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12 Social Genomics and the Life Course: Opportunities and Challenges for Multilevel Population Research--Michael J. Shanahan
Pages 255-276

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From page 255...
... Social genomics was chosen as the focus for this chapter because this subfield attempts to interrelate social settings with gene expression by way of chains of mediating factors, and thus illustrates the promise and challenges of multilevel research in sharp relief. The field of social genomics focuses on the mechanisms by which social experiences regulate genetic activity (Cole, 2009)
From page 256...
... Human studies of transcription often suffer from the same limitations; however, these human studies can then inform nonhuman animal studies that use experimental designs, and even human experimental designs. When these diverse types of studies converge on a mechanistic model that links social experiences with expression profiles, causal inferences about social context and health are indeed strengthened.
From page 257...
... Ideally, such studies will be designed to study multilevel, meditational processes as they extend over many decades of life. Socioeconomic Status, Gene Transcription, and Inflammatory Processes: Stages one and Two The Emergence of Transcription Studies of Social Experiences Transcription depends on RNA polymerase (RNAP)
From page 258...
... That is, psychosocial stressors and reactivity to stressors eventuate in faster progression of HIV-1 because of increased viral replication. Because the SNS is downstream from social stressors, however, this research suggested a broader possibility: that, beyond the specific example of HIV-1, social experiences could influence gene expression because of their effects on the nervous system.
From page 259...
... Thus, this study of social isolation joined two very different research traditions: a considerable body of population-based research on risk factors, and biological models of leukocytes, which offer a noninvasive window into the immune system and inflammatory processes associated with many common diseases of aging. The basic issue, then, was whether genes were expressed differentially among socially isolated versus socially integrated adults.
From page 260...
... . Transcriptional Studies of SES In addition to studies of acute and chronic stressors, research has also examined SES, of central interest to demography and social epidemiology in the study of health disparities.
From page 261...
... The results suggested that low-SES children with warm mothers showed reduced bioinformatic indications of pro-inflammatory transcription factor activity and immune activating transcription factor activity compared to those who were low in SES early in life but experienced low maternal warmth. In other words, high maternal warmth served as a protective factor for children from low SES households with respect to transcription patterns related to immune response and inflammation.
From page 262...
... Thus, Stage Three researchers should pay close attention to the extent to which nonexperimental results have replicated in experimental settings. STAGE THREE: POPULATION-BASED MULTILEVEL STUDIES This chapter has proposed a two-stage historiography according to which population-based research identified putative social risk factors (Stage One)
From page 263...
... The initial body of research was based, quite understandably, on relatively small samples drawn nonprobabilistically from communities, which renders inference and the study of diversity difficult. However, gene expression patterns may provide critical evidence of linking mechanisms that connect social experiences with health.
From page 264...
... At first glance, the results of gene transcription studies of SES appear largely consistent with a sensitive or perhaps critical period model. However, extant evidence is not decisive and indeed conceptual considerations suggest a hybrid model involving a sensitive or critical period followed by a "chain of insults," with perhaps accumulating disadvantage.
From page 265...
... One possibility is that transcription patterns change very soon after, or during, the sensitive period, a possibility for which there is presently no evidence. An additional possibility is that the sensitive period model is characterized by a longer induction period, meaning that there is an appreciable interval of time between the environmental exposure and altered transcription.
From page 266...
... All of these considerations suggest a highly nuanced life course model: a sensitive or critical period, with a possibly short induction period followed by chains of social, psychological, and biological risks with extensive positive feedback among them; the child's behaviors reflecting social
From page 267...
... First, as noted, early pronounced, chronic stressors may lead people to view ambiguous situations as threatening, which in turn activates neuroendocrine processes that eventuate in changes in inflammatory signaling pathways (Irwin and Cole, 2011)
From page 268...
... And, in turn, little is known about how sense of threat then creates more stressors for the person, contributing to the chain of risk model. Second, early chronic stressors are thought to influence the cortiostriatal circuitry, which is central to the processing of reward-related information and self-regulation (including, for example, impulse control and goal-directed behaviors)
From page 269...
... Because several different stressors appear to trigger GR resistance, it is unlikely that any one stressor is necessary and sufficient. Social isolation, parental stress due to a child's severe illness, low SES, and child maltreatment have all been associated with the upregulation of pro-inflammatory and down-regulation of anti-inflammatory transcriptional pathways.
From page 270...
... In the case of social genomics, for example, how do distinct macro-social contexts trigger pro-inflammatory transcription patterns? A central issue is the extent to which low-SES children are exposed to settings that heighten a sense of threat and vigilance, and these comparative strategies may shed light on this problem.
From page 271...
... CONCLUSIONS A large and complex body of research suggests that social experiences of early childhood may have lifelong implications for the immune system and the emergence of inflammatory diseases. This body of research began
From page 272...
... . On the one hand, Stage Two research provides evidence of linking mechanisms that may connect social experiences and health, mechanisms that are necessary for any convincing causal account of social risk factors and health.
From page 273...
... The reviewed studies also suggest very high levels of contingency among social experiences and the psychological and biological cascades that they initiate. That is, it may be that many different stressors are essentially substitutable, equally capable of instilling threat and increasing the likelihood of pro-inflammatory transcription patterns (i.e., equifinality)
From page 274...
... . Maternal warmth buffers the ef fects of low early-life socioeconomic status on pro-inflammatory signaling in adulthood.
From page 275...
... . Association of childhood socioeconomic status with subsequent coronary heart disease in physicians.
From page 276...
... . Specificity of putative psychosocial risk factors for psychiatric disorders in children and adolescents.


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