RESEARCH ARTICLE Eating Disorder Psychopathology, Brain Structure, Neuropsychological Correlates and Risk Mechanisms in Very Preterm Young Adults Nadia Micali 1 * , Radha Kothari 1 , Kie Woo Nam 2 , Elena Gioroukou 2 , Muriel Walshe 2 , Matthew Allin 2 , Larry Rifkin 2 , Robin M. Murray 2 & Chiara Nosarti 2 1 Behavioural and Brain Sciences Unit, Institute of Child Health, University College London, London, UK 2 Department of Psychiatry, Biomedical Research Centre for Mental Health, Institute of Psychiatry, King’s College London, London, UK Abstract This study investigates the prevalence of eating disorder (ED) psychopathology, neuropsychological function, structural brain correlates and risk mechanisms in a prospective cohort of very preterm (VPT) young adults. We assessed ED psychopathology and neuropsycho- logical correlates in 143 cohort individuals born at <33 weeks of gestation. Structural brain correlates and risk factors at birth, in child- hood and adolescence, were investigated using prospectively collected data throughout childhood/adolescence. VPT-born individuals had high levels of ED psychopathology at age 21 years. Executive function did not correlate with ED symptomatology. VPT adults pre- senting with ED psychopathology had smaller grey matter volume at age 14/15 years in the left posterior cerebellum and smaller white matter volume in the fusiform gyrus bilaterally, compared with VPT adults with no ED psychopathology. Caesarean delivery predicted engaging in compensatory behaviours, and severe eating difficulty at age 14 years predicted ED symptomatology in young adulthood. VPT individuals are at risk for ED symptomatology, with evidence of associated structural alterations in posterior brain regions. Further prospective studies are needed to clarify the pathways that lead from perinatal/obstetric complications to ED and relevant neurobiological mechanisms. Copyright © 2015 John Wiley & Sons, Ltd and Eating Disorders Association. Received 2 August 2014; Revised 19 December 2014; Accepted 27 December 2014 Keywords eating disorders; preterm; perinatal complications; neuropsychology; brain structure *Correspondence Nadia Micali, MD, MSc, MRCPsych, PhD, Behavioural and Brain Sciences Unit, Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK. Tel: +44 0207 905 2163. Email: N.micali@ucl.ac.uk The copyright line for this article was changed on 28 February 2015, after original online publication. Published online 19 January 2015 in Wiley Online Library (wileyonlinelibrary.com) DOI: 10.1002/erv.2346 Introduction Very preterm (VPT) birth and small size for gestational age at birth have been shown as risk factors for several psychiatric dis- orders, such as schizophrenia (Silverton, Mednick, Schulsinger, Parnas, & Harrington, 1988), attention deficit hyperactivity disorder (Breslau et al., 1996), depression (Costello, Worthman, Erkanli, & Angold, 2007; Walshe et al., 2008) and eating disorders (ED) (Favaro, Tenconi, & Santonastaso, 2006; Nosarti et al., 2012). Various hypotheses have been postulated to account for this increased risk. One is that perinatal insults adversely affect neurodevelopment (Murray & Lewis, 1987). The second is that altered brain development might lead to increased vulnerability to the effects of further environmental stressors (Costello et al., 2007; Sykes et al., 1997). These mechanisms might be similar across psychiatric disorders or vary across outcomes. The association between preterm birth and ED has been shown in register-based and clinical studies. Increased risk of anorexia nervosa (AN) was associated with being born at less than 32 weeks’ gestation (Cnattingius, Hultman, Dahl, & Sparen, 1999) and lower gestational age (Foley, Neale, & Kendler, 2000). Both AN and bulimia nervosa were associated with preterm birth in data-linkage studies (Favaro et al., 2006; Nosarti et al., 2012). In contrast to these investigations, a small prospective study did not find a higher prevalence of ED in preterm adolescents. However, participants were aged between 18 and 19 years and therefore not completely over the period of risk for ED (Feingold, Sheir-Neiss, Melnychuk, Bachrach, & Paul, 2002). A longitudinal follow-up of very-low-birthweight young adults interestingly found lower Eating Disorder Inventory-2 questionnaire scores in this group compared with healthy controls (Wehkalampi et al., 2010). Thus, although most studies suggest that preterm birth and/or low birthweight play a role in the aetiology of ED, the jury is still out. In a recent systematic review, we highlighted the methodological underpinning of possible discrepancies in the literature in this area of research (Krug, Taborelli, Sallis, Treasure, & Micali, 2013). The mechanisms through which preterm birth might increase risk for ED are still not known. Several hypotheses have been 147 Eur. Eat. Disorders Rev. 23 (2015) 147–155 © 2015 John Wiley & Sons, Ltd and Eating Disorders Association.