Emotion regulation and the association between PTSD, diet, and exercise: a longitudinal evaluation among US military veterans.

Background: Posttraumatic stress disorder (PTSD) is associated with premature onset of chronic health conditions such as cardiovascular disease. Diet and exercise are behavioural contributors to physical health, and research suggests they are influenced by psychiatric symptoms, including PTSD. Objectives: The aim of this study was to examine longitudinal associations between PTSD and exercise and diet quality and to test if emotion regulation strategies contribute to the link between PTSD and these health behaviours. Method: A representative sample of US military veterans (n = 860 at Time 1, n = 503 at Time 2, mean age = 63 years, 91.5% male) were assessed twice over the course of approximately three years. Results: Mediation models revealed that the association between baseline PTSD symptom severity and subsequent diet quality was mediated by emotion suppression (measured at Time 2; indirect B = -.03; 95% CI: -.059 to -.002). Trauma exposure also directly predicted diet quality (B = -.31; p = .003). There were no significant direct or indirect associations between PTSD severity or trauma exposure and exercise engagement. Conclusions: These results suggest that PTSD symptoms are associated with worse diet quality and that the consumption of unhealthy food may be driven by efforts to suppress emotion. This carries implications for understanding and treating medical comorbidities among those with traumatic stress.

Antecedentes: El trastorno de estrés postraumático (TEPT) está asociado con el inicio prematuro de condiciones crónicas de salud, como la enfermedad cardiovascular. La dieta y el ejercicio son contribuyentes conductuales para la salud física y las investigaciones sugieren que están influenciados por los síntomas psiquiátricos, incluyendo al TEPT.Objetivos: El objetivo de este estudio fue el de evaluar las asociaciones longitudinales entre el TEPT y el ejercicio y la calidad de la dieta; asimismo, evaluar si las estrategias de regulación emocional contribuyen al vínculo entre el TEPT y estas conductas de salud.Métodos: Se evaluó a una muestra representativa de veteranos de guerra estadounidenses (n = 860 en el Tiempo 1, n = 503 en el Tiempo 2, edad promedio = 63 años, 91,5% varones) en dos oportunidades en un periodo de tres años.Resultados: Los modelos de mediación mostraron que la asociación entre la severidad de los síntomas del TEPT de base y la calidad subsecuente de la dieta estaba mediada por la supresión de emociones (medidos en el Tiempo 2; B indirecta = −.03; 95% CI: − .059 to − .002). La exposición al trauma también predijo la calidad de la dieta de manera directa (B = = −.31; p = .003). No se encontraron asociaciones, directas o indirectas, entre la severidad del TEPT o la exposición al trauma con el compromiso con el ejercicio.Conclusiones: Estos resultados sugieren que los síntomas del TEPT están asociados a una peor calidad de la dieta y que el consumo de alimentos no saludables puede estar impulsado por esfuerzos para suprimir las emociones. Esto conlleva a implicaciones para comprender y tratar las comorbilidades médicas entre aquellos con estrés traumático.

Psychometric Performance of the Miller Forensic Assessment of Symptoms Test (M-FAST) in Veteran PTSD Assessment.

This study examined the psychometric properties of a widely used measure of symptom exaggeration, the Miller Forensic Assessment of Symptoms Test (M-FAST, Miller, 2001), in a sample of 209 (83.7% male) trauma-exposed veterans (57.9% probable current posttraumatic stress disorder; PTSD). M-FAST total scores evidenced acceptable internal consistency, but several subscales showed poor internal consistency. Factor analytic and item-response theory analyses identified seven poorly performing items. Comparisons with other measures of psychopathology and response validity (including subscales from the Minnesota Multiphasic Personality Inventory-2 Restructured Form) revealed that M-FAST scores were highly correlated with indices of psychopathology while less strongly associated with measures of symptom over-reporting. Empirically and clinically-derived (using a follow-up testing-the-limits procedure) revised M-FAST scores failed to improve the measure's psychometric performance. Results raise concerns about the validity of the M-FAST for identifying malingering in veterans with PTSD and carry implications for access to care and forensic evaluations in this population.

PTSD and the klotho longevity gene: Evaluation of longitudinal effects on inflammation via DNA methylation.

BACKGROUND: Longevity gene klotho (KL) is associated with age-related phenotypes including lifespan, cardiometabolic disorders, cognition, and brain morphology, in part, by conferring protection against inflammation. We hypothesized that the KL/inflammation association might be altered in the presence of psychiatric stress and operate via epigenetic pathways. We examined KL polymorphisms, and their interaction with posttraumatic stress disorder (PTSD) symptoms, in association with KL DNA methylation in blood. We further examined KL DNA methylation as a predictor of longitudinal changes in a peripheral biomarker of inflammation (C-reactive protein; CRP). METHODS: The sample comprised 309 white non-Hispanic military veterans (93.5 % male; mean age: 32 years, range: 19-65; 30 % PTSD per structured diagnostic interview); 111 were reassessed approximately two years later. RESULTS: Analyses revealed a methylation quantitative trait locus at rs9527025 (C370S, previously implicated in numerous studies of aging) in association with a Cytosine-phosphate-Guanine site (cg00129557; B = -.65, p = 1.29 X 10-20), located within a DNase hypersensitivity site in the body of KL. There was also a rs9527025 x PTSD severity interaction (B = .004, p = .035) on methylation at this locus such that the minor allele was associated with reduced cg00129557 methylation in individuals with few or no PTSD symptoms while this effect was attenuated in those with elevated levels of PTSD. Path models revealed that methylation at cg00129557 was inversely associated with CRP over time (B = -.14, p = .005), controlling for baseline CRP. There was also an indirect effect of rs9527025 X PTSD on subsequent CRP via cg00129557 methylation (indirect B = -.002, p = .033). CONCLUSIONS: Results contribute to our understanding of the epigenetic correlates of inflammation in PTSD and suggest that KL methylation may be a mechanism by which KL genotype confers risk vs. resilience to accelerated aging in those experiencing traumatic stress.