Understanding the Relation Between Anorexia Nervosa and Bulimia Nervosa in a Swedish National Twin Sample

Bulik, Cynthia M.; Thornton, Laura M.; Root, Tammy L.; Pisetsky, Emily M.; Lichtenstein, Paul; Pedersen, Nancy L.

doi:10.1016/j.biopsych.2009.08.010

Cited by 113 publications

(98 citation statements)

References 41 publications

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“…Traditionally, research focused on the role of psychosocial factors on the etiology of AN including parental education style, role model function, and traumata. However, recent studies demonstrated that AN is highly heritable showing heritability rates of 50-80 % [2][3][4]. These heritability rates are comparable with those of neurodevelopmental diseases such as schizophrenia [5].…”

Section: Introductionmentioning

confidence: 89%

Evidence for alterations of cortical folding in anorexia nervosa

Schultz

Wagner

Cruz

et al. 2015

Eur Arch Psychiatry Clin Neurosci

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Anorexia nervosa (AN) is highly heritable, and the perspective on the etiology of AN has changed from a behavioral to a neurobiological and neurodevelopmental view. However, cortical folding as an important marker for deviations in brain development has yet rarely been explored in AN. Hence, in order to determine potential cortical folding alterations, we investigated fine-grained cortical folding in a cohort of 26 patients with AN, of whom 6 patients were recovered regarding their weight at the time point of MRI measurement. MRI-derived cortical folding was computed and compared between patients and healthy controls at about 150,000 points per hemisphere using a surface-based technique (FreeSurfer). Patients with AN exhibited highly significant increased cortical folding in a right dorsolateral prefrontal cortex region (DLPFC). Furthermore, a statistical trend in the same direction was found in the right visual cortex. We did not find a correlation of local cortical folding and current symptoms of the disease. In conclusion, our analyses provide first evidence that altered DLPFC cortical folding plays a role in the etiology of AN. The absence of correlations with clinical parameters implicates a relatively independence of cortical folding alterations from the current symptomatology and might thus be regarded as a trait characteristic of the disease potentially related to other neurobiological features of AN.

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Section: Introductionmentioning

confidence: 89%

Evidence for alterations of cortical folding in anorexia nervosa

Schultz

Wagner

Cruz

et al. 2015

Eur Arch Psychiatry Clin Neurosci

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“…35 Individual items were adapted from the Structured Clinical Interview for DSM-IV (SCID-1) 79 and have been used previously for studies of eating disorders in the Swedish Twin Registry. 80,81 Diagnostic algorithms and hierarchies were constructed from the questionnaire items to determine the lifetime history of EDs, AN, BN, ENOS-P, and BED. The hierarchy was as follows.…”

Section: Edinburgh Postnatal Depression Scale (Epds)mentioning

confidence: 99%

Eating Disorders and Trauma History in Women with Perinatal Depression

Meltzer‐Brody

Zerwas

Leserman

et al. 2011

Journal of Women's Health

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Objective: Although the prevalence of perinatal depression (depression occurring during pregnancy and postpartum) is 10%, little is known about psychiatric comorbidity in these women. We examined the prevalence of comorbid eating disorders (ED) and trauma history in women with perinatal depression. Methods: A research questionnaire was administered to 158 consecutive patients seen in a perinatal psychiatry clinic during pregnancy (n = 99) or postpartum (n = 59). Measures included Structured Clinical Interview for DSM (SCID) IV-based questions for lifetime eating psychopathology and assessments of comorbid psychiatric illness including the State/Trait Anxiety Inventory (STAI), Patient Health Questionnaire (PHQ-9), Edinburgh Postnatal Depression Scale (EPDS), and Trauma Inventory. Results: In this cohort, 37.1% reported a putative lifetime ED history; 10.1% reported anorexia nervosa (AN), 10.1% reported bulimia nervosa (BN), 10.1% reported ED not otherwise specified-purging subtype (EDNOS-P), and 7.0% reported binge eating disorder (BED). Women with BN reported more severe depression (EPDS score, 19.1, standard deviation [SD 4.3], p = 0.02; PHQ-severity 14.5, SD 7.4, p = 0.02) than the referent group of women with perinatal depression and no ED history (EPDS 13.3, SD = 6.1; PHQ 9.0, SD = 6.2). Women with AN were more likely to report sexual trauma history than the referent group (62.5% vs. 29.3%, p < 0.05), and those with BN were more likely report physical (50.0%, p < 0.05) and sexual (66.7%, p < 0.05) trauma histories. Conclusions: ED histories were present in over one third of admissions to a perinatal psychiatry clinic. Women with BN reported more severe depression and histories of physical and sexual trauma. Screening for histories of eating psychopathology is important in women with perinatal depression.

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“…24,25 Genetic epidemiological studies have documented the familiality of AN (relative risk 11.3 in first-degree relatives of AN probands) 26,27 and the estimated twin-based heritability of AN ranges from 33 to 84%. [28][29][30][31][32] Genome-wide linkage studies did not narrow the genomic search space in a compelling manner. [33][34][35] Findings from candidate gene studies of AN resemble those for most complex biomedical diseases-initial intriguing findings diminished by the absence of rigorous replication.…”

Section: Introductionmentioning

confidence: 99%