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Rozenblat et al. 5-HTTLPR and Disordered Eating model of 5-HTTLPR, with some evidence that the tri-allelic may better represent activity of this polymorphism ( Wendland et al., 2006 ), as well as the use of self-report questionnaires to measure most constructs, with accounts of sexual abuse and parental physical punishment measured retrospectively. Accordingly, the measure of emotional control used in the present study does not have published psychometric properties, although it has been used in previous research ( O’Connor et al., 2011 ; Toumbourou et al., 2011 ). Finally, 5-HTTLPR is just one of numerous genetic factors that may be involved in the etiology of disordered eating. Implications and Future Directions Findings from this study suggest that psychological and environmental variables remain central in eating pathology, while evidence for specific candidate genes continues to be tentative at best. Although a statistically significant genetic interaction effect was identified in this study, evidence remains inconclusive because the subsample on which it was based was not in Hardy–Weinberg Equilibrium. It is important to note, however, that the null results reported in this study sit in contrast to the substantial genetic contribution to most psychiatric outcomes estimated in twin study designs ( Trace et al., 2013 ). This suggests that there is still much work to do in the area of eating pathology to adequately explain the variation reported in twin studies. Null findings from this study suggest a more complex picture of genetic determination, one that would benefit from a move to genome-wide approaches, with an emphasis on identifying polygenic effects that emerge from networks of genes, which may better reflect the genetic foundations of complex diseases. Future studies of candidate genes should prioritize increasing statistical power, which may be achieved via data sharing across consortiums of life-course studies. Studies such as the present investigation provide a valuable contribution that should form part of future meta-analytic investigations, and constitute an important step forward in progressing investigation of how psychosocial and genetic factors may be related to eating pathology. AUTHOR CONTRIBUTIONS VR was responsible for conducting all analyses and preparing all sections of the manuscript. IK, JR, EW, RK, and CO were involved in collecting data and revising the manuscript for important intellectual content. All authors contributed to and approved the final manuscript. FUNDING This work was supported by an Early Career Researcher Grant (1350035), an Australian Research Council Senior Research Fellowship (DP 130101459), and the Australian Postgraduate Award. None of these institutions had any role in the study design, collection, analysis and interpretation of data, preparation of the manuscript, or decision to submit the manuscript for publication. ACKNOWLEDGMENTS The ATP study is located at The Royal Children’s Hospital Melbourne and is a collaboration between Deakin University, The University of Melbourne, the Australian Institute of Family Studies, The University of New South Wales, The University of Otago (NZ), and The Royal Children’s Hospital; further information available at www.aifs.gov.au/atp. The views expressed in this paper are those of the authors and may not reflect those of their organizational affiliations, nor of other collaborating individuals or organizations. We acknowledge all collaborators who have contributed to the Australian Temperament Project, especially Professors Ann Sanson, Margot Prior, Frank Oberklaid, John Toumbourou and Ms. Diana Smart. We would also like to sincerely thank the participating families for their time and invaluable contribution to the study. This paper forms part of VR’s Ph.D. with publication undertaken at The University of Melbourne. SUPPLEMENTARY MATERIAL The Supplementary Material for this article can be found online at:
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