Neighborhood crime and depressive symptoms among African American women: Genetic moderation and epigenetic mediation of effects

Abstract

Introduction Social scientists have long recognized the important role that neighborhood crime can play in stress-related disease, but very little is known about potential biosocial mechanisms that may link the experience of living in high-crime neighborhoods with depression. Objective The current study introduces an integrated model that combines neighborhood, genetic, and epigenetic factors. Methods Hypotheses were tested with a sample of 99 African American women from the Family and Community Health Study (FACHS). Results Allele variants of the serotonin transporter gene (5-HTT) interact with neighborhood crime to predict depressive symptoms in a manner consonant with the differential susceptibility perspective. Furthermore, this association is mediated by DNA methylation of the promoter region of the serotonin transporter gene. Conclusion The findings provide support for an integrated model in which changes in DNA methylation, resulting from neighborhood crime, can result in an increase or decrease in gene activity which, in turn, influences depressive symptoms.

Biological embedding of neighborhood disadvantage and collective efficacy: Influences on chronic illness via accelerated cardiometabolic age

“…As hypothesized, long-term exposure to neighborhood disadvantage was related to chronic illness ( b = 0.203, IRR = 1.225, p =.004). The results are consistent with numerous studies (Aneshensel, 2009; Hill et al 2005; Lei et al, 2015; Ross & Mirowsky, 2001, 2009) reporting that residing in a disadvantaged neighborhood has a deleterious effect on physical health even after controlling for selection bias, socioeconomic status, and health-related behaviors.…”

“…However, while individuals living in disadvantaged neighborhoods are more likely to become ill than those residing in more advantaged areas, many, if not most, will remain healthy (Fone et al, 2007; Lei et al, 2015; Miller et al, 2011), a phenomenon labeled “neighborhood resilience” (Brody, Yu, Beach, 2016b; Masten & Coatsworth, 1998; Norris et al, 2008). This raises the question: Why and how do some people living in disadvantaged neighborhoods develop chronic illnesses whereas others do not?…”

A relationship between early life stress and depression: the role of the serotonin transporter gene polymorphism (5-HTTLPR)

“…Short allele carriers exposed to early life stress were more likely to display increased 5-HTT gene methylation than homozygous long allele carriers in a sample of 105 young adults [52]. Consistent with this finding, short allele carriers that have grown up in dangerous neighborhoods show greater methylation than long allele carriers [53]. This association conferred a significant risk for depressive symptoms in this sample.…”

Neighborhood characteristics influence DNA methylation of genes involved in stress response and inflammation: The Multi-Ethnic Study of Atherosclerosis

“… 18 Previous studies have demonstrated a link between global or site-specific DNA methylation patterns and socially patterned stressors including low childhood SES, 1-4 low adult SES, 3 , 4 perceived stress, 2 and neighborhood crime. 19 Differential DNA methylation patterns have also been demonstrated for a wide variety of physical and mental health indicators (e.g., cardiovascular disease, 20 inflammation, 21 cortisol levels, 2 and depression.) 22 In light of these associations, DNA methylation has been proposed as a mediator of the associations between social exposures and health.…”