Utilization of machine learning for prediction of post-traumatic stress: a re-examination of cortisol in the prediction and pathways to non-remitting PTSD.
To date, studies of biological risk factors have revealed inconsistent relationships with subsequent post-traumatic stress disorder (PTSD). The inconsistent signal may reflect the use of data analytic tools that are ill equipped for modeling the complex interactions between biological and environmental factors that underlay post-traumatic psychopathology. Further, using symptom-based diagnostic status as the group outcome overlooks the inherent heterogeneity of PTSD, potentially contributing to failures to replicate. To examine the potential yield of novel analytic tools, we reanalyzed data from a large longitudinal study of individuals identified following trauma in the general emergency room (ER) that failed to find a linear association between cortisol response to traumatic events and subsequent PTSD. First, latent growth mixture modeling empirically identified trajectories of post-traumatic symptoms, which then were used as the study outcome. Next, support vector machines with feature selection identified sets of features with stable predictive accuracy and built robust classifiers of trajectory membership (area under the receiver operator characteristic curve (AUC)=0.82 (95% confidence interval (CI)=0.80-0.85)) that combined clinical, neuroendocrine, psychophysiological and demographic information. Finally, graph induction algorithms revealed a unique path from childhood trauma via lower cortisol during ER admission, to non-remitting PTSD. Traditional general linear modeling methods then confirmed the newly revealed association, thereby delineating a specific target population for early endocrine interventions. Advanced computational approaches offer innovative ways for uncovering clinically significant, non-shared biological signals in heterogeneous samples.
Department of Psychiatry, New York University School of Medicine, New York, NY, USA.|Steven and Alexandra Cohen Center for the Study of Post-Traumatic Stress and Traumatic Brain Injury, New York, NY, USA.
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Galatzer-Levy
Department of Medicine, University of Minnesota, Minneapolis, MN, USA.
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Department of Medicine, New York University School of Medicine, New York, NY, USA.
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Statnikov
Traumatic Stress Studies Division, Mount Sinai School of Medicine, James J Peters VA Medical Center, Bronx, NY, USA.
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Yehuda
Department of Psychiatry, New York University School of Medicine, New York, NY, USA.|Steven and Alexandra Cohen Center for the Study of Post-Traumatic Stress and Traumatic Brain Injury, New York, NY, USA.
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Shalev
D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000328:Adult; D000465:Algorithms; D019540:Area Under Curve; D001794:Blood Pressure; D004636:Emergency Service, Hospital; D005260:Female; D006339:Heart Rate; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D016014:Linear Models; D008137:Longitudinal Studies; D008214:Lymphocytes / Q000378:metabolism; D000069550:Machine Learning; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D000067073:Psychological Trauma / Q000378:metabolism / Q000503:physiopathology / Q000523:psychology*; D012372:ROC Curve; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D018570:Risk Assessment; D012463:Saliva / Q000737:chemistry; D013313:Stress Disorders, Post-Traumatic / Q000453:epidemiology / Q000523:psychology*; D060388:Support Vector Machine; D014556:Urine / Q000737:chemistry; D014947:Wounds and Injuries / Q000378:metabolism / Q000503:physiopathology / Q000523:psychology*; D055815:Young Adult
D011965:Receptors, Glucocorticoid; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone; D009638:Norepinephrine