| 1. |
- 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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| 2. |
- 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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| 3. |
- Solmi, Francesca, et al.
(författare)
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Prevalence of purging at age 16 and associations with negative outcomes among girls in three community-based cohorts.
- 2015
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Ingår i: Journal of Child Psychology and Psychiatry. - : Wiley. - 0021-9630 .- 1469-7610. ; 56:1, s. 87-96
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The comorbidity of purging behaviours, such as vomiting, inappropriate use of laxatives, diuretics or slimming medications, has been examined in literature. However, most studies do not include adolescents, individuals who purge in the absence of binge eating, or those purging at subclinical frequency. This study examines the prevalence of purging among 16-year-old girls across three countries and their association with substance use and psychological comorbidity.METHODS: Data were obtained by questionnaire in 3 population-based cohorts (Avon Longitudinal Study of Parents and Children (ALSPAC), United Kingdom, n = 1,608; Growing Up Today Study (GUTS), USA, n = 3,504; North Finland Birth Cohort (NFBC85/86), Finland, n = 2,306). Multivariate logistic regressions were employed to estimate associations between purging and outcomes. Four models were fit adjusting for binge eating and potential confounders of these associations.RESULTS: In ALSPAC, 9.7% of girls reported purging in the 12-months prior to assessment, 7.3% in GUTS, and 3.5% in NFBC. In all 3 cohorts, purging was associated with adverse outcomes such as binge drinking (ALSPAC: odds ratio (OR) = 2.0, 95% confidence interval (CI) = 1.4-2.9; GUTS: OR = 2.5, 95% CI = 1.5-4.0; NFBC: OR = 1.7, 95% CI = 1.0-2.8), drug use (ALSPAC: OR = 2.9, 95% CI = 1.8-4.7; GUTS: OR = 4.5, 95% CI = 2.8-7.3; NFBC: OR = 4.1, 95% CI = 2.6-6.6), depressive symptoms in ALSPAC (OR = 2.2, 95% CI = 1.5-3.1) and GUTS(OR = 3.7, 95% CI = 2.2-6.3), and several psychopathology measures including clinical anxiety/depression in NFBC (OR = 11.2, 95% CI = 3.9, 31.7).CONCLUSIONS: Results show a higher prevalence of purging behaviours among girls in the United Kingdom compared to those in the United States and Finland. Our findings support evidence highlighting that purging in adolescence is associated with negative outcomes, independent of its frequency and binge eating.
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| 4. |
- Treasure, Janet, et al.
(författare)
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Anorexia nervosa
- 2015
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Ingår i: Nature Reviews Disease Primers. - : Springer Science and Business Media LLC. - 2056-676X. ; 1
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Tidskriftsartikel (refereegranskat)abstract
- Anorexia nervosa (AN) is a psychiatric condition characterized by severe weight loss and secondary problems associated with malnutrition. AN predominantly develops in adolescence in the peripubertal period. Without early effective treatment, the course is protracted with physical, psychological and social morbidity and high mortality. Despite these effects, patients are noted to value the beliefs and behaviours that contribute to their illness rather than regarding them as problematic, which interferes with screening, prevention and early intervention. Involving the family to support interventions early in the course of the illness can produce sustained changes; however, those with a severe and/or protracted illness might require inpatient nursing support and/or outpatient psychotherapy. Prevention programmes aim to moderate the overvaluation of ‘thinness’ and body dissatisfaction as one of the proximal risk factors. The low prevalence of AN limits the ability to identify risk factors and to study the timing and sex distribution of the condition. However, genetic profiles, premorbid features, and brain structures and functions of patients with AN show similarities with other psychiatric disorders and contrast with obesity and metabolic disorders. Such studies are informing approaches to address the neuroadaptation to starvation and the other various physical and psychosocial deficits associated with AN. This Primer describes the epidemiology, diagnosis, screening and prevention, aetiology, treatment and quality of life of patients with AN.
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| 5. |
- Watson, Hunna J., et al.
(författare)
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Common Genetic Variation and Age of Onset of Anorexia Nervosa
- 2022
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Ingår i: BIOLOGICAL PSYCHIATRY: GLOBAL OPEN SCIENCE. - : Elsevier BV. - 2667-1743. ; 2:4, s. 368-378
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Genetics and biology may influence the age of onset of anorexia nervosa (AN). The aims of this study were to determine whether common genetic variation contributes to age of onset of AN and to investigate the genetic associations between age of onset of AN and age at menarche.METHODS: A secondary analysis of the Psychiatric Genomics Consortium genome-wide association study (GWAS) of AN was performed, which included 9335 cases and 31,981 screened controls, all from European ancestries. We conducted GWASs of age of onset, early-onset AN (,13 years), and typical-onset AN, and genetic correlation, genetic risk score, and Mendelian randomization analyses.RESULTS: Two loci were genome-wide significant in the typical-onset AN GWAS. Heritability estimates (single nucleotide polymorphism-h2) were 0.01-0.04 for age of onset, 0.16-0.25 for early-onset AN, and 0.17-0.25 for typical-onset AN. Early-and typical-onset AN showed distinct genetic correlation patterns with putative risk factors for AN. Specifically, early-onset AN was significantly genetically correlated with younger age at menarche, and typical-onset AN was significantly negatively genetically correlated with anthropometric traits. Genetic risk scores for age of onset and early-onset AN estimated from independent GWASs significantly predicted age of onset. Mendelian randomization analysis suggested a causal link between younger age at menarche and early -onset AN.CONCLUSIONS: Our results provide evidence consistent with a common variant genetic basis for age of onset and implicate biological pathways regulating menarche and reproduction.
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| 6. |
- 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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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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