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Background Methods Results Conclusions Population‐based studies have observed sex biases in the diagnosis and treatment of attention‐deficit hyperactivity disorder (ADHD). Females are less likely to be diagnosed or prescribed ADHD medication. This study uses national healthcare records, to investigate sex differences in diagnosis and clinical care in young people with ADHD, particularly regarding recognition and treatment of other mental health conditions.The cohort included individuals diagnosed with ADHD, born between 1989 and 2013 and living in Wales between 2000 and 2019. Routine primary and secondary healthcare record data were used to derive diagnoses of ADHD and other neurodevelopmental and mental health conditions, as well as ADHD and antidepressant medications. Demographic variables included ethnicity, socioeconomic deprivation and contact with social services.There were 16,458 individuals diagnosed with ADHD (20.3% females, ages 3–30 years), with a male‐to‐female ratio of 3.9:1. Higher ratios (4.8:1) were seen in individuals diagnosed younger (<12 years), with the lowest ratio (1.9:1) in those diagnosed as adults (>18). Males were younger at first recorded ADHD diagnosis (mean = 10.9 vs. 12.6 years), more likely to be prescribed ADHD medication and younger at diagnosis of co‐occurring neurodevelopmental conditions. In contrast, females were more likely to receive a diagnosis of anxiety, depression or another mental health condition and to be prescribed antidepressant medications, prior to ADHD diagnosis. These sex differences were largely stable across demographic groups.This study adds to the evidence base that females with ADHD are experiencing later recognition and treatment of ADHD. The results indicate that this may be partly because of diagnostic overshadowing from other mental health conditions, such as anxiety and depression, or initial misdiagnosis. Further research and dissemination of findings to the public are needed to improve awareness, timely diagnosis and treatment of ADHD in females. [ABSTRACT FROM AUTHOR]

Purpose: Relative age within the school year ('relative age') is associated with increased rates of symptoms and diagnoses of mental health disorders, including ADHD. We aimed to investigate how relative age influences mental health and behaviour before, during and after school (age range: 4–25 years). Method: We used a regression discontinuity design to examine the effect of relative age on risk of mental health problems using data from a large UK population‐based cohort (Avon Longitudinal Study of Parents and Children (ALSPAC); N = 14,643). We compared risk of mental health problems between ages 4 and 25 years using the parent‐rated Strengths and Difficulties Questionnaire (SDQ), and depression using self‐rated and parent‐rated Short Mood and Feelings Questionnaire (SMFQ) by relative age. Results: The youngest children in the school year have greater parent‐rated risk of mental health problems, measured using parent‐rated SDQ total difficulties scores. We found no evidence of differences before school entry [estimated standardised mean difference (SMD) between those born on 31 August and 1 September:.02 (−.05,.08)]. We found that estimates of effect size for a 1‐year difference in relative age were greatest at 11 years [SMD:.22 (.15,.29)], but attenuated to the null at 25 years [SMD: −.02 (−.11,.07)]. We did not find consistent evidence of differences in self‐rated and parent‐rated depression by relative age. Conclusions: Younger relative age is associated with poorer parent‐rated general mental health, but not symptoms of depression. [ABSTRACT FROM AUTHOR]

Background: Attention‐deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are generally considered early‐onset disorders so most research has therefore tended to focus on children. Differences between ADHD/ASD in adult life and childhood have been noted, but few population‐based studies have examined them in adulthood. Furthermore, the interpretation of findings is hampered by changes in measure and from parent report to self‐report. Method: We examined continuous/trait measures of parent‐ and self‐rated ADHD and ASD in adulthood (age 25 years) in a UK prospective longitudinal sample ALPSAC (the Avon Longitudinal Study of Parents and Children), using many of the same measures that parents reported on in childhood (N = 6,064). Our aim was to investigate these traits in this population for mean‐level sex differences, overlaps with other cognitive, learning and communication problems and their associations with polygenic risk scores (PRS) for neuropsychiatric disorders (ADHD, ASD, schizophrenia, depression and anxiety). Results: ADHD and ASD traits in adulthood, as in childhood, showed associations with childhood cognitive, learning and communication problems and adult communication/language measures, although less so for self‐ratings than parent‐ratings. Males had higher ADHD and ASD trait levels, but this was not as marked as in childhood. In adulthood, ADHD (both parent‐ and self‐rated) and ASD (parent‐rated) symptoms showed associations with ADHD PRS; self‐reported ADHD also showed association with depression PRS, whereas self‐reported ASD did not show strong PRS associations. Conclusions: Our findings suggest that in young adults, ADHD and ASD symptoms have similar characteristics as they do in childhood. Associations with other cognitive, learning and communication problems, and ADHD PRS were somewhat less pronounced for self‐reported adult ADHD and ASD symptoms, suggesting that even at age 25, parent reports, where available, could be clinically useful. [ABSTRACT FROM AUTHOR]

Background: Adult ADHD has been assumed to be a continuation of childhood‐onset ADHD. However, recent studies have identified individuals with ADHD in adulthood who have not had ADHD in childhood. Whether or not these individuals have a ‘typical’ neurodevelopmental profile is not clear. Methods: We tested two explanations for the emergence of apparent late‐onset ADHD symptomatology using the ALSPAC epidemiological cohort, by grouping individuals according to their scores on the Strengths and Difficulties Questionnaire (SDQ) hyperactivity subscale at ages 12 and 17 years. First, we tested whether some of those with apparent late‐onset ADHD symptoms had been potentially misclassified on the basis of earlier SDQ hyperactivity scores (ages 7, 8 and 9 years) or of subthreshold symptoms at age 12 years. Second, we investigated the possibility that those with ‘genuine’ late‐onset ADHD symptoms had a delayed manifestation of the same liability that underlies childhood‐onset symptoms, by investigating whether they had a similar profile of neurodevelopmental impairments (in the domains of autistic symptomatology, language, reading, spelling, executive functioning and IQ) as those with typical childhood‐onset ADHD. Results: N = 56/75 (75%) of those with apparent late‐onset ADHD had had high ADHD scores at least one point in childhood, suggesting that they may have been misclassified on the basis of their score at age 12 years. The remaining 19 individuals (25%) with genuine late‐onset ADHD symptoms did not show a profile of neurodevelopmental impairment typically seen in ADHD, instead showing similar levels of autistic symptoms, language skills, executive functioning ability and IQ to those without ADHD symptoms. The only exceptions were that this group showed reading and spelling problems at age 9 years. Conclusions: Our work suggests that this small number of individuals with genuine late‐onset symptoms may not be most appropriately considered as having a typical neurodevelopmental disorder. [ABSTRACT FROM AUTHOR]

Background There is a known strong genetic contribution to aggression in those with ADHD. In a previous investigation of a large population cohort, impaired 'emotional/social cognitive' processing, assessed by questionnaire, was observed to mediate the link between COMT Val158Met and aggression in individuals with ADHD. We set out to replicate and extend this finding in a clinical sample, using task-based and physiological assessments of emotional and cognitive processing. Our aim was to test the hypothesis that directly assessed emotional processing mediates the link between COMT Val158Met and aggression in young people with ADHD. Methods Males aged 10-17 years with ADHD were recruited from UK community clinics ( n = 194). Research diagnostic interviews (parent and child) were used to assess psychopathology and generate DSM- IV Conduct Disorder symptom scores. Participants completed tasks assessing executive function (response inhibition and set shifting), empathy for fear, sadness and happiness, and fear conditioning [measured using skin conductance responses ( SCR) to aversive stimuli]. Results COMT V al allele carriers showed poorer response inhibition ( F = 5.27, p = .02) and set shifting abilities ( F = 6.45, p = .01), reduced fear empathy ( F = 4.33, p = .04) and reduced autonomic responsiveness (lower SCRs) to the conditioned aversive stimulus ( F = 11.74, p = .001). COMT Val158Met did not predict impairments in recognising others' emotions or affective empathy for happiness or sadness. Mediation analysis revealed that impaired fear-related mechanisms indirectly mediated the link between COMT Val158Met and aggression. Conclusion Our findings suggest fear mechanisms as possible targets for psychological interventions to disrupt links between genetic risk and aggressive outcomes in ADHD. Our findings also reveal the potential of hypothesis-driven approaches for identifying neuropsychological mechanisms that mediate genetic risk effects on behaviour and psychopathology. [ABSTRACT FROM AUTHOR]

Background Depression is typically more common in females and rates rise around puberty. However, studies of children and adolescents suggest that depression accompanied by conduct problems may represent a different subtype not characterised by a female preponderance, with differing risk factors and genetic architecture compared to pure-depression. This study aimed to identify aetiologically distinct profiles of depressive symptoms, distinguished by the presence or absence of co-occurring conduct problems. Methods Latent profile analysis was conducted on a school sample of 1648 children (11-12 years) and replicated in a sample of 2006 twins (8-17 years). Results In both samples pure-depressive and conduct-depressive profiles were identified. The pure-depressive profile was associated with female gender, while the conduct-depressive profile was associated with lower cognitive ability but not with gender. Twin analyses indicated possible differences in genetic aetiology. Conclusions There was evidence for aetiologically heterogeneous depression symptom profiles based on the presence or absence of co-occurring conduct problems. [ABSTRACT FROM AUTHOR]

Background: Attention deficit hyperactivity disorder (ADHD) and its possible causes still attract controversy. Genes, pre and perinatal risks, psychosocial factors and environmental toxins have all been considered as potential risk factors. Method: This review (focussing on literature published since 1997, selected from a search of PubMed) critically considers putative risk factors with a focus on genetics and selected environmental risks, examines their relationships with ADHD and discusses the likelihood that these risks are causal as well as some of the main implications. Results: No single risk factor explains ADHD. Both inherited and noninherited factors contribute and their effects are interdependent. ADHD is familial and heritable. Research into the inherited and molecular genetic contributions to ADHD suggest an important overlap with other neurodevelopmental problems, notably, autism spectrum disorders. Having a biological relative with ADHD, large, rare copy number variants, some small effect size candidate gene variants, extreme early adversity, pre and postnatal exposure to lead and low birth weight/prematurity have been most consistently found as risk factors, but none are yet known to be definitely causal. There is a large literature documenting associations between ADHD and a wide variety of putative environmental risks that can, at present, only be regarded as correlates. Findings from research designs that go beyond simply testing for association are beginning to contest the robustness of some environmental exposures previously thought to be ADHD risk factors. Conclusions: The genetic risks implicated in ADHD generally tend to have small effect sizes or be rare and often increase risk of many other types of psychopathology. Thus, they cannot be used for prediction, genetic testing or diagnostic purposes beyond what is predicted by a family history. There is a need to consider the possibility of parents and siblings being similarly affected and how this might impact on engagement with families, influence interventions and require integration with adult services. Genetic contributions to disorder do not necessarily mean that medications are the treatment of choice. We also consider how findings might influence the conceptualisation of ADHD, public health policy implications and why it is unhelpful and incorrect to dichotomise genetic/biological and environmental explanations. It is essential that practitioners can interpret genetic and aetiological research findings and impart informed explanations to families. [ABSTRACT FROM AUTHOR]