I am a social scientist with a passion for measurement, statistics, and data. I am always looking for interesting projects and am open to collaborations with researchers from Stanford, other places within the US, and abroad.

Academic Appointments

Administrative Appointments

  • Assistant Professor, Stanford Graduate School of Education (2015 - Present)

Professional Education

  • BS, University of Texas at Austin, Mathematics (2001)
  • MA, University of Texas at Austin, Mathematics (2006)
  • PhD, University of Colorado Boulder, Education (2012)

Current Research and Scholarly Interests

Ben Domingue is an assistant professor in the Graduate School of Education at Stanford University and a faculty fellow at Stanford's Center for Population Health Sciences. I am interested in how item responses collected via test or survey are leveraged to inform our understanding of human behavior (typically in the context of students or patients). I have a particular interest in the technical issues that make it challenging to draw simple inferences from such item responses. My work on student test scores has been done using data from both the US and abroad. While not analyzing item response data, I also work on projects pertaining to the implications for social science of the sudden increase in our capacity to measure human DNA and the promise and pitfalls associated with how this new data may change our understanding of human behavior.

2018-19 Courses

Stanford Advisees

All Publications

  • Genetic analysis of social-class mobility in five longitudinal studies PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Belsky, D. W., Domingue, B. W., Wedow, R., Arseneault, L., Boardman, J. D., Caspi, A., Conley, D., Fletcher, J. M., Freese, J., Herd, P., Moffitt, T. E., Poulton, R., Sicinski, K., Wertz, J., Harris, K. 2018; 115 (31): E7275–E7284


    A summary genetic measure, called a "polygenic score," derived from a genome-wide association study (GWAS) of education can modestly predict a person's educational and economic success. This prediction could signal a biological mechanism: Education-linked genetics could encode characteristics that help people get ahead in life. Alternatively, prediction could reflect social history: People from well-off families might stay well-off for social reasons, and these families might also look alike genetically. A key test to distinguish biological mechanism from social history is if people with higher education polygenic scores tend to climb the social ladder beyond their parents' position. Upward mobility would indicate education-linked genetics encodes characteristics that foster success. We tested if education-linked polygenic scores predicted social mobility in >20,000 individuals in five longitudinal studies in the United States, Britain, and New Zealand. Participants with higher polygenic scores achieved more education and career success and accumulated more wealth. However, they also tended to come from better-off families. In the key test, participants with higher polygenic scores tended to be upwardly mobile compared with their parents. Moreover, in sibling-difference analysis, the sibling with the higher polygenic score was more upwardly mobile. Thus, education GWAS discoveries are not mere correlates of privilege; they influence social mobility within a life. Additional analyses revealed that a mother's polygenic score predicted her child's attainment over and above the child's own polygenic score, suggesting parents' genetics can also affect their children's attainment through environmental pathways. Education GWAS discoveries affect socioeconomic attainment through influence on individuals' family-of-origin environments and their social mobility.

    View details for PubMedID 29987013

  • The social genome of friends and schoolmates in the National Longitudinal Study of Adolescent to Adult Health PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Domingue, B. W., Belsky, D. W., Fletcher, J. M., Conley, D., Boardman, J. D., Harris, K. 2018; 115 (4): 702–7


    Humans tend to form social relationships with others who resemble them. Whether this sorting of like with like arises from historical patterns of migration, meso-level social structures in modern society, or individual-level selection of similar peers remains unsettled. Recent research has evaluated the possibility that unobserved genotypes may play an important role in the creation of homophilous relationships. We extend this work by using data from 5,500 adolescents from the National Longitudinal Study of Adolescent to Adult Health (Add Health) to examine genetic similarities among pairs of friends. Although there is some evidence that friends have correlated genotypes, both at the whole-genome level as well as at trait-associated loci (via polygenic scores), further analysis suggests that meso-level forces, such as school assignment, are a principal source of genetic similarity between friends. We also observe apparent social-genetic effects in which polygenic scores of an individual's friends and schoolmates predict the individual's own educational attainment. In contrast, an individual's height is unassociated with the height genetics of peers.

    View details for PubMedID 29317533

  • Mortality selection in a genetic sample and implications for association studies. International journal of epidemiology Domingue, B. W., Belsky, D. W., Harrati, A., Conley, D., Weir, D. R., Boardman, J. D. 2017


    Mortality selection occurs when a non-random subset of a population of interest has died before data collection and is unobserved in the data. Mortality selection is of general concern in the social and health sciences, but has received little attention in genetic epidemiology. We tested the hypothesis that mortality selection may bias genetic association estimates, using data from the US-based Health and Retirement Study (HRS).We tested mortality selection into the HRS genetic database by comparing HRS respondents who survive until genetic data collection in 2006 with those who do not. We next modelled mortality selection on demographic, health and social characteristics to calculate mortality selection probability weights. We analysed polygenic score associations with several traits before and after applying inverse-probability weighting to account for mortality selection. We tested simple associations and time-varying genetic associations (i.e. gene-by-cohort interactions).We observed mortality selection into the HRS genetic database on demographic, health and social characteristics. Correction for mortality selection using inverse probability weighting methods did not change simple association estimates. However, using these methods did change estimates of gene-by-cohort interaction effects. Correction for mortality selection changed gene-by-cohort interaction estimates in the opposite direction from increased mortality selection based on analysis of HRS respondents surviving through 2012.Mortality selection may bias estimates of gene-by-cohort interaction effects. Analyses of HRS data can adjust for mortality selection associated with observables by including probability weights. Mortality selection is a potential confounder of genetic association studies, but the magnitude of confounding varies by trait.

    View details for DOI 10.1093/ije/dyx041

    View details for PubMedID 28402496

  • Genetic Heterogeneity in Depressive Symptoms Following the Death of a Spouse: Polygenic Score Analysis of the U.S. Health and Retirement Study. American journal of psychiatry Domingue, B. W., Liu, H., Okbay, A., Belsky, D. W. 2017: appiajp201716111209-?


    Experience of stressful life events is associated with risk of depression. Yet many exposed individuals do not become depressed. A controversial hypothesis is that genetic factors influence vulnerability to depression following stress. This hypothesis is often tested with a "diathesis-stress" model, in which genes confer excess vulnerability. The authors tested an alternative formulation of this model: genes may buffer against depressogenic effects of life stress.The hypothesized genetic buffer was measured using a polygenic score derived from a published genome-wide association study of subjective well-being. The authors tested whether married older adults who had higher polygenic scores were less vulnerable to depressive symptoms following the death of their spouse compared with age-matched peers who had also lost their spouse and who had lower polygenic scores. Data were analyzed from 8,588 non-Hispanic white adults in the Health and Retirement Study (HRS), a population-representative longitudinal study of older adults in the United States.HRS adults with higher well-being polygenic scores experienced fewer depressive symptoms during follow-up. Those who survived the death of their spouses (N=1,647) experienced a sharp increase in depressive symptoms following the death and returned toward baseline over the following 2 years. Having a higher well-being polygenic score buffered against increased depressive symptoms following a spouse's death.The effects were small, and the clinical relevance is uncertain, although polygenic score analyses may provide clues to behavioral pathways that can serve as therapeutic targets. Future studies of gene-environment interplay in depression may benefit from focus on genetics discovered for putative protective factors.

    View details for DOI 10.1176/appi.ajp.2017.16111209

    View details for PubMedID 28335623

  • Polygenic Risk Predicts Obesity in Both White and Black Young Adults PLOS ONE Domingue, B. W., Belsky, D. W., Harris, K. M., Smolen, A., McQueen, M. B., Boardman, J. D. 2014; 9 (7)


    To test transethnic replication of a genetic risk score for obesity in white and black young adults using a national sample with longitudinal data.A prospective longitudinal study using the National Longitudinal Study of Adolescent Health Sibling Pairs (n = 1,303). Obesity phenotypes were measured from anthropometric assessments when study members were aged 18-26 and again when they were 24-32. Genetic risk scores were computed based on published genome-wide association study discoveries for obesity. Analyses tested genetic associations with body-mass index (BMI), waist-height ratio, obesity, and change in BMI over time.White and black young adults with higher genetic risk scores had higher BMI and waist-height ratio and were more likely to be obese compared to lower genetic risk age-peers. Sibling analyses revealed that the genetic risk score was predictive of BMI net of risk factors shared by siblings. In white young adults only, higher genetic risk predicted increased risk of becoming obese during the study period. In black young adults, genetic risk scores constructed using loci identified in European and African American samples had similar predictive power.Cumulative information across the human genome can be used to characterize individual level risk for obesity. Measured genetic risk accounts for only a small amount of total variation in BMI among white and black young adults. Future research is needed to identify modifiable environmental exposures that amplify or mitigate genetic risk for elevated BMI.

    View details for DOI 10.1371/journal.pone.0101596

    View details for Web of Science ID 000341253400095

    View details for PubMedID 24992585

  • Genetic and educational assortative mating among US adults PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Domingue, B. W., Fletcher, J., Conley, D., Boardman, J. D. 2014; 111 (22): 7996-8000


    Understanding the social and biological mechanisms that lead to homogamy (similar individuals marrying one another) has been a long-standing issue across many fields of scientific inquiry. Using a nationally representative sample of non-Hispanic white US adults from the Health and Retirement Study and information from 1.7 million single-nucleotide polymorphisms, we compare genetic similarity among married couples to noncoupled pairs in the population. We provide evidence for genetic assortative mating in this population but the strength of this association is substantially smaller than the strength of educational assortative mating in the same sample. Furthermore, genetic similarity explains at most 10% of the assortative mating by education levels. Results are replicated using comparable data from the Framingham Heart Study.

    View details for DOI 10.1073/pnas.1321426111

    View details for Web of Science ID 000336687900041

    View details for PubMedID 24843128

  • Evaluating the Equal-Interval Hypothesis with Test Score Scales PSYCHOMETRIKA Domingue, B. 2014; 79 (1): 1-19


    The axioms of additive conjoint measurement provide a means of testing the hypothesis that testing data can be placed onto a scale with equal-interval properties. However, the axioms are difficult to verify given that item responses may be subject to measurement error. A Bayesian method exists for imposing order restrictions from additive conjoint measurement while estimating the probability of a correct response. In this study an improved version of that methodology is evaluated via simulation. The approach is then applied to data from a reading assessment intentionally designed to support an equal-interval scaling.

    View details for DOI 10.1007/s11336-013-9342-4

    View details for Web of Science ID 000331802000001

    View details for PubMedID 24532164

  • How social and genetic factors predict friendship networks PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Boardman, J. D., Domingue, B. W., Fletcher, J. M. 2012; 109 (43): 17377-17381


    Recent research suggests that the genotype of one individual in a friendship pair is predictive of the genotype of his/her friend. These results provide tentative support for the genetic homophily perspective, which has important implications for social and genetic epidemiology because it substantiates a particular form of gene-environment correlation. This process may also have important implications for social scientists who study the social factors related to health and health-related behaviors. We extend this work by considering the ways in which school context shapes genetically similar friendships. Using the network, school, and genetic information from the National Longitudinal Study of Adolescent Health, we show that genetic homophily for the TaqI A polymorphism within the DRD2 gene is stronger in schools with greater levels of inequality. Our results suggest that individuals with similar genotypes may not actively select into friendships; rather, they may be placed into these contexts by institutional mechanisms outside of their control. Our work highlights the fundamental role played by broad social structures in the extent to which genetic factors explain complex behaviors, such as friendships.

    View details for DOI 10.1073/pnas.1208975109

    View details for Web of Science ID 000311147800022

    View details for PubMedID 23045663

  • Genetic risk, body mass index, and weight control behaviors: Unlocking the triad. The International journal of eating disorders Nagata, J. M., Braudt, D. B., Domingue, B. W., Bibbins-Domingo, K., Garber, A. K., Griffiths, S., Murray, S. B. 2019


    BACKGROUND: The relationship between genetic risk for body mass index (BMI) and weight control behaviors remains unknown. The objectives of this study were to determine the association between genetic risk for BMI and weight control behaviors in young adults, and to examine actual measured BMI as a potential mediator variable.METHOD: We analyzed data from three data collection waves of the National Longitudinal Study of Adolescent to Adult Health. The BMI polygenic score (PGS) was based on published genome-wide association studies for BMI. BMI was collected at 11-18years and 18-26years. Weight control behaviors included self-reported: (a) weight loss behaviors (dieting, vomiting, fasting/skipping meals, diet pills, laxatives, or diuretic use to lose weight) and (b) weight gain behaviors (eating more or different foods than normal, taking supplements to gain weight).RESULTS: Among 4,397 participants, the BMI PGS was associated with higher odds of weight loss behaviors in females (OR 1.24, 95% CI 1.14-1.35) and males (OR 1.43, 95% CI 1.26-1.62), and this association was mediated by BMI (indirect effect 0.04, 95% CI 0.03-0.05 in females and 0.03, 95% CI 0.03-0.04 in males). The BMI PGS was associated with lower odds of weight gain behaviors in females and males, which was also mediated by actual BMI.CONCLUSIONS: The BMI PGS was associated with weight loss behaviors in both males and females, and this association was mediated by actual measured BMI. Clinical interventions to prevent high BMI, particularly for individuals with genetic risk, may also prevent subsequent development of potentially unhealthy weight loss behaviors.

    View details for PubMedID 30994932

  • Genetics and the geography of health, behaviour and attainment. Nature human behaviour Belsky, D. W., Caspi, A., Arseneault, L., Corcoran, D. L., Domingue, B. W., Harris, K. M., Houts, R. M., Mill, J. S., Moffitt, T. E., Prinz, J., Sugden, K., Wertz, J., Williams, B., Odgers, C. L. 2019


    Young people's life chances can be predicted by characteristics of their neighbourhood1. Children growing up in disadvantaged neighbourhoods exhibit worse physical and mental health and suffer poorer educational and economic outcomes than children growing up in advantaged neighbourhoods. Increasing recognition that aspects of social inequalities tend, in fact, to be geographical inequalities2-5 is stimulating research and focusing policy interest on the role of place in shaping health, behaviour and social outcomes. Where neighbourhood effects are causal, neighbourhood-level interventions can be effective. Where neighbourhood effects reflect selection of families with different characteristics into different neighbourhoods, interventions should instead target families or individuals directly. To test how selection may affect different neighbourhood-linked problems, we linked neighbourhood data with genetic, health and social outcome data for >7,000 European-descent UK and US young people in the E-Risk and Add Health studies. We tested selection/concentration of genetic risks for obesity, schizophrenia, teen pregnancy and poor educational outcomes in high-risk neighbourhoods, including genetic analysis of neighbourhood mobility. Findings argue against genetic selection/concentration as an explanation for neighbourhood gradients in obesity and mental health problems. By contrast, modest genetic selection/concentration was evident for teen pregnancy and poor educational outcomes, suggesting that neighbourhood effects for these outcomes should be interpreted with care.

    View details for PubMedID 30962612

  • New Evidence of Skin Color Bias and Health Outcomes Using Sibling Difference Models: A Research Note DEMOGRAPHY Laidley, T., Domingue, B., Sinsub, P., Harris, K., Conley, D. 2019; 56 (2): 753–62
  • Evaluation of the Preliminary Validity of Misuse of Prescription Pain Medication Items from the Patient-Reported Outcomes Measurement Information System (PROMIS). Pain medicine (Malden, Mass.) You, D. S., Hah, J. M., Collins, S., Ziadni, M. S., Domingue, B. W., Cook, K. F., Mackey, S. C. 2019


    OBJECTIVE: The National Institutes of Health's Patient-Reported Outcomes Measurement Information System (PROMIS) includes an item bank for measuring misuse of prescription pain medication (PROMIS-Rx Misuse). The bank was developed and its validity evaluated in samples of community-dwelling adults and patients in addiction treatment programs. The goal of the current study was to investigate the validity of the item bank among patients with mixed-etiology chronic pain conditions.METHOD: A consecutive sample of 288 patients who presented for initial medical evaluations at a tertiary pain clinic completed questionnaires using the open-source Collaborative Health Outcomes Information Registry. Participants were predominantly middle-aged (M [SD]=51.6 [15.5] years), female (62.2%), and white/non-Hispanic (51.7%). Validity was evaluated by estimating the association between PROMIS-Rx Misuse scores and scores on other measures and testing the ability of scores to distinguish among risk factor subgroups expected to have different levels of prescription pain medicine misuse (known groups analyses).RESULTS: Overall, score associations with other measures were as expected and scores effectively distinguished among patients with and without relevant risk factors.CONCLUSION: The study results supported the preliminary validity of PROMIS-Rx Misuse item bank scores for the assessment of prescription opioid misuse in patients visiting an outpatient pain clinic.

    View details for PubMedID 30856659

  • THE GENETIC RISK FOR BODY MASS INDEX AND WEIGHT LOSS BEHAVIORS Nagata, J., Domingue, B. W., Bibbins-Domingo, K., Garber, A. K., Griffiths, S., Murray, S. B. ELSEVIER SCIENCE INC. 2019: S53
  • New Evidence of Skin Color Bias and Health Outcomes Using Sibling Difference Models: A Research Note. Demography Laidley, T., Domingue, B., Sinsub, P., Harris, K. M., Conley, D. 2019


    In this research note, we use data from the National Longitudinal Study of Adolescent to Adult Health (Add Health) to determine whether darker skin tone predicts hypertension among siblings using a family fixed-effects analytic strategy. We find that even after we account for common family background and home environment, body mass index, age, sex, and outdoor activity, darker skin color significantly predicts hypertension incidence among siblings. In a supplementary analysis using newly released genetic data from Add Health, we find no evidence that our results are biased by genetic pleiotropy, whereby differences in alleles among siblings relate to coloration and directly to cardiovascular health simultaneously. These results add to the extant evidence on color biases that are distinct from those based on race alone and that will likely only heighten in importance in an increasingly multiracial environment as categorization becomes more complex.

    View details for PubMedID 30627966

  • Adolescent gender norms and adult health outcomes in the USA: a prospective cohort study. The Lancet. Child & adolescent health Shakya, H. B., Domingue, B., Nagata, J. M., Cislaghi, B., Weber, A., Darmstadt, G. L. 2019


    Previous research has documented differences in health behaviours between men and women, with differential risks and health outcomes between the sexes. Although some sex-specific differences in health outcomes are caused by biological factors, many others are socially driven through gender norms. We therefore aimed to assess whether gender expression as an adolescent, determined by the degree to which an individual's behvaiours were typical of their gender, were associated with health behaviours and outcomes in adulthood.In this prospective cohort study, we used data from the National Longitudinal Study of Adolescent to Adult Health, a nationally representative sample of US adolescents from whom data were collected during adolescence (ages 11-18 years) and adulthood (ages 24-32 years). We created a measure of gender expression that was based on the degree to which male and female adolescents and adults behave in stereotypically masculine (for men) or feminine (for women) ways relative to their same-gender peers. Adolescents were assessed for baseline sociodemographic characteristics and gender expression, and these participants were later assessed, during adulthood, for their gender expression and health behaviours and outcomes, which included depression, self-rated health, drug and alcohol use, cardiovascular risk factors, experience of sexual violence, diet, and obesity. These data were collected via surveys, except for body-mass index, cholesterol, and blood pressure, which were collected as biomarkers.Between April and December, 1995, self-reported data were collected from 10 480 female and 10 263 male adolescents; similar data were subsequently collected in several waves in this cohort, with a final collection between January, 2008, and February, 2009, when participants were aged 24-32 years. We used data from this final wave and from baseline, and our study represents a secondary analysis of these data. Of these participants, complete follow-up data from 6721 (80%) adult women and 5885 (80%) adult men were available. Gender expression was stable for men and women from adolescence to adulthood. High masculinity (vs low masculinity) in adolescent and adult men was positively associated with smoking in the past month, use of marijuana and recreational drugs, prescription drug misuse (adult gender expression only), and consumption of fast food and soda (adolescent gender expression only) in the past week. However, higher masculine gender expression in adult men was negatively associated with diagnosed depression and high cholesterol in adulthood, and masculine gender expression in adolescent and adult men was negatively associated with high blood pressure in adults. High femininity (vs low femininity) in adolescent or adult women was positively associated with high cholesterol and blood pressure (both adult gender expression only), depression, migraines (adult gender expression only), and physical limitations (ie, health problems that limited their daily activities). However, higher femininity in adolescence was negatively associated with self-rated good health in adulthood. Although feminine gender expression in adolescents was predictive of adult recreational and prescription drug and marijuana use and experience of sexual violence, feminine gender expression in adulthood was negatively associated with adult substance use and experience of sexual violence, suggesting that expressions of femininity typical of adolescents impart risks that expression of femininity as an adult does not. Individuals who are highly masculine or feminine seem to be at greatest risk of adverse health outcomes and behaviours.We found compelling evidence that adolescent gender expression is correlated with health in adulthood independently of gender expression as an adult. Although more research is needed to identify causal mechanisms, our results suggest that those designing health behaviour interventions should carefully consider integrating gender transformative components into interventions.Eunice Kennedy Shriver National Institute of Child Health and Human Development, Gender Equality, Integrated Delivery, HIV, Nutrition, Family Planning, and Water Sanitation and Hygiene Program Strategy Teams (Bill and Melinda Gates Foundation).

    View details for DOI 10.1016/S2352-4642(19)30160-9

    View details for PubMedID 31155319

  • Gender norms and health: insights from global survey data. Lancet (London, England) Weber, A. M., Cislaghi, B., Meausoone, V., Abdalla, S., Mejía-Guevara, I., Loftus, P., Hallgren, E., Seff, I., Stark, L., Victora, C. G., Buffarini, R., Barros, A. J., Domingue, B. W., Bhushan, D., Gupta, R., Nagata, J. M., Shakya, H. B., Richter, L. M., Norris, S. A., Ngo, T. D., Chae, S., Haberland, N., McCarthy, K., Cullen, M. R., Darmstadt, G. L. 2019


    Despite global commitments to achieving gender equality and improving health and wellbeing for all, quantitative data and methods to precisely estimate the effect of gender norms on health inequities are underdeveloped. Nonetheless, existing global, national, and subnational data provide some key opportunities for testing associations between gender norms and health. Using innovative approaches to analysing proxies for gender norms, we generated evidence that gender norms impact the health of women and men across life stages, health sectors, and world regions. Six case studies showed that: (1) gender norms are complex and can intersect with other social factors to impact health over the life course; (2) early gender-normative influences by parents and peers can have multiple and differing health consequences for girls and boys; (3) non-conformity with, and transgression of, gender norms can be harmful to health, particularly when they trigger negative sanctions; and (4) the impact of gender norms on health can be context-specific, demanding care when designing effective gender-transformative health policies and programmes. Limitations of survey-based data are described that resulted in missed opportunities for investigating certain populations and domains. Recommendations for optimising and advancing research on the health impacts of gender norms are made.

    View details for DOI 10.1016/S0140-6736(19)30765-2

    View details for PubMedID 31155273

  • Transancestral GWAS of alcohol dependence reveals common genetic underpinnings with psychiatric disorders. Nature neuroscience Walters, R. K., Polimanti, R., Johnson, E. C., McClintick, J. N., Adams, M. J., Adkins, A. E., Aliev, F., Bacanu, S., Batzler, A., Bertelsen, S., Biernacka, J. M., Bigdeli, T. B., Chen, L., Clarke, T., Chou, Y., Degenhardt, F., Docherty, A. R., Edwards, A. C., Fontanillas, P., Foo, J. C., Fox, L., Frank, J., Giegling, I., Gordon, S., Hack, L. M., Hartmann, A. M., Hartz, S. M., Heilmann-Heimbach, S., Herms, S., Hodgkinson, C., Hoffmann, P., Jan Hottenga, J., Kennedy, M. A., Alanne-Kinnunen, M., Konte, B., Lahti, J., Lahti-Pulkkinen, M., Lai, D., Ligthart, L., Loukola, A., Maher, B. S., Mbarek, H., McIntosh, A. M., McQueen, M. B., Meyers, J. L., Milaneschi, Y., Palviainen, T., Pearson, J. F., Peterson, R. E., Ripatti, S., Ryu, E., Saccone, N. L., Salvatore, J. E., Sanchez-Roige, S., Schwandt, M., Sherva, R., Streit, F., Strohmaier, J., Thomas, N., Wang, J., Webb, B. T., Wedow, R., Wetherill, L., Wills, A. G., 23andMe Research Team, Boardman, J. D., Chen, D., Choi, D., Copeland, W. E., Culverhouse, R. C., Dahmen, N., Degenhardt, L., Domingue, B. W., Elson, S. L., Frye, M. A., Gabel, W., Hayward, C., Ising, M., Keyes, M., Kiefer, F., Kramer, J., Kuperman, S., Lucae, S., Lynskey, M. T., Maier, W., Mann, K., Mannisto, S., Muller-Myhsok, B., Murray, A. D., Nurnberger, J. I., Palotie, A., Preuss, U., Raikkonen, K., Reynolds, M. D., Ridinger, M., Scherbaum, N., Schuckit, M. A., Soyka, M., Treutlein, J., Witt, S., Wodarz, N., Zill, P., Adkins, D. E., Boden, J. M., Boomsma, D. I., Bierut, L. J., Brown, S. A., Bucholz, K. K., Cichon, S., Costello, E. J., de Wit, H., Diazgranados, N., Dick, D. M., Eriksson, J. G., Farrer, L. A., Foroud, T. M., Gillespie, N. A., Goate, A. M., Goldman, D., Grucza, R. A., Hancock, D. B., Harris, K. M., Heath, A. C., Hesselbrock, V., Hewitt, J. K., Hopfer, C. J., Horwood, J., Iacono, W., Johnson, E. O., Kaprio, J. A., Karpyak, V. M., Kendler, K. S., Kranzler, H. R., Krauter, K., Lichtenstein, P., Lind, P. A., McGue, M., MacKillop, J., Madden, P. A., Maes, H. H., Magnusson, P., Martin, N. G., Medland, S. E., Montgomery, G. W., Nelson, E. C., Nothen, M. M., Palmer, A. A., Pedersen, N. L., Penninx, B. W., Porjesz, B., Rice, J. P., Rietschel, M., Riley, B. P., Rose, R., Rujescu, D., Shen, P., Silberg, J., Stallings, M. C., Tarter, R. E., Vanyukov, M. M., Vrieze, S., Wall, T. L., Whitfield, J. B., Zhao, H., Neale, B. M., Gelernter, J., Edenberg, H. J., Agrawal, A., Agee, M., Alipanahi, B., Auton, A., Bell, R. K., Bryc, K., Elson, S. L., Fontanillas, P., Furlotte, N. A., Hinds, D. A., Huber, K. E., Kleinman, A., Litterman, N. K., McCreight, J. C., McIntyre, M. H., Mountain, J. L., Noblin, E. S., Northover, C. A., Pitts, S. J., Sathirapongsasuti, J. F., Sazonova, O. V., Shelton, J. F., Shringarpure, S., Tian, C., Tung, J. Y., Vacic, V., Wilson, C. H. 2018; 21 (12): 1656–69


    Liability to alcohol dependence (AD) is heritable, but little is known about its complex polygenic architecture or its genetic relationship with other disorders. To discover loci associated with AD and characterize the relationship between AD and other psychiatric and behavioral outcomes, we carried out the largest genome-wide association study to date of DSM-IV-diagnosed AD. Genome-wide data on 14,904 individuals with AD and 37,944 controls from 28 case-control and family-based studies were meta-analyzed, stratified by genetic ancestry (European, n=46,568; African, n=6,280). Independent, genome-wide significant effects of different ADH1B variants were identified in European (rs1229984; P=9.8*10-13) and African ancestries (rs2066702; P=2.2*10-9). Significant genetic correlations were observed with 17 phenotypes, including schizophrenia, attention deficit-hyperactivity disorder, depression, and use of cigarettes and cannabis. The genetic underpinnings of AD only partially overlap with those for alcohol consumption, underscoring the genetic distinction between pathological and nonpathological drinking behaviors.

    View details for PubMedID 30482948

  • Schools as Moderators of Genetic Associations with Life Course Attainments: Evidence from the WLS and Add Heath SOCIOLOGICAL SCIENCE Trejo, S., Belsky, D. W., Boardman, J. D., Freese, J., Harris, K., Herd, P., Sicinski, K., Domingue, B. W. 2018; 5: 513–40

    View details for DOI 10.15195/v5.a22

    View details for Web of Science ID 000440607600001

  • Education, Smoking, and Cohort Change: Forwarding a Multidimensional Theory of the Environmental Moderation of Genetic Effects AMERICAN SOCIOLOGICAL REVIEW Wedow, R., Zacher, M., Huibregtse, B. M., Harris, K., Domingue, B. W., Boardman, J. D. 2018; 83 (4): 802–32
  • Wide educational disparities in young adult cardiovascular health SSM-POPULATION HEALTH Lawrence, E. M., Hummer, R. A., Domingue, B. W., Harris, K. 2018; 5: 249–56


    Widening educational differences in overall health and recent stagnation in cardiovascular disease mortality rates highlight the critical need to describe and understand educational disparities in cardiovascular health (CVH) among U.S. young adults. We use two data sets representative of the U.S. population to examine educational disparities in CVH among young adults (24-34) coming of age in the 21st century: the National Health and Nutrition Examination Survey (2005-2010; N= 689) and the National Longitudinal Study of Adolescent to Adult Health (2007-2008; N=11,200). We employ descriptive statistics and regression analysis. The results show that fewer than one in four young adults had good CVH (at least 5 out of 7 ideal cardiovascular indicators). Young adults who had not attained a college degree demonstrate particularly disadvantaged CVH compared with their college-educated peers. Such educational disparities persist after accounting for a range of confounders, including individuals' genetic propensity to develop coronary artery disease. The results indicate that the CVH of today's young adults is troubling and especially compromised for individuals with lower levels of educational attainment. These results generate substantial concern about the future CVH of the US population, particularly for young adults with a low level of education.

    View details for PubMedID 30094320

  • Father Absence and Accelerated Reproductive Development in Non-Hispanic White Women in the United States DEMOGRAPHY Gaydosh, L., Belsky, D. W., Domingue, B. W., Boardman, J. D., Harris, K. 2018; 55 (4): 1245–67


    Girls who experience father absence in childhood also experience accelerated reproductive development in comparison with peers with present fathers. One hypothesis advanced to explain this empirical pattern is genetic confounding, wherein gene-environment correlation (rGE) causes a spurious relationship between father absence and reproductive timing. We test this hypothesis by constructing polygenic scores for age at menarche and first birth using recently available genome-wide association study results and molecular genetic data on a sample of non-Hispanic white females from the National Longitudinal Study of Adolescent to Adult Health. We find that young women's accelerated menarche polygenic scores are unrelated to their exposure to father absence. In contrast, polygenic scores for earlier age at first birth tend to be higher in young women raised in homes with absent fathers. Nevertheless, father absence and the polygenic scores independently and additively predict reproductive timing. We find no evidence in support of the rGE hypothesis for accelerated menarche and only limited evidence in support of the rGE hypothesis for earlier age at first birth.

    View details for PubMedID 29978338

  • A sibling method for identifying vQTLs PLOS ONE Conley, D., Johnson, R., Domingue, B., Dawes, C., Boardman, J., Siegal, M. 2018; 13 (4): e0194541


    The propensity of a trait to vary within a population may have evolutionary, ecological, or clinical significance. In the present study we deploy sibling models to offer a novel and unbiased way to ascertain loci associated with the extent to which phenotypes vary (variance-controlling quantitative trait loci, or vQTLs). Previous methods for vQTL-mapping either exclude genetically related individuals or treat genetic relatedness among individuals as a complicating factor addressed by adjusting estimates for non-independence in phenotypes. The present method uses genetic relatedness as a tool to obtain unbiased estimates of variance effects rather than as a nuisance. The family-based approach, which utilizes random variation between siblings in minor allele counts at a locus, also allows controls for parental genotype, mean effects, and non-linear (dominance) effects that may spuriously appear to generate variation. Simulations show that the approach performs equally well as two existing methods (squared Z-score and DGLM) in controlling type I error rates when there is no unobserved confounding, and performs significantly better than these methods in the presence of small degrees of confounding. Using height and BMI as empirical applications, we investigate SNPs that alter within-family variation in height and BMI, as well as pathways that appear to be enriched. One significant SNP for BMI variability, in the MAST4 gene, replicated. Pathway analysis revealed one gene set, encoding members of several signaling pathways related to gap junction function, which appears significantly enriched for associations with within-family height variation in both datasets (while not enriched in analysis of mean levels). We recommend approximating laboratory random assignment of genotype using family data and more careful attention to the possible conflation of mean and variance effects.

    View details for PubMedID 29617452

  • Genetic Risks for Chronic Conditions: Implications for Long-term Wellbeing JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES Wehby, G. L., Domingue, B. W., Wolinsky, F. D. 2018; 73 (4): 477–83


    Relationships between genetic risks for chronic diseases and long-run wellbeing are largely unexplored. We examined the associations between genetic predispositions to several chronic conditions and long-term functional health and socioeconomic status (SES).We used data on a nationally representative sample of 9,317 adults aged 65 years or older from the 1992 to 2012 Health and Retirement Survey (HRS) in the US. Survey data were linked to genetic data on nearly 2 million single-nucleotide polymorphisms (SNPs). We measured individual-level genetic predispositions for coronary-artery disease, type 2 diabetes (T2D), obesity, rheumatoid arthritis (RA), Alzheimer's disease, and major depressive disorder (MDD) by polygenic risk scores (PRS) derived from genome-wide association studies (GWAS). The outcomes were self-rated health, depressive symptoms, cognitive ability, activities of everyday life, educational attainment, and wealth. We employed regression analyses for the outcomes including all polygenic scores and adjusting for gender, birth period, and genetic ancestry.The polygenic scores had important associations with functional health and SES. An increase in genetic risk for all conditions except T2D was significantly (p < .01) associated with reduced functional health and socioeconomic outcomes. The magnitudes of functional health declines were meaningful and in many cases equivalent in magnitude to several years of aging. These associations were robust to several sensitivity checks for ancestry and adjustment for parental educational attainment and age at death or the last interview if alive.Stronger genetic predispositions for leading chronic conditions are related to worse long-run health and SES outcomes, likely reflecting the adverse effects of the onset of these conditions on one's wellbeing.

    View details for PubMedID 28958056

    View details for PubMedCentralID PMC5861924

  • Geographic Clustering of Polygenic Scores at Different Stages of the Life Course. The Russell Sage Foundation journal of the social sciences : RSF Domingue, B. W., Rehkopf, D. H., Conley, D., Boardman, J. D. 2018; 4 (4): 137–49


    We interrogate state-level clustering of polygenic scores at different points in the life course and variation in the association of mean polygenic scores in a respondent's state of birth with corresponding phenotypes. The polygenic scores for height and smoking show the most state-level clustering (2 to 4 percent) with relatively little clustering observed for the other scores. However, even the small amounts of observed clustering are potentially meaningful. The state-mean polygenic score for educational attainment is strongly associated with an individual's educational attainment net of that person's polygenic score. The ecological clustering of polygenic scores may denote a new environmental factor in gene-environment research. We conclude by discussing possible mechanisms that underlie this association and the implications of our findings for social and genetic research.

    View details for PubMedID 30740524

  • Genetic Predisposition to Obesity and Medicare Expenditures JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES Wehby, G. L., Domingue, B. W., Ullrich, F., Wolinsky, F. D. 2018; 73 (1): 66–72


    The relationship between obesity and health expenditures is not well understood. We examined the relationship between genetic predisposition to obesity measured by a polygenic risk score for body mass index (BMI) and Medicare expenditures.Biennial interview data from the Health and Retirement Survey for a nationally representative sample of older adults enrolled in fee-for-service Medicare were obtained from 1991 through 2010 and linked to Medicare claims for the same period and to Genome-Wide Association Study (GWAS) data. The study included 6,628 Medicare beneficiaries who provided 68,627 complete person-year observations during the study period. Outcomes were total and service-specific Medicare expenditures and indicators for expenditures exceeding the 75th and 90th percentiles. The BMI polygenic risk score was derived from GWAS data. Regression models were used to examine how the BMI polygenic risk score was related to health expenditures adjusting for demographic factors and GWAS-derived ancestry.Greater genetic predisposition to obesity was associated with higher Medicare expenditures. Specifically, a 1 SD increase in the BMI polygenic risk score was associated with a $805 (p < .001) increase in annual Medicare expenditures per person in 2010 dollars (~15% increase), a $370 (p < .001) increase in inpatient expenses, and a $246 (p < .001) increase in outpatient services. A 1 SD increase in the polygenic risk score was also related to increased likelihood of expenditures exceeding the 75th percentile by 18% (95% CI: 10%-28%) and the 90th percentile by 27% (95% CI: 15%-40%).Greater genetic predisposition to obesity is associated with higher Medicare expenditures.

    View details for PubMedID 29240910

    View details for PubMedCentralID PMC5861952



    The Psychological Sense of School Membership (PSSM) scale is widely used to measure school belongingness among adolescents. However, previous studies identify inconsistencies in factor structures across different populations. The factor structure of the PSSM has yet to be examined with American Indian/Alaska Native (AI/AN) youth, a population of keen interest given reports of their educational and health disparities, and the potential of belongingness as a protective factor against risk behaviors. Thus, this study examined the factor structure of the PSSM in two samples of AI adolescents (N = 349). The two main aims of this study were to 1) determine if a comparable factor structure exists between the two AI groups and 2) examine the factor structure of the PSSM for use in AI/AN populations. Randomization analysis was used to test research aim one, and exploratory factor analysis was used to test research aim two. Analyses revealed that comparable factor structures existed based on responses from the two AI groups. Analyses also identified two factors: school identification/peer support and connection with teachers. Moreover, negatively worded statements were found to be unreliable and were removed from the final scale, reducing the PSSM to 13 items. Findings from this study will assist researchers and clinicians with assessing sense of school belongingness in AI/AN adolescents and with appropriately interpreting aspects of belongingness for this population.

    View details for Web of Science ID 000447634800002

    View details for PubMedID 30320875

  • Cohort Trends in the Gender Distribution of Household Tasks in the United States and the Implications for Understanding Disability. Journal of aging and health Sheehan, C., Domingue, B. W., Crimmins, E. 2018: 898264318793469


    Measures of disability depend on health and social roles in a given environment. Yet, social roles can change over time as they have by gender. We document how engagement in Instrumental Activities of Daily Living (IADLs) is shifting by gender and birth cohort among older adults, and the challenges these shifts can create for population-level estimates of disability.We used the Health and Retirement Study ( N = 25,047) and multinomial logistic regression models with an interaction term between gender and birth cohort to predict limitation and nonperformance relative to no difficulty conducting IADLs.Nonperformance of IADLs have significantly decreased among younger cohorts. Women in younger cohorts were more likely to use a map, whereas men in younger cohorts were more likely to prepare meals and shop.Failing to account for gender and cohort changes in IADL, performance may lead to systematic bias in estimates of population-level disability.

    View details for PubMedID 30141717

  • Schools as Moderators of Genetic Associations with Life Course Attainments: Evidence from the WLS and Add Health. Sociological science Trejo, S., Belsky, D. W., Boardman, J. D., Freese, J., Harris, K. M., Herd, P., Sicinski, K., Domingue, B. W. 2018; 5: 513–40


    Genetic variants identified in genome-wide association studies of educational attainment have been linked with a range of positive life course development outcomes. However, it remains unclear whether school environments may moderate these genetic associations. We analyze data from two biosocial surveys that contain both genetic data and follow students from secondary school through mid- to late life. We test if the magnitudes of the associations with educational and occupational attainments varied across the secondary schools that participants attended or with characteristics of those schools. Although we find little evidence that genetic associations with educational and occupational attainment varied across schools or with school characteristics, genetic associations with any postsecondary education and college completion were moderated by school-level socioeconomic status. Along similar lines, we observe substantial between-school variation in the average level of educational attainment students achieved for a fixed genotype. These findings emphasize the importance of social context in the interpretation of genetic associations. Specifically, our results suggest that though existing measures of individual genetic endowment have a linear relationship with years of schooling that is relatively consistent across school environments, school context is crucial in connecting an individual's genotype to his or her likelihood of crossing meaningful educational thresholds.

    View details for PubMedID 30613760

    View details for PubMedCentralID PMC6314676

  • The social genome: Current findings and implications for the study of human genetics PLOS GENETICS Domingue, B. W., Belsky, D. W. 2017; 13 (3): e1006615

    View details for PubMedID 28301508

  • The Genetics of Success: How Single-Nucleotide Polymorphisms Associated With Educational Attainment Relate to Life-Course Development. Psychological science Belsky, D. W., Moffitt, T. E., Corcoran, D. L., Domingue, B., Harrington, H., Hogan, S., Houts, R., Ramrakha, S., Sugden, K., Williams, B. S., Poulton, R., Caspi, A. 2016; 27 (7): 957-972


    A previous genome-wide association study (GWAS) of more than 100,000 individuals identified molecular-genetic predictors of educational attainment. We undertook in-depth life-course investigation of the polygenic score derived from this GWAS using the four-decade Dunedin Study (N = 918). There were five main findings. First, polygenic scores predicted adult economic outcomes even after accounting for educational attainments. Second, genes and environments were correlated: Children with higher polygenic scores were born into better-off homes. Third, children's polygenic scores predicted their adult outcomes even when analyses accounted for their social-class origins; social-mobility analysis showed that children with higher polygenic scores were more upwardly mobile than children with lower scores. Fourth, polygenic scores predicted behavior across the life course, from early acquisition of speech and reading skills through geographic mobility and mate choice and on to financial planning for retirement. Fifth, polygenic-score associations were mediated by psychological characteristics, including intelligence, self-control, and interpersonal skill. Effect sizes were small. Factors connecting DNA sequence with life outcomes may provide targets for interventions to promote population-wide positive development.

    View details for DOI 10.1177/0956797616643070

    View details for PubMedID 27251486

    View details for PubMedCentralID PMC4946990

  • Assortative mating and differential fertility by phenotype and genotype across the 20th century PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Conley, D., Laidley, T., Belsky, D. W., Fletcher, J. M., Boardman, J. D., Domingue, B. W. 2016; 113 (24): 6647-6652


    This study asks two related questions about the shifting landscape of marriage and reproduction in US society over the course of the last century with respect to a range of health and behavioral phenotypes and their associated genetic architecture: (i) Has assortment on measured genetic factors influencing reproductive and social fitness traits changed over the course of the 20th century? (ii) Has the genetic covariance between fitness (as measured by total fertility) and other traits changed over time? The answers to these questions inform our understanding of how the genetic landscape of American society has changed over the past century and have implications for population trends. We show that husbands and wives carry similar loadings for genetic factors related to education and height. However, the magnitude of this similarity is modest and has been fairly consistent over the course of the 20th century. This consistency is particularly notable in the case of education, for which phenotypic similarity among spouses has increased in recent years. Likewise, changing patterns of the number of children ever born by phenotype are not matched by shifts in genotype-fertility relationships over time. Taken together, these trends provide no evidence that social sorting is becoming increasingly genetic in nature or that dysgenic dynamics have accelerated.

    View details for DOI 10.1073/pnas.1523592113

    View details for Web of Science ID 000377948800037

    View details for PubMedID 27247411

    View details for PubMedCentralID PMC4914190

  • The Geographic Distribution of Genetic Risk as Compared to Social Risk for Chronic Diseases in the United States BIODEMOGRAPHY AND SOCIAL BIOLOGY Rehkopf, D. H., Domingue, B. W., Cullen, M. R. 2016; 62 (1): 126-142


    There is an association between chronic disease and geography, and there is evidence that the environment plays a critical role in this relationship. Yet at the same time, there is known to be substantial geographic variation by ancestry across the United States. Resulting geographic genetic variation-that is, the extent to which single nucleotide polymorphisms (SNPs) related to chronic disease vary spatially-could thus drive some part of the association between geography and disease. We describe the variation in chronic disease genetic risk by state of birth by taking risk SNPs from genome-wide association study meta-analyses for coronary artery disease, diabetes, and ischemic stroke and creating polygenic risk scores. We compare the amount of variability across state of birth in these polygenic scores to the variability in parental education, own education, earnings, and wealth. Our primary finding is that the polygenic risk scores are only weakly differentially distributed across U.S. states. The magnitude of the differences in geographic distribution is very small in comparison to the distribution of social and economic factors and thus is not likely sufficient to have a meaningful effect on geographic disease differences by U.S. state.

    View details for DOI 10.1080/19485565.2016.1141353

    View details for Web of Science ID 000373629600008

    View details for PubMedID 27050037

  • Genome-Wide Estimates of Heritability for Social Demographic Outcomes BIODEMOGRAPHY AND SOCIAL BIOLOGY Domingue, B. W., Wedow, R., Conley, D., McQueen, M., Hoffmann, T. J., Boardman, J. D. 2016; 62 (1): 1-18


    An increasing number of studies that are widely used in the demographic research community have collected genome-wide data from their respondents. It is therefore important that demographers have a proper understanding of some of the methodological tools needed to analyze such data. This article details the underlying methodology behind one of the most common techniques for analyzing genome-wide data, genome-wide complex trait analysis (GCTA). GCTA models provide heritability estimates for health, health behaviors, or indicators of attainment using data from unrelated persons. Our goal was to describe this model, highlight the utility of the model for biodemographic research, and demonstrate the performance of this approach under modifications to the underlying assumptions. The first set of modifications involved changing the nature of the genetic data used to compute genetic similarities between individuals (the genetic relationship matrix). We then explored the sensitivity of the model to heteroscedastic errors. In general, GCTA estimates are found to be robust to the modifications proposed here, but we also highlight potential limitations of GCTA estimates.

    View details for DOI 10.1080/19485565.2015.1068106

    View details for Web of Science ID 000373629600001

    View details for PubMedID 27050030

  • Cohort Effects in the Genetic Influence on Smoking BEHAVIOR GENETICS Domingue, B. W., Conley, D., Fletcher, J., Boardman, J. D. 2016; 46 (1): 31-42
  • Cohort Effects in the Genetic Influence on Smoking. Behavior genetics Domingue, B. W., Conley, D., Fletcher, J., Boardman, J. D. 2016; 46 (1): 31–42


    We examine the hypothesis that the heritability of smoking has varied over the course of recent history as a function of associated changes in the composition of the smoking and non-smoking populations. Classical twin-based heritability analysis has suggested that genetic basis of smoking has increased as the information about the harms of tobacco has become more prevalent-particularly after the issuance of the 1964 Surgeon General's Report. In the present paper we deploy alternative methods to test this claim. We use data from the Health and Retirement Study to estimate cohort differences in the genetic influence on smoking using both genomic-relatedness-matrix restricted maximum likelihood and a modified DeFries-Fulker approach. We perform a similar exercise deploying a polygenic score for smoking using results generated by the Tobacco and Genetics consortium. The results support earlier claims that the genetic influence in smoking behavior has increased over time. Emphasizing historical periods and birth cohorts as environmental factors has benefits over existing GxE research. Our results provide additional support for the idea that anti-smoking policies of the 1980s may not be as effective because of the increasingly important role of genotype as a determinant of smoking status.

    View details for PubMedID 26223473

    View details for PubMedCentralID PMC4720550

  • The Bell Curve Revisited: Testing Controversial Hypotheses with Molecular Genetic Data. Sociological science Conley, D., Domingue, B. 2016; 3: 520–39


    In 1994, the publication of Herrnstein's and Murray's The Bell Curve resulted in a social science maelstrom of responses. In the present study, we argue that Herrnstein's and Murray's assertions were made prematurely, on their own terms, given the lack of data available to test the role of genotype in the dynamics of achievement and attainment in U.S. society. Today, however, the scientific community has access to at least one dataset that is nationally representative and has genome-wide molecular markers. We deploy those data from the Health and Retirement Study in order to test the core series of propositions offered by Herrnstein and Murray in 1994. First, we ask whether the effect of genotype is increasing in predictive power across birth cohorts in the middle twentieth century. Second, we ask whether assortative mating on relevant genotypes is increasing across the same time period. Finally, we ask whether educational genotypes are increasingly predictive of fertility (number ever born [NEB]) in tandem with the rising (negative) association of educational outcomes and NEB. The answers to these questions are mostly no; while molecular genetic markers can predict educational attainment, we find little evidence for the proposition that we are becoming increasingly genetically stratified.

    View details for PubMedID 29130056

    View details for PubMedCentralID PMC5679002

  • Changing Polygenic Penetrance on Phenotypes in the 20(th) Century Among Adults in the US Population. Scientific reports Conley, D., Laidley, T. M., Boardman, J. D., Domingue, B. W. 2016; 6: 30348-?


    This study evaluates changes in genetic penetrance-defined as the association between an additive polygenic score and its associated phenotype-across birth cohorts. Situating our analysis within recent historical trends in the U.S., we show that, while height and BMI show increasing genotypic penetrance over the course of 20(th) Century, education and heart disease show declining genotypic effects. Meanwhile, we find genotypic penetrance to be historically stable with respect to depression. Our findings help inform our understanding of how the genetic and environmental landscape of American society has changed over the past century, and have implications for research which models gene-environment (GxE) interactions, as well as polygenic score calculations in consortia studies that include multiple birth cohorts.

    View details for DOI 10.1038/srep30348

    View details for PubMedID 27456657

    View details for PubMedCentralID PMC4960614

  • On the practices and challenges of measuring higher education value added: the case of Colombia ASSESSMENT & EVALUATION IN HIGHER EDUCATION Shavelson, R. J., Domingue, B. W., Marino, J. P., Molina Mantilla, A., Morales Forero, A., Wiley, E. E. 2016; 41 (5): 695-720
  • Breastfeeding is associated with waist-to-height ratio in young adults BMC PUBLIC HEALTH Bohr, A. D., Boardman, J. D., Domingue, B. W., McQueen, M. B. 2015; 15

    View details for DOI 10.1186/s12889-015-2611-7

    View details for PubMedID 26700003

  • Polygenic Influence on Educational Attainment: New evidence from The National Longitudinal Study of Adolescent to Adult Health. AERA open Domingue, B. W., Belsky, D., Conley, D., Harris, K. M., Boardman, J. D. 2015; 1 (3): 1-13


    Recent studies have begun to uncover the genetic architecture of educational attainment. We build on this work using genome-wide data from siblings in the National Longitudinal Study of Adolescent to Adult Health (Add Health). We measure the genetic predisposition of siblings to educational attainment using polygenic scores. We then test how polygenic scores are related to social environments and educational outcomes. In Add Health, genetic predisposition to educational attainment is patterned across the social environment. Participants with higher polygenic scores were more likely to grow up in socially advantaged families. Even so, the previously published genetic associations appear to be causal. Among pairs of siblings, the sibling with the higher polygenic score typically went on to complete more years of schooling as compared to their lower-scored co-sibling. We found subtle differences between sibling fixed effect estimates of the genetic effect versus those based on unrelated individuals.

    View details for DOI 10.1177/2332858415599972

    View details for PubMedID 28164148

    View details for PubMedCentralID PMC5291340

  • Prevention, Use of Health Services, and Genes: Implications of Genetics for Policy Formation JOURNAL OF POLICY ANALYSIS AND MANAGEMENT Wehby, G. L., Domingue, B. W., Boardman, J. D. 2015; 34 (3): 519-U228


    We evaluate the hypothesis that genetic factors influence the use of health services and prevention behaviors in a national sample of adult twins in the United States. The analysis compares the correlation of these outcomes between identical twins, who share all their genes, to the correlation between nonidentical twins, who share, on average, only one-half of their genes. Because the environmental similarities of twins are assumed to be the same for identical and nonidentical twin pairs, researchers can partition the variance in behavioral outcomes that are due to genetic and environmental factors. Using established methods in this field, we find evidence of significant genetic influences on preferences toward prevention, overall prevention effort, routine checkups, and prescription drug use. Use of curative services does not appear to be influenced by genes. Our findings offer several implications for policymakers and researchers and suggest that genetics could be informative for health services and policy research.

    View details for DOI 10.1002/pam.21835

    View details for Web of Science ID 000356005100005

    View details for PubMedID 26106669

  • What can genes tell us about the relationship between education and health? SOCIAL SCIENCE & MEDICINE Boardman, J. D., Domingue, B. W., Daw, J. 2015; 127: 171-180


    We use genome wide data from respondents of the Health and Retirement Study (HRS) to evaluate the possibility that common genetic influences are associated with education and three health outcomes: depression, self-rated health, and body mass index. We use a total of 1.7 million single nucleotide polymorphisms obtained from the Illumina HumanOmni2.5-4v1 chip from 4233 non-Hispanic white respondents to characterize genetic similarities among unrelated persons in the HRS. We then used the Genome Wide Complex Trait Analysis (GCTA) toolkit, to estimate univariate and bivariate heritability. We provide evidence that education (h(2) = 0.33), BMI (h(2) = 0.43), depression (h(2) = 0.19), and self-rated health (h(2) = 0.18) are all moderately heritable phenotypes. We also provide evidence that some of the correlation between depression and education as well as self-rated health and education is due to common genetic factors associated with one or both traits. We find no evidence that the correlation between education and BMI is influenced by common genetic factors.

    View details for DOI 10.1016/j.socscimed.2014.08.001

    View details for Web of Science ID 000350074800019

    View details for PubMedID 25113566

  • The National Longitudinal Study of Adolescent to Adult Health (Add Health) Sibling Pairs Genome-Wide Data BEHAVIOR GENETICS McQueen, M. B., Boardman, J. D., Domingue, B. W., Smolen, A., Tabor, J., Killeya-Jones, L., Halpern, C. T., Whitsel, E. A., Harris, K. M. 2015; 45 (1): 12-23


    Here we provide a detailed description of the genome-wide information available on the National Longitudinal Study of Adolescent to Adult Health (Add Health) sibling pair subsample (Harris et al. in Twin Res Hum Genet 16:391-398, 2013). A total of 2,020 samples were genotyped (including duplicates) arising from 1946 Add Health individuals from the sibling pairs subsample. After various steps for quality control (QC) and quality assurance (QA), we have high quality genome-wide data available on 1,888 individuals. In this report, we first highlight the QC and QA steps that were taken to prune the data of poorly performing samples and genetic markers. We further estimate the pairwise biological relationships using genome-wide data and compare those estimates to the assumed relationships in Add Health. Additionally, using genome-wide data from known regional reference populations from Europe, West Africa, North and South America, Japan and China, we estimate the relative genetic ancestry of the respondents. Finally, rather than conducting a traditional cross-sectional genome-wide association study (GWAS) of body mass index (BMI), we opted to utilize the extensive publicly available genome-wide information to conduct a weighted GWAS of longitudinal BMI while accounting for both family and ethnic variation.

    View details for DOI 10.1007/s10519-014-9692-4

    View details for Web of Science ID 000348279200002

    View details for PubMedID 25378290

  • Replicability and Robustness of Genome-Wide-Association Studies for Behavioral Traits PSYCHOLOGICAL SCIENCE Rietveld, C. A., Conley, D., Eriksson, N., Esko, T., Medland, S. E., Vinkhuyzen, A. A., Yang, J., Boardman, J. D., Chabris, C. F., Dawes, C. T., Domingue, B. W., Hinds, D. A., Johannesson, M., Kiefer, A. K., Laibson, D., Magnusson, P. K., Mountain, J. L., Oskarsson, S., Rostapshova, O., Teumer, A., Tung, J. Y., Visscher, P. M., Benjamin, D. J., Cesarini, D., Koellinger, P. D. 2014; 25 (11): 1975-1986


    A recent genome-wide-association study of educational attainment identified three single-nucleotide polymorphisms (SNPs) whose associations, despite their small effect sizes (each R (2) ≈ 0.02%), reached genome-wide significance (p < 5 × 10(-8)) in a large discovery sample and were replicated in an independent sample (p < .05). The study also reported associations between educational attainment and indices of SNPs called "polygenic scores." In three studies, we evaluated the robustness of these findings. Study 1 showed that the associations with all three SNPs were replicated in another large (N = 34,428) independent sample. We also found that the scores remained predictive (R (2) ≈ 2%) in regressions with stringent controls for stratification (Study 2) and in new within-family analyses (Study 3). Our results show that large and therefore well-powered genome-wide-association studies can identify replicable genetic associations with behavioral traits. The small effect sizes of individual SNPs are likely to be a major contributing factor explaining the striking contrast between our results and the disappointing replication record of most candidate-gene studies.

    View details for DOI 10.1177/0956797614545132

    View details for Web of Science ID 000344874900001

    View details for PubMedID 25287667

  • Norms as Group-Level Constructs: Investigating School-Level Teen Pregnancy Norms and Behaviors SOCIAL FORCES Mollborn, S., Domingue, B. W., Boardman, J. D. 2014; 93 (1): 241-267

    View details for DOI 10.1093/sf/sou063

    View details for Web of Science ID 000342988400039

  • Testing the key assumption of heritability estimates based on genome-wide genetic relatedness JOURNAL OF HUMAN GENETICS Conley, D., Siegal, M. L., Domingue, B. W., Harris, K. M., McQueen, M. B., Boardman, J. D. 2014; 59 (6): 342-345


    Comparing genetic and phenotypic similarity among unrelated individuals seems a promising way to quantify the genetic component of traits while avoiding the problematic assumptions plaguing twin- and other kin-based estimates of heritability. One approach uses a Genetic Relatedness Estimation through Maximum Likelihood (GREML) model for individuals who are related at less than 0.025 to predict their phenotypic similarity by their genetic similarity. Here we test the key underlying assumption of this approach: that genetic relatedness is orthogonal to environmental similarity. Using data from the Health and Retirement Study (and two other surveys), we show two unrelated individuals may be more likely to have been reared in a similar environment (urban versus nonurban setting) if they are genetically similar. This effect is not eliminated by controls for population structure. However, when we include this environmental confound in GREML models, heritabilities do not change substantially and thus potential bias in estimates of most biological phenotypes is probably minimal.

    View details for DOI 10.1038/jhg.2014.14

    View details for Web of Science ID 000338186000009

    View details for PubMedID 24599117

  • Understanding multiple levels of norms about teen pregnancy and their relationships to teens' sexual behaviors ADVANCES IN LIFE COURSE RESEARCH Mollborn, S., Domingue, B. W., Boardman, J. D. 2014; 20: 1-15
  • Is the Gene-Environment Interaction Paradigm Relevant to Genome-Wide Studies? The Case of Education and Body Mass Index DEMOGRAPHY Boardman, J. D., Domingue, B. W., Blalock, C. L., Haberstick, B. C., Harris, K. M., McQueen, M. B. 2014; 51 (1): 119-139


    This study uses data from the Framingham Heart Study to examine the relevance of the gene-environment interaction paradigm for genome-wide association studies (GWAS). We use completed college education as our environmental measure and estimate the interactive effect of genotype and education on body mass index (BMI) using 260,402 single-nucleotide polymorphisms (SNPs). Our results highlight the sensitivity of parameter estimates obtained from GWAS models and the difficulty of framing genome-wide results using the existing gene-environment interaction typology. We argue that SNP-environment interactions across the human genome are not likely to provide consistent evidence regarding genetic influences on health that differ by environment. Nevertheless, genome-wide data contain rich information about individual respondents, and we demonstrate the utility of this type of data. We highlight the fact that GWAS is just one use of genome-wide data, and we encourage demographers to develop methods that incorporate this vast amount of information from respondents into their analyses.

    View details for DOI 10.1007/s13524-013-0259-4

    View details for Web of Science ID 000330990200007

    View details for PubMedID 24281739

  • The Gains From Vertical Scaling JOURNAL OF EDUCATIONAL AND BEHAVIORAL STATISTICS Briggs, D. C., Domingue, B. 2013; 38 (6): 551-576
  • Gene-environment interactions related to body mass: School policies and social context as environmental moderators JOURNAL OF THEORETICAL POLITICS Boardman, J. D., Roettger, M. E., Domingue, B. W., McQueen, M. B., Haberstick, B. C., Harris, K. M. 2012; 24 (3): 370-388
  • Ethnicity, Body Mass, and Genome-Wide Data BIODEMOGRAPHY AND SOCIAL BIOLOGY Boardman, J. D., Blalock, C. L., Corley, R. P., Stallings, M. C., Domingue, B. W., McQueen, M. B., Crowley, T. J., Hewitt, J. K., Lu, Y., Field, S. H. 2010; 56 (2): 123-136


    This article combines social and genetic epidemiology to examine the influence of self-reported ethnicity on body mass index (BMI) among a sample of adolescents and young adults. We use genetic information from more than 5,000 single nucleotide polymorphisms in combination with principal components analysis to characterize population ancestry of individuals in this study. We show that non-Hispanic white and Mexican-American respondents differ significantly with respect to BMI and differ on the first principal component from the genetic data. This first component is positively associated with BMI and accounts for roughly 3% of the genetic variance in our sample. However, after controlling for this genetic measure, the observed ethnic differences in BMI remain large and statistically significant. This study demonstrates a parsimonious method to adjust for genetic differences among individual respondents that may contribute to observed differences in outcomes. In this case, adjusting for genetic background has no bearing on the influence of self-identified ethnicity.

    View details for DOI 10.1080/19485565.2010.524589

    View details for Web of Science ID 000288381100002

    View details for PubMedID 21387985