We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Recent changes to US research funding are having far-reaching consequences that imperil the integrity of science and the provision of care to vulnerable populations. Resisting these changes, the BJPsych Portfolio reaffirms its commitment to publishing mental science and advancing psychiatric knowledge that improves the mental health of one and all.
Irritability is a common symptom in children and adolescents, often resulting in referral to mental health services and is associated with depression. Depression in adolescents and adults at familial risk of, and with depression, is associated with reduced risk-taking on the Cambridge Gambling Task (CGT) particularly when the chance of winning is high. However, little is known about risk-taking in irritability. This study tests the hypothesis that increased irritability is longitudinally associated with later risk-taking behaviour on the CGT; specifically, that increasing irritability is associated with lower risk-taking when the chance of a favourable outcome is high.
Methods
We conducted a longitudinal study of the biological offspring of parents of children with depression (n = 337). Irritability, the exposure, was measured at wave one using the Child and Adolescent Psychiatric Assessment (CAPA). The primary outcome was risk-taking to obtain reward at varying probability ratios (6:4, 7:3, 8:2 and 9:1) measured by the Cambridge Gambling Task (CGT) at waves two and three. We investigated the longitudinal association between irritability at wave one and average risk-taking at each ratio across waves two and three using multi-level models. The extent to which risk-taking according to probability ratio varied with irritability was tested with interaction terms. We ran univariable models and then multivariable models.
Results
In univariable (n = 207; Coef. 0.006, 95%CI −0.011–0.023, p = 0.470), and fully adjusted (Coef. 0.011, 95%CI −0.007–0.029, p = 0.213) models there was no evidence of a main association between irritability and risk-taking on the CGT. There was evidence of an interaction between irritability and risk-taking ratio (p = 0.019). In fully adjusted models including the interaction, a one-point increase in irritability was associated with relatively higher risk-taking at the less favourable ratios (6:4 – 0.018 (95%CI −0.002–0.037) and 7:3 – 0.015 (95%CI −0.005–0.035)) relative to the more favourable ratios (9:1 – 0.001 (95%CI −0.019–0.021) and 8:1 – 0.011 (95%CI −0.008-0.031)).
Conclusion
We found no evidence of relationship between irritability and subsequent risk-taking on the CGT overall. However, there was some evidence that those with higher irritability were relatively more risk-taking when less likely to win compared with when a favourable outcome was more likely. These findings warrant further investigation of the association between prior irritability and later depression in a larger community cohort. If prior irritability and depression are both associated with risk-taking, this strengthens the case for focussing on risk-taking as a potential target for preventive intervention.
The prevalence of emotional problems, such as depressive and anxiety disorders, increases sharply during adolescence. There is evidence for familial clustering of mental health problems during early childhood and adulthood, however no studies have investigated whether adolescent mental health problems cluster within families. This study tests the hypotheses that i) emotional problems during adolescence cluster within families, and that ii) conduct, peer and hyperactivity problems, prosocial behaviour and overall emotional and behavioural difficulties during adolescence also cluster within families.
Methods
We used cross-sectional data from a nationally representative survey of UK households, collected between 2019 and 2021, with 4,088 participants aged 10–16 years. Analyses included 1,241 participants who had complete outcome data and complete data on all covariates of interest. The Strengths and Difficulties Questionnaire (SDQ) was used to examine emotional problems, as well as conduct, peer and hyperactivity problems, prosocial behaviour and total difficulties. Multilevel modelling was used to: estimate clustering of i) emotional problems and ii) conduct, peer and hyperactivity problems, prosocial behaviour and total difficulties, within families, after adjusting for several individual- and family-level covariates associated with adolescent mental health problems (including individual and family demographics, school and sibling bullying, quality of parent-child relationship, parent mental health and parent romantic relationship satisfaction).
Results
After adjusting for known covariates of adolescent mental health problems, there was substantial clustering of adolescent emotional problems (ICC: 0.439; CI95%: 0.36–0.52; SE: 0.042) and overall adolescent emotional and behavioural difficulties (ICC: 0.417; CI95%: 0.34–0.50; SE: 0.043) within families. There was also evidence of clustering of adolescent peer problems (ICC: 0.374; CI95%: 0.28–0.48; SE: 0.051), hyperactivity (ICC: 0.332; CI95%: 0.25–0.42; SE: 0.044), prosocial behaviour (ICC: 0.263; CI95%: 0.18–0.37; SE: 0.048) and conduct problems (ICC: 0.232; CI95%: 0.14–0.35; SE: 0.053) within families after adjustment.
Conclusion
We found strong evidence that adolescent emotional problems cluster within families even after accounting for individual- and family-level covariates which are associated with adolescent mental health problems. Over 40% of the variation was accounted for at the family level. This indicates how the contextual characteristics of the family environment may influence the mental health of young people. As such, social policy aiming to prevent or improve the mental health of young people should focus on family context.
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.
Methods
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.
Results
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).
Conclusion
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.
Methods
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.
Results
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).
Conclusion
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.
Children and young people (CYP) with intellectual and developmental disabilities (IDD) of known genetic origin experience complex physical and mental health problems; IMAGINE-ID has followed a national UK cohort from childhood to early adulthood. Parents completed structured online psychiatric assessments on repeated occasions. From these assessments, semi-automated personalised reports were generated summarising each child's strengths and difficulties, in collaboration with IMAGINE ID participants and the charity UNIQUE.
We aimed to discover whether providing a structured summary of our mental health and behavioural assessments would be beneficial to families of children with rare genetic conditions and IDD.
Methods
574 of the CYP's caregivers completed an online ‘impact’ survey, five years after receiving their initial report, comprising four areas of potential benefit: Quality of Care (whether the report led to an improvement in the child's quality of mental and/or physical health care); Social Impact (whether the report was used as evidence to support an EHCP, disability benefits etc.), Psychological Impact (whether it led to any change in understanding of the child's condition), and Referrals (whether the report led to a referral for Autism/ADHD etc.). We also invited qualitative feedback.
Results
82% of respondents rated the reports as helpful. 35% reported they had led to an improvement in their CYP's quality of care, 24% reported social impact using the report as supporting evidence, 99% reported a psychological impact – a change in their understanding of the child, and 17% used the report to initiate a referral for an assessment of ADHD and/or autism. In our qualitative analysis, families who found the report helpful mentioned it led to ‘reflection’ on their child's condition and that it provided ‘access to benefits’. For those who did not find the report helpful, issues such as ‘it lacked professional input’ and ‘forgetting the contents’ of the report were identified.
Conclusion
Personalised summary reports, based on a structured assessment of their child's behavioural, social and emotional adjustment, are valued by families of children with rare genetic conditions and IDD and can bring about tangible benefits to the child and the family's access to resources.
Edited by
David Kingdon, University of Southampton,Paul Rowlands, Derbyshire Healthcare NHS foundation Trust,George Stein, Emeritus of the Princess Royal University Hospital
Depression is a leading cause of disability in high- and middle-income countries and is of increasing relative burden in low-income countries. The Global Burden of Disease study illustrates how depression is increasing as a proportion of all the disabilities resulting from illness. This is because we know how to prevent other major causes of disability such as cardiovascular disease and infection and so their incidence is on the decline. Meanwhile, there is evidence that rates of depression are rising slightly. In order to have an impact on this major public health burden, we will need to devise preventative strategies to reduce the incidence. As depression is a continuum, much of the disability is experienced by the larger numbers of those with mild and moderate levels of depression who might not seek treatment for themselves. Therefore, effective preventative strategies applied to the whole population will have more widespread benefits than interventions simply targeted towards those at high risk. In order to develop preventative interventions, we need to know what causes depression.
Epidemiology tends to be primarily concerned with causes outside the individual or with genetic causes.
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.
Methods
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.
Results
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.
Conclusions
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.
Funding
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).
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.
Methods
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.
Results
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.
Conclusions
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.
To identify correlates of anaemia during the first trimester of pregnancy among 366 urban South Indian pregnant women.
Design
Cross-sectional study evaluating demographic, socio-economic, anthropometric and dietary intake data on haematological outcomes.
Setting
A government maternity health-care centre catering predominantly to the needs of pregnant women from the lower socio-economic strata of urban Bangalore.
Subjects
Pregnant women (n 366) aged ≥18 and ≤40 years, who registered for antenatal screening at ≤14 weeks of gestation.
Results
Mean age was 22·6 (sd 3·4) years, mean BMI was 20·4 (sd 3·3) kg/m2 and 236 (64·5 %) of the pregnant women were primiparous. The prevalence of anaemia (Hb <11·0 g/dl) was 30·3 % and of microcytic anaemia (anaemia with mean corpuscular volume <80 fl) 20·2 %. Mean dietary intakes of energy, Ca, Fe and folate were well below the Indian RDA. In multivariable log-binomial regression analysis, anaemia was independently associated with high dietary intakes of Ca (relative risk; 95 % CI: 1·79; 1·16, 2·76) and P (1·96; 1·31, 2·96) and high intake of meat, fish and poultry (1·94; 1·29, 2·91).
Conclusions
Low dietary intake of multiple micronutrients, but higher intakes of nutrients that inhibit Fe absorption such as Ca and P, may help explain high rates of maternal anaemia in India.
Recommend this
Email your librarian or administrator to recommend adding this to your organisation's collection.