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Research exploring the longitudinal course of posttraumatic stress disorder (PTSD) symptoms has documented four modal trajectories (low, remitting, high, and delayed), with proportions varying across studies. Heterogeneity could be due to differences in trauma types and patient demographic characteristics.
This analysis pooled data from six longitudinal studies of adult survivors of civilian-related injuries admitted to general hospital emergency departments (EDs) in six countries (pooled N = 3083). Each study included at least three assessments of the clinician-administered PTSD scale in the first post-trauma year. Latent class growth analysis determined the proportion of participants exhibiting various PTSD symptom trajectories within and across the datasets. Multinomial logistic regression analyses examined demographic characteristics, type of event leading to the injury, and trauma history as predictors of trajectories differentiated by their initial severity and course.
Five trajectories were found across the datasets: Low (64.5%), Remitting (16.9%), Moderate (6.7%), High (6.5%), and Delayed (5.5%). Female gender, non-white race, prior interpersonal trauma, and assaultive injuries were associated with increased risk for initial PTSD reactions. Female gender and assaultive injuries were associated with risk for membership in the Delayed (v. Low) trajectory, and lower education, prior interpersonal trauma, and assaultive injuries with risk for membership in the High (v. Remitting) trajectory.
The results suggest that over 30% of civilian-related injury survivors admitted to EDs experience moderate-to-high levels of PTSD symptoms within the first post-trauma year, with those reporting assaultive violence at increased risk of both immediate and longer-term symptoms.
Individuals with posttraumatic stress disorder (PTSD) are at increased risk of various chronic diseases. One hypothesized pathway is via changes in diet quality. This study evaluated whether PTSD was associated with deterioration in diet quality over time.
Data were from 51 965 women in the Nurses' Health Study II PTSD sub-study followed over 20 years. Diet, assessed at 4-year intervals, was characterized via the Alternative Healthy Eating Index-2010 (AHEI). Based on information from the Brief Trauma Questionnaire and Short Screening Scale for DSM-IV PTSD, trauma/PTSD status was classified as no trauma exposure, prevalent exposure (trauma/PTSD onset before study entry), or new-onset (trauma/PTSD onset during follow-up). We further categorized women with prevalent exposure as having trauma with no PTSD symptoms, trauma with low PTSD symptoms, and trauma with high PTSD symptoms, and created similar categories for women with new-onset exposure, resulting in seven comparison groups. Multivariable linear mixed-effects spline models tested differences in diet quality changes by trauma/PTSD status over follow-up.
Overall, diet quality improved over time regardless of PTSD status. In age-adjusted models, compared to those with no trauma, women with prevalent high PTSD and women with new-onset high PTSD symptoms had 3.3% and 3.6% lower improvement in diet quality, respectively, during follow-up. Associations remained consistent after adjusting for health conditions, sociodemographics, and behavioral characteristics.
PTSD is associated with less healthy changes in overall diet quality over time. Poor diet quality may be one pathway linking PTSD with a higher risk of chronic disease development.
Prospective population-based studies of psychiatric comorbidity following trauma and severe stress exposure in children are limited.
To examine incident psychiatric comorbidity following stress disorder diagnoses in Danish school-aged children using Danish national healthcare system registries.
Children (6–15 years of age) with a severe stress or adjustment disorder (ICD-10) between 1995 and 2011 (n = 11 292) were followed prospectively for an average of 5.8 years. Incident depressive, anxiety and behavioural disorder diagnoses were examined relative to an age- and gender-matched comparison cohort (n = 56 460) using Cox proportional hazards regression models. Effect modification by gender was examined through stratified analyses.
All severe stress and adjustment disorder diagnoses were associated with increased rates for all incident outcome disorders relative to the comparison cohort. For instance, adjustment disorders were associated with higher rates of incident depressive (rate ratio RR = 6.8; 95% CI 6.0–7.7), anxiety (RR = 5.3; 95% CI 4.5–6.4), and behavioural disorders (RR = 7.9; 95% CI 6.6–9.3). Similarly, PTSD was also associated with higher rates of depressive (RR = 7.4; 95% CI 4.2–13), anxiety (RR = 7.1; 95% CI 3.5–14) and behavioural disorder (RR = 4.9; 95% CI 2.3–11) diagnoses. There was no evidence of gender-related differences.
Stress disorders varying in symptom constellation and severity are associated with a range of incident psychiatric disorders in children. Transdiagnostic assessments within a longitudinal framework are needed to characterise the course of post-trauma or severe stressor psychopathology.
The term ‘global mental health’ came to the fore in 2007, when the Lancet published a series by that name.
To review all peer-reviewed articles using the term ‘global mental health’ and determine the implicit priorities of scientific literature that self-identifies with this term.
We conducted a systematic review to quantify all peer-reviewed articles using the English term ‘global mental health’ in their text published between 1 January 2007 and 31 December 2016, including by geographic regions and by mental health conditions.
A total of 467 articles met criteria. Use of the term ‘global mental health’ increased from 12 articles in 2007 to 114 articles in 2016. For the 111 empirical studies (23.8% of articles), the majority (78.4%) took place in low- and middle-income countries (LMICs), with the most in Sub-Saharan Africa (28.4%) and South Asia (25.5%) and none from Central Asia. The most commonly studied mental health conditions were depression (29.7%), psychoses (12.6%) and conditions specifically related to stress (12.6%), with fewer studies on epilepsy (2.7%), self-harm and suicide (1.8%) and dementia (0.9%). The majority of studies lacked contextual information, including specific region(s) within countries where studies took place (20.7% missing), specific language(s) in which studies were conducted (36.9% missing), and details on ethnic identities such as ethnicity, caste and/or tribe (79.6% missing) and on socioeconomic status (85.4% missing).
Research identifying itself as ‘global mental health’ has focused predominantly on depression in LMICs and lacked contextual and sociodemographic data that limit interpretation and application of findings.
Whereas genetic susceptibility increases the risk for major depressive disorder (MDD), non-genetic protective factors may mitigate this risk. In a large-scale prospective study of US Army soldiers, we examined whether trait resilience and/or unit cohesion could protect against the onset of MDD following combat deployment, even in soldiers at high polygenic risk.
Data were analyzed from 3079 soldiers of European ancestry assessed before and after their deployment to Afghanistan. Incident MDD was defined as no MDD episode at pre-deployment, followed by a MDD episode following deployment. Polygenic risk scores were constructed from a large-scale genome-wide association study of major depression. We first examined the main effects of the MDD PRS and each protective factor on incident MDD. We then tested the effects of each protective factor on incident MDD across strata of polygenic risk.
Polygenic risk showed a dose–response relationship to depression, such that soldiers at high polygenic risk had greatest odds for incident MDD. Both unit cohesion and trait resilience were prospectively associated with reduced risk for incident MDD. Notably, the protective effect of unit cohesion persisted even in soldiers at highest polygenic risk.
Polygenic risk was associated with new-onset MDD in deployed soldiers. However, unit cohesion – an index of perceived support and morale – was protective against incident MDD even among those at highest genetic risk, and may represent a potent target for promoting resilience in vulnerable soldiers. Findings illustrate the value of combining genomic and environmental data in a prospective design to identify robust protective factors for mental health.
Posttraumatic stress disorder (PTSD) is associated with higher risk of incident hypertension, but it is unclear whether specific aspects of PTSD are particularly cardiotoxic. PTSD is a heterogeneous disorder, comprising dimensions of fear and dysphoria. Because elevated fear after trauma may promote autonomic nervous system dysregulation, we hypothesized fear would predict hypertension onset, and associations with hypertension would be stronger with fear than dysphoria.
We examined fear and dysphoria symptom dimensions in relation to incident hypertension over 24 years in 2709 trauma-exposed women in the Nurses’ Health Study II. Posttraumatic fear and dysphoria symptom scores were derived from a PTSD diagnostic interview. We used proportional hazards models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for each symptom dimension (quintiles) with new-onset hypertension events (N = 925), using separate models. We also considered lower-order symptom dimensions of fear and dysphoria.
Higher levels of fear (P-trend = 0.02), but not dysphoria (P-trend = 0.22), symptoms were significantly associated with increased hypertension risk after adjusting for socio-demographics and family history of hypertension. Women in the highest v. lowest fear quintile had a 26% higher rate of developing hypertension [HR = 1.26 (95% CI 1.02–1.57)]; the increased incidence associated with greater fear was similar when further adjusted for biomedical and health behavior covariates (P-trend = 0.04) and dysphoria symptoms (P-trend = 0.04). Lower-order symptom dimension analyses provided preliminary evidence that the re-experiencing and avoidance components of fear were particularly associated with hypertension.
Fear symptoms associated with PTSD may be a critical driver of elevated cardiovascular risk in trauma-exposed individuals.
Abnormal thyroid function is prevalent among women and has been linked to increased risk of chronic disease. Posttraumatic stress disorder (PTSD) has been linked to thyroid dysfunction in some studies; however, the results have been inconsistent. Thus, we evaluated trauma exposure and PTSD symptoms in relation to incident thyroid dysfunction in a large longitudinal cohort of civilian women.
We used data from 45 992 women from the ongoing Nurses’ Health Study II, a longitudinal US cohort study that began in 1989. In 2008, history of trauma and PTSD were assessed with the Short Screening Scale for Diagnostic and Statistical Manual of Mental Disorders, fourth edition, PTSD, and incident thyroid dysfunction was determined by participants’ self-report in biennial questionnaires of physician-diagnosed hypothyroidism and Graves’ hyperthyroidism. The study period was from 1989 to 2013. Proportional hazard models were used to estimate multivariable-adjusted hazard ratios and 95% confidence intervals (CIs) for incident hypothyroidism and Graves’ hyperthyroidism.
In multivariable-adjusted models, we found significant associations for PTSD only with hypothyroidism [p-trend <0.001; trauma with no PTSD symptoms, 1.08 (95% CI 1.02–1.15); 1–3 PTSD symptoms, 1.12 (95% CI 1.04–1.21); 4–5 PTSD symptoms, 1.23 (95% CI 1.13–1.34); and 6–7 PTSD symptoms, 1.26 (95% CI 1.14–1.40)]. PTSD was not associated with risk of Graves’ hyperthyroidism (p-trend = 0.34). Associations were similar in sensitivity analyses restricted to outcomes with onset after 2008, when PTSD was assessed.
PTSD was associated with higher risk of hypothyroidism in a dose-dependent fashion. Highlighted awareness for thyroid dysfunction may be especially important in women with PTSD.