Speakers
The centerpiece of the meeting was a series of nine invited talks, given by renowned experts in the fields of psychology, biology, neuroscience, epidemiology, genetics, and related scientific disciplines. The speakers for this special event included:
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Steve Cole, PhD Vice President, Research and Development, Hope Lab & Associate Professor of Medicine University of California, Los Angeles Interests: Social regulation of gene expression, biochemical signaling pathways, HIV, inflammatory biology Links: UCLA Profile | Hope Lab |
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2007: Social
regulation of gene expression in human leukocytes,
Genome Biol 2009: Chronic interpersonal stress predicts activation of pro- and anti-inflammatory signaling..., Psychosom Med 2010: Computational identification of gene-social environment interactions at the human IL6 locus, PNAS |
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Abstract: Relationships between genes and social behavior have historically been viewed as a one-way street, with genes in control. Recent functional genomics studies have begun to challenge this view by discovering broad alterations in the expression of human genes as a function of differing socio-environmental conditions. My talk summarizes the developing field of social genomics, and its efforts to identify the types of genes subject to social regulation, the biological signaling pathways mediating those effects, and the genetic polymorphisms that moderate socio-environmental influences on human gene expression. These studies provide a concrete molecular perspective on how external social conditions interact with DNA to shape the functional characteristics of our bodies, and alter our future biological and behavioral responses based on our personal transcriptional histories. The presentation concludes by describing some new opportunities for in silico prediction of DNA polymorphisms that interact with transcription control pathways carrying socio-environmental information.
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Ahmad Hariri, PhD Professor of Psychology and Neuroscience & Director, Laboratory of Neurogenetics Duke University Interests: Neuroimaging, behavioral genetics, individual differences in behavior & risk for psychopathology Links: Laboratory of Neurogenetics |
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| 2002:
Serotonin
transporter genetic variation and the response of the human
amygdala, Science 2009: The neurobiology of individual differences in complex behavioral traits, Annu Rev Neurosci 2010: Genetic polymorphisms: a cornerstone of translational biobehavioral research, Sci Transl Med |
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Abstract: Two rapidly emerging and highly complementary strategies have accelerated progress into biological mechanisms mediating individual differences in behavior and related risk for psychopathology: imaging genetics and gene-environment interactions research. Through the systematic mapping of common genetic polymorphisms affecting brain chemistry onto variability in brain structure and function, imaging genetics has established multiple fundamental mechanisms through which individual differences in behavior emerge and bias responses to the environment. In parallel, gene-environment interactions research has demonstrated how such genetically mediated variability in behaviorally relevant brain function translates into individual risk for psychopathology upon exposure to environmental stress or adversity. In addition to reviewing findings at this research interface, I will illustrate how the application of a novel genetic profiling approach offers the opportunity to generate increasingly complete information regarding variability in behaviorally relevant brain function and related gene-environment interactions.
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Cole/Hariri Discussion Moderated by Greg Gibson, PhD Professor and Director, Center for Integrative Genomics Georgia Institute of Technology |
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Jeanne Brooks-Gunn, PhD Virginia and Leonard Marx Professor of Child Development Teachers College & College of Physicians and Surgeons Columbia University Interests: Biological & environmental influences in child development, menarcheal timing, stress responsivity, school functioning, policy work Links: Teachers College | National Center for Children and Families |
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| 2000:
The
neighborhoods they live in: the effects of neighborhood
residence on child and...,
Psychol Bull 2000. Depending on the kindness of strangers: current national data initiatives and..., Child Dev 2005: The contribution of parenting to ethnic and racial gaps in school readiness, Future Child |
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Abstract: Studies of human molecular genetics and social environment interactions on health have relied heavily on the classic diathesis-stress model that treats genetic variations and environments as being either risky or protective thereby diminishing the interactive space. We attempt to expand this space by 1) combining two polymorphisms (5-HTTLPR and STin2 VNTR) of the serotonin transporter gene (5-HTT) and 2) using a less truncated measure of the environment—socioeconomic status (SES). We find evidence of significant gene-environment interplay between the two 5-HTT polymorphisms and SES on depression in the first year after the birth of the child. More crucially, we find evidence that some people are genetically more or less reactive to the environment, resulting in a crossover of risks of PPD for the most reactive groups.
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Eric Turkheimer, PhD Professor, Department of Psychology & Director of Clinical Training University of Virginia Interests: GxE studies of mental illness, intelligence, & personality, methodological & statistical issues in GxE research Links: University of Virginia Homepage |
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| 2000:
Nonshared
environment: A theoretical, methodological, and quantitative
review,
Psychol Rev 2003. Socioeconomic status modifies heritability of IQ in young children, Psychol Sci 2005: Analysis and interpretation of twin studies including measures of the shared environment, Child Dev |
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Abstract: I will argue that as we have known for a long time that all behavior is heritable, and are learning now that all behavior is related in complex way to genetic variation at the level of DNA, the old null model of no genetic association has become meaningless. A new null model states our expectation that behavior is related to DNA through the accumulation of small associations that cannot be individually specified, and that the multivariate structure of genetic relations does not differ from the multivariate structure of the phenotype. I explore this multivariate null model through a variety of research projects using both population and molecular genetic methods. One outcome of my analysis is that more complex models of genetic transmission at the DNA level are not likely to solve the missing heritability problem, at least when it comes to complex phenotypes in humans.
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Brooks-Gunn/Turkheimer
Discussion Moderated by Greg Gibson, PhD Professor and Director, Center for Integrative Genomics Georgia Institute of Technology |
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Marcus Feldman, PhD Burnet C. and Mildred Finley Wohlford Professor of Biological Sciences & Director, Morrison Institute for Population and Resource Studies Stanford University Interests: Mathematical & computer modeling of evolution, complex genetic systems, interaction of cultural & biological evolution Links: Feldman Lab | Stanford Morrison Institute |
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1975:
The
heritability hang-up, Science 2002: Genetic structure of human populations, Science 2003: The application of molecular genetic approaches to the study of human evolution, Nat Genet |
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Abstract: Genotype-environment interactions are still largely discussed in terms of Fisher’s variance analysis. This leads to the phrasing of the apparent difference between the large number of SNPs with significant phenotypic risk and the low fraction of Fisherian genetic variance explained. Is this the way modern analysis of quantitative genetics should be carried out?
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David Goldstein, PhD Professor of Molecular Genetics and Microbiology & Director, Center for Human Genome Variation Duke University Interests: Human genetic diversity, HIV/AIDS genetics, genetics of neurological disease, pharmacogenetics Links: Goldstein Lab | Duke Center for Human Genome Variation |
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1995: An
evaluation of genetic distances for use with microsatellite
loci, Genetics 2003: Pharmacogenetics goes genomic, Nat Rev Genet 2007: A whole-genome association study of major determinants for host control of HIV-1, Science |
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Abstract: Genome wide association studies have proven successful in identifying regions of the genome that contain gene variants that influence both common diseases and drug responses. In most instances however, it has not been possible to track these associations down to the causal variants that are responsible, and this greatly reduces the utility of these findings in drug development and disease prediction.
Sequencing based strategies on the other hand offer the promise of identifying the precise mutations and the genes they influence that are responsible both for predisposition to common disease and drug responses. I outline how sequencing the entire genomes of patients is likely to change our understanding of human disease genetics over the next several years.
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Feldman/Goldstein Discussion Moderated by Greg Gibson, PhD Professor and Director, Center for Integrative Genomics Georgia Institute of Technology |
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Stephen Manuck, PhD Distinguished University Professor of Health Psychology and Behavioral Medicine & Director, Initiative for Neurobehavioral Genetics University of Pittsburgh Interests: Psychosocial factors in cardiovascular disease, genetics of behavior, neurobiology of personality & temperament Links: University of Pittsburgh Profile |
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| 1999:
Aggression
and anger-related traits associated with a polymorphism...,
Biol Psychiatry 2009. The reaction norm in gene x environment interaction, Mol Psychiatry 2010: Polymorphisms in the CRP gene moderate an association between depressive..., Brain Behav Immun |
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Abstract: Genetic effects on prominent behavioral phenotypes often vary by context, and such observations are frequently cited as instances of gene-environment interaction (GxE). According to one longstanding model of GxE in psychiatric genetics – termed diathesis-stress –some psychopathologies arise when individuals who carry certain genetic vulnerabilities (diathesis) encounter precipitating environmental adversities (stress). Several literatures framed within a diathesis-stress model have emerged recently, spawning mixed results and numerous narrative reviews, meta-analyses, and ‘expert’ commentaries. At the same time, others have faulted the diathesis-stress model for positing a truncated form of GxE that ignores “positive” environmental exposures – experiences that might analogously moderate genetic influences on psychological well-being and adjustment (referred to here as ‘vantage sensitivity’). Finally, a third model proposes that the same genotypes promoting negative outcomes in adverse environments may, conversely, potentiate positive outcomes in salubrious environments (‘differential susceptibility’), suggesting that the implicated genetic variation modulates behavioral or developmental plasticity under varying (good or bad) environmental circumstances. In my talk, I will summarize evidence for these several models and suggest a more general GxE framework, using as examples recent studies of context-dependent genetic associations involving pubertal timing, impulsive decision making, and adult antisocial and aggressive behaviors.
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Manuck Discussion Moderated by Greg Gibson, PhD Professor and Director, Center for Integrative Genomics Georgia Institute of Technology |
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Anne Wojcicki President & Co-Founder, 23andMe Board Member, Foundation for the National Institutes of Health Interests: Consumer Genomics, biotechnology, healthcare Links: 23andMe | Foundation for the National Institutes of Health |
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| 2009: A pragmatic consideration of ethical issues relating to personal genomics, Am J Bioeth | ||
Abstract: Anne Wojcicki, President and Co-Founder of 23andMe, a personal genetics company, will discuss how 23andMe is advancing disease research through a new kind of online research model that gives individuals the opportunity to actively participate in research that is meaningful to them. She will also address the company's long-term vision to help usher in personalized medicine.
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James Fowler, PhD Professor of Medical Genetics and Political Science University of California, San Diego Interests: Social networks & health, biological basis of behavior, genetic basis of political behavior ("genopolitics") Links: James Fowler Homepage | UCSD Division of Medical Genetics |
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| 2008:
Biology,
politics, and the emerging science of human nature,
Science 2009. Model of genetic variation in human social networks, PNAS 2010: Cooperative behavior cascades in human social networks, PNAS |
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Abstract: It is well known that humans tend to associate with other humans who have similar characteristics, but it is unclear whether this tendency has consequences for the distribution of genotypes in a population. Although geneticists have shown that populations tend to stratify genetically, this process results from assortative mating and it is unknown whether genotypes may be correlated as a consequence of non-reproductive associations. Here, we study six available genotypes from the National Longitudinal Study of Adolescent Health to test for genetic similarity between friends. Maps of the friendship networks show clustering of genotypes, and, after we apply strict controls for population stratification the results, show that two genotypes are positively correlated (homophily) and one genotype is negatively correlated (heterophily). A replication study on an independent sample from the Framingham Heart Study verifies that DRD2 exhibits significant homophily and CYP2A6 exhibits significant heterophily. These novel results show that homophily and heterophily operate on a genetic (indeed, an allelic) level, which has implications for the study of population genetics and social behavior. In particular, they suggest that association tests should include friends’ genes and that theories of evolution should take into account the fact that humans might, in some sense, be “metagenomic” with respect to the humans around them.
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Wojcicki/Fowler Discussion Moderated by Greg Gibson, PhD Professor and Director, Center for Integrative Genomics Georgia Institute of Technology |
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