61 research outputs found

    Decision-Making in Childhood Predicts Prodromal Eating Pathology in Adolescence

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    OBJECTIVE: Differences in decision-making under conditions of risk have been observed cross-sectionally in clinical groups of people with eating disorders but have never been studied longitudinally or in large cohorts. We investigated whether responses on the Cambridge Gambling Task (CGT), measured in the Millennium Cohort Study in childhood, would predict prodromal eating pathology in adolescence. METHOD: Regression models were built to explore relationships between CGT variables at age 11 years and prodromal eating pathology (body dissatisfaction, intention to lose weight, dietary restriction, significant under/overweight, and excessive exercise) at 14 years. RESULTS: In 11,303 boys and girls, those with better quality decision-making were 34% less likely to show an intention to lose weight (b = -0.40, odds ratio [OR] = 0.66, p < 0.05) and 34% less likely to be overweight (b = -0.41, relative risk ratio [RRR] = 0.66, p < 0.05). Those with higher risk-taking were 58% more likely to report dietary restriction (b = 0.45, OR = 1.58, p < 0.05) and 46% more likely to report excessive exercise (b = 0.38, OR = 1.46, p < 0.05). In the complete-cases sample, higher risk-adjustment scores were associated with a 47% increased risk of underweight (b = 0.39, RRR = 1.47, p < 0.05), and better quality of decision-making was associated with a 46% lower risk of overweight (b = -0.60, RRR = 0.54, p < 0.05). CONCLUSION: Disadvantageous decision-making in childhood may predict prodromal eating pathology in adolescence and might represent a prevention target

    Decision-making difficulties mediate the association between poor emotion regulation and eating disorder symptoms in adolescence

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    BACKGROUND: The emergence of eating problems during childhood increases the risk for eating disorders (EDs) during young adulthood. Previous studies highlight a relationship between poor self-regulation and onset of eating pathology. In this study, we investigated whether this association is mediated by decision-making difficulties. METHODS: To test this hypothesis, we used data from the Millennium Cohort Study. Decision-making performance was assessed with the Cambridge Gambling Task at age 11. Principal components analysis was used to derive an index of ED symptoms at age 14. The trajectories of scores of two subscales of the Child Social Behaviour Questionnaire, Independence and Self-Regulation (ISR) and Emotional Dysregulation (EmotDy), were modelled from ages 3 to 7 years in a latent growth curve analysis. The individual predicted values of the intercept (set at baseline, 3 years) and the slope (rate of annual change) were then used in the mediation analysis. RESULTS: In our sample of 11 303 individuals, there was evidence for mediation by three measures of decision-making at age 11 (poor quality of decision-making, delay aversion and low risk-adjustment) in the association between EmotDy across ages 3–7 and ED symptoms at age 14 even after the adjustment for relevant covariates. We found no evidence of association between ISR and ED symptoms. CONCLUSION: Our findings suggest that emotion regulation processes during childhood may be relevant for the future onset of ED symptoms via their association with decision-making skills. These findings, obtained from a large, representative, sample, shed light on the relationship between self-regulation, decision-making and symptoms of EDs

    The role of inflammation in the effects of peer victimisation and stressful life events on mental health in childhood

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    Background: Peer victimisation represents a salient stressor during childhood. However, studies investigating the mechanism of its impact on children’s mental health typically examine socio-cognitive factors as mediators. The current study sought to provide novel insight through testing a potential biological mechanism, inflammation. It also tested for pathway-specific effects by comparing how inflammation may mediate the effect of peer victimisation and that of another important stressor in childhood: adverse life events. Method: Data from 4,583 participants of the Avon Longitudinal Study of Parents and Children (ALSPAC) were used. Path analysis was carried out to investigate whether inflammation (IL-6 and CRP) at age 9 years mediates the effect of peer victimisation and stressful life events at age 8 years on internalising (peer and emotional) or externalising (hyperactivity and conduct) problems (measured at age 11 years), both before and after adjustment for potential confounders. Results: IL-6 partially mediated the effect of peer victimisation on peer problems, even after adjustment for potential confounders. Inflammation did not mediate the effect of stressful life events on either type of internalising problems. Neither stressor predicted externalising problems via inflammation. Conclusion: We did not find evidence that inflammation mediates the effect of stressful life events on mental health in childhood when they are considered alongside experiences of peer victimisation. Inflammation may already represent a form of biological embedding of peer victimisation in the early years

    Does decision-making at age 11 predict prodromal eating pathology at ages 14 and 17? A prospective, observational, UK population-based cohort study

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    OBJECTIVES: We examined whether decision-making at age 11 and 14 is associated with prodromal eating pathology at age 14 and whether it would persist across adolescence and also be present at age 17. DESIGN: This prospective, observational, population-based cohort study used a longitudinal design. SETTING: Data from the Millennium Cohort Study (MCS), a UK longitudinal cohort study involving 19 244 families from England, Scotland, Wales and Northern Ireland, were analysed. PARTICIPANTS: We modelled data from 8922 boys and girls aged 11, 14 and 17 (MCS sweeps 5, 6 and 7). PRIMARY AND SECONDARY OUTCOMES: We investigated decision-making using the risk-taking, quality of decision-making, deliberation time, delay aversion and risk adjustment subscales of the Cambridge Gambling Task and prodromal eating pathology through binary response items measuring: body dissatisfaction (whether the participant perceived their body as being too overweight); intention to lose weight (whether participants reported a strong desire to lose weight); dietary restriction (whether participants reported actively eating less to influence their shape/weight) and excessive exercise (whether participants reported exercising in a driven way in order to influence weight/shape). Data were analysed using latent class analysis and logistic regression. RESULTS: Lower scores on quality of decision-making (OR=0.46) and deliberation time (OR=0.99) at age 14 were associated with prodromal eating pathology at both ages 14 and 17 (all p<0.05), indicating an association between less frequently opting to bet on the most likely outcome and taking less time to decide on which bet to choose and the persistence of prodromal eating pathology over adolescence. Lower deliberation time (OR=0.99) and delay aversion (OR=0.62) at 11 and lower risk-taking scores at 14 (OR=0.43) were associated with the absence of prodromal eating pathology at 14 and 17 (all p<0.05), indicating that a moderate approach under conditions of risk in childhood and mid-adolescence is associated with reduced eating pathology across adolescence. CONCLUSIONS: Training advantageous decision-making might protect from later prodromal eating pathology

    Types of Eating Disorder Prodrome in Adolescence: The Role of Decision Making in Childhood

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    Psychiatric disorders like eating disorders (EDs) might be underpinned by differences in decision making. However, little previous research has investigated this potential relationship using longitudinal data. This study aimed to understand how components of decision making (delay aversion, risk adjustment, risk taking, quality of decision making and deliberation time) measured by the Cambridge Gambling Task in the United Kingdom’s Millennium Cohort Study (MCS; n = 11,303; female = 50.17%) at age 11 might explain clusters/types of ED prodrome involving body dissatisfaction, intention to lose weight, dietary restraint, excessive exercise and significant under/overweight measured in the MCS at age 14. Latent class analysis revealed two groups within the cohort: a non-prodromal eating pathology group, who were more likely to be of “average” weight, according to the UK90, with minimal disordered attitudes and behaviors in relation to eating and weight; and a second group with prodromal eating pathology, who had more body dissatisfaction, a desire to lose weight, were using dietary restriction and exercise to influence weight and were more likely to be “overweight” according to the UK90. Logistic regression showed that, after adjustment for confounding, higher risk-taking scores were associated with a 60% greater probability of being in the prodromal eating pathology group (b = 0.47, OR = 1.60, p &amp;lt; 0.01), and higher scores on quality of decision making were associated with a 30% lower probability of being in the prodromal eating pathology group (b = −0.34, OR = 0.70, p &amp;lt; 0.05). Helping young people to engage in moderate risk taking and improving decision making might reduce the later presence of ED prodromes

    The role of the built environment in the trajectories of cognitive ability and mental health across early and middle childhood: Results from a street audit tool in a general-population birth cohort

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    The research exploring the association between the built environment and children's mental health and cognitive abilities has produced mixed results. This may be due to the inconsistency in the approach taken to describe the built environment. This study, using data from the Millennium Cohort Study (MCS), a large general-population birth cohort, considered simultaneously several measures to describe it when the participant child was 3 years old, including neighbourhood disorder (assessed by an MCS interviewer by direct observation of several physical and social aspects of the immediate neighbourhood), area green space, air pollution, urbanicity and neighbourhood socio-economic disadvantage. It then explored its role in the trajectory of mental health (measured with the Strengths and Difficulties Questionnaire-SDQ) and cognitive ability (measured with the British Ability Scales-BAS) across ages 3–11 years in 4454 children of stayer families in England. Using growth curve modelling we found that neighbourhood disorder was associated with emotional symptoms and conduct problems at age 3 and with the trajectory of cognitive ability from ages 3 to 11. These associations were robust to controls for quality of the indoor housing environment and parental mental health and socio-economic status. Neither green space nor air pollution had any effect on our outcomes. Our findings shed light on the importance of specific aspects of the built environment for mental health and cognition during childhood. They also highlight the value of using direct observation of the immediate neighbourhood.The research exploring the association between the built environment and children's mental health and cognitive abilities has produced mixed results. This may be due to the inconsistency in the approach taken to describe the built environment. This study, using data from the Millennium Cohort Study (MCS), a large general-population birth cohort, considered simultaneously several measures to describe it when the participant child was 3 years old, including neighbourhood disorder (assessed by an MCS interviewer by direct observation of several physical and social aspects of the immediate neighbourhood), area green space, air pollution, urbanicity and neighbourhood socio-economic disadvantage. It then explored its role in the trajectory of mental health (measured with the Strengths and Difficulties Questionnaire-SDQ) and cognitive ability (measured with the British Ability Scales-BAS) across ages 3–11 years in 4454 children of stayer families in England. Using growth curve modelling we found that neighbourhood disorder was associated with emotional symptoms and conduct problems at age 3 and with the trajectory of cognitive ability from ages 3 to 11. These associations were robust to controls for quality of the indoor housing environment and parental mental health and socio-economic status. Neither green space nor air pollution had any effect on our outcomes. Our findings shed light on the importance of specific aspects of the built environment for mental health and cognition during childhood. They also highlight the value of using direct observation of the immediate neighbourhood

    The role of inflammatory markers and cortisol in the association between early social cognition abilities and later internalising or externalising problems: Evidence from a U.K. birth cohort

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    Objective: Deficits in social cognition are associated with internalising (emotional and peer problems) and externalising (conduct problems and hyperactivity/inattention) symptoms in youth. It has been suggested that stress may be one of the mechanisms underlying these associations. However, no empirical studies have investigated if physiological stress can explain the prospective associations between social cognition deficits and internalising and externalising symptoms in the general youth population. This study addressed this question and focused on two indicators of physiological stress, dysregulated diurnal cortisol patterns and systemic inflammation. Method: Participants were 714 individuals from the Avon Longitudinal Study of Parents and Children (ALSPAC), a UK population-based birth cohort. Bayesian structural equation modelling was used to investigate a) the associations of social cognition abilities at ages 8, 11, and 14 years with internalising and externalising problems at age 17 years and b) the potential mediating effects of cortisol parameters at age 15 years and inflammatory markers [interleukin 6 (IL-6) and C-reactive protein (CRP)] at ages 9 and 16 years. Results: We found that social cognition difficulties were associated with later internalising and externalising problems. Flattened diurnal cortisol slope was associated with hyperactivity/inattention problems two years later. Lower morning cortisol partially mediated the direct association between social communication deficits at 8 years and hyperactivity/inattention and conduct problems at 17 years, even after adjustments for inflammation and confounders (for hyperactivity/inattention: indirect effect = 0.07, 95% CI [0.00, 0.18], p = .042; for conduct problems: indirect effect = 0.04, 95% CI [0.00, 0.11], p = .040). We did not find a significant association between systemic inflammation and social cognition difficulties, internalising problems, or externalising problems. Conclusion: Our findings suggest that part of the effect of social communication difficulties in childhood on externalising problems in adolescence was mediated by lower morning cortisol. Hence, our study indicates that the hypoactivity of the hypothalamic-pituitary-adrenal (HPA) axis may be one of the physiological mechanisms linking some social cognition deficits to externalising problems

    Internalising symptoms mediate the longitudinal association between childhood inflammation and psychotic-like experiences in adulthood

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    Psychotic-like experiences (PLEs) are part of a continuum of psychosis. Previous longitudinal studies highlighted a relationship between peripheral inflammation during childhood and onset of PLEs in adulthood. In this study, we tested if this association is mediated by internalising and externalising symptoms experienced during childhood and adolescence. To test this hypothesis, we used data from the Avon Longitudinal Study of Parents and Children (ALSPAC). We investigated a subsample of 4525 individuals from this cohort with data on interleukin 6 (IL-6) and C-reactive protein (CRP) in childhood (age 9 years). We measured PLEs at age 18 years, and we used latent growth curve modelling to estimate longitudinal trajectories of internalising and externalising symptoms from ages 9 to 16 years. The individual predicted values of the intercept (set at baseline, 9 years) and the slope (rate of annual change) were then used in the mediation analysis. There was evidence for full mediation by the intercept of internalising symptoms. Our findings suggest that inflammation during childhood may be relevant for the future onset of PLEs via its association with a high level of internalising symptoms. These findings, although obtained from a non-clinical population, provide an additional step in advancing knowledge on the relationship between inflammation and symptoms of the psychosis continuum

    Investigating the link between drug-naive first episode psychoses (FEPs), weight gain abnormalities and brain structural damages: Relevance and implications for therapy

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    Evidence suggests that obesity and overweight may be associated with severe brain structural abnormalities and poor cognitive and functional outcomes in the general population. Despite these observations and the high prevalence of weight gain abnormalities in patients with psychosis spectrum disorders (PSDs), no studies have investigated the impact that these metabolic disturbances may have on brain structures and development in the earliest stages of PSDs. In the present review we shed light on the association between weight gain and brain structural abnormalities that may affect the course of illness in drug-naïve FEPs. Given the lack of studies directly investigating this issue, we firstly identified and critically evaluated the literature assessing weight gain abnormalities and gray or white matter (GM, WM) volumes (either globally or in specific regions of interest) in otherwise healthy obese/overweight adolescents and young adults. We then compared the results of this systematic review with those of two recent meta-analysis investigating GM and WM abnormalities in drug-naïve FEPs. Weight gain in otherwise healthy subjects was consistently associated with frontal and temporal GM atrophy and with reduced integrity of WM in the corpus callosum. Of relevance, all these brain regions are affected in drug-naïve FEPs, and their integrity is associated with clinical, cognitive and functional outcomes. The underlying mechanisms that may explain the association between weight gain, adiposity, and brain damage in both healthy subjects and drug-naïve FEPs are widely discussed. On the basis of this knowledge, we tried: a) to deduce an integrative model for the development of obesity in psychosis spectrum disorders; b) to identify the key vulnerability factors underlying the association between weight gain and psychosis; c) to provide information on new potential targets of intervention

    Prefronto-cerebellar transcranial direct current stimulation increases amplituded and decreases latency of P3b component in patients with euthymic bipolar disorder

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    INTRODUCTION: Neurocognitive impairments have been observed in patients with bipolar disorder (BD) even during the euthymic phase of the disease, potentially representing trait-associated rather than state-associated characteristics of the disorder. In the present study, we used transcranial direct current stimulation (tDCS) applied to cerebellar and prefrontal cortices to improve the neurophysiological performances of patients with euthymic BD. METHODS: Twenty-five outpatients with BD underwent open-label prefrontocerebellar tDCS for 3 consecutive weeks. Neurophysiological performances were assessed through the examination of the P3b and P3a subcomponents of P300 event-related potential at baseline and after stimulation. RESULTS: Compared to baseline, P3b component after tDCS showed significantly higher amplitude and shorter latency (latency: Fz P=0.02, Cz P=0.03, and Pz P=0.04; amplitude: Fz P=0.24, Cz P=0.02, and Pz P=0.35). CONCLUSION: In our sample of patients with euthymic BD, concomitant prefrontoexcitatory and cerebellar-inhibitory modulations led to improved brain information processing stream. This improvement may at least partially result from neuroplastic modulation of prefrontocerebellar circuitry activity
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