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Background: The coronavirus disease 2019 (COVID-19) pandemic led to measures that reduced social contact and support. We explored whether UK residents with more frequent or supportive social contact had fewer depressive symptoms during March−August 2020, and potential factors moderating the relationship. Methods: A convenience sample of UK dwelling participants aged ⩾18 in the internet-based longitudinal COVID-19 Social Study completed up to 22 weekly questionnaires about face-to-face and phone/video social contact frequency, perceived social support, and depressive symptoms using the PHQ-9. Mixed linear models examined associations between social contact and support, and depressive symptoms. We examined for interaction by empathic concern, perspective taking and pre-COVID social contact frequency. Results: In 71 117 people with mean age 49 years (standard deviation 15), those with high perceived social support scored 1.836 (1.801–1.871) points lower on PHQ-9 than those with low support. Daily face-to-face or phone/video contact was associated with lower depressive symptoms (0.258 (95% confidence interval 0.225–0.290) and 0.117 (0.080–0.154), respectively) compared to no contact. The negative association between social relationships and depressive symptoms was stronger for those with high empathic concern, perspective taking and usual sociability. Conclusions: We found during lockdown that those with higher quality or more face-to-face or phone/video contact had fewer depressive symptoms. Contact quality was more strongly associated than quantity. People who were usually more sociable or had higher empathy had more depressive symptoms during enforced reduced contact. The results have implications for COVID-19 and potential future pandemic management, and for understanding the relationship between social factors and mental health. [ABSTRACT FROM AUTHOR]

Background: Posttraumatic stress disorder (PTSD) is highly prevalent within prison settings, yet is often unidentified and undertreated. Complex PTSD (CPTSD) has been recently formally recognised in the International Classification of Diseases 11th revision (ICD-11) diagnostic framework but has never been explored in prison settings. We aimed to establish the prevalence of ICD-11 PTSD and CPTSD in a UK prison sample using a validated instrument (the International Trauma Questionnaire). We also explored the associations of these two diagnoses with their traumatic antecedents and psychiatric comorbidities. Method: Randomly selected male, sentenced prisoners in a large medium-security prison in south London (N = 221) took part in a clinical interview which assessed PTSD, CPTSD, trauma histories, and comorbid disorders. Multinomial logistic regression was performed to examine differences between those with PTSD or CPTSD, and those without symptoms. Results: A total of 7.7% (95% CI 4.5–12) of the male sentenced prisoners met diagnostic criteria for ICD-11 PTSD and 16.7% (95% CI 12.1–22.3) for CPTSD. A diagnosis of PTSD was associated with more recent traumatic exposure, comorbid generalised anxiety disorder, alcohol dependence, and Cluster B personality disorder. A diagnosis of CPTSD was associated with complex trauma exposure antecedents (developmental, interpersonal, repeated, or multiple forms), and comorbid with anxiety, depression, substance misuse, psychosis, and ADHD. Conclusions: This study confirms that CPTSD is a very common and comorbid condition in male prisoners. There is an urgent need to develop trauma-informed care in prisons. [ABSTRACT FROM AUTHOR]

Background: The Patient Health Questionnaire (PHQ-9), the Beck Depression Inventory (BDI-II) and the Generalised Anxiety Disorder Assessment (GAD-7) are widely used in the evaluation of interventions for depression and anxiety. The smallest reduction in depressive symptoms that matter to patients is known as the Minimum Clinically Important Difference (MCID). Little empirical study of the MCID for these scales exists. Methods: A prospective cohort of 400 patients in UK primary care were interviewed on four occasions, 2 weeks apart. At each time point, participants completed all three questionnaires and a 'global rating of change' scale (GRS). MCID estimation relied on estimated changes in symptoms according to reported improvement on the GRS scale, stratified by baseline severity on the Clinical Interview Schedule (CIS-R). Results: For moderate baseline severity, those who reported improvement on the GRS had a reduction of 21% (95% confidence interval (CI) −26.7 to −14.9) on the PHQ-9; 23% (95% CI −27.8 to −18.0) on the BDI-II and 26.8% (95% CI −33.5 to −20.1) on the GAD-7. The corresponding threshold scores below which participants were more likely to report improvement were −1.7, −3.5 and −1.5 points on the PHQ-9, BDI-II and GAD-7, respectively. Patients with milder symptoms require much larger reductions as percentage of their baseline to endorse improvement. Conclusions: An MCID representing 20% reduction of scores in these scales, is a useful guide for patients with moderately severe symptoms. If treatment had the same effect on patients irrespective of baseline severity, those with low symptoms are unlikely to notice a benefit. Funding: Funding. National Institute for Health Research. [ABSTRACT FROM AUTHOR]

Background. It is well-established that offspring of depressed mothers are at increased risk for suicidal ideation. However, pathways involved in the transmission of risk for suicidal ideation from depressed mothers to offspring are poorly understood. The aim of this study was to examine the contribution of potential mediators of this association, including maternal suicide attempt, offspring psychiatric disorder and the parent-child relationship. Method. Data were utilized from a population-based birth cohort (ALSPAC). Three distinct classes of maternal depression symptoms across the first 11 years of the child's life had already been identified (minimal, moderate, chronic-severe). Offspring suicidal ideation was assessed at age 16 years. Data were analysed using structural equation modelling. Results. There was evidence for increased risk of suicidal ideation in offspring of mothers with chronic-severe depression symptoms compared to offspring of mothers with minimal symptoms (odds ratio 3.04, 95% confidence interval 2.19- 4.21). The majority of this association was explained through maternal suicide attempt and offspring psychiatric disorder. There was also evidence for an independent indirect effect via the parent-child relationship in middle childhood. There was no longer evidence of a direct effect of maternal depression on offspring suicidal ideation after accounting for all three mediators. The pattern of results was similar when examining mechanisms for maternal moderate depression symptoms. Conclusions. Findings highlight that suicide prevention efforts in offspring of depressed mothers should be particularly targeted at both offspring with a psychiatric disorder and offspring whose mothers have made a suicide attempt. Interventions aimed at improving the parent-child relationship may also be beneficial. [ABSTRACT FROM AUTHOR]

Background Depression is expensive to treat, but providing ineffective treatment is more expensive. Such is the case for many patients who do not respond to antidepressant medication. Aims To assess the cost-effectiveness of cognitive-behavioural therapy (CBT) plus usual care for primary care patients with treatment-resistant depression compared with usual care alone. Method Economic evaluation at 12 months alongside a randomised controlled trial. Cost-effectiveness assessed using a cost-consequences framework comparing cost to the health and social care provider, patients and society, with a range of outcomes. Cost-utility analysis comparing health and social care costs with quality-adjusted life-years (QALYS). Results The mean cost of CBT per participant was £910. The difference in QALY gain between the groups was 0.057, equivalent to 21 days a year of good health. The incremental cost-effectiveness ratio was £14911 (representing a 74% probability of the intervention being cost-effective at the National Institute of Health and Care Excellence threshold of £20000 per QALY). Loss of earnings and productivity costs were substantial but there was no evidence of a difference between intervention and control groups. Conclusions The addition of CBT to usual care is cost-effective in patients who have not responded to antidepressants. Primary care physicians should therefore be encouraged to refer such individuals for CBT. [ABSTRACT FROM AUTHOR]

BackgroundIt has been argued that sleep disturbances are a risk factor for depression but previous longitudinal studies have had limitations and not addressed alternative explanations. The aim of this study was to examine the longitudinal association between sleep disturbances and depressive symptoms in a nationally representative sample.MethodData from the 18-month follow-up of the UK National Psychiatric Morbidity survey were used (n = 2406). Sleep disturbances, depressive and other psychiatric symptoms (fatigue, concentration problems, irritability, anxiety and pain symptoms) were assessed using the Revised Clinical Interview Schedule (CIS-R). The bidirectional association between symptoms was investigated with logistic regression analyses and path analysis.ResultsSleep disturbances and depressive symptoms were correlated with each other cross-sectionally (r = 0.52, p < 0.001). In the longitudinal analysis, sleep disturbances at baseline did not predict depressive symptoms at follow-up [odds ratio (OR) 1.27, 95% confidence interval (CI) 0.51–3.19] and the same was observed for the reciprocal association (OR 0.87, 95% CI 0.56–1.35). In the path analysis, the reciprocal model did not have a better fit compared to the simpler first-order model without cross-lagged paths. The path from sleep disturbances at baseline to depressive symptoms at follow-up had a minimal contribution to the explained variance of the latter (<1%).ConclusionsPrevious studies may have overestimated the importance of sleep disturbances as an independent risk factor of depression. The strong cross-sectional association is compatible with sleep disturbances being either a prodromal or a residual symptom of depression and this may have implications for recognition and treatment of depression. [ABSTRACT FROM PUBLISHER]

Background. It has been proposed that non-steroidal anti-inflammatory drugs (NSAIDs) may interfere with the efficacy of antidepressants and contribute to treatment resistance in major depressive disorder (MDD). This effect requires replication and a test of whether it is specific to serotonin-reuptake inhibiting (SRI) antidepressants. Method. We tested the effect of concomitant medication with NSAIDs on the efficacy of escitalopram, a SRI antidepressant, and nortriptyline, a tricyclic antidepressant, among 811 subjects with MDD treated for up to 12 weeks in the GENDEP study. Effects of NSAIDs on improvement of depressive symptoms were tested in mixed-effect linear models. Effects on remission were tested in logistic regression. Age, sex, baseline severity and centre of recruitment were considered as potential confounding factors. Results. Ten percent (n = 78) of subjects were taking NSAIDs during the antidepressant treatment. Older subjects were significantly more likely to take NSAIDs. After controlling for age, sex, centre of recruitment and baseline severity, concomitant medication with NSAIDs did not significantly influence the efficacy of escitalopram [β=0.035, 95% confidence interval (CI) -0.145 to 0.215, p=0.704] or nortriptyline (β=0.075, 95% CI -0.131 to 0.281, p=0.476). Although slightly fewer subjects who took NSAIDs reached remission [odds ratio (OR) 0.80, 95% CI 0.49-1.31, p=0.383], this non-significant effect was reversed after controlling for age, sex, baseline severity and recruitment centre effects (OR 1.04, 95% CI 0.61-1.77, p=0.882). Conclusions. NSAIDs are unlikely to affect the efficacy of SRI or other antidepressants. Concurrent use of NSAIDs and antidepressants does not need to be avoided. [ABSTRACT FROM AUTHOR]

BackgroundLower cognitive functioning in early childhood has been proposed as a risk factor for depression in later life but its association with depressive symptoms during adolescence has rarely been investigated. Our study examines the relationship between total intelligence quotient (IQ) score at age 8 years, and depressive symptoms at 11, 13, 14 and 17 years.MethodStudy participants were 5250 children and adolescents from the Avon Longitudinal Study of Parents and their Children (ALSPAC), UK, for whom longitudinal data on depressive symptoms were available. IQ was assessed with the Wechsler Intelligence Scale for Children III, and self-reported depressive symptoms were measured with the Short Mood and Feelings Questionnaire (SMFQ).ResultsMulti-level analysis on continuous SMFQ scores showed that IQ at age 8 years was inversely associated with depressive symptoms at age 11 years, but the association changed direction by age 13 and 14 years (age–IQ interaction, p<0.0001; age squared–IQ interaction, p<0.0001) when a higher IQ score was associated with a higher risk of depressive symptoms. This change in IQ effect was also found in relation to pubertal stage (pubertal stage–IQ interaction, 0.00049