Browsing by Subject "ANOREXIA-NERVOSA"

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  • Brainstorm Consortium; Anttila, Verneri; Bulik-Sullivan, Brendan; Finucane, Hilary K.; Walters, Raymond K.; Bras, Jose; Duncan, Laramie; Escott-Price, Valentina; Falcone, Guido J.; Gormley, Padhraig; Malik, Rainer; Patsopoulos, Nikolaos A.; Ripke, Stephan; Wei, Zhi; Yu, Dongmei; Lee, Phil H.; Turley, Patrick; Grenier-Boley, Benjamin; Chouraki, Vincent; Kamatani, Yoichiro; Berr, Claudine; Letenneur, Luc; Hannequin, Didier; Amouyel, Philippe; Boland, Anne; Deleuze, Jean-Francois; Duron, Emmanuelle; Vardarajan, Badri N.; Reitz, Christiane; Goate, Alison M.; Huentelman, Matthew J.; Kamboh, M. Ilyas; Larson, Eric B.; Rogaeva, Ekaterina; St George-Hyslop, Peter; Hakonarson, Hakon; Kukull, Walter A.; Palta, Priit; Wedenoja, Juho; Artto, Ville; Kaunisto, Mari; Vepsäläinen, Salli; Kurki, Mitja I.; Hämäläinen, Eija; Kaprio, Jaakko; Metspalu, Andres; Keski-Rahkonen, Anna; Raevuori, Anu; Ripatti, Samuli; Lönnqvist, Jouko; Daly, Mark; Palotie, Aarno; Neale, Benjamin M. (2018)
    Disorders of the brain can exhibit considerable epidemiological comorbidity and often share symptoms, provoking debate about their etiologic overlap. We quantified the genetic sharing of 25 brain disorders from genome-wide association studies of 265,218 patients and 784,643 control participants and assessed their relationship to 17 phenotypes from 1,191,588 individuals. Psychiatric disorders share common variant risk, whereas neurological disorders appear more distinct from one another and from the psychiatric disorders. We also identified significant sharing between disorders and a number of brain phenotypes, including cognitive measures. Further, we conducted simulations to explore how statistical power, diagnostic misclassification, and phenotypic heterogeneity affect genetic correlations. These results highlight the importance of common genetic variation as a risk factor for brain disorders and the value of heritability-based methods in understanding their etiology.
  • Psychiat Genomics Consortium; Yao, Shuyang; Kuja-Halkola, Ralf; Martin, Joanna; Kaprio, Jaakko; Keski-Rahkonen, Anna; Raevuori, Anu; Ripatti, Samuli; Widen, Elisabeth (2019)
    BACKGROUND: Although attention-deficit/hyperactivity disorder (ADHD) and eating disorders (EDs) frequently cooccur, little is known about the shared etiology. In this study, we comprehensively investigated the genetic association between ADHD and various EDs, including anorexia nervosa (AN) and other EDs such as bulimia nervosa. METHODS: We applied different genetically informative designs to register-based information of a Swedish nationwide population (N = 3,550,118). We first examined the familial coaggregation of clinically diagnosed ADHD and EDs across multiple types of relatives. We then applied quantitative genetic modeling in full-sisters and maternal half-sisters to estimate the genetic correlations between ADHD and EDs. We further tested the associations between ADHD polygenic risk scores and ED symptoms, and between AN polygenic risk scores and ADHD symptoms, in a genotyped population-based sample (N = 13,472). RESULTS: Increased risk of all types of EDs was found in individuals with ADHD (any ED: odds ratio [OR] = 3.97, 95% confidence interval [CI] = 3.81, 4.14; AN: OR = 2.68, 95% CI = 2.15, 2.86; other EDs: OR = 4.66, 95% CI = 4.47, 4.87; bulimia nervosa: OR = 5.01, 95% CI = 4.63, 5.41) and their relatives compared with individuals without ADHD and their relatives. The magnitude of the associations decreased as the degree of relatedness decreased, suggesting shared familial liability between ADHD and EDs. Quantitative genetic models revealed stronger genetic correlation of ADHD with other EDs (.37, 95% CI = .31, .42) than with AN (.14, 95% CI = .05, .22). ADHD polygenic risk scores correlated positively with ED symptom measures overall and with the subscales Drive for Thinness and Body Dissatisfaction despite small effect sizes. CONCLUSIONS: We observed stronger genetic association with ADHD for non-AN EDs than for AN, highlighting specific genetic correlation beyond a general genetic factor across psychiatric disorders.
  • Linna, Milla S.; Kaprio, Jaakko; Raevuori, Anu; Sihvola, Elina; Keski-Rahkonen, Anna; Rissanen, Aila (2013)
  • Silén, Yasmina; Sipilä, Pyry N; Raevuori, Anu; Mustelin, Linda; Marttunen, Mauri; Kaprio, Jaakko; Keski-Rahkonen, Anna (2020)
    OBJECTIVE: We aimed to assess the lifetime prevalence, 10-year incidence, and peak periods of onset for eating disorders as defined by the Fifth Diagnostic and Statistical Manual of Mental Disorders (DSM-5) among adolescents and young adults born in the 1980s in Finland. METHOD: Virtually all Finnish twins born in 1983-1987 (n = 5,600) were followed prospectively from the age of 12 years. A subsample of participants (n = 1,347) was interviewed using a semi-structured diagnostic interview in their early twenties. RESULTS: The prevalence of lifetime DSM-5 eating disorders was 17.9% for females and 2.4% for males (pooled across genders, 10.5%). The estimated lifetime prevalences for females and males, respectively, were 6.2 and 0.3% for anorexia nervosa (AN), 2.4 and 0.16% for bulimia nervosa (BN), 0.6 and 0.3% for binge-eating disorder (BED), 4.5 and 0.16% for other specified feeding or eating disorder (OSFED), and 4.5 and 1.6% for unspecified feeding or eating disorder (UFED). Among females, the prevalence of OSFED subcategories was as follows: atypical AN 2.1%, purging disorder 1.3%, BED of low frequency/limited duration 0.7%, and BN of low frequency/limited duration 0.4%. The 10-year incidence rate of eating disorders was 1,700 per 100,000 person-years among females (peak age of onset 16-19 years) and 220 per 100,000 person-years among males. DISCUSSION: Eating disorders are a common public health concern among youth and young adults, affecting one in six females and one in 40 males. Adequate screening efforts, prevention, and interventions are urgently needed.
  • Mustelin, Linda; Kärkkäinen, Ulla; Kaprio, Jaakko; Keski-Rahkonen, Anna (2016)
    Background: We assessed whether the Eating Disorder Inventory (EDI) is suitable for screening binge eating disorder (BED) in young women. Method: Young women (N = 2825) from the 1975-79 birth cohorts of Finnish twins were assessed by questionnaires, including subscales of the EDI. For a subset of women (N = 548), we established DSM-5 diagnoses of BED; 16 women had lifetime BED. We compared screening properties of the EDI scales using receiver operating characteristic (ROC) analysis, determined optimal cutoff points, and calculated sensitivities and specificities. Results: The best screen for DSM-5 BED was the global score of three subscales (Bulimia, Drive for Thinness, Body Dissatisfaction) with an area under the curve (AUC) of 0.86. Its sensitivity was 87% and specificity 76% at cutoff >= 21. Three individual subscales had acceptable screening properties: Bulimia (AUC 0.83; sensitivity 80%, specificity 78% at cutoff >= 2), Drive For Thinness (AUC 0.82; sensitivity 87%, specificity 72% at cutoff >= 7), and Body Dissatisfaction (AUC 0.81; sensitivity 93%, specificity 60% at cutoff >= 8). Conclusion: The EDI performed well as a screening tool for BED in our community-based sample of young twin women. Future studies should assess its value in other populations and in clinical settings. (C) 2016 Elsevier Ltd. All rights reserved.
  • Hulmi, Juha; Isola, Ville; Suonpaa, Marianna; Jarvinen, Neea J.; Kokkonen, Marja; Wennerstrom, Annika; Nyman, Kai; Perola, Markus; Ahtiainen, Juha P.; Hakkinen, Keijo (2017)
    Worries about the potential negative consequences of popular fat loss regimens for aesthetic purposes in normal weight females have been surfacing in the media. However, longitudinal studies investigating these kinds of diets are lacking. The purpose of the present study was to investigate the effects of a 4-month fat-loss diet in normal weight females competing in fitness-sport. In total 50 participants finished the study with 27 females (27.2 +/- 4.1 years) dieting for a competition and 23 (27.7 +/- 3.7 years) acting as weight-stable controls. The energy deficit of the diet group was achieved by reducing carbohydrate intake and increasing aerobic exercise while maintaining a high level of protein intake and resistance training in addition to moderate fat intake. The diet led to a similar to 12% decrease in body weight (P <0.001) and a similar to 3550% decrease in fat mass (DXA, bioimpedance, skinfolds, P <0.001) whereas the control group maintained their body and fat mass (diet x group interaction P <0.001). A small decrease in lean mass (bioimpedance and skinfolds) and in vastus lateralis muscle cross-sectional area (ultrasound) were observed in diet (P <0.05), whereas other results were unaltered (DXA: lean mass, ultrasound: triceps brachii thickness). The hormonal system was altered during the diet with decreased serum concentrations of leptin, triiodothyronine (T3), testosterone (P <0.001), and estradiol (P <0.01) coinciding with an increased incidence of menstrual irregularities (P <0.05). Body weight and all hormones except T3 and testosterone returned to baseline during a 34 month recovery period including increased energy intake and decreased levels aerobic exercise. This study shows for the first time that most of the hormonal changes after a 3550% decrease in body fat in previously normal-weight females can recover within 34 months of increased energy intake.
  • Raevuori, Anu; Haukka, Jari; Vaarala, Outi; Suvisaari, Jaana M.; Gissler, Mika; Grainger, Marjut; Linna, Milla S.; Suokas, Jaana T. (2014)