Ashley Winning1, Paola Gilsanz2, Karestan C Koenen3, Andrea L Roberts2, Qixuan Chen4, Jennifer A Sumner5, Eric B Rimm6, M Maria Glymour7, Laura D Kubzansky2. 1. Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Department of Research and Evaluation, EMPath (Economic Mobility Pathways), Boston, Massachusetts. Electronic address: awinning@empathways.org. 2. Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. 3. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. 4. Department of Biostatistics, Mailman School of Public Health, Columbia University, New York, New York. 5. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Center for Behavioral Cardiovascular Health, Columbia University Medical Center, New York, New York. 6. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts. 7. Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, California.
Abstract
INTRODUCTION: Post-traumatic stress disorder (PTSD) may be associated with physical inactivity, a modifiable lifestyle factor that contributes to risk of cardiovascular and other chronic diseases; however, no study has evaluated the association between PTSD onset and subsequent physical activity (PA) changes. METHOD: Analyses were conducted between October 2014 and April 2016, using data from the ongoing Nurses' Health Study II (N=50,327). Trauma exposure and PTSD symptoms were assessed using two previously validated measures, the Brief Trauma Questionnaire and Short Screening Scale for DSM-IV PTSD. Average PA (hours/week) was assessed using self-report measures at six time points across 20 years (1989-2009). Linear mixed models with time-updated PTSD assessed differences in PA trajectories by trauma/PTSD status. Among a subsample of women whose trauma/PTSD onset during follow-up, group differences in PA patterns before and after onset were assessed using linear spline models. RESULTS: PA decreased more steeply over time among trauma-exposed women reporting four or five (β= -2.5E-3, SE=1.0E-3, p=0.007) or six or seven PTSD symptoms (β= -6.7E-3, SE=1.1E-3, p<0.001) versus women without trauma exposure, adjusting for potential confounders. Among a subsample of women whose trauma/PTSD symptoms onset during follow-up, no differences in PA were observed prior to onset; after onset, women with six or seven PTSD symptoms had a steeper decline (β= -17.1E-3, SE=4.2E-3, p<0.001) in PA over time than trauma-exposed women without PTSD. CONCLUSIONS: Decreases in PA associated with PTSD symptoms may be a pathway through which PTSD influences cardiovascular and other chronic diseases.
INTRODUCTION: Post-traumatic stress disorder (PTSD) may be associated with physical inactivity, a modifiable lifestyle factor that contributes to risk of cardiovascular and other chronic diseases; however, no study has evaluated the association between PTSD onset and subsequent physical activity (PA) changes. METHOD: Analyses were conducted between October 2014 and April 2016, using data from the ongoing Nurses' Health Study II (N=50,327). Trauma exposure and PTSD symptoms were assessed using two previously validated measures, the Brief Trauma Questionnaire and Short Screening Scale for DSM-IV PTSD. Average PA (hours/week) was assessed using self-report measures at six time points across 20 years (1989-2009). Linear mixed models with time-updated PTSD assessed differences in PA trajectories by trauma/PTSD status. Among a subsample of women whose trauma/PTSD onset during follow-up, group differences in PA patterns before and after onset were assessed using linear spline models. RESULTS: PA decreased more steeply over time among trauma-exposed women reporting four or five (β= -2.5E-3, SE=1.0E-3, p=0.007) or six or seven PTSD symptoms (β= -6.7E-3, SE=1.1E-3, p<0.001) versus women without trauma exposure, adjusting for potential confounders. Among a subsample of women whose trauma/PTSD symptoms onset during follow-up, no differences in PA were observed prior to onset; after onset, women with six or seven PTSD symptoms had a steeper decline (β= -17.1E-3, SE=4.2E-3, p<0.001) in PA over time than trauma-exposed women without PTSD. CONCLUSIONS: Decreases in PA associated with PTSD symptoms may be a pathway through which PTSD influences cardiovascular and other chronic diseases.
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