Conduct disorder carries significant individual and societal repercussions. Despite heightened risk-taking and challenges in adapting to changing probabilities of choice outcomes being linked to maladaptive behaviours such as conduct disorder, no study to date has examined the association behind childhood decision-making and adolescent conduct disorder. This study seeks to address this gap by exploring the longitudinal association between these two variables. Understanding the mechanisms underlying conduct disorder could help with developing new preventive interventions.

We used data from the Millennium Cohort Study, a nationally representative UK cohort; participants included those with complete data on exposure, outcome and confounding variables (n = 7,237). The exposure, childhood decision-making at 11 years was measured using the Cambridge Gambling Task risk-taking and risk-adjustment measures. The outcome, a binary measure of adolescent conduct disorder was created using items from the risky and antisocial behaviour interview sections at age 17. We used logistic regression to examine the association between childhood decision-making and adolescent conduct disorder and adjusted for relevant confounders.

The univariable model showed that at age 11, each 20-point increase in risk-taking score increased the odds of conduct disorder behaviour at age 17 by 32% (OR = 1.32, 95% CI 1.18–1.44, p < 0.0001). In the multivariable model, there was strong evidence that a 20-point increase in risk-taking at 11 years was associated with 18% higher odds of conduct disorder behaviour at 17 years (OR = 1.18, 95% CI 1.05–1.33, p = 0.005). There was no evidence that this association differed by sex. Risk adjustment at 11 years showed no association with conduct disorder behaviours at age 17 both in the univariable model (OR = 0.96, 95% CI 0.88–1.06, p = 0.440) and the multivariable model (OR = 0.96, 95% CI 0.88–1.06, p = 0.433).

We found that risk-taking at 11 years was associated with conduct disorder behaviour at 17 years. If causal, our findings suggest that risk-taking might be a potential mechanism underlying adolescent conduct disorder behaviours. This may be useful in informing the design of preventive strategies, such as encouraging positive risk-taking in children and discouraging negative risk-taking behaviours.

Irritability is common and easily identified in childhood. It is transdiagnostic and a common reason for referral to mental health services. Irritability which does not decrease during early childhood is associated with adolescent depression. We hypothesised that irritability would be associated with increased risk-taking overall but reduced risk-taking in response to loss.

We used data from the Millennium Cohort Study, a population-based cohort of 18,552 children born in 2000–02. We examined whether irritability at 3, 5 and 7 years is associated with risk-taking on the CGT using multilevel mixed effect generalised linear models (MEGLMs). We also calculated the change in irritability between 3–7 years for each participant using multilevel mixed models. We then examined the association between this change measure and risk-taking on the CGT using MEGLMs. Analyses were adjusted for a broad range of confounders.

We found that children whose irritability did not decrease as would be expected from 3 to 7 years were more likely to stake a higher number of points per trial on the CGT at 11 years. This increase was most evident when the previous trial had been won. Irritability at 7 years was associated with staking a higher number of points per trial on the CGT (coefficient 0.52, 95%CI −0.04–1.08, p = 0.067) in fully adjusted model, whereas irritability at 3 and 5 years were not (3 years – coefficient 0.02, 95%CI -0.62–0.65, p = 0.961; 5 years – coefficient 0.14, 95%CI −0.45–0.73, p = 0.641). There was evidence of an interaction between irritability at seven years and whether the previous trial was won (p = 0.014). Childhood irritability which did not decrease between 3–7 years was associated with staking a higher number of points per trial on the CGT (coefficient 1.36, 95%CI 0.44–2.28, p = 0.004); there was evidence of an interaction between change in irritability and whether the previous trial was won (p = 0.056).

This is the first longitudinal population-based study examining the relationship between changes in irritability during early childhood and risk-taking behaviour measured by the CGT. Our findings illustrate that irritability in children is characterised by an increase in risk-taking at age 11 years, reflecting differences in how children behave in relation to rewards and losses based on prior irritability. Further understanding of how the processes such as risk-taking which link childhood phenotypes such as irritability, relate to future mental health, may enable the development of new interventions focussing on reactions to rewards and losses.

Selective serotonin reuptake inhibitors (SSRIs) are first-line pharmacological treatments for depression and anxiety. However, little is known about how pharmacological action is related to cognitive and affective processes. Here, we examine whether specific reinforcement learning processes mediate the treatment effects of SSRIs.

The PANDA trial was a multicentre, double-blind, randomized clinical trial in UK primary care comparing the SSRI sertraline with placebo for depression and anxiety. Participants (N = 655) performed an affective Go/NoGo task three times during the trial and computational models were used to infer reinforcement learning processes.

There was poor task performance: only 54% of the task runs were informative, with more informative task runs in the placebo than in the active group. There was no evidence for the preregistered hypothesis that Pavlovian inhibition was affected by sertraline. Exploratory analyses revealed that in the sertraline group, early increases in Pavlovian inhibition were associated with improvements in depression after 12 weeks. Furthermore, sertraline increased how fast participants learned from losses and faster learning from losses was associated with more severe generalized anxiety symptoms.

The study findings indicate a relationship between aversive reinforcement learning mechanisms and aspects of depression, anxiety, and SSRI treatment, but these relationships did not align with the initial hypotheses. Poor task performance limits the interpretability and likely generalizability of the findings, and highlights the critical importance of developing acceptable and reliable tasks for use in clinical studies.

This article presents research supported by NIHR Program Grants for Applied Research (RP-PG-0610-10048), the NIHR BRC, and UCL, with additional support from IMPRS COMP2PSYCH (JM, QH) and a Wellcome Trust grant (QH).

Although suicide bereavement is associated with suicide and self-harm, evidence regarding mechanisms is lacking. We investigated whether depression and substance use (alcohol and/or other drugs) explain the association between partner suicide bereavement and suicide.

Linkage of nationwide, longitudinal data from Denmark for the period 1980–2016 facilitated a comparison of 22 668 individuals exposed to bereavement by a partner's suicide with 913 402 individuals bereaved by a partner's death due to other causes. Using causal mediation models, we estimated the degree to which depression and substance use (considered separately) mediated the association between suicide bereavement and suicide.

Suicide-bereaved partners were found to have a higher risk of suicide (HRadj = 1.59, 95% CI 1.36–1.86) and of depression (ORadj 1.16, 95% CI 1.09–1.25) when compared to other-bereaved partners, but a lower risk of substance use (ORadj 0.83; 95% CI 0.78–0.88). An increased risk of suicide was found among any bereaved individuals with a depression diagnosis recorded post-bereavement (ORadj 3.92, 95% CI 3.55–4.34). Mediation analysis revealed that depression mediated 2% (1.68%; 95% CI 0.23%–3.14%; p = 0.024) of the association between suicide bereavement and suicide in partners when using bereaved controls.

Depression is a partial mediator of the association between suicide bereavement and suicide. Efforts to prevent and optimize the treatment of depression in suicide-bereaved people could reduce their suicide risk. Our findings might be conservative because we did not include cases of depression diagnosed in primary care. Further work is needed to understand this and other mediators.

This paper investigates whether age of onset of depression, duration of the last episode, number of episodes, and residual symptoms of depression and anxiety are associated with depression relapse in primary care patients who have been on long–term maintenance antidepressant treatment and no longer meet ICD10 criteria for depression.

An observational cohort using data from ANTLER (N = 478), a double-blind placebo-controlled trial. The primary outcome was time to relapse using the retrospective CIS-R. Participants were followed for 12 months.

Primary outcome was available for 468 participants. Time to relapse in those with more than five previous episodes of depression was shorter, hazard ratio (HR) 1.84 (95% confidence interval [CI] 1.23–2.75) compared to people with two episodes; HR 1.57 (95% CI 1.01–2.43) after adjustment. The residual symptoms of depression at baseline were also associated with increased relapse: HR 1.05 (95% CI 1.01–1.09) and HR 1.06 (95% CI 1.01–1.12) in the adjusted model. There was evidence of reduced rate of relapse in older age of onset group: HR 0.86 (95% CI 0.78–0.95); HR attenuated after adjustment HR 0.91 (95% CI 0.81–1.02). There was no evidence of an association between duration of the current episode and residual anxiety symptoms with relapse.

The number of previous episodes and residual symptoms of depression were associated with increased likelihood of relapse. These factors could inform joint decision making when patients are considering tapering off maintenance antidepressant treatment or considering other treatments to prevent relapse.

To investigate mechanisms of suicide risk in people bereaved by suicide, prompted by observations that bereaved people experience higher levels of distress around dates of emotional significance. We hypothesised that suicide-bereaved first-degree relatives and partners experience an increased risk of self-harm and suicide around dates of (i) anniversaries of the death and (ii) the deceased’s birthday, compared with intervening periods.

We conducted a self-controlled case series study using national register data on all individuals living in Denmark from 1 January 1980 to 31 December 2016 and who were bereaved by the suicide of a first-degree relative or partner (spouse or cohabitee) during that period, and who had the outcome (any episode of self-harm or suicide) within 5 years and 6 weeks of the bereavement. We compared relative incidence of suicidal behaviour in (i) the first 30 days after bereavement and (ii) in the aggregated exposed periods (6 weeks either side of death anniversaries; 6 weeks either side of the deceased’s birthdays) to the reference (aggregated unexposed intervening periods). As an indirect comparison, we repeated these models in people bereaved by other causes.

We found no evidence of an elevated risk of suicidal behaviour during periods around anniversaries of a death or the deceased’s birthdays in people bereaved by suicide (adjusted incidence rate ratio [IRRadj] = 1.00; 95% confidence interval [CI] = 0.87–1.16) or other causes (IRRadj = 1.04; 95% CI = 1.00–1.08) compared with intervening periods. Rates were elevated in the 30 days immediately after bereavement by other causes (IRRadj: 1.95, 95% CI: 1.77–2.22).

Although people bereaved by suicide are at elevated risk of self-harm and suicide, our findings do not suggest that this risk is heightened around emotionally significant anniversaries. Bereavement care should be accessible at all points after a traumatic loss as needs will differ over the grief trajectory.

Increased rates of visual impairment are observed in people with schizophrenia.

We assessed whether genetically predicted poor distance acuity is causally associated with schizophrenia, and whether genetically predicted schizophrenia is causally associated with poorer visual acuity.

We used bidirectional, two-sample Mendelian randomisation to assess the effect of poor distance acuity on schizophrenia risk, poorer visual acuity on schizophrenia risk and schizophrenia on visual acuity, in European and East Asian ancestry samples ranging from approximately 14 000 to 500 000 participants. Genetic instrumental variables were obtained from the largest available summary statistics: for schizophrenia, from the Psychiatric Genomics Consortium; for visual acuity, from the UK Biobank; and for poor distance acuity, from a meta-analysis of case–control samples. We used the inverse variance-weighted method and sensitivity analyses to test validity of results.

We found little evidence that poor distance acuity was causally associated with schizophrenia (odds ratio 1.00, 95% CI 0.91–1.10). Genetically predicted schizophrenia was associated with poorer visual acuity (mean difference in logMAR score: 0.024, 95% CI 0.014–0.033) in European ancestry samples, with a similar but less precise effect that in smaller East Asian ancestry samples (mean difference: 0.186, 95% CI –0.008 to 0.379).

Genetic evidence supports schizophrenia being a causal risk factor for poorer visual acuity, but not the converse. This highlights the importance of visual care for people with psychosis and refutes previous hypotheses that visual impairment is a potential target for prevention of schizophrenia.

Antidepressants have been proposed to act via their influence on emotional processing. We investigated the effect of discontinuing maintenance antidepressant treatment on positive and negative self-referential recall and the association between self-referential recall and risk of relapse.

The ANTLER trial was a large (N = 478) pragmatic double-blind trial investigating the clinical effectiveness of long-term antidepressant treatment for preventing relapse in primary care patients. Participants were randomised to continue their maintenance antidepressants or discontinue via a taper to placebo. We analysed memory for positive and negative personality descriptors, assessed at baseline, 12- and 52-week follow-up.

The recall task was completed by 437 participants. There was no evidence of an effect of discontinuation on self-referential recall at 12 [positive recall ratio 1.00, 95% CI (0.90–1.11), p = 0.93; negative recall ratio 1.00 (0.87–1.14), p = 0.87] or 52 weeks [positive recall ratio 1.03 (0.91–1.17), p = 0.62; negative recall ratio 1.00 (0.86–1.15), p = 0.96; ratios larger than one indicate higher recall in the discontinuation group], and no evidence of an association between recall at baseline or 12 weeks and later relapse [baseline, positive hazard ratio (HR) 1.02 (0.93–1.12), p = 0.74; negative HR 1.01 (0.90–1.13), p = 0.87; 12 weeks, positive HR 0.99 (0.89–1.09), p = 0.81; negative HR 0.98 (0.84–1.14), p = 0.78; ratios larger than one indicate a higher frequency of relapse in those with higher recall].

We found no evidence that discontinuing long-term antidepressants altered self-referential recall or that self-referential recall was associated with risk of relapse. These findings suggest that self-referential recall is not a neuropsychological marker of antidepressant action.

Psychotic experiences are reported by 5–10% of young people, although only a minority persist and develop into psychotic disorders. It is unclear what characteristics differentiate those with transient psychotic experiences from those with persistent psychotic experiences that are more likely to be of clinical relevance.

To investigate how longitudinal profiles of psychotic experiences, created from assessments at three different time points, are influenced by early life and co-occurring factors.

Using data from 8045 individuals from a birth cohort study, longitudinal profiles of psychotic experiences based on semi-structured interviews conducted at 12, 18 and 24 years were defined. Environmental, cognitive, psychopathological and genetic determinants of these profiles were investigated, along with concurrent changes in psychopathology and cognition.

Following multiple imputations, the distribution of longitudinal profiles of psychotic experiences was none (65.7%), transient (24.1%), low-frequency persistent (8.4%) and high-frequency persistent (1.7%). Individuals with high-frequency persistent psychotic experiences were more likely to report traumatic experiences, other psychopathology, a more externalised locus of control, reduced emotional stability and conscientious personality traits in childhood, compared with those with transient psychotic experiences. These characteristics also differed between those who had any psychotic experiences and those who did not.

These findings indicate that the same risk factors are associated with incidence as with persistence of psychotic experiences. Thus, it might be that the severity of exposure, rather than the presence of specific disease-modifying factors, is most likely to determine whether psychotic experiences are transient or persist, and potentially develop into a clinical disorder over time.

Evidence on inequalities in mental health in lesbian, gay, and bisexual people arises primarily from non-random samples.

To use a probability sample to study change in mental health inequalities between two survey points, 7 years apart; the contribution of minority stress; and whether associations vary by age, gender, childhood sexual abuse, and religious identification.

We analysed data from 10 443 people, in two English population-based surveys (2007 and 2014), on common mental disorder (CMD), hazardous alcohol use, and illicit drug use. Multivariable models were adjusted for age, gender, and economic factors, adding interaction terms for survey year, age, gender, childhood sexual abuse, and religious identification. We explored bullying and discrimination as mediators.

Inequalities in risks of CMD or substance misuse were unchanged between 2007 and 2014. Compared to heterosexuals, bisexual, and lesbian/gay people were more likely to have CMD, particularly bisexual people [adjusted odds ratio (AOR) = 2.86; 95% CI 1.83–4.46], and to report alcohol misuse and illicit drug use. When adjusted for bullying, odds of CMD remained elevated only for bisexual people (AOR = 3.21; 95% CI 1.64–6.30), whilst odds of alcohol and drug misuse were unchanged. When adjusted for discrimination, odds of CMD and alcohol misuse remained elevated only for bisexual people (AOR = 2.91; 95% CI 1.80–4.72; and AOR = 1.63; 95% CI 1.03–2.57 respectively), whilst odds of illicit drug use remained unchanged. There were no interactions with age, gender, childhood sexual abuse, or religious identification.

Mental health inequalities in non-heterosexuals have not narrowed, despite increasing societal acceptance. Bullying and discrimination may help explain the elevated rate of CMD in lesbian women and gay men but not in bisexual people.

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.

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.

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.

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.

According to the cognitive neuropsychological model, antidepressants reduce symptoms of depression and anxiety by increasing positive relative to negative information processing. Most studies of whether antidepressants alter emotional processing use small samples of healthy individuals, which lead to low statistical power and selection bias and are difficult to generalise to clinical practice. We tested whether the selective serotonin reuptake inhibitor (SSRI) sertraline altered recall of positive and negative information in a large randomised controlled trial (RCT) of patients with depressive symptoms recruited from primary care.

The PANDA trial was a pragmatic multicentre double-blind RCT comparing sertraline with placebo. Memory for personality descriptors was tested at baseline and 2 and 6 weeks after randomisation using a computerised emotional categorisation task followed by a free recall. We measured the number of positive and negative words correctly recalled (hits). Poisson mixed models were used to analyse longitudinal associations between treatment allocation and hits.

A total of 576 participants (88% of those randomised) completed the recall task at 2 and 6 weeks. We found no evidence that positive or negative hits differed according to treatment allocation at 2 or 6 weeks (adjusted positive hits ratio = 0.97, 95% CI 0.90–1.05, p = 0.52; adjusted negative hits ratio = 0.99, 95% CI 0.90–1.08, p = 0.76).

In the largest individual placebo-controlled trial of an antidepressant not funded by the pharmaceutical industry, we found no evidence that sertraline altered positive or negative recall early in treatment. These findings challenge some assumptions of the cognitive neuropsychological model of antidepressant action.

Cognitive mechanisms that characterize or precede depressive symptoms are poorly understood. We investigated cross-sectional and longitudinal associations between risk taking to obtain reward and adolescent depressive symptoms in a large prospective cohort, using the Cambridge Gambling Task (CGT). We also explored sex differences.

The Millennium Cohort Study (MCS) is an ongoing UK study, following the lives of 19 000 individuals born 2000/02. The CGT was completed at ages 11 (n = 12 355) and 14 (n = 10 578). Our main exposure was the proportion of points gambled, when the odds of winning were above chance (risk-taking to obtain reward). Outcomes were emotional symptoms (Strengths and Difficulties Questionnaire, SDQ) at age 11 and depressive symptoms (short Mood and Feelings Questionnaire, sMFQ) at age 14. We calculated cross-sectional and longitudinal associations, using linear regressions.

In univariable models, there was evidence of cross-sectional associations between risk-taking and SDQ/sMFQ scores, but these associations disappeared after we adjusted for sex. Longitudinally, there was weak evidence of an association between risk-taking and depressive symptoms in females only [a 20-point increase in risk-taking at age 11 was associated with a reduction of 0.31 sMFQ points at age 14 (95% CI −0.60 to −0.02)]. At both time-points, females were less risk-taking than males.

We found no convincing evidence of a relationship between risk-taking to obtain reward and depressive symptoms. There were large sex differences in risk-taking, but these do not appear to contribute to the female preponderance of depressive symptoms in adolescence.

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.

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).

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.

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. National Institute for Health Research.

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.

Self-administered questionnaires are widely used in primary care and other clinical settings to assess the severity of depressive symptoms and monitor treatment outcomes. Qualitative studies have found that changes in questionnaire scores might not fully capture patients' experience of changes in their mood but there are no quantitative studies of this issue. We examined the extent to which changes in scores from depression questionnaires disagreed with primary care patients' perceptions of changes in their mood and investigated factors influencing this relationship.

Prospective cohort study assessing patients on four occasions, 2 weeks apart. Patients (N = 554) were recruited from primary care surgeries in three UK sites (Bristol, Liverpool and York) and had reported depressive symptoms or low mood in the past year [68% female, mean age 48.3 (s.d. 12.6)]. Main outcome measures were changes in scores on patient health questionnaire (PHQ-9) and beck depression inventory (BDI-II) and the patients' own ratings of change.

There was marked disagreement between clinically important changes in questionnaire scores and patient-rated change, with disagreement of 51% (95% CI 46–55%) on PHQ-9 and 55% (95% CI 51–60%) on BDI-II. Patients with more severe anxiety were less likely, and those with better mental and physical health-related quality of life were more likely, to report feeling better, having controlled for depression scores.

Our results illustrate the limitations of self-reported depression scales to assess clinical change. Clinicians should be cautious in interpreting changes in questionnaire scores without further clinical assessment.

People with sensory impairments may be at increased risk of depression and anxiety but experience barriers to accessing treatment.

To investigate whether people with sensory impairment have more depressive and anxiety symptoms than people without, whether this is mediated by social functioning and whether they report greater non-treatment.

We analysed data from the English 2014 Adult Psychiatric Morbidity Survey using regression models, with the Clinical Interview Schedule-Revised (CIS-R) score as the primary outcome and self-reported hearing and vision impairment as exposures. A secondary outcome was self-reported receipt of mental health diagnosis and treatment. We used structural equation modelling to assess for mediation by social functioning.

A total of 19.0% of people with hearing impairment, and 30.9% and 24.5% with distance and near visual impairments, respectively, had clinically significant psychological morbidity. Adjusted mean CIS-R score was 1.86 points higher in people with hearing impairment compared with those without (95% CI 1.30–2.42, P<0.001). People with distance and near vision impairment had mean CIS-R scores 3.61 (95% CI 2.58–4.63, P<0.001) and 2.74 (95% CI 2.12–3.37, P<0.001) points higher, respectively, than those without. Social functioning accounted for approximately 50% of these relationships between sensory impairment and psychological morbidity. We found no evidence of an increased treatment gap for people with sensory impairment.

Social functioning, a potentially modifiable target, may mediate an association between sensory impairment and depressive and anxiety symptoms.

Two longitudinal studies have shown that depressive symptoms in women with eating disorders might improve in the antenatal and early postnatal periods. No study has followed up women beyond 8 months postnatal.

To investigate long-term trajectories of depressive symptoms in mothers with lifetime self-reported eating disorders.

Using data from the Avon Longitudinal Study of Parents and Children and multilevel growth curves we modelled trajectories of depressive symptoms from the 18th week of pregnancy to 18 years postnatal in women with lifetime self-reported anorexia nervosa, bulimia nervosa or both anorexia and bulimia nervosa. As sensitivity analyses we also investigated these trajectories using quintiles of a continuous measure of body image in pregnancy.

Of the 9276 women in our main sample, 126 (1.4%) reported a lifetime diagnosis of anorexia nervosa, 153 (1.6%) of bulimia nervosa and 60 (0.6%) of both anorexia and bulimia nervosa. Women with lifetime eating disorders had greater depressive symptoms scores than women with no eating disorders, before and after adjustment for confounders (anorexia nervosa: 2.10, 95% CI 1.36–2.83; bulimia nervosa: 2.28, 95% CI: 1.61–2.94, both anorexia and bulimia nervosa: 2.86, 95% CI 1.81–3.90). We also observed a dose–response association between greater body image and eating concerns in pregnancy and more severe trajectories of depressive symptoms, even after adjusting for lifetime eating disorders which also remained independently associated with greater depressive symptoms.

Women with eating disorders experience persistently greater depressive symptoms across the life-course. More training for practitioners and midwives on how to recognise eating disorders in pregnancy could help to identify depressive symptoms and reduce the long-term burden of disease resulting from this comorbidity.