Perceived stress affects emotional eating and food choices. However, the extent to which stress associates with food choice motives is not completely understood. This study assessed whether emotional eating mediates the associations between perceived stress levels and food choice motives (i.e., health, mood, convenience, natural content, price, sensory appeal, familiarities, weight control, and ethical concerns) during the Coronavirus Disease 2019 pandemic. A total of 800 respondents were surveyed in the United States in June 2020. Their perceived stress, emotional eating, and food choice motives were assessed by the Perceived Stress Scale, Dutch Eating Behavior Questionnaire, and Food Choice Questionnaire, respectively. Moderate to high levels of perceived stress were experienced by the majority (73.6%) of respondents. Perceived stress was significantly correlated with emotional eating (r = 0.26) as well as five out of nine food choice motives: mood (r = 0.32), convenience (r = 0.28), natural content (r = −0.14), price (r = 0.27), and familiarity (r = 0.15). Emotional eating was significantly correlated with four out of nine food choice motives: mood (r = 0.27), convenience (r = 0.23), price (r = 0.16), and familiarity (r = 0.16). The mediation analyses showed that emotional eating mediates the associations between perceived stress and five food choices motives: mood, convenience, sensory appeal, price, and familiarity. Findings were interpreted using theories and concepts from the humanities, specifically, folklore studies, ritual studies, and symbolic anthropology.

The hypothalamus is critical for regulation of the hypothalamic-pituitary-adrenal (HPA) axis and response to stress. Adverse childhood experience (ACE) can affect brain structure, which may contribute to development of posttraumatic stress disorder (PTSD) after subsequent adult trauma. It is unclear, however, if ACE history is particularly associated with aspects of hypothalamic structure which contribute to development of PTSD. To address this issue, the present study longitudinally assessed hypothalamic volumes and their associations with ACE and early post-trauma stress symptoms in subjects who did or did not develop PTSD during 12 months after adult trauma. 109 subjects (18–60 years, F/M = 75/34) completed the PTSD Checklist (PCL) questionnaire for post-trauma stress symptoms, the Childhood Trauma Questionnaire (CTQ) for ACE assessment, and an initial MRI brain scan for hypothalamic volume measurement, within 2 weeks after adult trauma. At post-trauma 12 months, subjects underwent a subsequent PTSD diagnosis interview using the Clinician-Administered PTSD Scale (CAPS), and a follow-up MRI scan. Left and right hypothalamus volumes at 2 weeks after adult trauma negatively correlated with CTQ scores. Right hypothalamus volume at this early time mediated an association between ACE and PTSD symptoms 12 months later. Right hypothalamus volumes also remained persistently smaller from 2 weeks to 12 months after trauma in survivors who developed PTSD. These results suggest that smaller right hypothalamus volume may be related to ACE history in ways that contribute to PTSD development after trauma in adulthood.

Background: Trauma exposure can cause post-traumatic stress symptoms (PTSS), and persistently experiencing PTSS may lead to the development of post-traumatic stress disorder (PTSD). Research has shown that PTSS that emerged within days of trauma was a robust predictor of PTSD development. Aims: To investigate patterns of early stress responses to trauma and their associations with development of PTSD. Method: We recruited 247 civilian trauma survivors from a local hospital emergency department. The PTSD Checklist for DSM-5 (PCL-5) and Acute Stress Disorder Scale (ASDS) were completed within 2 weeks after the traumatic event. Additionally, 3 months post-trauma 146 of these participants completed a PTSD diagnostic interview using the Clinician Administered PTSD Scale for DSM-5. Results: We first used latent profile analysis on four symptom clusters of the PCL-5 and the dissociation symptom cluster of the ASDS and determined that a four-profile model (‘severe symptoms’, ‘moderate symptoms’, ‘mild symptoms’, ‘minimal symptoms’) was optimal based on multiple fit indices. Gender was found to be predictive of profile membership. We then found a significant association between subgroup membership and PTSD diagnosis (χ²(3) = 11.85, P < 0.01, Cramer's V = 0.263). Post hoc analysis revealed that this association was driven by participants in the ‘severe symptoms’ profile, who had a greater likelihood of developing PTSD. Conclusions: These findings fill the knowledge gap of identifying possible subgroups of individuals based on their PTSS severity during the early post-trauma period and investigating the relationship between subgroup membership and PTSD development, which have important implications for clinical practice.

Background: The presence of mild traumatic brain injury (mTBI) increases post-traumatic stress disorder (PTSD) symptoms in the months following injury. However, factors that link mTBI and PTSD development are still unclear. Acute stress responses after trauma have been associated with PTSD development. mTBI may impair cognitive functions and increase anxiety immediately after trauma. Objective: This research aimed to test the possibility that mTBI increases acute stress symptoms rapidly, which in turn results in PTSD development in the subsequent months. Method: Fifty-nine patients were recruited from the emergency rooms of local hospitals. Post-mTBI, acute stress, and PTSD symptom severity were measured using the Rivermead Post-Concussion Symptoms Questionnaire (RPQ), Acute Stress Disorder Scale (ASDS), and PTSD Checklist for DSM-5 (PCL-5), respectively. Results: Moderated mediation analysis indicated that ASDS, at 2 weeks post-trauma, mediated the relationship between RPQ scores at 2 weeks and PCL-5 scores at 3 months post-trauma, only for patients who met mTBI diagnostic criteria. Conclusions: These findings present preliminary evidence suggesting that acute stress disorder symptoms may be one of the mechanisms involved in the development of PTSD among trauma survivors who have experienced mTBI, which provides a theoretical basis for early intervention of PTSD prevention after mTBI.

Background: Sleep disturbance is common within days to weeks following a traumatic event and has been associated with emotion dysregulation, a strong risk factor for PTSD development. This study aims to examine if emotion dysregulation mediates the relationship between early post-trauma sleep disturbance and subsequent PTSD symptom severity. Methods: Adult participants (n = 125) completed questionnaires regarding sleep disturbance (via Pittsburgh Sleep Quality Index Addendum; PSQI-A) and emotion dysregulation (via Difficulties in Emotion Regulation Scale; DERS) within 2 weeks after exposure to traumatic events. Results: PTSD symptom severity was assessed with PTSD Checklist for DSM-5 (PCL-5) at 3-month follow-up. There were strong correlations between PSQI-A, DERS, and PCL-5 (r ranges between .38 and .45). Mediation analysis further revealed significant indirect effects of overall emotion regulation difficulties in the relationship between sleep disturbance at 2 weeks and PTSD symptom severity at 3 months (B = .372, SE = .136, 95% CI: [.128, .655]). Importantly, limited access to emotion regulation strategies emerged as the single, significant indirect effect in this relationship (B = .465, SE = .204, 95% CI [.127, .910]) while modelling DERS subscales as multiple parallel mediators. Conclusions: Early post-trauma sleep disturbance is associated with PTSD symptoms over months, and acute emotion dysregulation explains part of this association. Those with limited emotion regulation strategies are at particular risk of developing PTSD symptoms. Early interventions focusing on the appropriate strategies for emotion regulation may be crucial for trauma-exposed individuals.