| 1. |
- Brimo, Katarzyna, et al.
(författare)
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The co-occurrence of neurodevelopmental problems in dyslexia
- 2021
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Ingår i: Dyslexia. - : Wiley. - 1076-9242 .- 1099-0909. ; 27:3, s. 277-293
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Tidskriftsartikel (refereegranskat)abstract
- The primary aim of this study was to explore the overlaps between dyslexia and a range of neurodevelopmental disorders and problems (NDPs), specifically symptoms of attention-deficit/hyperactivity disorder, autism spectrum disorder, atypical sensory perception and developmental coordination disorder. Capitalizing on a population-based sample of twins, secondary aims included estimating the heritability of dyslexia and reporting on the measurement characteristics of the scale used to assess dyslexia. A telephone interview regarding symptoms of dyslexia and other NDPs was conducted with parents of 1,688 nine-year-old twins. The prevalence and the heritability of dyslexia were estimated at 8 and 52%, respectively. The boy: girl ratio was 1.5:1. Results revealed that there was more than an eightfold increase in (diagnostic proxy) NDPs prevalence in the dyslexia group as compared to typical readers. Quantitatively measured symptoms of inattention, oral language problems and atypical sensory perception significantly predicted dyslexia status in a multivariate analysis. By contrast, ASD-related inflexibility was inversely associated with dyslexia in the multivariate model. In sum, dyslexia often overlaps with other NDPs. The current study provides new knowledge supporting the position to move beyond isolated diagnostic categories into behavioural profiles of co-occurring problems when trying to understand the pattern of strengths and needs in individuals with dyslexia.
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| 2. |
- Dinkler, Lisa, et al.
(författare)
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Anorexia nervosa and autism: a prospective twin cohort study
- 2021
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Ingår i: Journal of Child Psychology and Psychiatry and Allied Disciplines. - : Wiley. - 0021-9630 .- 1469-7610. ; 62:3, s. 316-326
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Tidskriftsartikel (refereegranskat)abstract
- © 2020 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health. Background: Anorexia nervosa (AN) and autism spectrum disorder (ASD) may be phenotypically and etiologically linked. However, due to the absence of prospective studies, it remains unclear whether the elevation of autistic traits in AN is evident in early childhood. Here, we prospectively investigated autistic traits before and after the first diagnosis of AN. Methods: In a population-based sample of 5,987 individuals (52.4% female) from the Child and Adolescent Twin Study in Sweden, parents reported autistic traits at ages 9 and 18. AN and ASD diagnoses were retrieved from the Swedish National Patient Register. In addition, AN diagnoses were ascertained by parent-reported treatment for AN. We compared whether individuals with and without AN differed in autistic traits before the first diagnosis of AN (age 9) and after the first diagnosis of AN (age 18). Results: We did not find evidence for elevated autistic traits in 9-year-old children later diagnosed with AN. At age 18, however, there was a marked elevation in restricted/repetitive behavior and interests, but only in the subgroup of individuals with acute AN. A less pronounced elevation was observed for social communication problems. Conclusions: Coping strategies in individuals with ASD and the somewhat different female ASD phenotype may explain why we did not find elevated autistic traits in children who later developed AN. Alternatively, it is possible that elevated autistic traits were not present prior to the onset of AN, thus questioning the previously reported elevated prevalence of ASD in AN. Future studies should use tailored measurements in order to investigate whether autistic traits in individuals with AN are best conceptualized as an epiphenomenon of the acute AN phase or whether these symptoms indeed represent ASD as a clinically verifiable neurodevelopmental disorder.
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| 3. |
- Dinkler, Lisa, et al.
(författare)
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Association of etiological factors across the extreme end and continuous variation in disordered eating in female Swedish twins
- 2021
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Ingår i: Psychological Medicine. - 0033-2917 .- 1469-8978. ; 51:5, s. 750-760
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundAccumulating evidence suggests that many psychiatric disorders etiologically represent the extreme end of dimensionally distributed features rather than distinct entities. The extent to which this applies to eating disorders (EDs) is unknown.MethodsWe investigated if there is similar etiology in (a) the continuous distribution of the Eating Disorder Inventory-2 (EDI-2), (b) the extremes of EDI-2 score, and (c) registered ED diagnoses, in 1481 female twin pairs at age 18 years (born 1992-1999). EDI-2 scores were self-reported at age 18. ED diagnoses were identified through the Swedish National Patient Register, parent-reported treatment and/or self-reported purging behavior of a frequency and duration consistent with DSM-IV criteria. We differentiated between anorexia nervosa (AN) and other EDs.ResultsThe heritability of the EDI-2 score was 0.65 (95% CI 0.61-0.68). The group heritabilities in DeFries-Fulker extremes analyses were consistent over different percentile-based extreme groups [0.59 (95% CI 0.37-0.81) to 0.65 (95% CI 0.55-0.75)]. Similarly, the heritabilities in liability threshold models were consistent over different levels of severity. In joint categorical-continuous models, the twin-based genetic correlation was 0.52 (95% CI 0.39-0.65) between EDI-2 score and diagnoses of other EDs, and 0.26 (95% CI 0.08-0.42) between EDI-2 score and diagnoses of AN. The non-shared environmental correlations were 0.52 (95% CI 0.32-0.70) and 0.60 (95% CI 0.38-0.79), respectively.ConclusionsOur findings suggest that some EDs can partly be conceptualized as the extreme manifestation of continuously distributed ED features. AN, however, might be more distinctly genetically demarcated from ED features in the general population than other EDs.
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| 4. |
- Dinkler, Lisa, et al.
(författare)
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Etiology of the Broad Avoidant Restrictive Food Intake Disorder Phenotype in Swedish Twins Aged 6 to 12 Years
- 2023
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Ingår i: JAMA psychiatry. - : American Medical Association. - 2168-6238 .- 2168-622X. ; 80:3, s. 260-269
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Tidskriftsartikel (refereegranskat)abstract
- IMPORTANCE: Avoidant restrictive food intake disorder (ARFID) is characterized by an extremely limited range and/or amount of food eaten, resulting in the persistent failure to meet nutritional and/or energy needs. Its etiology is poorly understood, and knowledge of genetic and environmental contributions to ARFID is needed to guide future research. OBJECTIVE: To estimate the extent to which genetic and environmental factors contribute to the liability to the broad ARFID phenotype.DESIGN, SETTING, AND PARTICIPANTS: This nationwide Swedish twin study includes 16 951 twin pairs born between 1992 and 2010 whose parents participated in the Child and Adolescent Twin Study in Sweden (CATSS) at twin age 9 or 12 years. CATSS was linked to the National Patient Register (NPR) and the Prescribed Drug Register (PDR). Data were collected from July 2004 to April 2020, and data were analyzed from October 2021 to October 2022.MAIN OUTCOMES AND MEASURES: From CATSS, NPR, and PDR, all parent reports, diagnoses, procedures, and prescribed drugs that were relevant to the DSM-5 ARFID criteria were extracted when twin pairs were aged 6 to 12 years and integrated into a composite measure for the ARFID phenotype (ie, avoidant/restrictive eating with clinically significant impact, such as low weight or nutritional deficiency, and with fear of weight gain as an exclusion). In sensitivity analyses, autism and medical conditions that could account for the eating disturbance were controlled for. Univariate liability threshold models were fitted to estimate the relative contribution of genetic and environmental variation to the liability to the ARFID phenotype.RESULTS: Of 33 902 included children, 17 151 (50.6%) were male. A total of 682 children (2.0%) with the ARFID phenotype were identified. The heritability of ARFID was 0.79 (95% CI, 0.70-0.85), with significant contributions from nonshared environmental factors (0.21; 95% CI, 0.15-0.30). Heritability was very similar when excluding children with autism (0.77; 95% CI, 0.67-0.84) or medical illnesses that could account for the eating disturbance (0.79; 95% CI, 0.70-0.86).CONCLUSIONS AND RELEVANCE: Prevalence and sex distribution of the broad ARFID phenotype were similar to previous studies, supporting the use of existing epidemiological data to identify children with ARFID. This study of the estimated genetic and environmental etiology of ARFID suggests that ARFID is highly heritable, encouraging future twin and molecular genetic studies.
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| 5. |
- Dinkler, Lisa, et al.
(författare)
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Heritability of the Avoidant/Restrictive Food Intake Disorder (ARFID) Phenotype in 6-to-12-Year-Old Swedish Twins
- 2022
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 52:6, s. 357-357
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Little is known about the etiology of avoidant/restrictive food intake disorder (ARFID) and no twin studies of ARFID exist yet. Validated screening instruments for ARFID are only starting to emerge and accordingly, few large-scale epidemiological studies specifically aimed at measuring ARFID are available. We leveraged the rich existing datasets of the Swedish Twin Registry to develop a proxy for the ARFID phenotype and determine its twin-based heritability. We extracted all data relevant to ARFID from the Child and Adolescent Twin Study in Sweden and national health registers, and identified children with avoidant/restrictive eating with clinically significant impact, but without body image concerns such as fear of weight gain and excluding major medical illnesses that could account for the eating behavior. Among 34,382 twins born 1992–2010, 678 children (2.0%, 39% female) were identified with the ARFID phenotype between age 6 and 12 years. In the best fitting model, variation in the liability to ARFID was largely explained by additive genetic factors (0.80, 95% confidence interval [CI] 0.71–0.86), with significant contributions from non-shared environmental factors (0.20, 95% CI 0.14–0.29) and sibling contrast effects (-0.11, 95% CI -0.16—-0.04). Prevalence and sex distribution of the ARFID phenotype were similar to previous studies, supporting the use of epidemiological data to identify ARFID. This first heritability estimate of ARFID suggests that ARFID is highly heritable, encouraging future twin and molecular genetic studies. In a next step we will use multivariate twinmodels to test whether, etiologically, ARFID is related to neurod-velopmental disorders.
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| 6. |
- Dinkler, Lisa, et al.
(författare)
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Maltreatment-associated neurodevelopmental disorders : a co-twin control analysis
- 2017
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Ingår i: Journal of Child Psychology and Psychiatry. - Stockholm : Karolinska Institutet, Dept of Medical Epidemiology and Biostatistics. - 0021-9630 .- 1469-7610.
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Childhood maltreatment (CM) is strongly associated with psychiatric disorders in childhood and adulthood. Previous findings suggest that the association between CM and psychiatric disorders is partly causal and partly due to familial confounding, but few studies have investigated the mechanisms behind the association between CM and neurodevelopmental disorders (NDDs). Our objective was to determine whether maltreated children have an elevated number of NDDs and whether CM is a risk factor for an increased NDD 'load' and increased NDD symptoms when controlling for familial effects. METHODS: We used a cross-sectional sample from a population-representative Swedish twin study, comprising 8,192 nine-year-old twins born in Sweden between 1997 and 2005. CM was defined as parent-reported exposure to emotional abuse/neglect, physical neglect, physical abuse, and/or sexual abuse. Four NDDs were measured with the Autism-Tics, AD/HD, and other comorbidities inventory. RESULTS: Maltreated children had a greater mean number of NDDs than nonmaltreated children. In a co-twin control design, CM-discordant monozygotic twins did not differ significantly for their number of NDDs, suggesting that CM is not associated with an increased load of NDDs when genetic and shared environmental factors are taken into account. However, CM was associated with a small increase in symptoms of attention-deficit/hyperactivity disorder and autism spectrum disorder in CM-discordant MZ twins, although most of the covariance of CM with NDD symptoms was explained by common genetic effects. CONCLUSIONS: Maltreated children are at higher risk of having multiple NDDs. Our findings are, however, not consistent with the notion that CM causes the increased NDD load in maltreated children. Maltreated children should receive a full neurodevelopmental assessment, and clinicians should be aware that children with multiple NDDs are at higher risk of maltreatment.
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| 7. |
- Gajwani, Ruchika, et al.
(författare)
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Mania symptoms in a Swedish longitudinal population study: The roles of childhood trauma and neurodevelopmental disorders.
- 2021
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Ingår i: Journal of affective disorders. - : Elsevier BV. - 1573-2517 .- 0165-0327. ; 280:Part A, s. 450-456
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Tidskriftsartikel (refereegranskat)abstract
- Adult psychiatric disorders are associated with both childhood traumatic experiences (CTEs) and neurodevelopmental disorders (NDDs). CTEs and NDDs frequently co-occur in childhood, but their combined risk effect on the emergence of juvenile mania symptoms has not yet been examined.In a population-representative Swedish twin study, CTEs and NDDs were assessed in 3,348 nine-year old twins born between 1998 and 2001, and treated as dichotomous predictors (any CTEs, any NDDs). Follow-up data were gathered at age 15 through parental reports of mania symptoms, yielding a symptom count score.Both CTEs and NDDs at age 9 contributed uniquely to an increase in mania symptoms at age 15. Children with both risk factors had 1.6 times the rate of mania symptoms as children with CTEs-only (Incidence rate ratio [IRR] 1.63, 95% CI 1.37-1.93), and 1.3 times the rate of mania symptoms as children with NDDs-only (IRR 1.26, 95% CI 1.06-1.50). There was no evidence for an interactive effect of CTEs and NDDs. NDDs showed a trend towards having a larger effect on mania symptoms than CTEs (NDDs-only vs. CTEs-only: IRR 1.29, 95% CI 0.99-1.68).Although it is a strength of the study that the data on exposures and outcome were collected prospectively, parental recall of CTEs was required and CTEs may be under-reported.NDDs are at least as important as CTEs in the development of mania symptoms, and their risk is additive. Those with a history of both CTEs and NDDs should be monitored closely for the development of more severe psychiatric presentations.
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| 8. |
- Wronski, Marie-Louis, et al.
(författare)
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Co-existing mental and somatic conditions in Swedish children with the avoidant restrictive food intake disorder phenotype
- 2024
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Ingår i: medRxiv : the preprint server for health sciences.
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- BACKGROUND: Avoidant restrictive food intake disorder (ARFID) is a feeding and eating disorder, characterized by limited variety and/or quantity of food intake impacting physical health and psychosocial functioning. Children with ARFID often present with a range of psychiatric and somatic symptoms, and therefore consult various pediatric subspecialties; large-scale studies mapping comorbidities are however lacking. To characterize health care needs of people with ARFID, we systematically investigated ARFID-related mental and somatic conditions in 616 children with ARFID and >30,000 children without ARFID.METHODS: In a Swedish twin cohort, we identified the ARFID phenotype in 6-12-year-old children based on parent-reports and register data. From >1,000 diagnostic ICD-codes, we specified mental and somatic conditions within/across ICD-chapters, number of distinct per-person diagnoses, and inpatient treatment days between birth and 18th birthday (90 outcomes). Hazard ratios (HR) and incidence rate ratios (IRR) were calculated.FINDINGS: Relative risks of neurodevelopmental, gastrointestinal, endocrine/metabolic, respiratory, neurological, and allergic disorders were substantially increased in ARFID (e.g., autism HR[CI95%]=9.7[7.5-12.5], intellectual disability 10.3[7.6-13.9], gastroesophageal reflux disease 6.7[4.6-9.9], pituitary conditions 5.6[2.7-11.3], chronic lower respiratory diseases 4.9[2.4-10.1], epilepsy 5.8[4.1-8.2]). ARFID was not associated with elevated risks of autoimmune illnesses and obsessive-compulsive disorder. Children with ARFID had a significantly higher number of distinct mental diagnoses (IRR[CI95%]=4.7[4.0-5.4]) and longer duration of hospitalizations (IRR[CI95%]=5.5[1.7-17.6]) compared with children without ARFID. Children with ARFID were diagnosed earlier with a mental condition than children without ARFID. No sex-specific differences emerged.INTERPRETATION: This study yields the broadest and most detailed evidence of co-existing mental and somatic conditions in the largest sample of children with ARFID to date. Findings suggest a complex pattern of health needs in youth with ARFID, underscoring the critical importance of attention to the illness across all pediatric specialties.FUNDING: Fredrik and Ingrid Thurings Foundation, Mental Health Foundation.
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