Abstract
Anorexia nervosa and bulimia nervosa are two severe eating disorders associated with high premature mortality, suicidal risk and serious medical complications. Transition between anorexia nervosa and bulimia nervosa over the illness course and familial co-aggregation of the two eating disorders imply aetiological overlap. However, genetic and environmental liabilities to the overlap are poorly understood. Quantitative genetic research using clinical diagnosis is needed. We acquired a clinical diagnosis of anorexia nervosa (prevalence = 0.90%) and bulimia nervosa (prevalence = 0.48%) in a large population-based sample (N = 782 938) of randomly selected full-sisters and maternal half-sisters born in Sweden between 1970 and 2005. Structural equation modelling was applied to quantify heritability of clinically diagnosed anorexia nervosa and bulimia nervosa and the contributions of genetic and environmental effects on their overlap. The heritability of clinically diagnosed anorexia nervosa and bulimia nervosa was estimated at 43% [95% confidence interval (CI) (36-50%)] and 41% (31-52%), respectively, in the study population, with the remaining variance explained by variance in unique environmental effects. We found statistically significant genetic [0.66, 95% CI (0.49-0.82)] and unique environmental correlations [0.55 (0.43-0.66)] between the two clinically diagnosed eating disorders; and their overlap was about equally explained by genetic and unique environmental effects [co-heritability 47% (35-58%)]. Our study supports shared mechanisms for anorexia nervosa and bulimia nervosa and extends the literature from self-reported behavioural measures to clinical diagnosis. The findings encourage future molecular genetic research on both eating disorders and emphasize clinical vigilance for symptom fluctuation between them.
Highlights
Eating disorders are psychiatric illnesses marked by dysregulated appetite, eating behaviours, and shape and weight concerns
Contribute to the liability to the eating disorders, because full-sisters on average share more segregating genes than maternal half-sisters, whereas the environmental contribution within a pair was assumed to be equal between the two types of sisters
The AE model was selected for interpretation because it had the lowest Akaike Information Criterion (AIC) (Table 2)
Summary
Eating disorders are psychiatric illnesses marked by dysregulated appetite, eating behaviours, and shape and weight concerns. Bulimia nervosa, affecting approximately 1.5% females and 0.5% males (Hudson et al, 2007; Preti et al, 2009; Thomas et al, 2016), is characterized by recurrent episodes of uncontrollable binge eating coupled with compensatory behaviours (e.g. purging, fasting and excessive exercise) to prevent consequent weight gain (Dalle Grave et al, 2013) Both eating disorders have been associated with increased premature mortality and suicidal risk (Arcelus et al, 2011; Whiteford et al, 2013; Keshaviah et al, 2014; Yao et al, 2016) and medical (Kessler et al, 2013; Sheehan and Herman, 2015; Westmoreland et al, 2016) and psychiatric comorbidities (Herzog et al, 1992; Striegel-Moore et al, 1999; Kaye et al, 2004; Keel et al, 2005; Hudson et al, 2007; Bulik-Sullivan et al, 2015; Cederlof et al, 2015). The findings encourage future molecular genetic research on both eating disorders and emphasize clinical vigilance for symptom fluctuation between them
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