Depression is strongly associated with chronic disease; yet, the direction of this relationship is poorly understood. Allostatic load (AL) provides a framework for elucidating depression-disease pathways. We aimed to investigate bidirectional, longitudinal associations of baseline depressive symptoms or AL with 5-year AL or depressive symptoms, respectively.

Data were from baseline, 2-year, and 5-year visits of 620 adults (45–75 years) enrolled in the Boston Puerto Rican Health Study. The Center for Epidemiology Studies Depression (CES-D) scale (0–60) captured depressive symptoms, which were categorized at baseline as low (<8), subthreshold (8–15), or depression-likely (⩾16) symptoms. AL was calculated from 11 parameters of biological functioning, representing five physiological systems. Baseline AL scores were categorized by the number of dysregulated parameters: low (0–2), moderate (3–5), or high (⩾6) AL. Multivariable, multilevel random intercept and slope linear regression models were used to examine associations between 3-category baseline CES-D score and 5-year continuous AL score, and between baseline 3-category AL and 5-year continuous CES-D score.

Baseline subthreshold depressive symptoms [(mean (95% CI)): 4.8 (4.5–5.2)], but not depression-likely symptoms [4.5 (4.2–4.9)], was significantly associated with higher 5-year AL scores, compared to low depressive symptoms [4.3 (3.9–4.7)]. Baseline high AL [19.4 (17.6–21.2)], but not low AL [18.5 (16.5–20.6)], was significantly associated with higher 5-year CES-D score, compared to baseline moderate AL [16.9 (15.3–18.5)].

Depressive symptoms and AL had a bi-directional relationship over time, indicating a nuanced pathway linking depression with chronic diseases among a minority population.

This study examined the associations between accelerometer-derived sedentary time (ST), lower intensity physical activity (LPA), higher intensity physical activity (HPA) and the incidence of depressive symptoms over 4 years of follow-up.

We included 2082 participants from The Maastricht Study (mean ± s.d. age 60.1 ± 8.0 years; 51.2% men) without depressive symptoms at baseline. ST, LPA and HPA were measured with the ActivPAL3 activity monitor. Depressive symptoms were measured annually over 4 years of follow-up with the 9-item Patient Health Questionnaire (PHQ-9). Cox regression analysis was performed to examine the associations between ST, LPA, HPA and incident depressive symptoms (PHQ-9 ⩾ 10). Analyses were adjusted for total waking time per day, age, sex, education level, type 2 diabetes mellitus, body mass index, total energy intake, smoking status and alcohol use.

During 7812.81 person-years of follow-up, 203 (9.8%) participants developed incident depressive symptoms. No significant associations [Hazard Ratio (95% confidence interval)] were found between sex-specific tertiles of ST (lowest v. highest tertile) [1.13 (0.76–1.66], or HPA (highest v. lowest tertile) [1.14 (0.78–1.69)] and incident depressive symptoms. LPA (highest v. lowest tertile) was statistically significantly associated with incident depressive symptoms in women [1.98 (1.19–3.29)], but not in men (p-interaction <0.01).

We did not observe an association between ST or HPA and incident depressive symptoms. Lower levels of daily LPA were associated with an increased risk of incident depressive symptoms in women. Future research is needed to investigate accelerometer-derived measured physical activity and ST with incident depressive symptoms, preferably stratified by sex.

Stress is a risk factor for numerous negative health outcomes, including cognitive impairment in late-life. The negative association between stress and cognition may be mediated by depressive symptoms, which separate studies have identified as both a consequence of perceived stress and a risk factor for cognitive decline. Pathways linking perceived stress, depressive symptoms, and cognition may be moderated by sociodemographics and psychosocial resources. The goal of this cross-sectional study was to identify modifying factors and enhance understanding of the mechanisms underlying the stress–cognition association in a racially and ethnically diverse sample of older adults.

A linear regression estimated the association between perceived stress and episodic memory in 578 older adults (M age = 74.58) in the Washington Heights-Inwood Columbia Aging Project. Subsequent models tested whether depressive symptoms mediated the stress–memory relationship and whether sociodemographics (gender, race, and ethnicity) or perceived control moderated these pathways.

Independent of sociodemographics and chronic diseases, greater perceived stress was associated with worse episodic memory. This relationship was mediated by more depressive symptoms. Higher perceived control buffered the association between stress and depressive symptoms. There was no significant moderation by gender, race, or ethnicity.

Depressive symptoms may play a role in the negative association between perceived stress and cognition among older adults; however, longitudinal analyses and studies using experimental designs are needed. Perceived control is a modifiable psychological resource that may offset the negative impact of stress.

To investigate the cross-sectional association between dietary intakes of antioxidants and fiber and depressive symptoms among Iranian adolescent girls.

A cross-sectional population-based study.

Primary schools in two different cities located in northeastern Iran (Mashhad and Sabzevar).

A total of 988 adolescent girls aged 12-18 years were included in the study.

Subjects with no or minimal depression symptoms had significantly higher dietary intakes of α-carotene (p=0.01), β-carotene (p=0.006), lutein (p=0.03), and vitamin C (p=0.04) when compared with subjects with mild to severe depression symptoms. Soluble dietary fiber and insoluble dietary fiber intakes were also significantly higher in healthy adolescents compared to those with depression symptoms (p<0.001). In multivariate-adjusted model 2, the odds ratios (95% confidence intervals) of depressive symptoms were 0.61 (0.37–1.01), 0.42 (0.26–0.69), 0.50 (0.31–0.79), 0.71 (0.44–1.15), 0.51 (0.32-0.82) and 0.42 (0.25-0.68) for the highest versus lowest quartile of vitamin C, β-carotene, α-carotene, lutein, soluble dietary fiber, and insoluble dietary fiber cereal intakes, respectively.

Dietary intake of some antioxidants and dietary fiber intake were inversely associated with depression symptoms among Iranian adolescent girls.

Geriatric depression complicates cognitive health in older adults. This study aims to investigate the impact of depressive symptoms on cognitive impairment in community-dwelling older adults, depending on whether cognitive dysfunction accompanied.

A community-based longitudinal cohort study.

This study analyzed data from the Korean Longitudinal Study of Aging (KLoSA) from 2006 to 2018.

Among 10,254 individuals who were registered in the KLoSA study, a total of 9119 subjects met the criteria, and 4547 subjects were included in the final analysis. The subjects were grouped into 4 categories based on depressive symptoms and cognitive dysfunction at baseline assessment: “normal control” (NC, n = 3341), “depression only” (Dep-only, n = 652), “cognitive dysfunction only” (CD-only, n = 393), and “depression with cognitive dysfunction” (Dep-CD, n = 161).

Cognitive impairment 10 years later was defined as K-MMSE scores below two percentile on demographically adjusted norms.

Ten-year survival, that is, not experiencing cognitive impairment, was 80 $$ \pm \,$$ 1% in NC group, 72 $$ \pm $$ 2% in Dep-only group, 52 $$ \pm $$ 3% in CD-only group, and 44 $$ \pm $$ 5% in Dep-CD group. The hazard ratio (HR) of the Dep-only group (HR = 1.18, 95% CI, 0.97–1.43, n.s.) did not differ from that of the NC group, but the HR of the Dep-CD group was significantly higher (HR = 2.85, 95% CI, 2.23–3.66, p < 0.001) than the NC group. When the Dep-CD group was compared to the CD-only group, the HR was 1.13 (95% CI, 0.85–1.49, n.s.), which indicates that it did not significantly differ from the CD-only group.

Our findings suggest that depressive symptoms with cognitive dysfunction are associated with a higher risk of cognitive impairment. Furthermore, cognitive dysfunction occurring with depressive symptoms is as much a risk for cognitive impairment as is pure cognitive dysfunction. Thus, healthcare providers should pay close attention to the community-dwelling elderly when depressive symptoms occur with cognitive dysfunction.

Childhood infections are associated with adult psychosis and depression, but studies of psychotic experiences (PEs) and depressive symptoms in childhood, adolescence, and early-adulthood are scarce. Previous studies have typically examined severe infections, but studies of common infections are also scarce.

Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) birth cohort, we examined associations of the number of infections in childhood from age 1.5 to 7.5 years with depressive symptom scores at age 10, 13, 14, 17, 18, and 19 years, and with PEs at 12 and 18 years. We performed additional analysis using infection burden (‘low’ = 0–4 infections, ‘medium’ = 5–6, ‘high’ = 7–9, or ‘very high’ = 10–22 infections) as the exposure.

The risk set comprised 11 786 individuals with childhood infection data. Number of childhood infections was associated with depressive symptoms from age 10 (adjusted beta = 0.14; standard error (s.e.) = 0.04; p = <0.01) to 17 years (adjusted beta = 0.17; s.e. = 0.08; p = 0.04), and with PEs at age 12 (suspected/definite PEs: adjusted odds ratio (OR) = 1.18; 95% confidence interval (CI) = 1.09–1.27). These effect sizes were larger when the exposure was defined as very high infection burden (depressive symptoms age 17: adjusted beta = 0.79; s.e. = 0.29; p = 0.01; suspected/definite PEs at age 12: adjusted OR = 1.60; 95% CI = 1.25–2.05). Childhood infections were not associated with depressive/psychotic outcomes at age 18 or 19.

Common early-childhood infections are associated with depressive symptoms up to mid-adolescence and with PEs subsequently in childhood, but not with these outcomes in early-adulthood. These findings require replication including larger samples with outcomes in adulthood.

Large population-based cohort studies of neuropsychological factors that characterise or precede depressive symptoms are rare. Most studies use small case-control or cross-sectional designs, which may cause selection bias and cannot test temporality. In a large UK population-based cohort, we investigated cross-sectional and longitudinal associations between inhibitory control of positive and negative information and adolescent depressive symptoms.

Cohort study of 2328 UK adolescents who completed an affective go/no-go task at age 18. Depressive symptoms were assessed with the Clinical Interview Schedule Revised (CIS-R) and short Mood and Feeling Questionnaire (sMFQ) at age 18, and with the sMFQ 1 year later (age 19). Analyses were multilevel and traditional linear regressions, before and after adjusting for confounders.

Cross-sectionally, we found little evidence that adolescents with more depressive symptoms made more inhibitory control errors [after adjustments, errors increased by 0.04% per 1 s.d. increase in sMFQ score (95% confidence interval 0.02–0.06)], but this association was not observed for the CIS-R. There was no evidence for an influence of valence. Longitudinally, there was no evidence that reduced inhibitory control was associated with future depressive symptoms.

Inhibitory control of positive and negative information does not appear to be a marker of current or future depressive symptoms in adolescents and would not be a useful target in interventions to prevent adolescent depression. Our lack of convincing evidence for associations with depressive symptoms suggests that the affective go/no-go task is not a promising candidate for future neuroimaging studies of adolescent depression.

Although there is growing interest in mental health problems in university students there is limited understanding of the scope of need and determinants to inform intervention efforts.

To longitudinally examine the extent and persistence of mental health symptoms and the importance of psychosocial and lifestyle factors for student mental health and academic outcomes.

Undergraduates at a Canadian university were invited to complete electronic surveys at entry and completion of their first year. The baseline survey measured important distal and proximal risk factors and the follow-up assessed mental health and well-being. Surveys were linked to academic grades. Multivariable models of risk factors and mental health and academic outcomes were fit and adjusted for confounders.

In 1530 students surveyed at entry to university 28% and 33% screened positive for clinically significant depressive and anxiety symptoms respectively, which increased to 36% and 39% at the completion of first year. Over the academic year, 14% of students reported suicidal thoughts and 1.6% suicide attempts. Moreover, there was persistence and overlap in these mental health outcomes. Modifiable psychosocial and lifestyle factors at entry were associated with positive screens for mental health outcomes at completion of first year, while anxiety and depressive symptoms were associated with lower grades and university well-being.

Clinically significant mental health symptoms are common and persistent among first-year university students and have a negative impact on academic performance and well-being. A comprehensive mental health strategy that includes a whole university approach to prevention and targeted early-intervention measures and associated research is justified.

Network analysis (NA) conceptualizes psychiatric disorders as complex dynamic systems of mutually interacting symptoms. Major depressive disorder (MDD) is a heterogeneous clinical condition, and very few studies to date have assessed putative changes in its psychopathological network structure in response to antidepressant (AD) treatment.

In this randomized trial with adult depressed outpatients (n = 151), we estimated Gaussian graphical models among nine core MDD symptom-domains before and after 8 weeks of treatment with either escitalopram or desvenlafaxine. Networks were examined with the measures of cross-sectional and longitudinal structure and connectivity, centrality and predictability as well as stability and accuracy.

At baseline, the most connected MDD symptom-domains were fatigue–cognitive disturbance, whereas at week 8 they were depressed mood–suicidality. Overall, the most central MDD symptom-domains at baseline and week 8 were, respectively, fatigue and depressed mood; in contrast, the most peripheral symptom-domain across both timepoints was appetite/weight disturbance. Furthermore, the psychopathological network at week 8 was significantly more interconnected than at baseline, and they were also structurally dissimilar.

Our findings highlight the utility of focusing on the dynamic interaction between depressive symptoms to better understand how the treatment with ADs unfolds over time. In addition, depressed mood, fatigue, and cognitive/psychomotor disturbance seem to be central MDD symptoms that may be viable targets for novel, focused therapeutic interventions.

Previous studies have found a relationship between job-related stress and depressive symptoms in different occupational groups, and that personality may modify the risk of developing depressive symptoms. We aimed to examine the association of personality and other individual and work conditions with depressive symptoms.

A sample of 498 teachers answered a questionnaire concerning individual and work characteristics, some job-related perceptions, and the wish to change jobs. Depressive symptoms were measured by the Center for Epidemiologic Studies Depression scale (CES-D) and personality was measured by the Temperament and Character Inventory (TCI-125).

Depressive symptoms were associated with female gender, age, low job satisfaction, high job stress, the wish to change jobs, working at a public school, and with higher scores on harm avoidance and novelty seeking and lower scores on self-directedness.

Our results underline the influence of personality traits on the development of depressive symptoms independently of other individual characteristics and the occupational context.

Familial aggregation of major depression might indicate a genetic liability for the disorder. The complete disorder or, alternatively, only some individual symptoms might be inherited. Under the latter condition, an increased frequency of inherited symptoms might consecutively increase the likelihood to reach the threshold for depression in relatives and, thus, might cause the familial aggregation of depression. Up to now, no study investigated the possibility of a relationship between individual depressive symptoms and the familial aggregation of depression.

The familial aggregation of early-onset depression (age-at-onset < 60 years, EOD) but less so of late-onset depression (LOD) has been shown in this sample. To assess the hypothesis of an inheritance of individual depressive symptoms as a possible cause of the familial aggregation of depression, frequencies of symptoms were compared in relatives of depressed patients and of controls using forward logistic regression analyses.

Some individual depressive symptoms showed clustering in relatives of patients with depression, but the pattern of inheritance was inconsistent, i.e. the clustering of symptoms was different between non-depressed and depressed relatives of patients with EOD and LOD, respectively. No intra-familial clustering of specific depressive symptoms within families of depressed subjects could be observed.

Due to the inconsistencies in the clustering of individual symptoms in non-depressed and depressed relatives and the lack of intra-familial clustering, the familial aggregation of depression is unlikely to be caused by the aggregation of individual depressive symptoms. An inheritance of the vulnerability for complete depressive disorders influenced by environmental factors is more likely.

Depressive disorders (DD) in adolescence are often misdiagnosed and under-recognised. A major clinical problem regards the high rate of co-morbidity with other disorders, namely substance abuse. The aim of this study was to assess the discriminative power of the Beck Depression Inventory II (BDI-II) to characterise specific social–demographic variables related to DD in adolescence.

A Portuguese version of the BDI-II and a social–demographic questionnaire were administered to 775 Portuguese adolescents (312 males, 463 females; mean age: 16.9 years); 83 adolescents performed a clinical interview following DSM-IV criteria.

Mean BDI-II Portuguese version (BDI-II-P) total score was 10.31 (standard deviation: 8.4), with females reporting more depressive symptoms than males (P < 0.001). Low academic achievement, sleep disturbances, and alcohol consumption were consistently associated with depressive symptoms for both genders. Higher tobacco consumption was significantly associated with depressive symptoms in females. Familial factors did not appear to be associated with depressive symptoms in males. However, a higher frequency of siblings, having separated parents as well as a more extreme perception of the mother's educational style were consistently associated with depressive symptoms in females.

The BDI-II-P showed discriminative power to characterise social–demographic variables related to DD especially in adolescent females.