Hunna J Watson, Elisabeth Welch, Elin Monell, Emma Forsén Mantilla, Lisa Dinkler, Johanna Levallius, Lauren Breithaupt, Camilla A Wiklund, Afrouz Abbaspour, Christopher Hübel, Christina Ralph Nearman, Annelie Billger, Jessica Pege, Ralf Kuja-Halkola, Johan Zvrskovec, Androula Savva, Martin Schaefer, Elin Hedlund, Ricard Nergårdh, Laura M Thornton, Maria Seidel, Stefan Ehrlich, Jamie D Feusner, Ata Ghaderi, Cynthia M Bulik
Findings support a multifactorial model of AN involving individual-specific influences and shared familial liability. Perfectionism, goal-directed drive, and competency-related teasing emerged as candidate individual-specific risk factors, while the pattern of elevations, with unaffected co-twins often falling between affected twins and healthy controls, suggests that several clinical and phenotypic features may reflect familial liability for AN.
OBJECTIVE: To characterise the clinical and phenotypic profile of the Comprehensive Risk Evaluation for Anorexia nervosa in Twins (CREAT) cohort, identify candidate risk and illness-related correlates of AN, and establish a foundation for forthcoming biological, neuroimaging, endocrinological, and microbiota studies.
METHODS: MZ twins discordant for lifetime AN (44 individuals) and control MZ twin pairs (42 individuals) were recruited. Analyses included total-sample associations with AN, between-group comparisons (affected, unaffected co-twins, controls), and within-pair analyses of discordant twins.
RESULTS: Affected twins, most of whom were weight-restored and non-acute, differed markedly from unaffected co-twins and controls. Lifetime AN was associated with higher perfectionism, goal-directed drive, neuroticism, behavioural inhibition, impulsivity, broader psychiatric symptoms, teasing history, autism symptoms, and lower quality of life. Within-pair analyses implicated perfectionism, goal-directed drive, and competency-related teasing as candidate individual-specific risk factors for AN, with evidence of additional associations with impulsivity, behavioural inhibition, neuroticism, broader psychiatric symptoms, and autism symptoms.
CONCLUSION: Findings support a multifactorial model of AN involving individual-specific influences and shared familial liability. Perfectionism, goal-directed drive, and competency-related teasing emerged as candidate individual-specific risk factors, while the pattern of elevations, with unaffected co-twins often falling between affected twins and healthy controls, suggests that several clinical and phenotypic features may reflect familial liability for AN.