| 1. |
- Dinkler, Lisa, et al.
(author)
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Anorexia nervosa and autism: a prospective twin cohort study
- 2021
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In: Journal of Child Psychology and Psychiatry and Allied Disciplines. - : Wiley. - 0021-9630 .- 1469-7610. ; 62:3, s. 316-326
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Journal article (peer-reviewed)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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| 2. |
- Dinkler, Lisa, et al.
(author)
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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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In: Psychological Medicine. - 0033-2917 .- 1469-8978. ; 51:5, s. 750-760
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Journal article (peer-reviewed)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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| 3. |
- Javaras, Kristin N., et al.
(author)
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Sex- and age-specific incidence of healthcare-register-recorded eating disorders in the complete swedish 1979-2001 birth cohort
- 2015
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In: International Journal of Eating Disorders. - : Wiley-Blackwell. - 0276-3478 .- 1098-108X. ; 48:8, s. 1070-81
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Journal article (peer-reviewed)abstract
- OBJECTIVE: To investigate the sex- and age-specific incidence of healthcare-register-recorded anorexia nervosa (AN) and other eating disorders (OED) in a complete birth cohort, and assess whether incidence varies by diagnostic period and (sub-) birth cohort.METHOD: We used the actuarial method and Poisson models to examine the incidence of AN and OED from 1987 to 2009 (when individuals were 8-30 years old) for a cohort of 2.3 million individuals (48.7% female) born from 1979 to 2001 in Sweden, identified using Swedish registers.RESULTS: For both sexes, incidences of AN and OED increased considerably for diagnostic periods after 2000, but differed little by birth cohort. In 2009, AN incidence in the peak age category was 205.9 cases/100,000 persons (95% CI: 178.2, 233.5) for females (14-15 years), versus 12.8 cases/100,000 (95% CI: 5.6, 20.1) for males (12-13 years). OED incidence in the peak age category was 372.1 cases/100,000 (95% CI: 336.4, 407.9) for females (16-17 years), versus 22.2 cases/100,000 (95% CI: 13.3, 31.1) for males (14-15 years).DISCUSSION: Our finding of an increase in healthcare-register-recorded eating disorders for diagnostic periods after 2000 likely reflects improved detection and expanded register coverage in Sweden. The peak of eating disorder incidence in adolescence, which began unexpectedly early for AN in males, suggests the importance of vigilance for signs of AN in young boys and early primary prevention efforts. Waiting until later could miss critical windows for intervention that could prevent disorders from taking root.
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