Iraq and Afghanistan Veterans with posttraumatic stress disorder (PTSD) and traumatic brain injury (TBI) history have high rates of performance validity test (PVT) failure. The study aimed to determine whether those with scores in the invalid versus valid range on PVTs show similar benefit from psychotherapy and if psychotherapy improves PVT performance.

Veterans (N = 100) with PTSD, mild-to-moderate TBI history, and cognitive complaints underwent neuropsychological testing at baseline, post-treatment, and 3-month post-treatment. Veterans were randomly assigned to cognitive processing therapy (CPT) or a novel hybrid intervention integrating CPT with TBI psychoeducation and cognitive rehabilitation strategies from Cognitive Symptom Management and Rehabilitation Therapy (CogSMART). Performance below standard cutoffs on any PVT trial across three different PVT measures was considered invalid (PVT-Fail), whereas performance above cutoffs on all measures was considered valid (PVT-Pass).

Although both PVT groups exhibited clinically significant improvement in PTSD symptoms, the PVT-Pass group demonstrated greater symptom reduction than the PVT-Fail group. Measures of post-concussive and depressive symptoms improved to a similar degree across groups. Treatment condition did not moderate these results. Rate of valid test performance increased from baseline to follow-up across conditions, with a stronger effect in the SMART-CPT compared to CPT condition.

Both PVT groups experienced improved psychological symptoms following treatment. Veterans who failed PVTs at baseline demonstrated better test engagement following treatment, resulting in higher rates of valid PVTs at follow-up. Veterans with invalid PVTs should be enrolled in trauma-focused treatment and may benefit from neuropsychological assessment after, rather than before, treatment.

Group-based trajectory modeling holds promise for the study of prognostic indicators in the mood disorders because the courses that the individuals with these disorders follow are so highly variable. However, trajectory analyses of major depressive disorder have so far not included some of the more robust predictors of mood disorder outcome, nor have they described interactions between these predictors.

A group of 186 individuals aged 15–20 years with past or current depressive symptoms, who had recently begun taking a serotonin reuptake inhibitors antidepressant, underwent extensive baseline evaluations and were then followed for up to 2 years. Trajectory analyses used weekly ratings of depressive symptoms and the resulting groups were compared by the risk factors of sex, psychiatric comorbidity, negative emotionality, and childhood adversity.

A three-group solution provided the best statistical fit to the 2-year symptom trajectory. Negative emotionality and childhood adversity, though correlated, independently predicted membership in higher-morbidity groups. Female sex and comorbidity with generalized anxiety disorder (GAD) were also significantly more likely in the trajectory groups with higher symptom levels. However, the presence of GAD, rather than female sex, was the most important determinant of group membership. Negative emotionality was predictive of group membership only among women.

Trajectory analyses indicated that week-to-week variations in depressive symptoms across individuals could best be condensed into low, remitting and persistent symptom patterns. Female sex, anxiety symptoms, negative emotionality and childhood adversity were each independently associated with trajectories of higher morbidity but negative emotionality may be prognostically important only among women.

Depression is a clinically heterogeneous disorder. Previous large-scale genetic studies of depression have explored genetic risk factors of depression case–control status or aggregated sums of depressive symptoms, ignoring possible clinical or genetic heterogeneity.

We analyse data from 148 752 subjects of white British ancestry in the UK Biobank who completed nine items of a self-rated measure of current depressive symptoms: the Patient Health Questionnaire (PHQ-9). Genome-Wide Association analyses were conducted for nine symptoms and two composite measures. LD Score Regression was used to calculate SNP-based heritability (h2SNP) and genetic correlations (rg) across symptoms and to investigate genetic correlations with 25 external phenotypes. Genomic structural equation modelling was used to test the genetic factor structure across the nine symptoms.

We identified nine genome-wide significant genomic loci (8 novel), with no overlap in loci across symptoms. h2SNP ranged from 6% (concentration problems) to 9% (appetite changes). Genetic correlations ranged from 0.54 to 0.96 (all p < 1.39 × 10−3) with 30 of 36 correlations being significantly smaller than one. A two-factor model provided the best fit to the genetic covariance matrix, with factors representing ‘psychological’ and ‘somatic’ symptoms. The genetic correlations with external phenotypes showed large variation across the nine symptoms.

Patterns of SNP associations and genetic correlations differ across the nine symptoms, suggesting that current depressive symptoms are genetically heterogeneous. Our study highlights the value of symptom-level analyses in understanding the genetic architecture of a psychiatric trait. Future studies should investigate whether genetic heterogeneity is recapitulated in clinical symptoms of major depression.

Previous research has shown an association between subjective wellbeing and incident diabetes. Less is known about the role of wellbeing for subclinical disease trajectories as captured via glycated hemoglobin (HbA1c). We aimed to explore the association between subjective wellbeing and future HbA1c levels, and the role of sociodemographic, behavioral and clinical factors in this association.

We used data from the English Longitudinal Study of Ageing for this study (N = 2161). Subjective wellbeing (CASP-19) was measured at wave 2 and HbA1c was measured 8 years later at wave 6. Participants were free from diabetes at baseline. We conducted a series of analyses to examine the extent to which the association was accounted for by a range of sociodemographic, behavioral and clinical factors in linear regression models.

Models showed that subjective wellbeing (CASP-19 total score) was inversely associated with HbA1c 8 years later after controlling for depressive symptoms, age, sex, and baseline HbA1c (B = −0.035, 95% CI −0.060 to –0.011, p = 0.005). Inclusion of sociodemographic variables and behavioral factors in models accounted for a large proportion (17.0% and 24.5%, respectively) of the relationship between wellbeing and later HbA1c; clinical risk factors explained a smaller proportion of the relationship (3.4%).

Poorer subjective wellbeing is associated with greater HbA1c over 8 years of follow-up and this relationship can in part be explained by sociodemographic, behavioral and clinical factors among older adults.

Despite extensive research, symptom structure of posttraumatic stress disorder (PTSD) is highly debated. The network approach to psychopathology offers a novel method for understanding and conceptualizing PTSD. However, extant studies have mainly used small samples and self-report measures among sub-clinical populations, while also overlooking co-morbid depressive symptoms.

PTSD symptom network topology was estimated in a sample of 1489 treatment-seeking veteran patients based on a clinician-rated PTSD measure. Next, clinician-rated depressive symptoms were incorporated into the network to assess their influence on PTSD network structure. The PTSD-symptom network was then contrasted with the network of 306 trauma-exposed (TE) treatment-seeking patients not meeting full criteria for PTSD to assess corresponding network differences. Finally, a directed acyclic graph (DAG) was computed to estimate potential directionality among symptoms, including depressive symptoms and daily functioning.

The PTSD symptom network evidenced robust reliability. Flashbacks and getting emotionally upset by trauma reminders emerged as the most central nodes in the PTSD network, regardless of the inclusion of depressive symptoms. Distinct clustering emerged for PTSD and depressive symptoms within the comorbidity network. DAG analysis suggested a key triggering role for re-experiencing symptoms. Network topology in the PTSD sample was significantly distinct from that of the TE sample.

Flashbacks and psychological reactions to trauma reminders, along with their strong connections to other re-experiencing symptoms, have a pivotal role in the clinical presentation of combat-related PTSD among veterans. Depressive and posttraumatic symptoms constitute two separate diagnostic entities, but with meaningful between-disorder connections, suggesting two mutually-influential systems.

Maternal depression during pregnancy increases the risk for adverse developmental outcomes in children. However, the underpinning biological mechanisms remain unknown. We tested whether depression was associated with levels of and change in the inflammatory state during pregnancy, if early pregnancy overweight/obesity or diabetes/hypertensive pregnancy disorders accounted for/mediated these effects, and if depression added to the inflammation that typically accompanies these conditions.

We analyzed plasma high-sensitivity C-reactive protein (hsCRP) and glycoprotein acetyls at three consecutive stages during pregnancy, derived history of depression diagnoses before pregnancy from Care Register for Healthcare (HILMO) (N = 375) and self-reports (N = 347) and depressive symptoms during pregnancy using the Center for Epidemiological Studies Depression Scale completed concurrently to blood samplings (N = 295). Data on early pregnancy body mass index (BMI) and diabetes/hypertensive pregnancy disorders came from medical records.

Higher overall hsCRP levels, but not change, during pregnancy were predicted by history of depression diagnosis before pregnancy [HILMO: mean difference (MD) = 0.69 standard deviation (s.d.) units; 95% confidence interval (CI) 0.26–1.11, self-report: MD = 0.56 s.d.; 95% CI 0.17–0.94] and higher depressive symptoms during pregnancy (0.06 s.d. per s.d. increase; 95% CI 0.00–0.13). History of depression diagnosis before pregnancy also predicted higher overall glycoprotein acetyls (HILMO: MD = 0.52 s.d.; 95% CI 0.12–0.93). These associations were not explained by diabetes/hypertensive disorders, but were accounted for and mediated by early pregnancy BMI. Furthermore, in obese women, overall hsCRP levels increased as depressive symptoms during pregnancy increased (p = 0.006 for interaction).

Depression is associated with a proinflammatory state during pregnancy. These associations are mediated by early pregnancy BMI, and depressive symptoms during pregnancy aggravate the inflammation related to obesity.

The current study examined whether self-reported memory problems among cognitively intact older adults changed concurrently with, preceded, or followed depressive symptoms over time.

Data were collected annually via in-person comprehensive medical and neuropsychological examinations as part of the Einstein Aging Study.

Community-dwelling older adults in an urban, multi-ethnic area of New York City were interviewed.

The current study included a total of 1,162 older adults (Mage = 77.65, SD = 5.03, 63.39% female; 74.12% White). Data were utilized from up to 11 annual waves per participant.

Multilevel modeling tested concurrent and lagged associations between three types of memory self-report (frequency of memory problems, perceived one-year decline, and perceived ten-year decline) and depressive symptoms.

Results showed that self-reported frequency of memory problems covaried with depressive symptoms only in participants who were older at baseline. Changes in perceived one-year and ten-year memory decline were related to changes in depressive symptoms across all ages. Depressive symptoms increased the likelihood of perceived ten-year memory decline the next year; however, perceived ten-year memory decline did not predict future depressive symptoms. Additionally, no significant temporal relationship was observed between depressive symptoms and self-reported frequency of memory problems or perceived one-year memory decline.

Our findings highlight the importance of testing the unique associations of different types of self-reported memory problems with depressive symptoms.

More people remain in the workforce into their late life as people’s life expectancy increases. This study examined the relationship between work stress and depressive symptoms of older workers in mainland China, focusing on the interplay between work stress with family and community factors in three (i.e., urban, rural, and migrant) settings.

National representative survey data on the Chinese labor force collected by the Social Science Research Center of Sun-Yetsen University in 2014 were used. The sample consisted of 5,751 workers aged 50 and above recruited from 29 out of 31 provinces in mainland China.

Work stress had a consistent and robust effect on depressive symptoms across older worker groups. Moreover, it interacted with family and community factors differentially in three settings. For migrant older workers, work stress was a dominant factor affecting their depressive symptoms. Among rural older workers, the influence of work stress on depressive symptoms depended on their family debt and neighborhood cohesion levels.

Stressors from work, family, and community comprised a general model that explains depressive symptoms in Chinese older workers. Interventions or service programs aimed at reducing work stress and improving mental health among older adults should consider the complexity of intertwining family and community dynamics as well as respective strengths in urban, rural, and migrant communities.

Lay opinions and published papers alike suggest mood varies with the seasons, commonly framed as higher rates of depression mood in winter. Memory and confirmation bias may have influenced previous studies. We therefore systematically searched for and reviewed studies on the topic, but excluded study designs where explicit referrals to seasonality were included in questions, interviews or data collection.

Systematic literature search in Cochrane database, DARE, Medline, Embase, PsychINFO and CINAHL, reporting according to the PRISMA framework, and study quality assessment using the Newcastle-Ottawa scale. Two authors independently assessed each study for inclusion and quality assessment. Due to large heterogeneity, we used a descriptive review of the studies.

Among the 41 included studies, there was great heterogeneity in regards to included symptoms and disorder definitions, operationalisation and measurement. We also observed important heterogeneity in how definitions of ‘seasons’ as well as study design, reporting and quality. This heterogeneity precluded meta-analysis and publication bias analysis. Thirteen of the studies suggested more depression in winter. The remaining studies suggested no seasonal pattern, seasonality outside winter, or inconclusive results.

The results of this review suggest that the research field of seasonal variations in mood disorders is fragmented, and important questions remain unanswered. There is some support for seasonal variation in clinical depression, but our results contest a general population shift towards lower mood and more sub-threshold symptoms at regular intervals throughout the year. We suggest future research on this issue should be aware of potential bias by design and take into account other biological and behavioural seasonal changes that may nullify or exacerbate any impact on mood.

The apolipoprotein E (APOE) genotype provides information about Alzheimer’s disease risk, yet genotype disclosure is discouraged due to concerns about possible distress. This is the first study investigating the psychological and behavioral impacts that genetic susceptibility testing for Alzheimer’s disease has in an Asian population.

From March 2016 to November 2017, we ran a prospective cohort study at Duke-National University of Singapore Medical School. 280 healthy Chinese elderly filled in questionnaires that measured psychological symptoms and health behaviors, 1 week before and 6 weeks after APOE genotype disclosure. Responses from ε4-positive subjects (associated with greater Alzheimer’s disease risk) were compared to responses from ε4-negative subjects.

ε4 presence was not significantly associated with anxiety (p = 0.09) or depression (p = 0.25). No associations were found for changes to diet (p = 0.36), dietary supplements consumption (p = 0.90), physical activity (p = 0.15), or cognitive activity (p = 0.18).

There is no evidence to suggest that disclosure of APOE to Asian populations was associated with any short-term adverse psychological or behavioral impacts.

The Pain Catastrophizing Scale (PCS) measures three aspects of catastrophic cognitions about pain—rumination, magnification, and helplessness. To facilitate assessment and clinical application, we aimed to (a) develop a short version on the basis of its factorial structure and the items’ correlations with key pain-related outcomes, and (b) identify the threshold on the short form indicative of risk for depression.

Cross-sectional survey.

Social centers for older people.

664 Chinese older adults with chronic pain.

Besides the PCS, pain intensity, pain disability, and depressive symptoms were assessed.

For the full scale, confirmatory factor analysis showed that the hypothesized 3-factor model fit the data moderately well. On the basis of the factor loadings, two items were selected from each of the three dimensions. An additional item significantly associated with pain disability and depressive symptoms, over and above these six items, was identified through regression analyses. A short-PCS composed of seven items was formed, which correlated at r=0.97 with the full scale. Subsequently, receiver operating characteristic (ROC) curves were plotted against clinically significant depressive symptoms, defined as a score of ≥12 on a 10-item version of the Center for Epidemiologic Studies-Depression Scale. This analysis showed a score of ≥7 to be the optimal cutoff for the short-PCS, with sensitivity = 81.6% and specificity = 78.3% when predicting clinically significant depressive symptoms.

The short-PCS may be used in lieu of the full scale and as a brief screen to identify individuals with serious catastrophizing.

A complex interaction exists between age, body mass index, medical conditions, polypharmacotherapy, smoking, alcohol use, education, nutrition, depressive symptoms, functioning and quality of life (QoL). We aimed to examine the inter-relationships among these variables, test whether depressive symptomology plays a central role in a large sample of adults, and determine the degree of association with life-style and health variables.

Regularised network analysis was applied to 3532 North-American adults aged ⩾45 years drawn from the Osteoarthritis Initiative. Network stability (autocorrelation after case-dropping), centrality of nodes (strength, M, the sum of weight of the connections for each node), and edges/regularised partial correlations connecting the nodes were assessed.

Physical and mental health-related QoL (M = 1.681; M = 1.342), income (M = 1.891), age (M = 1.416), depressive symptoms (M = 1.214) and education (M = 1.173) were central nodes. Depressive symptoms’ stronger negative connections were found with mental health-related QoL (−0.702), income (−0.090), education (−0.068) and physical health-related QoL (−0.354). This latter was a ‘bridge node’ that connected depressive symptoms with Charlson comorbidity index, and number of medications. Physical activity and Mediterranean diet adherence were associated with income and physical health-related QoL. This latter was a ‘bridge node’ between the former two and depressive symptoms. The network was stable (stability coefficient = 0.75, i.e. highest possible value) for all centrality measures.

A stable network exists between life-style behaviors and social, environmental, medical and psychiatric variables. QoL, income, age and depressive symptoms were central in the multidimensional network. Physical health-related QoL seems to be a ‘bridge node’ connecting depressive symptoms with several life-style and health variables. Further studies should assess such interactions in the general population.

To examine whether previously established associations between experiences of meaning in life on the one hand and life satisfaction and depressive symptoms on the other hand are transferable to a population of older residential care residents with Alzheimer’s disease (AD).

Cross-sectional study using questionnaires administered in a structured interview format.

Nine residential care settings in Flanders, Belgium.

Convenience sample of 138 older adults (+65) living in residential care with a diagnosis of AD.

Meaning in life was measured using the Presence of Meaning (PoM) subscale of the Meaning in Life Questionnaire-Short Form, life satisfaction was measured using the Satisfaction With Life Scale (SWLS), depressive symptoms were measured using a five-item short form of the Geriatric Depression Scale (GDS), and general cognitive status was measured using the Mini-Mental State Examination (MMSE).

Controlling for demographic variables (age, sex, and marital status) and cognitive status, meaning in life scores were positively predictive of life satisfaction scores and negatively predictive of depressive symptoms. Post-hoc analyses suggested a possible interaction between meaning in life and cognitive status in predicting both outcomes of psychological functioning (GDS and SWLS).

The presence of meaning in life is related to important well-being outcomes for older adults with AD living in residential care. More awareness for the importance of existential themes and interventions fostering meaning might be warranted for this population.

Vulnerability to depression can be measured in different ways. We here examine how genetic risk factors are inter-related for lifetime major depression (MD), self-report current depressive symptoms and the personality trait Neuroticism.

We obtained data from three population-based adult twin samples (Virginia n = 4672, Australia #1 n = 3598 and Australia #2 n = 1878) to which we fitted a common factor model where risk for ‘broadly defined depression’ was indexed by (i) lifetime MD assessed at personal interview, (ii) depressive symptoms, and (iii) neuroticism. We examined the proportion of genetic risk for MD deriving from the common factor v. specific to MD in each sample and then analyzed them jointly. Structural equation modeling was conducted in Mx.

The best fit models in all samples included additive genetic and unique environmental effects. The proportion of genetic effects unique to lifetime MD and not shared with the broad depression common factor in the three samples were estimated as 77, 61, and 65%, respectively. A cross-sample mega-analysis model fit well and estimated that 65% of the genetic risk for MD was unique.

A large proportion of genetic risk factors for lifetime MD was not, in the samples studied, captured by a common factor for broadly defined depression utilizing MD and self-report measures of current depressive symptoms and Neuroticism. The genetic substrate for MD may reflect neurobiological processes underlying the episodic nature of its cognitive, motor and neurovegetative manifestations, which are not well indexed by current depressive symptom and neuroticism.