Chronicity Of Depressive Symptoms Research Articles

Low-grade inflammation and endothelial dysfunction predict four-year risk and course of depressive symptoms: The Maastricht study

BackgroundLow-grade inflammation (LGI) and endothelial dysfunction (ED) might play a key role in the development of depression. We investigated the associations and mediation of LGI and ED with four-year incidence and course of depressive symptoms (remitted, recurrent or persistent). Design, setting, participants, measurementsIn this prospective cohort study (mean age 59.6 ± 8.2 years, 48.9% women, 26.6% diabetes by design), Cox and multinomial regression analyses, adjusted for age, sex, educational level and diabetes status were used to investigate the associations of LGI and ED with onset and course of depressive symptoms as assessed by the PHQ-9 questionnaire. ResultsDuring 10,847 person-years of follow-up, 264 participants developed incident depression. Higher levels of LGI (OR [95%CI] per SD 1.32[1.16–1.49], p < 0.001) and ED (1.26[1.11–1.43], p < 0.001) were associated with incident depressive symptoms. In mediation analysis, 60% of the total effect of ED with incident depressive symptoms could be attributed to LGI. 76 out of 2637 participants had a persistent course of depressive symptoms. Higher levels of LGI (1.75[1.40–2.19], p < 0.001) and ED (1.33[1.04–1.71], p = 0.021) were associated with a persistent course of depressive symptoms. Higher ED was more strongly associated with persistent depressive symptoms (1.33[1.04–1.71], p = 0.021), while LGI was associated with remission of depression symptoms. ConclusionsLGI and ED were both associated with incident depressive symptoms, where the latter association was substantially mediated by LGI. ED was further associated with a persistent course of depressive symptoms, while LGI was not. These results suggest a temporal, vascular contribution of both LGI and ED to the etiology and chronicity of depressive symptoms.

Longitudinal course of depressive symptom severity among youths with bipolar disorders: Moderating influences of sustained attention and history of child maltreatment

BackgroundPediatric bipolar disorders are often characterized by disruptions in cognitive functioning, and exposure to child maltreatment (e.g., physical and sexual abuse) is associated with a significantly poorer course of illness. Although clinical and developmental research has shown maltreatment to be robustly associated with poorer cognitive functioning, it is unclear whether maltreatment and cognitive function jointly influence the clinical course of bipolar symptoms. MethodsThis secondary analysis examined moderating effects of lifetime childhood physical and sexual abuse, and cognitive disruptions (sustained attention, affective information processing), on longitudinal ratings of depression symptom severity in youths from the Course and Outcome of Bipolar Youth (COBY) study, examined from intake (M = 12.24 years) through age 22 (N = 198; 43.9% female; Mean age of bipolar onset = 8.85 years). ResultsA significant moderating effect was detected for sustained attention and maltreatment history. In the context of lower sustained attention, maltreatment exposure was associated with higher depression symptom severity during childhood, but not late adolescence. There was no association between maltreatment and symptom severity in the context of higher sustained attention, and no association between attention and depression symptom severity for non-maltreated youths. LimitationsDepression symptom ratings at each assessment were subject to retrospective recall bias despite the longitudinal design. Cognitive assessments were administered at different ages across youths. ConclusionsDepressive symptoms in pediatric bipolar may be jointly moderated by impairments in attention and exposure to maltreatment. Assessment of these risks, particularly in childhood, may be beneficial for considering risk of recurrence or chronicity of depressive symptoms.

Depression, smoking, and lung cancer risk over 24 years among women.

Studies evaluating depression's role in lung cancer risk revealed contradictory findings, partly because of the small number of cases, short follow-up periods, and failure to account for key covariates including smoking exposure. We investigated the association of depressive symptoms with lung cancer risk in a large prospective cohort over 24 years while considering the role of smoking. Women from the Nurses' Health Study completed measures of depressive symptoms, sociodemographics, and other factors including smoking in 1992 (N = 42 913). Depressive symptoms were also queried in 1996 and 2000, whereas regular antidepressant use and physician-diagnosed depression were collected starting in 1996. Multivariable Cox regression models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) of lung cancer risk until 2016. We identified 1009 cases of lung cancer. Women with the highest v. lowest level of depressive symptoms had an increased lung cancer risk (HRsociodemographics-adjusted = 1.62, 95% CI 1.34-1.95; HRfully-adjusted = 1.25, 95% CI 1.04-1.51). In a test of mediation, lifetime pack-years of smoking accounted for 38% of the overall association between depressive symptoms and disease risk. When stratifying by smoking status, the elevated risk was evident among former smokers but not current or never smokers; however, the interaction term suggested no meaningful differences across groups (p = 0.29). Results were similar or stronger when considering time-updated depression status (using depressive symptoms, physician diagnosis, and regular antidepressant use) and chronicity of depressive symptoms. These findings suggest that greater depressive symptoms may contribute to lung cancer incidence, directly and indirectly via smoking habits, which accounted for over a third of the association.

Neuroticism polygenic risk score predicts 20-year burden of depressive symptoms for Whites but not Blacks

Black-White differences are reported in social, psychological, behavioral, medical, and biological correlates of depression. This study was conducted to compare Black and White older adults for the association between neuroticism polygenic risk score (N-PRS) and chronicity of depressive symptoms over 20 years. Data came from the Health and Retirement Study (HRS), 1990 - 2012, a nationally representative sample of Americans above age 50. Current analysis followed 9,249 individuals (7,924 Whites and 1,325 Blacks) for up to 22 years. Depressive symptoms were measured every two years between 1992 and 2012 using the 8-item Center for Epidemiological Studies-Depression Scale (CES-D-8). The independent variable was N-PRS. The dependent variable was average depressive symptoms between 1992 and 2012. Linear regression was used for data analysis. In the pooled sample, higher N-PRS was associated with higher average depressive symptoms over the 20-year follow up period [b=0.01, 95%CI=0.00 to 0.04], net of all covariates. We also found an interaction between race and N-PRS [b=-0.02, 95%CI=-0.03 to 0.00], suggesting a stronger effect of N-PRS on 20-year average depressive symptoms for Whites than Blacks. Based on our race-specific linear regression models, higher N-PRS was associated with higher depressive symptoms from 1992 to 2012 for Whites [b=0.01, 95%CI=0.01 to 0.02] but not Blacks [b=0.00, 95%CI=-0.02 to 0.02]. Black and White older adults may differ in the salience of the existing N-PRS for depressive symptoms, which better reflects the burden of depression for Whites than Blacks. This may be because the existing PRSs are derived from mostly or exclusively White samples, limiting their applicability in other race groups. Racial variation in psychosocial, clinical, and biological correlates of depression needs further research.

CHRONICITY OF DEPRESSION AND MOLECULAR MARKERS IN A LARGE SAMPLE OF HAN CHINESE WOMEN.

Major depressive disorder (MDD) has been associated with changes in mean telomere length and mitochondrial DNA (mtDNA) copy number. This study investigates if clinical features of MDD differentially impact these molecular markers. Data from a large, clinically ascertained sample of Han Chinese women with recurrent MDD were used to examine whether symptom presentation, severity, and comorbidity were related to salivary telomere length and/or mtDNA copy number (maximum N=5,284 for both molecular and phenotypic data). Structural equation modeling revealed that duration of longest episode was positively associated with mtDNA copy number, while earlier age of onset of most severe episode and a history of dysthymia were associated with shorter telomeres. Other factors, such as symptom presentation, family history of depression, and other comorbid internalizing disorders, were not associated with these molecular markers. Chronicity of depressive symptoms is related to more pronounced telomere shortening and increased mtDNA copy number among individuals with a history of recurrent MDD. As these molecular markers have previously been implicated in physiological aging and morbidity, individuals who experience prolonged depressive symptoms are potentially at greater risk of adverse medical outcomes.

It is time to focus on maternal mental health: optimising maternal and child health outcomes.

With maternal mental health so clearly and consistently associated with child health outcomes, it is imperative that science and society prioritise support for mothers of young children. In this issue of BJOG, Woolhouse et al. provide just such a welcome call to arms by documenting the prevalence and chronicity of depressive symptoms in women not just in the first postpartum year, but throughout the first 4 years of motherhood. Expanding our focus beyond the perinatal period is critical to ensure optimal health outcomes for both mother and child. Only within the last year one group of investigators reported that 61% of the children of chronically depressed mothers met criteria for Axis I disorders (compared with 15% of those with nondepressed mothers), and also identified neurobiological mechanisms associated with depressed families (Apter-Levy et al. Am J Psychiatry 2013;170:1161–8). Further, data from the STAR*-D cohort study of adult depression confirmed that not only do the children (ages 7–18 years) of chronically depressed mothers have significantly worse outcomes, but the treatment and remission of maternal depression had positive effects on both mothers and their children (Weissman et al. J Am Med Assoc 2006;295:1389–98). Given this body of knowledge, it is highly troubling that so little attention has been paid to the recognition or systematic intervention of maternal depression outside the acute perinatal period. Woolhouse et al. recruited 1507 Australian nulliparous women during the first trimester of pregnancy, collecting data at five postpartum time-points (3, 6, 12, 18 months and 4 years). The investigators found a disturbingly high prevalence of maternal depressive symptoms, with one in three mothers reporting symptoms at some point during the course of the study and one in seven (14.5%) still reporting symptoms at the 4-year follow-up period. Robust associations were reported between depressive symptoms and co-occurring intimate partner violence, psychosocial adverse events and chronicity of the symptoms. Although an association between intimate partner violence and maternal depression has been previously documented (Meltzer-Brody et al. Arch Womens Ment Health 2013;16:465–73; Silverman et al. Arch Womens Ment Health 2010;13:411–15), more than a quarter (28.4%) of the Australian cohort had a history of intimate partner violence. In other words, the most vulnerable women (those with past and current trauma histories and persistent mental illness) remained the most depressed over time. These figures highlight an epidemic mandating our response as scientists, clinicians and members of society. One of the most important ways in which we can address the neglect of maternal mental health is by examining the delivery of our healthcare services to children and families and finding ways to incorporate psychosocial and mental health assessment and intervention across mother–child units. It is extremely naive to believe that mothers can provide optimal care for their children without having adequate support and treatment for the widely prevalent societal and mental health concerns that challenge women during their reproductive years. Second, if we are to mitigate the intergenerational consequences of violence against women, we must take an active stance against intimate partner violence. Across healthcare settings, we can only optimise mother and child outcomes through tireless advocacy, careful assessment and immediate intervention. The authors report no conflict of interest.

A prospective longitudinal study of the impact of early postnatal vs. chronic maternal depressive symptoms on child development

Background Few studies of the effects of postnatal depression on child development have considered the chronicity of depressive symptoms. We investigated whether early postnatal depressive symptoms (PNDS) predicted child developmental outcome independently of later maternal depressive symptoms. Methods In a prospective, longitudinal study, mothers and children were followed-up from birth to 2 years; repeated measures of PNDS were made using the Edinburgh Postnatal Depression Scale (EPDS); child development was assessed using the Bayley Scales II. Multilevel modelling techniques were used to examine the association between 6 week PNDS, and child development, taking subsequent depressive symptoms into account. Results Children of mothers with 6 week PNDS were significantly more likely than children of non-symptomatic mothers to have poor cognitive outcome; however, this association was reduced to trend level when adjusted for later maternal depressive symptoms. Conclusion Effects of early PNDS on infant development may be partly explained by subsequent depressive symptoms.

Differential Association of Concurrent, Baseline, and Average Depressive Symptoms With Cognitive Decline in Older Adults

The impact of depressive symptoms on cognitive decline in older adults remains unclear due to inconsistent findings in the literature. It is also unclear whether effects of depressive symptoms on cognitive decline vary with age. This study investigated the effect of concurrent, baseline, and average depressive symptoms on cognitive functioning and decline, and examined the interactive effect of age and depressive symptoms on cognition. Prospective observational design with examination of cognitive performance and depressive symptoms at 1- to 2-year intervals for up to 26 years. Baltimore Longitudinal Study of Aging, National Institute on Aging. One thousand five hundred eighty-six dementia-free adults 50 years of age and older. Scores over time on the Center for Epidemiologic Studies Depression Scale and measures of learning and memory, attention and executive functions, verbal and language abilities, visuospatial functioning, and general cognitive status. Increased depressive symptoms were associated with poor cognitive functioning and cognitive decline in multiple domains. Concurrent, baseline, and average depressive symptoms had differential associations with cognition. Average depressive symptoms, a measure of chronic symptoms, seemed to show the most widespread effects on cognitive abilities. Effects of depressive symptoms on some frontal functions were greater with advancing age. Depressive symptoms are associated with poor cognitive functioning and cognitive decline, particularly with advancing age. The widespread impact of average depressive symptoms on cognition suggests that clinicians should consider the chronicity of depressive symptoms when evaluating cognitive functioning in older adults.

First onset of common pain symptoms: a prospective study of depression as a risk factor

This report examined first onset rates of 5 common pain symptoms and assessed, on a prospective basis, whether depressive symptoms at baseline were associated with onset risks. Adult Health Maintenance Organization (HMO) enrollees (n = 1016) were interviewed in 1986 about their history of each of 5 pain conditions (back pain, severe headache, chest pain, abdominal pain and temporomandibular disorder (TMD) pain). Three years later, this sample was re-interviewed (n = 803) to measure site-specific first onset rates. The Symptom Checklist 90-Revised (SCL-90-R) Depression scale was administered at baseline and at 3 year follow-up. Over the three year follow-up interval, rates of first onset were: 17.7% for back pain; 4.2% for severe headache; 3.0% for chest pain; 3.1% for abdominal pain; and 6.5% for TMD pain. Onset rates of persistent pain and of chronic pain dysfunction were substantially lower, but over 1% experienced onset of chronic pain dysfunction for back pain and for headache. There were not significant differences in onset rates of back pain, abdominal pain or TMD pain by severity or chronicity of depressive symptoms. Relative to the non-depressed, persons with moderate-to-severe depressive symptoms were more likely to develop headache and chest pain (adjusted odds ratios of 1.7 to 5.0). For headache and chest pain, onset risks were highest among the chronically depressed. After adjusting for age, gender, education and depression severity, persons with a pain condition at baseline were more likely to report first onset of a new pain condition over the follow-up period (adjusted odds ratios of 2.1 for back pain, 4.3 for headache, 1.4 for chest pain, 6.3 for abdominal pain and 3.7 for TMD pain). Thus, presence of a pain condition was a more consistent predictor of subsequent risks of developing a new pain condition than was the severity or chronicity of depressive symptoms. Possible explanations for this relationship are considered.