Pervasive exposure to violence and posttraumatic stress disorder in a predominantly African American Urban Community: the Detroit Neighborhood Health Study.

Columbia University Mailman School of Public Health, New York, NY 10032, USA.
Journal of Traumatic Stress (Impact Factor: 2.72). 12/2011; 24(6):747-51. DOI: 10.1002/jts.20705
Source: PubMed

ABSTRACT Exposure to traumatic events is common, particularly among economically disadvantaged, urban African Americans. There is, however, scant data on the psychological consequences of exposure to traumatic events in this group. We assessed experience with traumatic events and posttraumatic stress disorder (PTSD) among 1,306 randomly selected, African American residents of Detroit. Lifetime prevalence of exposure to at least 1 traumatic event was 87.2% (assault = 51.0%). African Americans from Detroit have a relatively high burden of PTSD; 17.1% of those who experienced a traumatic event met criteria for probable lifetime PTSD. Assaultive violence is pervasive and is more likely to be associated with subsequent PTSD than other types of events. Further efforts to prevent violence and increase access to mental health treatment could reduce the mental health burden in economically disadvantaged urban areas.

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    • "We found a significant association between PTSD diagnosis and SLC18A2 after correction for multiple testing. We identified a risk haplotype in SLC18A2 and found a consistent result in the Detroit Neighborhood Health Study (DNHS) (N ¼ 748), an epidemiologic sample of primarily African-American adults residing in urban Detroit (Goldmann et al, 2011). Our polygenic analyses suggest that there are shared genetic factors between PTSD severity and BP. "
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    ABSTRACT: The genetic architecture of post-traumatic stress disorder (PTSD) remains poorly understood with the vast majority of genetic association studies reporting on single candidate genes. We conducted a large genetic study in trauma exposed European American women (N=2538; 845 PTSD cases, 1693 controls) by testing 3742 SNPs across more than 300 genes and conducting polygenic analyses using results from the Psychiatric GWAS Consortium. We tested the association between each SNP and two measures of PTSD, a severity score and diagnosis. We found a significant association between PTSD (diagnosis) and SNPs (top SNP: rs363276, OR=1.4, p=2.1E-05) in SLC18A2 (vesicular monoamine transporter 2). A haplotype analysis of 9 SNPs in SLC18A2, including rs363276, identified a risk haplotype (CGGCGGAAG, p=0.0046), and the same risk haplotype was associated with PTSD in an independent cohort of trauma-exposed African Americans (p=0.049; N=748, men and women). SLC18A2 is involved in transporting monoamines to synaptic vesicles and has been implicated in a number of neuropsychiatric disorders including major depression. Eight genes previously associated with PTSD had SNPs with nominally significant associations (p<0.05). The polygenic analyses suggested that there are SNPs in common between PTSD severity and bipolar disorder. Our data are consistent with a genetic architecture for PTSD that is highly polygenic, influenced by numerous SNPs with weak effects, and may overlap with mood disorders. Genome-wide studies with very large samples sizes are needed to detectthese types of effects.Neuropsychopharmacology accepted article preview online, 14 February 2014; doi:10.1038/npp.2014.34.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 02/2014; DOI:10.1038/npp.2014.34 · 7.83 Impact Factor
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    • "Participants were recruited from the DNHS (N = 1547), a longitudinal cohort of predominately African American men and women adults (18+) living in Detroit, Michigan and screened for lifetime trauma exposure using procedures described in more detail elsewhere (Uddin et al., 2010; Goldmann et al., 2011). The analytic sample for this paper is 413 women, who signed consent to provide DNA samples that were viable for analysis and were exposed to at least one traumatic event. "
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    ABSTRACT: Posttraumatic stress disorder (PTSD) is a common and debilitating mental disorder with a particularly high burden for women. Emerging evidence suggests PTSD may be more heritable among women and evidence from animal models and human correlational studies suggest connections between sex-linked biology and PTSD vulnerability, which may extend to the disorder's genetic architecture. We conducted a genome-wide association study (GWAS) of PTSD in a primarily African American sample of women from the Detroit Neighborhood Health Study (DNHS) and tested for replication in an independent cohort of primarily European American women from the Nurses Health Study II (NHSII). We genotyped 413 DNHS women - 94 PTSD cases and 319 controls exposed to at least one traumatic event - on the Illumina HumanOmniExpress BeadChip for >700,000 markers and tested 578 PTSD cases and 1963 controls from NHSII for replication. We performed a network-based analysis integrating data from GWAS-derived independent regions of association and the Reactome database of functional interactions. We found genome-wide significant association for one marker mapping to a novel RNA gene, lincRNA AC068718.1, for which we found suggestive evidence of replication in NHSII. Our network-based analysis indicates that our top GWAS results were enriched for pathways related to telomere maintenance and immune function. Our findings implicate a novel RNA gene, lincRNA AC068718.1, as risk factor for PTSD in women and add to emerging evidence that non-coding RNA genes may play a crucial role in shaping the landscape of gene regulation with putative pathological effects that lead to phenotypic differences.
    Psychoneuroendocrinology 09/2013; 38(12). DOI:10.1016/j.psyneuen.2013.08.014 · 5.59 Impact Factor
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    • "Although initially identified among combat veterans, research now indicates that a number of populations are at high risk for PTSD based on high levels of trauma exposure. One of these populations is low-income African-Americans living in urban environments [Goldmann et al., 2011]. Over the last 5 years we have examined the prevalence and comorbidity of PTSD in over 4,000 low-income, primarily African-American men and women in Atlanta, documenting an extremely high prevalence of trauma exposure (>85%) and of PTSD. "
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    ABSTRACT: Pituitary adenylate cyclase-activating polypeptide (PACAP) and its receptor (PAC1) play a critical role in biological processes that mediate stress response and have been implicated in psychological outcome following trauma. Our previous work [Ressler et al. (2011); Nature 470:492-497] demonstrated that a variant, rs2267735, in the gene encoding PAC1 (ADCYAP1R1) is associated with post-traumatic stress disorder (PTSD) in a primarily African-American cohort of highly traumatized females. We sought to extend and replicate our previous finding in a similarly trauma-exposed, replicate sample of 1,160 African-American adult male and female patients. Self-reported psychiatric measures were collected, and DNA was obtained for genetic analysis. Using linear regression models to test for association with PTSD symptom severity under an additive (allelic) model, we found a genotype × trauma interaction in females (P < 0.001), but not males (P > 0.1); however, there was no main effect of genotype as in our previous study. The observed interaction suggests a genetic association that increases with the degree of trauma exposure in females only. This interaction remained significant in females, but not males, after controlling for age (P < 0.001), income (P < 0.01), past substance abuse (P < 0.001), depression severity (P = 0.02), or child abuse (P < 0.0005), and all five combined (P = 0.01). No significant effects of genotype (or interactions) were found when modeling depression severity when controlling for comorbid PTSD symptom severity (P > 0.1), demonstrating the relative specificity of this variant for PTSD symptoms. A meta-analysis with the previously reported African-American samples revealed a strong association between PTSD symptom severity and the interaction between trauma and genotype in females (N = 1424, P < 0.0001). © 2013 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 04/2013; 162(3). DOI:10.1002/ajmg.b.32145 · 3.27 Impact Factor