statistical significance from 0.05 to 0.005 for claims of new discoveries.


Proceedings of the National Academy of Sciences of the United States of America | 2014

Common genetic variants associated with cognitive performance identified using the proxy-phenotype method

Cornelius A. Rietveld; Tonu Esko; Gail Davies; Tune H. Pers; Patrick Turley; Beben Benyamin; Christopher F. Chabris; Valur Emilsson; Andrew D. Johnson; James J. Lee; Christiaan de Leeuw; Riccardo E. Marioni; Sarah E. Medland; Michael B. Miller; Olga Rostapshova; Sven J. van der Lee; Anna A. E. Vinkhuyzen; Najaf Amin; Dalton Conley; Jaime Derringer; Cornelia M. van Duijn; Rudolf S. N. Fehrmann; Lude Franke; Edward L. Glaeser; Narelle K. Hansell; Caroline Hayward; William G. Iacono; Carla A. Ibrahim-Verbaas; Vincent W. V. Jaddoe; Juha Karjalainen

Significance We identify several common genetic variants associated with cognitive performance using a two-stage approach: we conduct a genome-wide association study of educational attainment to generate a set of candidates, and then we estimate the association of these variants with cognitive performance. In older Americans, we find that these variants are jointly associated with cognitive health. Bioinformatics analyses implicate a set of genes that is associated with a particular neurotransmitter pathway involved in synaptic plasticity, the main cellular mechanism for learning and memory. In addition to the substantive contribution, this work also serves to show a proxy-phenotype approach to discovering common genetic variants that is likely to be useful for many phenotypes of interest to social scientists (such as personality traits). We identify common genetic variants associated with cognitive performance using a two-stage approach, which we call the proxy-phenotype method. First, we conduct a genome-wide association study of educational attainment in a large sample (n = 106,736), which produces a set of 69 education-associated SNPs. Second, using independent samples (n = 24,189), we measure the association of these education-associated SNPs with cognitive performance. Three SNPs (rs1487441, rs7923609, and rs2721173) are significantly associated with cognitive performance after correction for multiple hypothesis testing. In an independent sample of older Americans (n = 8,652), we also show that a polygenic score derived from the education-associated SNPs is associated with memory and absence of dementia. Convergent evidence from a set of bioinformatics analyses implicates four specific genes (KNCMA1, NRXN1, POU2F3, and SCRT). All of these genes are associated with a particular neurotransmitter pathway involved in synaptic plasticity, the main cellular mechanism for learning and memory.


Journal of the European Economic Association | 2013

WHO IS ‘BEHAVIORAL’? COGNITIVE ABILITY AND ANOMALOUS PREFERENCES: Who is ‘Behavioral’?

Daniel J. Benjamin; Sebastian A. Brown; Jesse M. Shapiro

In this paper, we ask whether variation in preference anomalies is related to variation in cognitive ability. Evidence from a new laboratory study of Chilean high-school students with similar schooling backgrounds shows that small-stakes risk aversion and short-run discounting are less common among those with higher standardized test scores. The relationship with test scores survives controls for parental education and wealth. We find some evidence that elementary-school GPA is predictive of preferences measured at the end of high school. Two laboratory interventions provide suggestive evidence of a possible causal impact of cognitive resources on expressed preferences. (JEL: J24, D14, C91).


Nature Neuroscience | 2015

Polygenic risk scores for schizophrenia and bipolar disorder predict creativity

Robert A. Power; Stacy Steinberg; Gyda Bjornsdottir; Cornelius A. Rietveld; Abdel Abdellaoui; Michel Nivard; Magnus Johannesson; Tessel E. Galesloot; Jouke J. Hottenga; Gonneke Willemsen; David Cesarini; Daniel J. Benjamin; Patrik K. E. Magnusson; Fredrik Ullén; Henning Tiemeier; Albert Hofman; Frank J. A. van Rooij; G. Bragi Walters; Engilbert Sigurdsson; Thorgeir E. Thorgeirsson; Andres Ingason; Agnar Helgason; Augustine Kong; Lambertus A. Kiemeney; Philipp Koellinger; Dorret I. Boomsma; Daniel F. Gudbjartsson; Hreinn Stefansson; Kari Stefansson

We tested whether polygenic risk scores for schizophrenia and bipolar disorder would predict creativity. Higher scores were associated with artistic society membership or creative profession in both Icelandic (P = 5.2 × 10−6 and 3.8 × 10−6 for schizophrenia and bipolar disorder scores, respectively) and replication cohorts (P = 0.0021 and 0.00086). This could not be accounted for by increased relatedness between creative individuals and those with psychoses, indicating that creativity and psychosis share genetic roots.


Current Directions in Psychological Science | 2015

The Fourth Law of Behavior Genetics

Christopher F. Chabris; James J. Lee; David Cesarini; Daniel J. Benjamin; David Laibson

Behavior genetics is the study of the relationship between genetic variation and psychological traits. Turkheimer (2000) proposed “Three Laws of Behavior Genetics” based on empirical regularities observed in studies of twins and other kinships. On the basis of molecular studies that have measured DNA variation directly, we propose a Fourth Law of Behavior Genetics: “A typical human behavioral trait is associated with very many genetic variants, each of which accounts for a very small percentage of the behavioral variability.” This law explains several consistent patterns in the results of gene-discovery studies, including the failure of candidate-gene studies to robustly replicate, the need for genome-wide association studies (and why such studies have a much stronger replication record), and the crucial importance of extremely large samples in these endeavors. We review the evidence in favor of the Fourth Law and discuss its implications for the design and interpretation of gene-behavior research.


Proceedings of the National Academy of Sciences of the United States of America | 2013

Molecular genetics and subjective well-being

Cornelius A. Rietveld; David Cesarini; Daniel J. Benjamin; Philipp Koellinger; Jan-Emmanuel De Neve; Henning Tiemeier; Magnus Johannesson; Patrik K. E. Magnusson; Nancy L. Pedersen; Robert F. Krueger; Meike Bartels

Subjective well-being (SWB) is a major topic of research across the social sciences. Twin and family studies have found that genetic factors may account for as much as 30–40% of the variance in SWB. Here, we study genetic contributions to SWB in a pooled sample of ≈11,500 unrelated, comprehensively-genotyped Swedish and Dutch individuals. We apply a recently developed method to estimate “common narrow heritability”: the fraction of variance in SWB that can be explained by the cumulative additive effects of genetic polymorphisms that are common in the population. Our estimates are 5–10% for single-question survey measures of SWB, and 12–18% after correction for measurement error in the SWB measures. Our results suggest guarded optimism about the prospects of using genetic data in SWB research because, although the common narrow heritability is not large, the polymorphisms that contribute to it could feasibly be discovered with a sufficiently large sample of individuals.


Journal of Mathematical Psychology | 2016

Rejection Odds and Rejection Ratios: A Proposal for Statistical Practice in Testing Hypotheses

M. J. Bayarri; Daniel J. Benjamin; James O. Berger; Thomas Sellke

Much of science is (rightly or wrongly) driven by hypothesis testing. Even in situations where the hypothesis testing paradigm is correct, the common practice of basing inferences solely on p-values has been under intense criticism for over 50 years. We propose, as an alternative, the use of the odds of a correct rejection of the null hypothesis to incorrect rejection. Both pre-experimental versions (involving the power and Type I error) and post-experimental versions (depending on the actual data) are considered. Implementations are provided that range from depending only on the p-value to consideration of full Bayesian analysis. A surprise is that all implementations – even the full Bayesian analysis – have complete frequentist justification. Versions of our proposal can be implemented that require only minor modifications to existing practices yet overcome some of their most severe shortcomings.


PLOS ONE | 2013

The Molecular Genetic Architecture of Self-Employment

Matthijs J. H. M. van der Loos; Cornelius A. Rietveld; Niina Eklund; Philipp Koellinger; Fernando Rivadeneira; Gonçalo R. Abecasis; Georgina A. Ankra-Badu; Sebastian E. Baumeister; Daniel J. Benjamin; Reiner Biffar; Stefan Blankenberg; Dorret I. Boomsma; David Cesarini; Francesco Cucca; Eco J. C. de Geus; George V. Dedoussis; Panos Deloukas; Maria Dimitriou; Gudny Eiriksdottir; Johan G. Eriksson; Christian Gieger; Vilmundur Gudnason; Birgit Höhne; Rolf Holle; Jouke-Jan Hottenga; Aaron Isaacs; Marjo-Riitta Järvelin; Magnus Johannesson; Marika Kaakinen; Mika Kähönen

Economic variables such as income, education, and occupation are known to affect mortality and morbidity, such as cardiovascular disease, and have also been shown to be partly heritable. However, very little is known about which genes influence economic variables, although these genes may have both a direct and an indirect effect on health. We report results from the first large-scale collaboration that studies the molecular genetic architecture of an economic variable–entrepreneurship–that was operationalized using self-employment, a widely-available proxy. Our results suggest that common SNPs when considered jointly explain about half of the narrow-sense heritability of self-employment estimated in twin data (σg 2/σP 2 = 25%, h 2 = 55%). However, a meta-analysis of genome-wide association studies across sixteen studies comprising 50,627 participants did not identify genome-wide significant SNPs. 58 SNPs with p<10−5 were tested in a replication sample (n = 3,271), but none replicated. Furthermore, a gene-based test shows that none of the genes that were previously suggested in the literature to influence entrepreneurship reveal significant associations. Finally, SNP-based genetic scores that use results from the meta-analysis capture less than 0.2% of the variance in self-employment in an independent sample (p≥0.039). Our results are consistent with a highly polygenic molecular genetic architecture of self-employment, with many genetic variants of small effect. Although self-employment is a multi-faceted, heavily environmentally influenced, and biologically distal trait, our results are similar to those for other genetically complex and biologically more proximate outcomes, such as height, intelligence, personality, and several diseases.

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Magnus Johannesson

Stockholm School of Economics

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Aysu Okbay

VU University Amsterdam

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Mark Alan Fontana

Hospital for Special Surgery

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