Person:

Christakis, Nicholas A.

Objective: We examined body mass index (BMI) across place and time to determine the pattern of BMI mean and standard deviation trajectories. Methods: We included participants in the Framingham Heart Study (FHS) Offspring Cohort over eight waves of follow-up, from 1971 to 2008. After exclusions, the final sample size was 4569 subjects with 28,625 observations. We used multi-level models to examine population means and variation at the individual and neighborhood (census tracts) levels across time with measured BMI as the outcome, controlling for individual demographics and behaviors and neighborhood poverty. Because neighborhoods accounted for limited BMI variance, we removed this level as a source of variation in final models. We examined sex-stratified models with all subjects and models stratified by sex and baseline weight classification. Results: Mean BMI increased from 24.0 kg/m2 at Wave 1 to 27.7 at Wave 8 for women and from 26.6 kg/m2 to 29.0 for men. In final models, BMI variation also increased from Waves 1 to 8, with the standard deviation increasing from 4.18 kg/m2 to 6.15 for women and 3.31 kg/m2 to 4.73 for men. BMI means increased in parallel across most baseline BMI weight classifications, except for more rapid increases through middle-age for obese women followed by declines in the last wave. BMI standard deviations also increased in parallel across baseline BMI classifications for women, with greater divergence of BMI variance for obese men compared to other weight classifications. Conclusion: Over nearly 40 years, BMI mean and variation increased in parallel across most baseline weight classifications in our sample. Individual-level characteristics, especially baseline BMI, were the primary factors in rising BMI. These findings have important implications not only for understanding the sources of the obesity epidemic in the United States but also for the targeting of interventions to address the epidemic.

Many human diseases, arising from mutations of disease susceptibility genes (genetic diseases), are also associated with viral infections (virally implicated diseases), either in a directly causal manner or by indirect associations. Here we examine whether viral perturbations of host interactome may underlie such virally implicated disease relationships. Using as models two different human viruses, Epstein-Barr virus (EBV) and human papillomavirus (HPV), we find that host targets of viral proteins reside in network proximity to products of disease susceptibility genes. Expression changes in virally implicated disease tissues and comorbidity patterns cluster significantly in the network vicinity of viral targets. The topological proximity found between cellular targets of viral proteins and disease genes was exploited to uncover a novel pathway linking HPV to Fanconi anemia.

Many behavioral phenomena have been found to spread interpersonally through social networks, in a manner similar to infectious diseases. An important difference between social contagion and traditional infectious diseases, however, is that behavioral phenomena can be acquired by non-social mechanisms as well as through social transmission. We introduce a novel theoretical framework for studying these phenomena (the SISa model) by adapting a classic disease model to include the possibility for ‘automatic’ (or ‘spontaneous’) non-social infection. We provide an example of the use of this framework by examining the spread of obesity in the Framingham Heart Study Network. The interaction assumptions of the model are validated using longitudinal network transmission data. We find that the current rate of becoming obese is 2% per year and increases by 0.5 percentage points for each obese social contact. The rate of recovering from obesity is 4% per year, and does not depend on the number of non-obese contacts. The model predicts a long-term obesity prevalence of approximately 42, and can be used to evaluate the effect of different interventions on steady-state obesity. Model predictions quantitatively reproduce the actual historical time course for the prevalence of obesity. We find that since the 1970s, the rate of recovery from obesity has remained relatively constant, while the rates of both spontaneous infection and transmission have steadily increased over time. This suggests that the obesity epidemic may be driven by increasing rates of becoming obese, both spontaneously and transmissively, rather than by decreasing rates of losing weight. A key feature of the SISa model is its ability to characterize the relative importance of social transmission by quantitatively comparing rates of spontaneous versus contagious infection. It provides a theoretical framework for studying the interpersonal spread of any state that may also arise spontaneously, such as emotions, behaviors, health states, ideas or diseases with reservoirs.

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.

Using a population-based, panel survey, we study how egocentric social networks change over time, and the relationship between egocentric network properties and health and pro-social behaviors. We find that the number of prosocial activities is strongly positively associated with having more friends, or an increase in degree, with approximately 0.04 more prosocial behaviors expected for every friend added. Moreover, having more friends is associated with an improvement in health, while being healthy and prosocial is associated with closer relationships. Specifically, a unit increase in health is associated with an expected 0.45 percentage-point increase in average closeness, while adding a prosocial activity is associated with a 0.46 percentage-point increase in the closeness of one’s relationships. Furthermore, a tradeoff between degree and closeness of social contacts was observed. As the number of close social contacts increases by one, the estimated average closeness of each individual contact decreases by approximately three percentage-points. The increased awareness of the importance of spillover effects in health and health care makes the ascertainment of egocentric social networks a valuable complement to investigations of the relationship between socioeconomic factors and health.

Scholars in many fields have long noted the importance of social context in the development of political ideology. Recent work suggests that political ideology also has a heritable component, but no specific gene variant or combination of variants associated with political ideology have so far been identified. Here, we hypothesize that individuals with a genetic predisposition toward seeking out new experiences will tend to be more liberal, but only if they are embedded in a social context that provides them with multiple points of view. Using data from the National Longitudinal Study of Adolescent Health, we test this hypothesis by investigating an association between self-reported political ideology and the 7R variant of the dopamine receptor D4 gene (DRD4), which has previously been associated with novelty seeking. Among those with DRD4-7R, we find that the number of friendships a person has in adolescence is significantly associated with liberal political ideology. Among those without the gene variant, there is no association. This is the first study to elaborate a specific gene-environment interaction that contributes to ideological self-identification, and it highlights the importance of incorporating both nature and nurture into the study of political preferences.

In-group favoritism is a central aspect of human behavior. People often help members of their own group more than members of other groups. Here we propose a mathematical framework for the evolution of in-group favoritism from a continuum of strategies. Unlike previous models, we do not pre-suppose that players never cooperate with out-group members. Instead, we determine the conditions under which preferential in-group cooperation emerges, and also explore situations where preferential out-group helping could evolve. Our approach is not based on explicit intergroup conflict, but instead uses evolutionary set theory. People can move between sets. Successful sets attract members, and successful strategies gain imitators. Individuals can employ different strategies when interacting with in-group versus out-group members. Our framework also allows us to implement different games for these two types of interactions. We prove general results and derive specific conditions for the evolution of cooperation based on in-group favoritism.

Objectives. We examined the effects of community socioeconomic conditions, air pollution, and the physical environment on elderly health and survival in China. Methods. We analyzed data from a nationally representative sample of 15973 elderly residents of 866 counties and cities with multilevel logistic regression models in which individuals were nested within each county or city. Results. After control for individual-level factors, communities’ gross domestic product per capita, adult labor force participation rate, and illiteracy rate were significantly associated with physical, mental, and overall health and mortality among the elderly in China. We also found that air pollution increased the odds of disability in activities of daily living (ADLs), cognitive impairment, and health deficits; more rainfall was protective, reducing the odds of ADL disability and cognitive impairment; low seasonal temperatures increased the odds of ADL disability and mortality; high seasonal temperatures increased the odds of cognitive impairment and deficits; and living in hilly areas decreased the odds of ADL disability and health deficits. Conclusions. Efforts to reduce pollution and improve socioeconomic conditions could significantly improve elderly health and survival.

Objectives. We assessed whether widowhood is associated with risk of diagnosis with a sexually transmitted infection (STI) among older adults in the United States and whether the associations observed in men differed before and after the introduction of sildenafil, the first oral erectile dysfunction medication approved by the Food and Drug Administration. Methods. We used Cox proportional hazards regression to analyze the time to first STI diagnosis in a random sample of married, Medicare-eligible couples aged 67 to 99 years in 1993 (N = 420 790 couples). Results. Twenty-one percent of male and 43% of female participants lost a spouse during the 9-year study period. Only 0.65% of men and 0.97% of women were diagnosed with an STI. Widowhood was associated with an increased risk of STI diagnosis for men only, with the largest effects found 0.5 to 1 year after a wife’s death. Effects for men were larger after the introduction of sildenafil. Conclusions. Widowhood in older men, but not women, increased the risk for STIs, especially in the postsildenafil era. Clinicians should address sexual health issues with older patients, especially bereaved men taking erectile dysfunction medications.

Theoretical models suggest that social networks influence the evolution of cooperation, but to date there have been few experimental studies. Observational data suggest that a wide variety of behaviors may spread in human social networks, but subjects in such studies can choose to befriend people with similar behaviors, posing difficulty for causal inference. Here, we exploit a seminal set of laboratory experiments that originally showed that voluntary costly punishment can help sustain cooperation. In these experiments, subjects were randomly assigned to a sequence of different groups to play a series of single-shot public goods games with strangers; this feature allowed us to draw networks of interactions to explore how cooperative and uncooperative behaviors spread from person to person to person. We show that, in both an ordinary public goods game and in a public goods game with punishment, focal individuals are influenced by fellow group members’ contribution behavior in future interactions with other individuals who were not a party to the initial interaction. Furthermore, this influence persists formultiple periods and spreads up to three degrees of separation (from person to person to person to person). The results suggest that each additional contribution a subject makes to the public good in the first period is tripled over the course of the experiment by other subjects who are directly or indirectly influenced to contribute more as a consequence. These results show experimentally that cooperative behavior cascades in human social networks.