Linn B. Norbom, Jaroslav Rokicki, Espen M. Eilertsen, Thea Wiker, Jamie Hanson, Andreas Dahl, Dag Alnæs, Sara Fernández-Cabello, Dani Beck, Ingrid Agartz, Ole A. Andreassen, Lars T. Westlye, Christian K. Tamnes
Background
A child's socioeconomic environment can shape central aspects of their life, including vulnerability to mental disorders. Negative environmental influences in youth may interfere with the extensive and dynamic brain development occurring at this time. Indeed, there are numerous yet diverging reports of associations between parental socioeconomic status (SES) and child cortical brain morphometry. Most of these studies have used single metric- or unimodal analyses of standard cortical morphometry that downplay the probable scenario where numerous biological pathways in sum account for SES-related cortical differences in youth.
Methods
To comprehensively capture such variability, using data from 9758 children aged 8.9–11.1 years from the ABCD Study®, we employed linked independent component analysis (LICA) and fused vertex-wise cortical thickness, surface area, curvature and grey-/white-matter contrast (GWC). LICA revealed 70 uni- and multimodal components. We then assessed the linear relationships between parental education, parental income and each of the cortical components, controlling for age, sex, genetic ancestry, and family relatedness. We also assessed whether cortical structure moderated the negative relationships between parental SES and child general psychopathology.
Results
Parental education and income were both associated with larger surface area and higher GWC globally, in addition to local increases in surface area and to a lesser extent bidirectional GWC and cortical thickness patterns. The negative relation between parental income and child psychopathology were attenuated in children with a multimodal pattern of larger frontal- and smaller occipital surface area, and lower medial occipital thickness and GWC.
Conclusion
Structural brain MRI is sensitive to SES diversity in childhood, with GWC emerging as a particularly relevant marker together with surface area. In low-income families, having a more developed cortex across MRI metrics, appears beneficial for mental health.
{"title":"Parental education and income are linked to offspring cortical brain structure and psychopathology at 9–11 years","authors":"Linn B. Norbom, Jaroslav Rokicki, Espen M. Eilertsen, Thea Wiker, Jamie Hanson, Andreas Dahl, Dag Alnæs, Sara Fernández-Cabello, Dani Beck, Ingrid Agartz, Ole A. Andreassen, Lars T. Westlye, Christian K. Tamnes","doi":"10.1002/jcv2.12220","DOIUrl":"https://doi.org/10.1002/jcv2.12220","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>A child's socioeconomic environment can shape central aspects of their life, including vulnerability to mental disorders. Negative environmental influences in youth may interfere with the extensive and dynamic brain development occurring at this time. Indeed, there are numerous yet diverging reports of associations between parental socioeconomic status (SES) and child cortical brain morphometry. Most of these studies have used single metric- or unimodal analyses of standard cortical morphometry that downplay the probable scenario where numerous biological pathways <i>in sum</i> account for SES-related cortical differences in youth.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>To comprehensively capture such variability, using data from 9758 children aged 8.9–11.1 years from the ABCD Study<sup>®</sup>, we employed linked independent component analysis (LICA) and fused vertex-wise cortical thickness, surface area, curvature and grey-/white-matter contrast (GWC). LICA revealed 70 uni- and multimodal components. We then assessed the linear relationships between parental education, parental income and each of the cortical components, controlling for age, sex, genetic ancestry, and family relatedness. We also assessed whether cortical structure moderated the negative relationships between parental SES and child general psychopathology.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Parental education and income were both associated with larger surface area and higher GWC globally, in addition to local increases in surface area and to a lesser extent bidirectional GWC and cortical thickness patterns. The negative relation between parental income and child psychopathology were attenuated in children with a multimodal pattern of larger frontal- and smaller occipital surface area, and lower medial occipital thickness and GWC.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Structural brain MRI is sensitive to SES diversity in childhood, with GWC emerging as a particularly relevant marker together with surface area. In low-income families, having a more developed cortex across MRI metrics, appears beneficial for mental health.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12220","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140114184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ian A. Apperly, Robert Lee, Sanne W. van der Kleij, Rory T. Devine
Background
The concept of neurodiversity draws upon scientific research, and lessons from practice and lived experience to suggest new ways of thinking about neurodevelopmental conditions. Among the formative observations are that characteristics associated with neurodevelopmental conditions are part of a “broader phenotype” of variation across the whole population, and that there appear to be “transdiagnostic” similarities as well as differences in these characteristics. These observations raise important questions that have implications for understanding diversity in neurodevelopmental conditions and in neurocognitive phenotypes across the whole population.
Method
The present work examines broader phenotypes using seven widely used self-report assessments of traits associated with autism, ADHD, dyslexia, Developmental Coordination Disorder/dyspraxia, tic disorders/Tourette's, cortical hyperexcitability associated with subclinical epilepsy, and sensory sensitivities. A representative sample of 995 adults (aged 17–77) in the UK completed self-report measures of neurodiversity, wellbeing, generalized anxiety, and depression, and cognitive abilities (nonverbal intelligence and executive functioning).
Results
We used confirmatory factor analysis to test whether variation and covariation was better characterized (1) by traditional diagnostic labels, or (2) transdiagnostically according to similarities in functions, behaviours, or phenomena. Results indicated that neurodiversity characteristics were best explained using a bifactor model with one general “N” factor and four condition-specific factors.
Conclusion
This was the largest examination to date of the factor structure of broader phenotypes relevant to neurodevelopmental conditions. It provides critical benchmark data, and a framework approach for asking systematic questions about the structure of neurocognitive diversities seen in the whole population and in people with one or more diagnoses.
{"title":"A transdiagnostic approach to neurodiversity in a representative population sample: The N+ 4 model","authors":"Ian A. Apperly, Robert Lee, Sanne W. van der Kleij, Rory T. Devine","doi":"10.1002/jcv2.12219","DOIUrl":"10.1002/jcv2.12219","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The concept of neurodiversity draws upon scientific research, and lessons from practice and lived experience to suggest new ways of thinking about neurodevelopmental conditions. Among the formative observations are that characteristics associated with neurodevelopmental conditions are part of a “broader phenotype” of variation across the whole population, and that there appear to be “transdiagnostic” similarities as well as differences in these characteristics. These observations raise important questions that have implications for understanding diversity in neurodevelopmental conditions and in neurocognitive phenotypes across the whole population.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>The present work examines broader phenotypes using seven widely used self-report assessments of traits associated with autism, ADHD, dyslexia, Developmental Coordination Disorder/dyspraxia, tic disorders/Tourette's, cortical hyperexcitability associated with subclinical epilepsy, and sensory sensitivities. A representative sample of 995 adults (aged 17–77) in the UK completed self-report measures of neurodiversity, wellbeing, generalized anxiety, and depression, and cognitive abilities (nonverbal intelligence and executive functioning).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We used confirmatory factor analysis to test whether variation and covariation was better characterized (1) by traditional diagnostic labels, or (2) transdiagnostically according to similarities in functions, behaviours, or phenomena. Results indicated that neurodiversity characteristics were best explained using a bifactor model with one general “N” factor and four condition-specific factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This was the largest examination to date of the factor structure of broader phenotypes relevant to neurodevelopmental conditions. It provides critical benchmark data, and a framework approach for asking systematic questions about the structure of neurocognitive diversities seen in the whole population and in people with one or more diagnoses.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12219","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139872537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ian A. Apperly, Robert Lee, Sanne W. van der Kleij, R. Devine
The concept of neurodiversity draws upon scientific research, and lessons from practice and lived experience to suggest new ways of thinking about neurodevelopmental conditions. Among the formative observations are that characteristics associated with neurodevelopmental conditions are part of a “broader phenotype” of variation across the whole population, and that there appear to be “transdiagnostic” similarities as well as differences in these characteristics. These observations raise important questions that have implications for understanding diversity in neurodevelopmental conditions and in neurocognitive phenotypes across the whole population.The present work examines broader phenotypes using seven widely used self‐report assessments of traits associated with autism, ADHD, dyslexia, Developmental Coordination Disorder/dyspraxia, tic disorders/Tourette's, cortical hyperexcitability associated with subclinical epilepsy, and sensory sensitivities. A representative sample of 995 adults (aged 17–77) in the UK completed self‐report measures of neurodiversity, wellbeing, generalized anxiety, and depression, and cognitive abilities (nonverbal intelligence and executive functioning).We used confirmatory factor analysis to test whether variation and covariation was better characterized (1) by traditional diagnostic labels, or (2) transdiagnostically according to similarities in functions, behaviours, or phenomena. Results indicated that neurodiversity characteristics were best explained using a bifactor model with one general “N” factor and four condition‐specific factors.This was the largest examination to date of the factor structure of broader phenotypes relevant to neurodevelopmental conditions. It provides critical benchmark data, and a framework approach for asking systematic questions about the structure of neurocognitive diversities seen in the whole population and in people with one or more diagnoses.
{"title":"A transdiagnostic approach to neurodiversity in a representative population sample: The N+ 4 model","authors":"Ian A. Apperly, Robert Lee, Sanne W. van der Kleij, R. Devine","doi":"10.1002/jcv2.12219","DOIUrl":"https://doi.org/10.1002/jcv2.12219","url":null,"abstract":"The concept of neurodiversity draws upon scientific research, and lessons from practice and lived experience to suggest new ways of thinking about neurodevelopmental conditions. Among the formative observations are that characteristics associated with neurodevelopmental conditions are part of a “broader phenotype” of variation across the whole population, and that there appear to be “transdiagnostic” similarities as well as differences in these characteristics. These observations raise important questions that have implications for understanding diversity in neurodevelopmental conditions and in neurocognitive phenotypes across the whole population.The present work examines broader phenotypes using seven widely used self‐report assessments of traits associated with autism, ADHD, dyslexia, Developmental Coordination Disorder/dyspraxia, tic disorders/Tourette's, cortical hyperexcitability associated with subclinical epilepsy, and sensory sensitivities. A representative sample of 995 adults (aged 17–77) in the UK completed self‐report measures of neurodiversity, wellbeing, generalized anxiety, and depression, and cognitive abilities (nonverbal intelligence and executive functioning).We used confirmatory factor analysis to test whether variation and covariation was better characterized (1) by traditional diagnostic labels, or (2) transdiagnostically according to similarities in functions, behaviours, or phenomena. Results indicated that neurodiversity characteristics were best explained using a bifactor model with one general “N” factor and four condition‐specific factors.This was the largest examination to date of the factor structure of broader phenotypes relevant to neurodevelopmental conditions. It provides critical benchmark data, and a framework approach for asking systematic questions about the structure of neurocognitive diversities seen in the whole population and in people with one or more diagnoses.","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"58 11","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139812388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rebecka Keijser, Jakob Åsberg Johnels, Marika Habbe, Paul Lichtenstein, Henrik Larsson, Sebastian Lundström, Mark J. Taylor, Kristiina Tammimies
Background
Research on genetic and environmental influences on speech and/or language difficulties (SaLD) is sparse, with inconsistent heritability estimates. We aimed to estimate the prevalence of parental reported SaLD and the relative contributions of genetic and environmental factors for the phenotype using a Swedish population-based twin sample. We hypothesized that there would be a stronger genetic than environmental effect on SaLD.
Methods
Data were collected from The Child and Adolescent Twin Study in Sweden. The study sample included 16,774 twin pairs (16,946 males, 16,602 females), of which 5141 were monozygotic, 5861 dizygotic (DZ), and 5772 opposite-sex DZ pairs. The language items in the Autism–Tics, Attention-Deficit Hyperactivity Disorder, and other Comorbidities inventory were used to categorize individuals as having parental-reported SaLD. A classical twin design was used to estimate the relative contribution of genetic and environmental factors to the liability of SaLD.
Results
The prevalence of SaLD was 7.85% (95% confidence interval (CI) [7.57%–8.15%]) and 7.27% (95% CI [6.99%–7.55%]) when excluding individuals with autism and intellectual disability (ID). We also found that SaLD were significantly more prevalent in males than females with a ratio of 2:1. The heritability was estimated to be 75% (95% CI [67%–83%]) for SaLD. Shared environment played a significant role with an estimated contribution of 22% (95% CI [14%–30%]). The heritability estimate was reduced to 70% but with overlapping CI when excluding individuals with autism and ID.
Conclusions
We provide evidence that SaLD is common in the population and under strong genetic influence. Future studies should focus on mapping the genetic architecture of SaLD and related disorders.
有关遗传和环境对言语和/或语言障碍（SaLD）影响的研究很少，对遗传率的估计也不一致。我们的目的是通过瑞典人口中的双胞胎样本，估计父母报告的SaLD患病率，以及遗传和环境因素对表型的相对贡献。我们假设，遗传因素对SaLD的影响要强于环境因素。研究样本包括16774对双胞胎（男性16946对，女性16602对），其中单卵双胞胎5141对，双卵双胞胎5861对，异性双卵双胞胎5772对。自闭症-抽动障碍、注意缺陷多动障碍和其他合并症量表中的语言项目被用来对父母报告的SaLD患者进行分类。在排除自闭症和智力障碍（ID）患者后，SaLD的患病率为7.85%（95%置信区间[7.57%-8.15%]），而SaLD的患病率为7.27%（95%置信区间[6.99%-7.55%]）。我们还发现，SaLD 在男性中的发病率明显高于女性，比例为 2:1。据估计，SaLD 的遗传率为 75%（95% CI [67%-83%]）。共同环境起着重要作用，估计占 22%（95% CI [14%-30%]）。我们提供的证据表明，SaLD在人群中很常见，并受到遗传因素的强烈影响。未来的研究应侧重于绘制SaLD及相关疾病的遗传结构图。
{"title":"Prevalence and heritability of parental-reported speech and/or language difficulties in a Swedish population-based twin sample","authors":"Rebecka Keijser, Jakob Åsberg Johnels, Marika Habbe, Paul Lichtenstein, Henrik Larsson, Sebastian Lundström, Mark J. Taylor, Kristiina Tammimies","doi":"10.1002/jcv2.12221","DOIUrl":"10.1002/jcv2.12221","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Research on genetic and environmental influences on speech and/or language difficulties (SaLD) is sparse, with inconsistent heritability estimates. We aimed to estimate the prevalence of parental reported SaLD and the relative contributions of genetic and environmental factors for the phenotype using a Swedish population-based twin sample. We hypothesized that there would be a stronger genetic than environmental effect on SaLD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data were collected from The Child and Adolescent Twin Study in Sweden. The study sample included 16,774 twin pairs (16,946 males, 16,602 females), of which 5141 were monozygotic, 5861 dizygotic (DZ), and 5772 opposite-sex DZ pairs. The language items in the Autism–Tics, Attention-Deficit Hyperactivity Disorder, and other Comorbidities inventory were used to categorize individuals as having parental-reported SaLD. A classical twin design was used to estimate the relative contribution of genetic and environmental factors to the liability of SaLD.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The prevalence of SaLD was 7.85% (95% confidence interval (CI) [7.57%–8.15%]) and 7.27% (95% CI [6.99%–7.55%]) when excluding individuals with autism and intellectual disability (ID). We also found that SaLD were significantly more prevalent in males than females with a ratio of 2:1. The heritability was estimated to be 75% (95% CI [67%–83%]) for SaLD. Shared environment played a significant role with an estimated contribution of 22% (95% CI [14%–30%]). The heritability estimate was reduced to 70% but with overlapping CI when excluding individuals with autism and ID.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We provide evidence that SaLD is common in the population and under strong genetic influence. Future studies should focus on mapping the genetic architecture of SaLD and related disorders.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12221","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140479705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anna-Karin Ångström, Anneli Andersson, Miguel Garcia-Argibay, Zheng Chang, Paul Lichtenstein, Brian M. D’Onofrio, Catherine Tuvblad, Laura Ghirardi, Henrik Larsson
Background
Individuals with Attention-Deficit/Hyperactivity Disorder (ADHD) face an elevated risk of criminal convictions compared to those without ADHD. However, understanding this link involves considering sex differences, coexisting psychiatric conditions, and unmeasured familial factors. This study aimed to explore the connection between ADHD and criminal convictions (both violent and non-violent) in males and females, while also assessing the impact of comorbid psychiatric disorders and familial factors.
Methods
Using Swedish national registers, we identified individuals born between 1986 and 1997 (635,391 males and 600,548 females). ADHD was defined through clinical diagnosis and prescribed medications, while criminal convictions were determined based on Swedish lower court records. Unmeasured familial factors were accounted for using a sibling design approach.
Results
Findings revealed that individuals with ADHD had a notably higher absolute and relative risk of both violent and non-violent criminal convictions compared to those without ADHD. While criminal convictions were more frequent among males with ADHD, females with ADHD exhibited higher relative risks (HR violent 10.50, non-violent 4.04) than their male counterparts (HR violent 6.03, non-violent 3.57). Additionally, lower socioeconomic status (SES) in individuals with ADHD was associated with increased relative risks for criminal convictions compared to individuals with ADHD who had higher SES. Adjusting for childhood and internalizing psychiatric disorders partially attenuated these associations, while substance use disorders (SUD) substantially attenuated them. SUD also contributed to an elevated absolute risk of criminal convictions in both male and female individuals with ADHD. Accounting for unmeasured shared familial factors slightly reduced the estimates, but the association between ADHD and criminal convictions persisted.
Conclusion
In conclusion, ADHD remains a potent independent risk factor for criminal convictions, with varying effects based on gender. This underscores the importance of tailored crime prevention strategies and early interventions for individuals with ADHD, especially when comorbid SUD is present.
{"title":"Criminal convictions in males and females diagnosed with attention deficit hyperactivity disorder: A Swedish national registry study","authors":"Anna-Karin Ångström, Anneli Andersson, Miguel Garcia-Argibay, Zheng Chang, Paul Lichtenstein, Brian M. D’Onofrio, Catherine Tuvblad, Laura Ghirardi, Henrik Larsson","doi":"10.1002/jcv2.12217","DOIUrl":"10.1002/jcv2.12217","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Individuals with Attention-Deficit/Hyperactivity Disorder (ADHD) face an elevated risk of criminal convictions compared to those without ADHD. However, understanding this link involves considering sex differences, coexisting psychiatric conditions, and unmeasured familial factors. This study aimed to explore the connection between ADHD and criminal convictions (both violent and non-violent) in males and females, while also assessing the impact of comorbid psychiatric disorders and familial factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Using Swedish national registers, we identified individuals born between 1986 and 1997 (635,391 males and 600,548 females). ADHD was defined through clinical diagnosis and prescribed medications, while criminal convictions were determined based on Swedish lower court records. Unmeasured familial factors were accounted for using a sibling design approach.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Findings revealed that individuals with ADHD had a notably higher absolute and relative risk of both violent and non-violent criminal convictions compared to those without ADHD. While criminal convictions were more frequent among males with ADHD, females with ADHD exhibited higher relative risks (HR violent 10.50, non-violent 4.04) than their male counterparts (HR violent 6.03, non-violent 3.57). Additionally, lower socioeconomic status (SES) in individuals with ADHD was associated with increased relative risks for criminal convictions compared to individuals with ADHD who had higher SES. Adjusting for childhood and internalizing psychiatric disorders partially attenuated these associations, while substance use disorders (SUD) substantially attenuated them. SUD also contributed to an elevated absolute risk of criminal convictions in both male and female individuals with ADHD. Accounting for unmeasured shared familial factors slightly reduced the estimates, but the association between ADHD and criminal convictions persisted.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In conclusion, ADHD remains a potent independent risk factor for criminal convictions, with varying effects based on gender. This underscores the importance of tailored crime prevention strategies and early interventions for individuals with ADHD, especially when comorbid SUD is present.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12217","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139524082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This perspective considers complexities in the relationship between impaired cognitive abilities and autism from a maturational, developmental perspective, and aims to serve as a helpful guide for the complex and growing investigation of cognitive abilities and Autism Spectrum Disorder (ASD). Low Intelligence Quotient (IQ) and ASD are frequently co-occurring. About 37% of 8-year old children and 48% of 4-year old children diagnosed with ASD also have Intellectual Disability, with IQ below 70. And, low IQ in early infancy, including below 1 year of age, carries a 40% greater chance of receiving ASD diagnosis in early childhood. We consider the evidence that may explain this co-occurrence, including the possibility that high IQ may “rescue” the social communication issues, as well as the possible role of critical periods during growth and development. We consider how early low IQ may subsume a part of a subgroup of individuals with ASD, in particular, those diagnosed with autism in very early childhood, and we provide neurobiological evidence in support of this subtype. Moreover, we distinguish the concept of early low IQ from the delay in speech onset in preschool and school-aged children, based on (i) age and (ii) impairments in both verbal and non-verbal domains. The etiology of these early-diagnosed, early low IQ ASD cases is different from later-diagnosed, average or higher-IQ cases, and from children with speech delay onset. Given recent interest in formulating new subtypes of autism, rather than continuing to conceive of ASD as a spectrum, as well as new subtypes that vary in the degree of severity along the spectrum, we identify gaps in knowledge and directions for future work in this complex and growing area.
{"title":"Neurobiology of cognitive abilities in early childhood autism","authors":"Kristina Denisova","doi":"10.1002/jcv2.12214","DOIUrl":"10.1002/jcv2.12214","url":null,"abstract":"<p>This perspective considers complexities in the relationship between impaired cognitive abilities and autism from a maturational, developmental perspective, and aims to serve as a helpful guide for the complex and growing investigation of cognitive abilities and Autism Spectrum Disorder (ASD). Low Intelligence Quotient (IQ) and ASD are frequently co-occurring. About 37% of 8-year old children and 48% of 4-year old children diagnosed with ASD also have Intellectual Disability, with IQ below 70. And, low IQ in early infancy, including below 1 year of age, carries a 40% greater chance of receiving ASD diagnosis in early childhood. We consider the evidence that may explain this co-occurrence, including the possibility that high IQ may “rescue” the social communication issues, as well as the possible role of critical periods during growth and development. We consider how early low IQ may subsume a part of a subgroup of individuals with ASD, in particular, those diagnosed with autism in very early childhood, and we provide neurobiological evidence in support of this subtype. Moreover, we distinguish the concept of early low IQ from the delay in speech onset in preschool and school-aged children, based on (<i>i</i>) age and (<i>ii</i>) impairments in both verbal and non-verbal domains. The etiology of these early-diagnosed, early low IQ ASD cases is different from later-diagnosed, average or higher-IQ cases, and from children with speech delay onset. Given recent interest in formulating new subtypes of autism, rather than continuing to conceive of ASD as a spectrum, as well as new subtypes that vary in the degree of severity along the spectrum, we identify gaps in knowledge and directions for future work in this complex and growing area.</p>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12214","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139524854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hedy A. van Oers, Hekmat Alrouh, Jacintha M. Tieskens, Michiel A. J. Luijten, Rowdy de Groot, Emma Broek, Daniël van der Doelen, Helen Klip, Ronald De Meyer, Malindi van der Mheen, I. Hyun Ruisch, Germie van den Berg, Hilgo Bruining, Jan Buitelaar, Rachel van der Rijken, Pieter J. Hoekstra, Marloes Kleinjan, Ramón Lindauer, Kim J. Oostrom, Wouter Staal, Robert Vermeiren, Ronald Cornet, Lotte Haverman, Arne Popma, Meike Bartels, Tinca J. C. Polderman, Josjan Zijlmans
Background
The COVID-19 pandemic negatively affected child and adolescent mental health and at the end of the pandemic (April 2022) child mental health had not returned to pre-pandemic levels. We investigated whether this observed increase in mental health problems has continued, halted, or reversed after the end of the pandemic in children from the general population and in children in psychiatric care.
Methods
We collected parent-reported and child-reported data at two additional post-pandemic time points (November/December 2022 and March/April 2023) in children (8–18 years) from two general population samples (N = 818–1056 per measurement) and one clinical sample receiving psychiatric care (N = 320–370) and compared these with data from before the pandemic. We collected parent-reported data on internalizing and externalizing problems with the Brief Problem Monitor and self-reported data on Anxiety, Depressive symptoms, Sleep-related impairments, Anger, Global health, and Peer relations with the Patient-Reported Outcomes Measurement Information System (PROMIS®).
Results
In the general population, parents reported no changes in externalizing problems but did report higher internalizing problems post-pandemic than pre-pandemic (p < 0.001). Children also reported increased mental health problems post-pandemic, especially in anxiety and depression, to a lesser extent in sleep-related impairment and global health, and least in anger (all ps < 0.01). In the clinical sample, parents reported higher internalizing (p < 0.001), but not externalizing problems post-pandemic compared to the start of the pandemic. Children reported greatest increases in problems in anxiety, depression, and global health, to a lesser extent on sleep-related impairment, and least on anger (all ps < 0.05).
Conclusions
Child mental health problems in the general population are substantially higher post-pandemic compared to pre-pandemic measurements. In children in psychiatric care mental health problems have increased during the pandemic and are substantially higher post-pandemic than at the start of the pandemic. Longitudinal and comparative studies are needed to assess what the most important drivers of these changes are.
{"title":"Changes in child and adolescent mental health across the COVID-19 pandemic (2018–2023): Insights from general population and clinical samples in the Netherlands","authors":"Hedy A. van Oers, Hekmat Alrouh, Jacintha M. Tieskens, Michiel A. J. Luijten, Rowdy de Groot, Emma Broek, Daniël van der Doelen, Helen Klip, Ronald De Meyer, Malindi van der Mheen, I. Hyun Ruisch, Germie van den Berg, Hilgo Bruining, Jan Buitelaar, Rachel van der Rijken, Pieter J. Hoekstra, Marloes Kleinjan, Ramón Lindauer, Kim J. Oostrom, Wouter Staal, Robert Vermeiren, Ronald Cornet, Lotte Haverman, Arne Popma, Meike Bartels, Tinca J. C. Polderman, Josjan Zijlmans","doi":"10.1002/jcv2.12213","DOIUrl":"https://doi.org/10.1002/jcv2.12213","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The COVID-19 pandemic negatively affected child and adolescent mental health and at the end of the pandemic (April 2022) child mental health had not returned to pre-pandemic levels. We investigated whether this observed increase in mental health problems has continued, halted, or reversed after the end of the pandemic in children from the general population and in children in psychiatric care.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We collected parent-reported and child-reported data at two additional post-pandemic time points (November/December 2022 and March/April 2023) in children (8–18 years) from two general population samples (<i>N</i> = 818–1056 per measurement) and one clinical sample receiving psychiatric care (<i>N</i> = 320–370) and compared these with data from before the pandemic. We collected parent-reported data on internalizing and externalizing problems with the Brief Problem Monitor and self-reported data on Anxiety, Depressive symptoms, Sleep-related impairments, Anger, Global health, and Peer relations with the Patient-Reported Outcomes Measurement Information System (PROMIS<sup>®</sup>).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In the general population, parents reported no changes in externalizing problems but did report higher internalizing problems post-pandemic than pre-pandemic (<i>p</i> < 0.001). Children also reported increased mental health problems post-pandemic, especially in anxiety and depression, to a lesser extent in sleep-related impairment and global health, and least in anger (all <i>p</i>s < 0.01). In the clinical sample, parents reported higher internalizing (<i>p</i> < 0.001), but not externalizing problems post-pandemic compared to the start of the pandemic. Children reported greatest increases in problems in anxiety, depression, and global health, to a lesser extent on sleep-related impairment, and least on anger (all <i>p</i>s < 0.05).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Child mental health problems in the general population are substantially higher post-pandemic compared to pre-pandemic measurements. In children in psychiatric care mental health problems have increased during the pandemic and are substantially higher post-pandemic than at the start of the pandemic. Longitudinal and comparative studies are needed to assess what the most important drivers of these changes are.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12213","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142169849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yun-Ju Chen, Eric Duku, Peter Szatmari, Mackenzie Salt, Isabel Smith, Annie Richard, Lonnie Zwaigenbaum, Tracy Vaillancourt, Anat Zaidman-Zait, Terry Bennett, Mayada Elsabbagh, Connor Kerns, Stelios Georgiades
Background
Previous research has demonstrated heterogeneous adaptive outcomes across the autism spectrum; however, the current literature remains limited in elucidating turning points and associated factors for longitudinal variability (chronogeneity). To address these empirical gaps, we aimed to provide a finer-grained characterization of trajectories of adaptive functioning from early childhood to adolescence in autism.
Methods
Our sample (N = 406) was drawn from an inception cohort of children diagnosed Autistic at ages 2–5. Adaptive functioning was assessed with Vineland Adaptive Behavior Scales (VABS, 2nd Edition) across 6 visits from the time of diagnosis by age 18. Parallel-process latent growth curve modeling were used to estimate domain-level VABS trajectories, followed by latent class growth analysis to identify trajectory subgroups. Child characteristics at diagnosis, family demographics, and participation outcomes at adolescence were compared across subgroups.
Results
Piecewise latent growth models best described VABS trajectories with two turning points identified at around ages 5-6 and 9–10, respectively reflecting transitions into school age and early adolescence. We parsed four VABS trajectory subgroups that vary by level of functioning and change rate for certain domains and periods. Around 16% of the sample exhibited overall adequate functioning (standard score >85) with notable early growth and social adaptation during adolescence. About 21% showed low adaptive functioning (standard score ≤70), with decreasing slopes by age 6 followed by improvements in communication and daily-living skills by age 10. The other two subgroups (63% in total) were characterized by adaptive functioning between low and adequate levels, with relatively stable trajectories entering school age. These subgroups differed most in their cognitive ability at diagnosis, household income, and social participation in adolescence.
Conclusions
We identified key individual and family characteristics and time windows associated with distinct adaptive functioning trajectories, which have important implications for providing timely and tailored supports to Autistic people across developmental stages.
{"title":"Trajectories of adaptive functioning from early childhood to adolescence in autism: Identifying turning points and key correlates of chronogeneity","authors":"Yun-Ju Chen, Eric Duku, Peter Szatmari, Mackenzie Salt, Isabel Smith, Annie Richard, Lonnie Zwaigenbaum, Tracy Vaillancourt, Anat Zaidman-Zait, Terry Bennett, Mayada Elsabbagh, Connor Kerns, Stelios Georgiades","doi":"10.1002/jcv2.12212","DOIUrl":"10.1002/jcv2.12212","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Previous research has demonstrated heterogeneous adaptive outcomes across the autism spectrum; however, the current literature remains limited in elucidating turning points and associated factors for longitudinal variability (chronogeneity). To address these empirical gaps, we aimed to provide a finer-grained characterization of trajectories of adaptive functioning from early childhood to adolescence in autism.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Our sample (<i>N</i> = 406) was drawn from an inception cohort of children diagnosed Autistic at ages 2–5. Adaptive functioning was assessed with Vineland Adaptive Behavior Scales (VABS, 2<sup>nd</sup> Edition) across 6 visits from the time of diagnosis by age 18. Parallel-process latent growth curve modeling were used to estimate domain-level VABS trajectories, followed by latent class growth analysis to identify trajectory subgroups. Child characteristics at diagnosis, family demographics, and participation outcomes at adolescence were compared across subgroups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Piecewise latent growth models best described VABS trajectories with two turning points identified at around ages 5-6 and 9–10, respectively reflecting transitions into school age and early adolescence. We parsed four VABS trajectory subgroups that vary by level of functioning and change rate for certain domains and periods. Around 16% of the sample exhibited overall adequate functioning (standard score >85) with notable early growth and social adaptation during adolescence. About 21% showed low adaptive functioning (standard score ≤70), with decreasing slopes by age 6 followed by improvements in communication and daily-living skills by age 10. The other two subgroups (63% in total) were characterized by adaptive functioning between low and adequate levels, with relatively stable trajectories entering school age. These subgroups differed most in their cognitive ability at diagnosis, household income, and social participation in adolescence.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We identified key individual and family characteristics and time windows associated with distinct adaptive functioning trajectories, which have important implications for providing timely and tailored supports to Autistic people across developmental stages.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12212","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138973956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lea L. Backhausen, Jonas Granzow, Juliane H. Fröhner, Eric Artiges, Marie-Laure Paillère-Martinot, Hervé Lemaître, Fabio Sticca, Tobias Banaschewski, Sylvane Desrivières, Antoine Grigis, Andreas Heinz, Rüdiger Brühl, Dimitri Papadopoulos-Orfanos, Luise Poustka, Sarah Hohmann, Lauren Robinson, Henrik Walter, Jeanne Winterer, Gunter Schumann, Jean-Luc Martinot, Michael N. Smolka, Nora C. Vetter, the IMAGEN Consortium
Background
Early negative life events (NLE) have long-lasting influences on neurodevelopment and psychopathology. Reduced orbitofrontal cortex (OFC) thickness was frequently associated with NLE and depressive symptoms. OFC thinning might mediate the effect of NLE on depressive symptoms, although few longitudinal studies exist. Using a complete longitudinal design with four time points, we examined whether NLE during childhood and early adolescence predict depressive symptoms in young adulthood through accelerated OFC thinning across adolescence.
Methods
We acquired structural MRI from 321 participants at two sites across four time points from ages 14 to 22. We measured NLE with the Life Events Questionnaire at the first time point and depressive symptoms with the Center for Epidemiologic Studies Depression Scale at the fourth time point. Modeling latent growth curves, we tested whether OFC thinning mediates the effect of NLE on depressive symptoms.
Results
A higher burden of NLE, a thicker OFC at the age of 14, and an accelerated OFC thinning across adolescence predicted young adults' depressive symptoms. We did not identify an effect of NLE on OFC thickness nor OFC thickness mediating effects of NLE on depressive symptoms.
Conclusions
Using a complete longitudinal design with four waves, we show that NLE in childhood and early adolescence predict depressive symptoms in the long term. Results indicate that an accelerated OFC thinning may precede depressive symptoms. Assessment of early additionally to acute NLEs and neurodevelopment may be warranted in clinical settings to identify risk factors for depression.
{"title":"Interplay of early negative life events, development of orbitofrontal cortical thickness and depression in young adulthood","authors":"Lea L. Backhausen, Jonas Granzow, Juliane H. Fröhner, Eric Artiges, Marie-Laure Paillère-Martinot, Hervé Lemaître, Fabio Sticca, Tobias Banaschewski, Sylvane Desrivières, Antoine Grigis, Andreas Heinz, Rüdiger Brühl, Dimitri Papadopoulos-Orfanos, Luise Poustka, Sarah Hohmann, Lauren Robinson, Henrik Walter, Jeanne Winterer, Gunter Schumann, Jean-Luc Martinot, Michael N. Smolka, Nora C. Vetter, the IMAGEN Consortium","doi":"10.1002/jcv2.12210","DOIUrl":"10.1002/jcv2.12210","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Early negative life events (NLE) have long-lasting influences on neurodevelopment and psychopathology. Reduced orbitofrontal cortex (OFC) thickness was frequently associated with NLE and depressive symptoms. OFC thinning might mediate the effect of NLE on depressive symptoms, although few longitudinal studies exist. Using a complete longitudinal design with four time points, we examined whether NLE during childhood and early adolescence predict depressive symptoms in young adulthood through accelerated OFC thinning across adolescence.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We acquired structural MRI from 321 participants at two sites across four time points from ages 14 to 22. We measured NLE with the Life Events Questionnaire at the first time point and depressive symptoms with the Center for Epidemiologic Studies Depression Scale at the fourth time point. Modeling latent growth curves, we tested whether OFC thinning mediates the effect of NLE on depressive symptoms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A higher burden of NLE, a thicker OFC at the age of 14, and an accelerated OFC thinning across adolescence predicted young adults' depressive symptoms. We did not identify an effect of NLE on OFC thickness nor OFC thickness mediating effects of NLE on depressive symptoms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Using a complete longitudinal design with four waves, we show that NLE in childhood and early adolescence predict depressive symptoms in the long term. Results indicate that an accelerated OFC thinning may precede depressive symptoms. Assessment of early additionally to acute NLEs and neurodevelopment may be warranted in clinical settings to identify risk factors for depression.</p>\u0000 </section>\u0000 </div>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12210","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138596801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Three papers in the December issue (2023) of JCPP Advances focus on children of parents with depression or anxiety. They highlight the value of using prospective longitudinal data to improve the understanding about the development of children of parents with depression or anxiety from early childhood to young adulthood. They contribute to an advanced understanding of long-term outcomes, causality and resilience for children of parents with depression or anxiety.
{"title":"Children of parents with depression or anxiety: Long-term follow-up, causality and resilience","authors":"Henrik Larsson","doi":"10.1002/jcv2.12211","DOIUrl":"https://doi.org/10.1002/jcv2.12211","url":null,"abstract":"<p>Three papers in the December issue (2023) of <i>JCPP Advances</i> focus on children of parents with depression or anxiety. They highlight the value of using prospective longitudinal data to improve the understanding about the development of children of parents with depression or anxiety from early childhood to young adulthood. They contribute to an advanced understanding of long-term outcomes, causality and resilience for children of parents with depression or anxiety.</p>","PeriodicalId":73542,"journal":{"name":"JCPP advances","volume":"3 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://acamh.onlinelibrary.wiley.com/doi/epdf/10.1002/jcv2.12211","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138480945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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