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.

It has been hypothesised that refugees have an increased risk of suicide.

To investigate whether risk of suicide is higher among refugees compared with non-refugee migrants from the same areas of origin and with the Swedish-born population, and to examine whether suicide rates among migrants converge to the Swedish-born population over time.

A population-based cohort design using linked national registers to follow 1 457 898 people born between 1 January 1970 and 31 December 1984, classified by migrant status as refugees, non-refugee migrants or Swedish-born. Participants were followed from their 16th birthday or date of arrival in Sweden until death, emigration or 31 December 2015, whichever came first. Cox regression models estimated adjusted hazard ratios for suicide by migrant status, controlling for age, gender, region of origin and income.

There were no significant differences in suicide risk between refugee and non-refugee migrants (hazard ratio 1.28, 95% CI 0.93–1.76) and both groups had a lower risk of suicide than Swedish born. During their first 5 years in Sweden no migrants died by suicide; however, after 21–31 years their suicide risk was equivalent to the Swedish-born population (hazard ratio 0.94, 95% CI 0.79–1.22). After adjustment for income this risk was significantly lower for migrants than the Swedish-born population.

Being a refugee was not an additional risk factor for suicide. Our findings regarding temporal changes in suicide risk suggest that acculturation and socioeconomic deprivation may account for a convergence of suicide risk between migrants and the host population over time.

None.

Peripheral low-grade inflammation in depression is increasingly seen as a therapeutic target. We aimed to establish the prevalence of low-grade inflammation in depression, using different C-reactive protein (CRP) levels, through a systematic literature review and meta-analysis.

We searched the PubMed database from its inception to July 2018, and selected studies that assessed depression using a validated tool/scale, and allowed the calculation of the proportion of patients with low-grade inflammation (CRP >3 mg/L) or elevated CRP (>1 mg/L).

After quality assessment, 37 studies comprising 13 541 depressed patients and 155 728 controls were included. Based on the meta-analysis of 30 studies, the prevalence of low-grade inflammation (CRP >3 mg/L) in depression was 27% (95% CI 21–34%); this prevalence was not associated with sample source (inpatient, outpatient or population-based), antidepressant treatment, participant age, BMI or ethnicity. Based on the meta-analysis of 17 studies of depression and matched healthy controls, the odds ratio for low-grade inflammation in depression was 1.46 (95% CI 1.22–1.75). The prevalence of elevated CRP (>1 mg/L) in depression was 58% (95% CI 47–69%), and the meta-analytic odds ratio for elevated CRP in depression compared with controls was 1.47 (95% CI 1.18–1.82).

About a quarter of patients with depression show evidence of low-grade inflammation, and over half of patients show mildly elevated CRP levels. There are significant differences in the prevalence of low-grade inflammation between patients and matched healthy controls. These findings suggest that inflammation could be relevant to a large number of patients with depression.

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.

Prenatal infections have been proposed as a putative risk factor for a number of psychiatric outcomes across a continuum of severity. Evidence on eating disorders is scarce. We investigated whether exposure to prenatal maternal infections is associated with an increased risk of disordered eating and weight and shape concerns in adolescence in a large UK birth cohort.

We used data from the Avon Longitudinal Study of Parents and Children. The primary exposure was maternal experience of infections at any time in pregnancy. Study outcomes were presence of any, monthly or weekly disordered eating at 14 and 16 years of age, and weight and shape concerns at 14 years. We defined the causal effect of the exposure on these outcomes using a counterfactual framework adjusting our analyses for a number of hypothesised confounders, and imputing missing confounder data using multiple imputation.

In total, 4884 children had complete exposure and outcome data at age 14 years, and 4124 at 16 years. Exposed children had a greater risk of reporting weekly disordered eating at both age 14 [risk difference (RD) 0.9%, 95% confidence interval (CI) −0.01 to 1.9, p = 0.08] and 16 (RD 2.3%, 95% CI 0.6–3.9, p < 0.01), though evidence of an association was weak at age 14 years. Exposed children also had greater weight and shape concerns at age 14 years (mean difference 0.15, 95% CI 0.05–0.26, p < 0.01).

Exposure to prenatal maternal infection is associated with greater risk of disordered eating in adolescence. This association could be explained by in utero processes leading to impaired neurodevelopment or altered immunological profiles. Residual confounding cannot be excluded.

Recent studies suggest psychotic and eating disorders can be comorbid and could have shared genetic liability. However, this comorbidity has been overlooked in the epidemiological literature.

To test whether polygenic risk scores (PRS) for schizophrenia are associated with disordered eating behaviours and body mass index (BMI) in the general population.

Using data from the Avon Longitudinal Study of Parents and Children and random-effects logistic and linear regression models, we investigated the association between PRS for schizophrenia and self-reported disordered eating behaviours (binge eating, purging, fasting and excessive exercise) and BMI at 14, 16 and 18 years.

Of the 6920 children with available genetic data, 4473 (64.6%) and 5069 (73.3%) had at least one disordered eating and one BMI outcome measurement, respectively. An s.d. increase in PRS was associated with greater odds of having binge eating behaviours (odds ratio, 1.36; 95% CI 1.16–1.60) and lower BMI (coefficient, −0.03; 95% CI, −0.06 to −0.01).

Our findings suggest the presence of shared genetic risk between schizophrenia and binge eating behaviours. Intermediate phenotypes such as impaired social cognition and irritability, previously shown to be positively correlated in this sample with schizophrenia PRS, could represent risk factors for both phenotypes. Shared genetic liability between binge eating and schizophrenia could also explain higher rates of metabolic syndrome in individuals with schizophrenia, as binge eating could be a mediator of this association in drug-naïve individuals. The finding of an association between greater PRS and lower BMI, although consistent with existing epidemiological and genetic literature, requires further investigation.

None.

Cognitive ability and problem behaviour (externalising and internalising problems) are variable and inter-related in children. However, it is not known if they mutually influence one another, if difficulties in one cause difficulties in the other, or if they are related only because they share causes.

Random-intercept cross-lagged models adjusted for confounding were fitted to explore this in 17,318 (51% male) children of the UK’s Millennium Cohort Study at ages 3, 5, 7, 11 and 14 years. Externalising and internalising problems were assessed using the parent-reported Strengths and Difficulties Questionnaire. Cognitive ability was measured using standardised scores of age-appropriate validated cognitive ability assessments. Where multiple cognitive assessments were available a single score was derived using principal components analysis.

There was much evidence for cross-domain longitudinal effects in childhood, especially for cognitive ability (on both internalising and externalising problems and in both males and females) and externalising problems (on internalising problems in both genders and cognitive ability in males). Bidirectional effects were childhood-limited, gender-specific and less consistent. The consistent bidirectional associations were, in males, between externalising problems and cognitive ability, and, in females, between externalising and internalising problems (although the effects of internalising problems were weak). In adolescence, only externalising problems had cross-domain effects such that, in both genders, they were associated with lower cognitive ability in subsequent measurements and increased levels of internalising problems.

In either childhood or adolescence, reducing behavioural problems could have both emotional and cognitive benefits. In childhood, improving cognitive skills could reduce both emotional and behavioural problems.

We assessed whether the risk of various psychotic disorders and non-psychotic bipolar disorder (including mania) varied by migrant status, a region of origin, or age-at-migration, hypothesizing that risk would only be elevated for psychotic disorders.

We established a prospective cohort of 1 796 257 Swedish residents born between 1982 and 1996, followed from their 15th birthday, or immigration to Sweden after age 15, until diagnosis, emigration, death, or end of 2011. Cox proportional hazards models were used to model hazard ratios by migration-related factors, adjusted for covariates.

All psychotic disorders were elevated among migrants and their children compared with Swedish-born individuals, including schizophrenia and schizoaffective disorder (adjusted hazard ratio [aHR]migrants: 2.20, 95% CI 1.96–2.47; aHRchildren : 2.00, 95% CI 1.79–2.25), affective psychotic disorders (aHRmigrant1.42, 95% CI 1.25–1.63; aHRchildren: 1.22 95% CI 1.07–1.40), and other non-affective psychotic disorders (aHRmigrant: 1.97, 95% CI 1.81–2.14; aHRchildren: 1.68, 95% CI 1.54–1.83). For all psychotic disorders, risks were generally highest in migrants from Africa (i.e. aHRschizophrenia: 5.24, 95% CI 4.26–6.45) and elevated at most ages-of-migration. By contrast, risk of non-psychotic bipolar disorders was lower for migrants (aHR: 0.58, 95% CI 0.52–0.64) overall, and across all ages-of-migration except infancy (aHR: 1.20; 95% CI 1.01–1.42), while risk for their children was similar to the Swedish-born population (aHR: 1.00, 95% CI 0.93–1.08).

Increased risk of psychiatric disorders associated with migration and minority status may be specific to psychotic disorders, with exact risk dependent on the region of origin.

Depressive symptoms and inflammation are risk factors for cardiovascular disease (CVD) and mortality. We investigated the combined association of these factors with the prediction of CVD and all-cause mortality in a representative cohort of older men and women.

We measured C-reactive protein (CRP) and depressive symptoms in 5328 men and women aged 52–89 years in the English Longitudinal Study of Ageing. Depressive symptoms were measured using the eight-item Centre for Epidemiological Studies Depression Scale. CRP was analysed from peripheral blood. Mortality was ascertained from national registers and associations with depressive symptoms and inflammation were estimated using Cox proportional hazard models.

We identified 112 CVD related deaths out of 420 all-cause deaths in men and 109 CVD related deaths out of 334 all-cause deaths in women over a mean follow-up of 7.7 years. Men with both depressive symptoms and high CRP (3–20 mg/L) had an increased risk of CVD mortality (hazard ratio; 95% confidence interval: 3.89; 2.04–7.44) and all-cause mortality (2.40; 1.65–3.48) after adjusting for age, socioeconomic variables and health behaviours. This considerably exceeds the risks associated with high CRP alone (CVD 2.43; 1.59–3.71, all-cause 1.49; 1.20–1.84). There was no significant increase in mortality risk associated with depressive symptoms alone in men. In women, neither depressive symptoms or inflammation alone or the combination of both significantly predicted CVD or all-cause mortality.

The combination of depressive symptoms and increased inflammation confers a considerable increase in CVD mortality risk for men. These effects appear to be independent, suggesting an additive role.

Anxiety disorders are prevalent yet under-recognized in late life. We examined the prevalence of anxiety disorders in a representative sample of community dwelling older adults in Hong Kong.

Data on 1,158 non-demented respondents aged 60–75 years were extracted from the Hong Kong Mental Morbidity survey (HKMMS). Anxiety was assessed with the revised Clinical Interview Schedule (CIS-R).

One hundred and thirty-seven respondents (11.9%, 95% CI = 10–13.7%) had common mental disorders with a CIS-R score of 12 or above. 8% (95% CI = 6.5–9.6%) had anxiety, 2.2% (95% CI = 1.3–3%) had an anxiety disorder comorbid with depressive disorder, and 1.7% (95% CI = 1–2.5%) had depression. Anxious individuals were more likely to be females (χ 2 = 25.3, p < 0.001), had higher chronic physical burden (t = −9.3, p < 0.001), lower SF-12 physical functioning score (t = 9.2, p < 0.001), and poorer delayed recall (t = 2.3, p = 0.022). The risk of anxiety was higher for females (OR 2.8, 95% C.I. 1.7–4.6, p < 0.001) and those with physical illnesses (OR 1.4, 95% C.I. 1.3–1.6, p < 0.001). The risk of anxiety disorders increased in those with disorders of cardiovascular (OR 1.9, 95% C.I. 1.2–2.9, p = 0.003), musculoskeletal (OR 2.0, 95% C.I. 1.5–2.7, p < 0.001), and genitourinary system (OR 2.0, 95% C.I. 1.3–3.2, p = 0.002).

The prevalence of anxiety disorders in Hong Kong older population was 8%. Female gender and those with poor physical health were at a greater risk of developing anxiety disorders. Our findings also suggested potential risk for early sign of memory impairment in cognitively healthy individuals with anxiety disorders.

Pathways from early-life conduct problems to young adult depression remain poorly understood.

To test developmental pathways from early-life conduct problems to depression at age 18.

Data (n = 3542) came from the Avon Longitudinal Study of Parents and Children (ALSPAC). Previously derived conduct problem trajectories (ages 4–13 years) were used to examine associations with depression from ages 10 to 18 years, and the role of early childhood factors as potential confounders.

Over 43% of young adults with depression in the ALSPAC cohort had a history of child or adolescent conduct problems, yielding a population attributable fraction of 0.15 (95% CI 0.08–0.22). The association between conduct problems and depression at age 18 was considerable even after adjusting for prior depression (odds ratio 1.55, 95% CI 1.24–1.94). Early-onset persistent conduct problems carried the highest risk for later depression. Irritability characterised depression for those with a history of conduct problems.

Early-life conduct problems are robustly associated with later depressive disorder and may be useful targets for early intervention.

1. Understand the difference between process measurement and outcome measurement.
2. Understand the limitation of using outcome measures to assess and promote quality of services.
3. Understand the difficulties in assessing the psychometric properties and validity of outcome measures.

Some studies have found an association between elevated cortisol and subsequent depression, but findings are inconsistent. The cortisol awakening response may be a more stable measure of hypothalamic–pituitary–adrenal function and potentially of stress reactivity.

To investigate whether salivary cortisol, particularly the cortisol awakening response, is associated with subsequent depression in a large population cohort.

Young people (aged 15 years, n = 841) from the Avon Longitudinal Study of Parents and Children (ALSPAC) collected salivary cortisol at four time points for 3 school days. Logistic regression was used to calculate odds ratios for developing depression meeting ICD-10 criteria at 18 years.

We found no evidence for an association between salivary cortisol and subsequent depression. Odds ratios for the cortisol awakening response were 1.24 per standard deviation (95% CI 0.93–1.66, P = 0.14) before and 1.12 (95% CI 0.73–1.72, P = 0.61) after adjustment for confounding factors. There was no evidence that the other cortisol measures, including cortisol at each time point, diurnal drop and area under the curve, were associated with subsequent depression.

Our findings do not support the hypothesis that elevated salivary cortisol increases the short-term risk of subsequent depressive illness. The results suggest that if an association does exist, it is small and unlikely to be of clinical significance.