eating disorders research articles

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

• View all journals
• Explore content
• About the journal
• Publish with us
• Sign up for alerts
• Review Article
• Published: 06 May 2022

Genetics and neurobiology of eating disorders

• Cynthia M. Bulik   ORCID: orcid.org/0000-0001-7772-3264 1 , 2 , 3 ,
• Jonathan R. I. Coleman   ORCID: orcid.org/0000-0002-6759-0944 4 , 5 ,
• J. Andrew Hardaway 6 ,
• Lauren Breithaupt 7 , 8 ,
• Hunna J. Watson 1 , 9 , 10 ,
• Camron D. Bryant   ORCID: orcid.org/0000-0003-4505-5809 11 &
• Gerome Breen   ORCID: orcid.org/0000-0003-2053-1792 4 , 5  

Nature Neuroscience volume  25 ,  pages 543–554 ( 2022 ) Cite this article

9994 Accesses

28 Citations

58 Altmetric

Metrics details

• Feeding behaviour
• Psychiatric disorders

Eating disorders (anorexia nervosa, bulimia nervosa and binge-eating disorder) are a heterogeneous class of complex illnesses marked by weight and appetite dysregulation coupled with distinctive behavioral and psychological features. Our understanding of their genetics and neurobiology is evolving thanks to global cooperation on genome-wide association studies, neuroimaging, and animal models. Until now, however, these approaches have advanced the field in parallel, with inadequate cross-talk. This review covers overlapping advances in these key domains and encourages greater integration of hypotheses and findings to create a more unified science of eating disorders. We highlight ongoing and future work designed to identify implicated biological pathways that will inform staging models based on biology as well as targeted prevention and tailored intervention, and will galvanize interest in the development of pharmacologic agents that target the core biology of the illnesses, for which we currently have few effective pharmacotherapeutics.

This is a preview of subscription content, access via your institution

Access options

Access Nature and 54 other Nature Portfolio journals

Get Nature+, our best-value online-access subscription

24,99 € / 30 days

cancel any time

Subscribe to this journal

Receive 12 print issues and online access

195,33 € per year

only 16,28 € per issue

Buy this article

• Purchase on Springer Link
• Instant access to full article PDF

Prices may be subject to local taxes which are calculated during checkout

Similar content being viewed by others

GLP-1-directed NMDA receptor antagonism for obesity treatment

Temporal dynamics of the multi-omic response to endurance exercise training

Associations of dietary patterns with brain health from behavioral, neuroimaging, biochemical and genetic analyses

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (5th edn) (American Psychiatric Publishing, 2013).

Erskine, H. E., Whiteford, H. A. & Pike, K. M. The global burden of eating disorders. Curr. Opin. Psychiatry 29 , 346–353 (2016).

Article   PubMed   Google Scholar  

Santomauro, D. F. et al. The hidden burden of eating disorders: an extension of estimates from the Global Burden of Disease Study 2019. Lancet Psychiatry 8 , 320–328 (2021).

Article   PubMed   PubMed Central   Google Scholar  

Schaumberg, K. et al. Patterns of diagnostic flux in eating disorders: a longitudinal population study in Sweden. Psychol. Med. 49 , 432–450 (2019).

Article   Google Scholar  

Southern, J. et al. Multi-scale computational modelling in biology and physiology. Prog. Biophys. Mol. Biol. 96 , 60–89 (2008).

Article   CAS   PubMed   Google Scholar  

Yilmaz, Z., Hardaway, J. & Bulik, C. Genetics and epigenetics of eating disorders. Adv. Genomics Genet. 5 , 131–150 (2015).

PubMed   PubMed Central   Google Scholar  

Dellava, J. E., Thornton, L. M., Lichtenstein, P., Pedersen, N. L. & Bulik, C. M. Impact of broadening definitions of anorexia nervosa on sample characteristics. J. Psychiatr. Res. 45 , 691–698 (2011).

Watson, H. et al. Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa. Nat. Genet. 51 , 1207–1214 (2019).

Article   CAS   PubMed   PubMed Central   Google Scholar  

Duncan, L. et al. Significant locus and metabolic genetic correlations revealed in genome-wide association study of anorexia nervosa. Am. J. Psychiatry 174 , 850–858 (2017).

Thornton, L. et al. The Anorexia Nervosa Genetics Initiative: overview and methods. Contemp. Clin. Trials 74 , 61–69 (2018).

Song, W., Wang, W., Yu, S. & Lin, G. N. Dissection of the genetic association between anorexia nervosa and obsessive–compulsive disorder at the network and cellular levels. Genes 12 , 491 (2021).

Munn-Chernoff, M. A. et al. Shared genetic risk between eating disorder- and substance-use-related phenotypes: evidence from genome-wide association studies. Addict. Biol. 26 , e12880 (2021).

Kaye, W. et al. Comorbidity of anxiety disorders with anorexia and bulimia nervosa. Am. J. Psychiatry 161 , 2215–2221 (2004).

Cederlöf, M. et al. Etiological overlap between obsessive–compulsive disorder and anorexia nervosa: a longitudinal cohort, family and twin study. World Psychiatry 14 , 333–338 (2015).

Thornton, L. M., Welch, E., Munn-Chernoff, M. A., Lichtenstein, P. & Bulik, C. M. Anorexia nervosa, major depression, and suicide attempts: shared genetic factors. Suicide Life Threat. Behav. 46 , 525–534 (2016).

Dellava, J., Kendler, K. & Neale, M. Generalized anxiety disorder and anorexia nervosa: evidence of shared genetic variation. Depress. Anxiety 28 , 728–733 (2011).

Bulik-Sullivan, B. et al. An atlas of genetic correlations across human diseases and traits. Nat. Genet. 47 , 1236–1241 (2015).

Watson, H. J. et al. Common genetic variation and age at onset of anorexia nervosa. Biol. Psychiatry https://doi.org/10.1016/j.bpsgos.2021.09.001 (2021).

Solmi, F., Mascarell, M. C., Zammit, S., Kirkbride, J. B. & Lewis, G. Polygenic risk for schizophrenia, disordered eating behaviours and body mass index in adolescents. Br. J. Psychiatry 215 , 428–433 (2019).

Yilmaz, Z., Gottfredson, N., Zerwas, S., Bulik, C. & Micali, N. Developmental premorbid body mass index trajectories of adolescents with eating disorders in a longitudinal population cohort. J. Am. Acad. Child Adolesc. Psychiatry 58 , 191–199 (2019).

Abdulkadir, M. et al. Polygenic score for body mass index is associated with disordered eating in a general population cohort. J. Clin. Med. 9 , 1187 (2020).

Article   PubMed Central   Google Scholar  

Hübel, C. et al. One size does not fit all. Genomics differentiates among anorexia nervosa, bulimia nervosa, and binge-eating disorder. Int. J. Eat. Disord. 54 , 785–793 (2021).

Murray, G. K. et al. Could polygenic risk scores be useful in psychiatry?: a review. JAMA Psychiatry 78 , 210–219 (2020).

Wray, N. et al. Research review: polygenic methods and their application to psychiatric traits. J. Child Psychol. Psychiatry 55 , 1068–1087 (2014).

Lee, P. H. et al. Genomic relationships, novel loci, and pleiotropic mechanisms across eight psychiatric disorders. Cell 179 , 1469–1482 (2019).

Article   CAS   Google Scholar  

Lee, J. E., Namkoong, K. & Jung, Y.-C. Impaired prefrontal cognitive control over interference by food images in binge-eating disorder and bulimia nervosa. Neurosci. Lett. 651 , 95–101 (2017).

Yilmaz, Z. et al. Examination of the shared genetic basis of anorexia nervosa and obsessive–compulsive disorder. Mol. Psychiatry 25 , 2036–2046 (2020).

Reed, Z. E., Micali, N., Bulik, C. M., Davey Smith, G. & Wade, K. H. Assessing the causal role of adiposity on disordered eating in childhood, adolescence, and adulthood: a Mendelian randomization analysis. Am. J. Clin. Nutr. 106 , 764–772 (2017).

CAS   PubMed   PubMed Central   Google Scholar  

Tyrrell, J. et al. Genetic evidence for causal relationships between maternal obesity-related traits and birth weight. JAMA 315 , 1129–1140 (2016).

Adams, D. M., Reay, W. R., Geaghan, M. P. & Cairns, M. J. Investigating the effect of glycaemic traits on the risk of psychiatric illness using Mendelian randomisation. Neuropsychopharmacology 46 , 1093–1102 (2020).

Article   PubMed   PubMed Central   CAS   Google Scholar  

Huckins, L. M. et al. Investigation of common, low-frequency and rare genome-wide variation in anorexia nervosa. Mol. Psychiatry 23 , 1169–1180 (2018).

PubMed   Google Scholar  

Scott-Van Zeeland, A. A. et al. Evidence for the role of EPHX2 gene variants in anorexia nervosa. Mol. Psychiatry 19 , 724–732 (2013).

Lutter, M. et al. Novel and ultra-rare damaging variants in neuropeptide signaling are associated with disordered eating behaviors. PLoS ONE 12 , e0181556 (2017).

Cui, H. et al. Eating disorder predisposition is associated with ESRRA and HDAC4 mutations. J. Clin. Invest. 123 , 4706–4713 (2013).

Lombardi, L. et al. Anorexia nervosa is associated with Neuronatin variants. Psychiatr. Genet. 29 , 103–110 (2019).

Wang, K. et al. A genome-wide association study on common SNPs and rare CNVs in anorexia nervosa. Mol. Psychiatry 16 , 949–959 (2011).

Yilmaz, Z. et al. Exploration of large, rare CNVs associated with psychiatric and neurodevelopmental disorders in individuals with anorexia nervosa. Psychiatr. Genet 27 , 152–158 (2017).

Boraska, V. et al. A genome-wide association study of anorexia nervosa. Mol. Psychiatry 19 , 1085–1094 (2014).

Chang, X. et al. Microduplications at the 15q11.2 BP1–BP2 locus are enriched in patients with anorexia nervosa. J. Psychiatr. Res. 113 , 34–38 (2019).

Bulik, C. M. et al. The Eating Disorders Genetics Initiative (EDGI): study protocol. BMC Psychiatry 21 , 234 (2021).

Co, M., Anderson, A. G. & Konopka, G. FOXP transcription factors in vertebrate brain development, function, and disorders. Wiley Interdiscip. Rev. Dev. Biol. 9 , e375 (2020).

Yengo, L. et al. Meta-analysis of genome-wide association studies for height and body mass index in ∼ 700,000 individuals of European ancestry. Hum. Mol. Genet. 27 , 3641–3649 (2018).

Zhang, M. et al. Axonogenesis is coordinated by neuron-specific alternative splicing programming and splicing regulator PTBP2. Neuron 101 , 690–706 (2019).

Arends, R. M. et al. Associations between the CADM2 gene, substance use, risky sexual behavior and self-control: a phenome-wide association study. Addict. Biol. 26 , e13015 (2021).

Rathjen, T. et al. Regulation of body weight and energy homeostasis by neuronal cell adhesion molecule 1. Nat. Neurosci. 20 , 1096–1103 (2017).

Gerson, S. L. MGMT: its role in cancer aetiology and cancer therapeutics. Nat. Rev. Cancer 4 , 296–307 (2004).

Reid, D. A. et al. Incorporation of a nucleoside analog maps genome repair sites in postmitotic human neurons. Science 372 , 91–94 (2021).

Wu, W. et al. Neuronal enhancers are hotspots for DNA single-strand break repair. Nature 593 , 440–444 (2021).

Finucane, H. et al. Partitioning heritability by functional annotation using genome-wide association summary statistics. Nat. Genet. 47 , 1228–1235 (2015).

Skene, N. G. et al. Genetic identification of brain cell types underlying schizophrenia. Nat. Genet. 50 , 825–833 (2018).

Chowdhury, T. G. et al. Voluntary wheel running exercise evoked by food-restriction stress exacerbates weight loss of adolescent female rats but also promotes resilience by enhancing GABAergic inhibition of pyramidal neurons in the dorsal hippocampus. Cereb. Cortex 29 , 4035–4049 (2019).

Klenowski, P. M. et al. Prolonged consumption of sucrose in a binge-like manner, alters the morphology of medium spiny neurons in the nucleus accumbens shell. Front. Behav. Neurosci. 10 , 54 (2016).

Wang, D. et al. Comprehensive functional genomic resource and integrative model for the human brain. Science 362 , eaat8464 (2018).

Rossi, M. A. & Stuber, G. D. Overlapping brain circuits for homeostatic and hedonic feeding. Cell Metab. 27 , 42–56 (2018).

Frank, G. K., Shott, M. E. & DeGuzman, M. C. Recent advances in understanding anorexia nervosa. F1000Res. 8 , 504 (2019).

Kaye, W. H., Wagner, A., Fudge, J. L. & Paulus, M. Neurocircuity of eating disorders. Curr. Top. Behav. Neurosci. 6 , 37–57 (2010).

Lammel, S., Lim, B. K. & Malenka, R. C. Reward and aversion in a heterogeneous midbrain dopamine system. Neuropharmacol 76 , 351–359 (2014).

Cowdrey, F. A., Park, R. J., Harmer, C. J. & McCabe, C. Increased neural processing of rewarding and aversive food stimuli in recovered anorexia nervosa. Biol. Psychiatry 70 , 736–743 (2011).

Kaye, W. H. et al. Neural insensitivity to the effects of hunger in women remitted from anorexia nervosa. Am. J. Psychiatry 177 , 601–610 (2020).

Bohon, C. & Stice, E. Reward abnormalities among women with full and subthreshold bulimia nervosa: a functional magnetic resonance imaging study. Int. J. Eat. Disord. 44 , 585–595 (2011).

Simon, J. J. et al. Neural signature of food reward processing in bulimic-type eating disorders. Soc. Cogn. Affect. Neurosci. 11 , 1393–1401 (2016).

Bailer, U. F. et al. Exaggerated 5-HT 1A but normal 5-HT 2 A receptor activity in individuals ill with anorexia nervosa. Biol. Psychiatry 61 , 1090–1099 (2007).

Broft, A. et al. Striatal dopamine type 2 receptor availability in anorexia nervosa. Psychiatry Res. 233 , 380–387 (2015).

Bailer, U. F. et al. Amphetamine induced dopamine release increases anxiety in individuals recovered from anorexia nervosa. Int. J. Eat. Disord. 45 , 263–271 (2012).

Broft, A. et al. Striatal dopamine in bulimia nervosa: a PET imaging study. Int. J. Eat. Disord. 45 , 648–656 (2012).

Mihov, Y. et al. Metabotropic glutamate receptor 5 in bulimia nervosa. Sci. Rep. 10 , 1–10 (2020).

Frank, G. K., Shott, M. E., Hagman, J. O. & Mittal, V. A. Alterations in brain structures related to taste reward circuitry in ill and recovered anorexia nervosa and in bulimia nervosa. Am. J. Psychiatry 170 , 1152–1160 (2013).

Craig, A. D. & Craig, A. How do you feel—now? The anterior insula and human awareness. Nat. Rev. Neurosci. 10 , 59–70 (2009).

Kerr, K. L. et al. Altered insula activity during visceral interoception in weight-restored patients with anorexia nervosa. Neuropsychopharmacology 41 , 521–528 (2016).

Zucker, N. L. et al. The clinical significance of posterior insular volume in adolescent anorexia nervosa. Psychosom. Med. 79 , 1025–1035 (2017).

Berner, L. A. et al. Altered anticipation and processing of aversive interoceptive experience among women remitted from bulimia nervosa. Neuropsychopharmacology 44 , 1265–1273 (2019).

Ting, J. T. & Feng, G. Neurobiology of obsessive–compulsive disorder: insights into neural circuitry dysfunction through mouse genetics. Curr. Opin. Neurobiol. 21 , 842–848 (2011).

Marsh, R. et al. An fMRI study of self-regulatory control and conflict resolution in adolescents with bulimia nervosa. Am. J. Psychiatry 168 , 1210–1220 (2011).

Skunde, M. et al. Neural signature of behavioural inhibition in women with bulimia nervosa. J. Psychiatry Neurosci. 41 , E69–E78 (2016).

Wierenga, C. et al. Altered BOLD response during inhibitory and error processing in adolescents with anorexia nervosa. PLoS ONE 9 , e92017 (2014).

Oberndorfer, T. A., Kaye, W. H., Simmons, A. N., Strigo, I. A. & Matthews, S. C. Demand‐specific alteration of medial prefrontal cortex response during an inhibition task in recovered anorexic women. Int. J. Eat. Disord. 44 , 1–8 (2011).

Finch, J. E., Palumbo, I. M., Tobin, K. E. & Latzman, R. D. Structural brain correlates of eating pathology symptom dimensions: a systematic review. Psychiatry Res. Neuroimaging 317 , 111379 (2021).

Geisler, D. et al. Altered white matter connectivity in young acutely underweight patients with anorexia nervosa. J. Am. Acad. Child Adolesc. Psychiatry 61 , 331–340 (2022).

Goodkind, M. et al. Identification of a common neurobiological substrate for mental illness. JAMA Psychiatry 72 , 305–315 (2015).

McTeague, L. M. et al. Identification of common neural circuit disruptions in emotional processing across psychiatric disorders. Am. J. Psychiatry 177 , 411–421 (2020).

Shanmugan, S. et al. Common and dissociable mechanisms of executive system dysfunction across psychiatric disorders in youth. Am. J. Psychiatry 173 , 517–526 (2016).

Wang, S. et al. Neurobiological commonalities and distinctions among 3 major psychiatric disorders: a graph theoretical analysis of the structural connectome. J. Psychiatry Neurosci. 45 , 15–22 (2020).

Xia, M. et al. Shared and distinct functional architectures of brain networks across psychiatric disorders. Schizophr Bull. 45 , 450–463 (2019).

Hudson, J. I., Hiripi, E., Pope, H. G. Jr. & Kessler, R. C. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol. Psychiatry 61 , 348–358 (2007).

Frank, G. K., Favaro, A., Marsh, R., Ehrlich, S. & Lawson, E. A. Toward valid and reliable brain imaging results in eating disorders. Int. J. Eat. Disord. 51 , 250–261 (2018).

Kaufmann, L.-K. et al. Fornix under water? Ventricular enlargement biases forniceal diffusion magnetic resonance imaging indices in anorexia nervosa. Biol. Psychiatry Cogn. Neurosci. Neuroimaging 2 , 430–437 (2017).

Gaudio, S., Carducci, F., Piervincenzi, C., Olivo, G. & Schiöth, H. B. Altered thalamo–cortical and occipital–parietal–temporal–frontal white matter connections in patients with anorexia and bulimia nervosa: a systematic review of diffusion tensor imaging studies. J. Psychiatry Neurosci. 44 , 324–339 (2019).

Thompson, P. M. et al. ENIGMA and global neuroscience: a decade of large-scale studies of the brain in health and disease across more than 40 countries. Transl. Psychiatry 10 , 100 (2020).

Gelegen, C. et al. Difference in susceptibility to activity-based anorexia in two inbred strains of mice. Eur. Neuropsychopharmacol. 17 , 199–205 (2007).

Gelegen, C. et al. Chromosomal mapping of excessive physical activity in mice in response to a restricted feeding schedule. Eur. Neuropsychopharmacol. 20 , 317–326 (2010).

Pjetri, E. et al. Identifying predictors of activity based anorexia susceptibility in diverse genetic rodent populations. PLoS ONE 7 , e50453 (2012).

Babbs, R. K. et al. Genetic differences in the behavioral organization of binge eating, conditioned food reward, and compulsive-like eating in C57BL/6J and DBA/2J strains. Physiol. Behav. 197 , 51–66 (2018).

Newmyer, B. A., Whindleton, C. M., Srinivasa, N., Jones, M. K. & Scott, M. M. Genetic variation affects binge feeding behavior in female inbred mouse strains. Sci. Rep. 9 , 1–10 (2019).

Kirkpatrick, S. L. et al. Cytoplasmic FMR1-interacting protein 2 is a major genetic factor underlying binge eating. Biol. Psychiatry 81 , 757–769 (2017).

Babbs, R. K. et al. Cyfip1 haploinsufficiency increases compulsive-like behavior and modulates palatable food intake in mice: dependence on Cyfip2 genetic background, parent of origin and sex. G3 9 , 3009–3022 (2019).

Farrell, M. et al. Treatment-resistant psychotic symptoms and the 15q11.2 BP1–BP2 (Burnside–Butler) deletion syndrome: case report and review of the literature. Transl. Psychiatry 10 , 1–8 (2020).

Yao, E. J. et al. Systems genetic analysis of binge-like eating in a C57BL/6J × DBA/2J-F2 cross. Genes Brain Behav. e12751 (2021).

Nobis, S. et al. Alterations of proteome, mitochondrial dynamic and autophagy in the hypothalamus during activity-based anorexia. Sci. Rep. 8 , 1–15 (2018).

Nobis, S. et al. Colonic mucosal proteome signature reveals reduced energy metabolism and protein synthesis but activated autophagy during anorexia‐induced malnutrition in mice. Proteomics 18 , 1700395 (2018).

Breton, J. et al. Proteome modifications of gut microbiota in mice with activity-based anorexia and starvation: role in ATP production. Nutrition 67 , 110557 (2019).

Article   PubMed   CAS   Google Scholar  

Schroeder, M. et al. Placental miR-340 mediates vulnerability to activity based anorexia in mice. Nat. Commun. 9 , 1–15 (2018).

He, X., Stefan, M., Terranova, K., Steinglass, J. & Marsh, R. Altered white matter microstructure in adolescents and adults with bulimia nervosa. Neuropsychopharmacology 41 , 1841–1848 (2015).

Kaakoush, N. O. et al. Alternating or continuous exposure to cafeteria diet leads to similar shifts in gut microbiota compared to chow diet. Mol. Nutr. Food Res. 61 , 1500815 (2017).

Sweeney, P. & Yang, Y. Neural circuit mechanisms underlying emotional regulation of homeostatic feeding. Trends Endocrinol. Metab. 28 , 437–448 (2017).

Webber, E. S., Bonci, A. & Krashes, M. J. The elegance of energy balance: insight from circuit‐level manipulations. Synapse 69 , 461–474 (2015).

Andermann, M. L. & Lowell, B. B. Toward a wiring diagram understanding of appetite control. Neuron 95 , 757–778 (2017).

Welch, A. C. et al. Dopamine D2 receptor overexpression in the nucleus accumbens core induces robust weight loss during scheduled fasting selectively in female mice. Mol. Psychiatry 26 , 3765–3777 (2019).

Milton, L. K. et al. Suppression of corticostriatal circuit activity improves cognitive flexibility and prevents body weight loss in activity-based anorexia in rats. Biol. Psychiatry 90 , 819–828 (2021).

Zhang, J. & Dulawa, S. C. The utility of animal models for studying the metabo-psychiatric origins of anorexia nervosa. Front. Psychiatry 12 , 711181 (2021).

Foldi, C. J., Milton, L. K. & Oldfield, B. J. The role of mesolimbic reward neurocircuitry in prevention and rescue of the activity-based anorexia phenotype in rats. Neuropsychopharmacology 42 , 2292–2300 (2017).

Hebebrand, J., Muller, T., Holtkamp, K. & Herpertz-Dahlmann, B. The role of leptin in anorexia nervosa: clinical implications. Mol. Psychiatry 12 , 23–35 (2007).

Verhagen, L. A., Luijendijk, M. C. & Adan, R. A. Leptin reduces hyperactivity in an animal model for anorexia nervosa via the ventral tegmental area. Eur. Neuropsychopharmacol. 21 , 274–281 (2011).

Antel, J. et al. Rapid amelioration of anorexia nervosa in a male adolescent during metreleptin treatment including recovery from hypogonadotropic hypogonadism. Eur. Child Adolesc. Psychiatry https://doi.org/10.1007/s00787-021-01778-7 (2021).

Burghardt, P. R. et al. Leptin regulates dopamine responses to sustained stress in humans. J. Neurosci. 32 , 15369–15376 (2012).

Wu, Q., Han, Y. & Tong, Q. in Neural Regulation of Metabolism (eds. Wu, Q. & Zheng, R.) 211–233 (Springer, 2018).

Xu, P. et al. Activation of serotonin 2C receptors in dopamine neurons inhibits binge-like eating in mice. Biol. Psychiatry 81 , 737–747 (2017).

Marino, R. A. M. et al. Control of food approach and eating by a GABAergic projection from lateral hypothalamus to dorsal pons. Proc. Natl Acad. Sci. USA 117 , 8611–8615 (2020).

Wu, H. et al. Closing the loop on impulsivity via nucleus accumbens delta-band activity in mice and man. Proc. Natl Acad. Sci. USA 115 , 192–197 (2018).

Halpern, C. H. et al. Amelioration of binge eating by nucleus accumbens shell deep brain stimulation in mice involves D2 receptor modulation. J. Neurosci. 33 , 7122–7129 (2013).

London, T. D. et al. Coordinated ramping of dorsal striatal pathways preceding food approach and consumption. J. Neurosci. 38 , 3547–3558 (2018).

Livneh, Y. et al. Homeostatic circuits selectively gate food cue responses in insular cortex. Nature 546 , 611–616 (2017).

Kusumoto-Yoshida, I., Liu, H., Chen, B. T., Fontanini, A. & Bonci, A. Central role for the insular cortex in mediating conditioned responses to anticipatory cues. Proc. Natl Acad. Sci. USA 112 , 1190–1195 (2015).

Price, A. E., Stutz, S. J., Hommel, J. D., Anastasio, N. C. & Cunningham, K. A. Anterior insula activity regulates the associated behaviors of high fat food binge intake and cue reactivity in male rats. Appetite 133 , 231–239 (2019).

Wu, Y. et al. The anterior insular cortex unilaterally controls feeding in response to aversive visceral stimuli in mice. Nat. Commun. 11 , 640 (2020).

Spierling, S. et al. Insula to ventral striatal projections mediate compulsive eating produced by intermittent access to palatable food. Neuropsychopharmacology 45 , 579–588 (2020).

Anastasio, N. C. et al. Convergent neural connectivity in motor impulsivity and high-fat food binge-like eating in male Sprague-Dawley rats. Neuropsychopharmacology 44 , 1752–1761 (2019).

Newmyer, B. A. et al. VIPergic neurons of the infralimbic and prelimbic cortices control palatable food intake through separate cognitive pathways. JCI Insight 5 , e126283 (2019).

Mathis, A. et al. DeepLabCut: markerless pose estimation of user-defined body parts with deep learning. Nat. Neurosci. 21 , 1281–1289 (2018).

Maussion, G., Demirova, I., Gorwood, P. & Ramoz, N. Induced pluripotent stem cells: new tools for investigating molecular mechanisms in anorexia nervosa. Front. Nutr. 6 , 118 (2019).

Breen, G. et al. Translating genome-wide association findings into new therapeutics for psychiatry. Nat. Neurosci. 19 , 1392–1396 (2016).

Galmiche, M., Déchelotte, P., Lambert, G. & Tavolacci, M. P. Prevalence of eating disorders over the 2000–2018 period: a systematic literature review. Am. J. Clin. Nutr. 109 , 1402–1413 (2019).

Papadopoulos, F., Ekbom, A., Brandt, L. & Ekselius, L. Excess mortality, causes of death and prognostic factors in anorexia nervosa. Br. J. Psychiatry 194 , 10–17 (2009).

Yao, S. et al. Familial liability for eating disorders and suicide attempts: evidence from a population registry in Sweden. JAMA Psychiatry 73 , 284–291 (2016).

Fichter, M. M., Quadflieg, N., Crosby, R. D. & Koch, S. Long-term outcome of anorexia nervosa: results from a large clinical longitudinal study. Int J. Eat. Disord. 50 , 1018–1030 (2017).

Berkman, N. et al. Management of eating disorders. Evid. Rep. Technol. Assess. 135 , 1–166 (2006).

Keski-Rahkonen, A. et al. Epidemiology and course of anorexia nervosa in the community. Am. J. Psychiatry 164 , 1259–1265 (2007).

Brownley, K. et al. Binge-eating disorder in adults: a systematic review and meta-analysis. Ann. Intern. Med. 165 , 409–420 (2016).

Fornaro, M. et al. Lisdexamfetamine in the treatment of moderate-to-severe binge eating disorder in adults: systematic review and exploratory meta-analysis of publicly available placebo-controlled, randomized clinical trials. Neuropsychiatr. Dis. Treat. 12 , 1827–1836 (2016).

Hall, J. F., Smith, K., Schnitzer, S. B. & Hanford, P. V. Elevation of activity level in the rat following transition from ad libitum to restricted feeding. J. Comp. Physiol. Psychol. 46 , 429–433 (1953).

Schalla, M. A. & Stengel, A. Activity based anorexia as an animal model for anorexia nervosa—a systematic review. Front Nutr. 6 , 69 (2019).

Novelle, M. G. & Diéguez, C. Food addiction and binge eating: lessons learned from animal models. Nutrients 10 , 71 (2018).

Article   PubMed Central   CAS   Google Scholar  

Corwin, R. L. & Babbs, R. K. Rodent models of binge eating: are they models of addiction? ILAR J. 53 , 23–34 (2012).

Moore, C. F., Sabino, V., Koob, G. F. & Cottone, P. Pathological overeating: emerging evidence for a compulsivity construct. Neuropsychopharmacology 42 , 1375–1389 (2017).

Rospond, B., Szpigiel, J., Sadakierska-Chudy, A. & Filip, M. Binge eating in preclinical models. Pharmacol. Rep. 67 , 504–512 (2015).

Cottone, P., Sabino, V., Steardo, L. & Zorrilla, E. P. Intermittent access to preferred food reduces the reinforcing efficacy of chow in rats. Am. J. Physiol. Regul. Integr. Comp. Physiol. 295 , R1066–R1076 (2008).

Hardaway, J. A. et al. Nociceptin receptor antagonist SB 612111 decreases high-fat diet binge eating. Behav. Brain Res. 307 , 25–34 (2016).

Download references

Acknowledgements

C.M.B. is supported by the National Institute of Mental Health (R01MH120170, R01MH124871, R01MH119084, R01MH118278 and R01MH124871), a Brain and Behavior Research Foundation Distinguished Investigator grant, the Swedish Research Council (Vetenskapsrådet, award no. 538-2013-8864), and the Lundbeck Foundation (grant no. R276-2018-4581). J.R.I.C. and G.B. acknowledge that the paper represents independent research part funded by the National Institute for Health Research (NIHR) Maudsley Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health and Social Care. J.A.H. is supported by K01DK115902. C.D.B. is supported by U01DA050243 and U01DA055299. L.B. is supported by T32MH112485, a Harvard Medical School Livingston Fellowship and the International OCD Foundation. G.B. is also supported by the UK Medical Research Council (MR/V012878/1, MR/V03605X/1 and MR/R024804/1) and Charlotte’s Helix.

Author information

Authors and affiliations.

Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Cynthia M. Bulik & Hunna J. Watson

Department of Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA

Cynthia M. Bulik

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden

Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK

Jonathan R. I. Coleman & Gerome Breen

National Institute of Health Research Maudsley Biomedical Research Centre, South London and Maudsley National Health Service Trust, London, UK

Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL, USA

J. Andrew Hardaway

Department of Psychiatry, Harvard Medical School, Boston, MA, USA

Lauren Breithaupt

Eating Disorders Clinical and Research Program, Massachusetts General Hospital, Boston, MA, USA

School of Psychology, Curtin University, Perth, Western Australia, Australia

Hunna J. Watson

Division of Paediatrics, School of Medicine, The University of Western Australia, Perth, Western Australia, Australia

Department of Pharmacology and Experimental Therapeutics and Psychiatry, Boston University School of Medicine, Boston, MA, USA

Camron D. Bryant

You can also search for this author in PubMed   Google Scholar

Contributions

C.M.B., J.R.I.C., J.A.H., L.B., C.D.B., H.W. and G.B. all substantially contributed to the writing of the manuscript, approved the submitted version, are personally accountable for their own contribution, and ensure that questions related to the accuracy or integrity of any part of the work, even ones in which the author was not personally involved, are appropriately investigated, resolved, and the resolution documented in the literature.

Corresponding author

Correspondence to Cynthia M. Bulik .

Ethics declarations

Competing interests.

C.M.B. reports the following competing interests: Shire (grant recipient, Scientific Advisory Board member); Idorsia (consultant); Pearson (author, royalty recipient); Equip Health (Clinical Advisory Board Member). G.B. reports the following competing interests: Otsuka Pharma (advisory board); Illumina (grant recipient, conference sponsorship). The other authors declare no competing interests.

Peer review

Peer review information.

Nature Neuroscience thanks Roger Adan, Sandra Sanchez-Roige, and the other, anonymous, reviewer(s) for their contribution to the peer review of this work.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Reprints and permissions

About this article

Cite this article.

Bulik, C.M., Coleman, J.R.I., Hardaway, J.A. et al. Genetics and neurobiology of eating disorders. Nat Neurosci 25 , 543–554 (2022). https://doi.org/10.1038/s41593-022-01071-z

Download citation

Received : 03 May 2020

Accepted : 01 April 2022

Published : 06 May 2022

Issue Date : May 2022

DOI : https://doi.org/10.1038/s41593-022-01071-z

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

This article is cited by

Unexpected identification of obesity-associated mutations in lep and mc4r genes in patients with anorexia nervosa.

• Luisa Sophie Rajcsanyi
• Yiran Zheng
• Anke Hinney

Scientific Reports (2024)

The multisensory mind: a systematic review of multisensory integration processing in Anorexia and Bulimia Nervosa

• Giulia Brizzi
• Maria Sansoni
• Giuseppe Riva

Journal of Eating Disorders (2023)

Psilocybin for the treatment of anorexia nervosa

• Tomislav Majić
• Stefan Ehrlich

Nature Medicine (2023)

Quick links

• Explore articles by subject
• Guide to authors
• Editorial policies

Sign up for the Nature Briefing: Translational Research newsletter — top stories in biotechnology, drug discovery and pharma.

Eating disorders

Affiliations.

• 1 Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK. Electronic address: [email protected].
• 2 Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; Serviço de Psiquiatria e Saúde Mental, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, Lisbon, Portugal.
• 3 Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; South London and Maudsley NHS Foundation Trust, London, UK.
• PMID: 32171414
• DOI: 10.1016/S0140-6736(20)30059-3

Eating disorders are disabling, deadly, and costly mental disorders that considerably impair physical health and disrupt psychosocial functioning. Disturbed attitudes towards weight, body shape, and eating play a key role in the origin and maintenance of eating disorders. Eating disorders have been increasing over the past 50 years and changes in the food environment have been implicated. All health-care providers should routinely enquire about eating habits as a component of overall health assessment. Six main feeding and eating disorders are now recognised in diagnostic systems: anorexia nervosa, bulimia nervosa, binge eating disorder, avoidant-restrictive food intake disorder, pica, and rumination disorder. The presentation form of eating disorders might vary for men versus women, for example. As eating disorders are under-researched, there is a great deal of uncertainty as to their pathophysiology, treatment, and management. Future challenges, emerging treatments, and outstanding research questions are addressed.

Copyright © 2020 Elsevier Ltd. All rights reserved.

Publication types

• Research Support, Non-U.S. Gov't
• Diagnosis, Differential
• Feeding and Eating Disorders* / diagnosis
• Feeding and Eating Disorders* / physiopathology
• Feeding and Eating Disorders* / psychology
• Feeding and Eating Disorders* / therapy
• Nutritional Status

Transforming the understanding and treatment of mental illnesses.

Información en español

Celebrating 75 Years! Learn More >>

• Health Topics
• Brochures and Fact Sheets
• Help for Mental Illnesses
• Clinical Trials

Eating Disorders: About More Than Food

• Download PDF
• Order a free hardcopy

What are eating disorders?

Eating disorders are serious, biologically influenced medical illnesses marked by severe disturbances to one’s eating behaviors. Although many people may be concerned about their health, weight, or appearance from time to time, some people become fixated or obsessed with weight loss, body weight or shape, and controlling their food intake. These may be signs of an eating disorder.

Eating disorders are not a choice. These disorders can affect a person’s physical and mental health. In some cases, they can be life-threatening. With treatment, however, people can recover completely from eating disorders.

Who is at risk for eating disorders?

Eating disorders can affect people of all ages, racial and ethnic backgrounds, body weights, and genders. Even people who appear healthy, such as athletes, can have eating disorders and be extremely ill. People with eating disorders can be underweight, normal weight, or overweight. In other words, you can’t tell if someone has an eating disorder by looking at them.

The exact cause of eating disorders is not fully understood.  Research suggests a combination of genetic, biological, behavioral, psychological, and social factors can raise a person’s risk. 

What are the common types of eating disorders?

Common eating disorders include anorexia nervosa, bulimia nervosa, binge-eating disorder, and avoidant restrictive food intake disorder. Each of these disorders is associated with different but sometimes overlapping symptoms. People exhibiting any combination of these symptoms may have an eating disorder and should be evaluated by a health care provider.

What is anorexia nervosa?

Anorexia nervosa is a condition where people avoid food, severely restrict food, or eat very small quantities of only certain foods. They also may weigh themselves repeatedly. Even when dangerously underweight, they may see themselves as overweight.

There are two subtypes of anorexia nervosa: a restrictive subtype and a binge-purge subtype.

Restrictive : People with the restrictive subtype of anorexia nervosa severely limit the amount and type of food they consume.

Binge-Purge : People with the binge-purge subtype of anorexia nervosa also greatly restrict the amount and type of food they consume. In addition, they may have binge-eating and purging episodes—eating large amounts of food in a short time followed by vomiting or using laxatives or diuretics to get rid of what was consumed.

Symptoms of anorexia nervosa include:

• Extremely restricted eating and/or intensive and excessive exercise
• Extreme thinness (emaciation)
• A relentless pursuit of thinness and unwillingness to maintain a normal or healthy weight
• Intense fear of gaining weight
• Distorted body or self-image that is heavily influenced by perceptions of body weight and shape
• Denial of the seriousness of low body weight

Over time, anorexia nervosa can lead to numerous serious health consequences, including:

• Thinning of the bones (osteopenia or osteoporosis)
• Mild anemia
• Muscle wasting and weakness
• Brittle hair and nails
• Dry and yellowish skin
• Growth of fine hair all over the body (lanugo)
• Severe constipation
• Low blood pressure
• Slowed breathing and pulse
• Damage to the structure and function of the heart
• Drop in internal body temperature, causing a person to feel cold all the time
• Lethargy, sluggishness, or feeling tired all the time
• Infertility
• Brain damage
• Multiple organ failure

Anorexia nervosa can be fatal. It has an extremely high death (mortality) rate compared with other mental disorders. People with anorexia are at risk of dying from medical complications associated with starvation. Suicide is the second leading cause of death for people diagnosed with anorexia nervosa.

If you or someone you know is in immediate distress or is thinking about hurting themselves, call the National Suicide Prevention Lifeline toll-free at 1-800-273-TALK (8255). You also can text the Crisis Text Line (HELLO to 741741) or use the Lifeline Chat on the National Suicide Prevention Lifeline   website. If you suspect a medical emergency, seek medical attention or call 911 immediately.

What is bulimia nervosa?

Bulimia nervosa is a condition where people have recurrent episodes of eating unusually large amounts of food and feeling a lack of control over their eating. This binge eating is followed by behaviors that compensate for the overeating to prevent weight gain, such as forced vomiting, excessive use of laxatives or diuretics, fasting, excessive exercise, or a combination of these behaviors. Unlike those with anorexia nervosa, people with bulimia nervosa may maintain a normal weight or be overweight.

Symptoms and health consequences of bulimia nervosa include:

• Chronically inflamed and sore throat
• Swollen salivary glands in the neck and jaw area
• Worn tooth enamel and increasingly sensitive and decaying teeth from exposure to stomach acid when vomiting
• Acid reflux disorder and other gastrointestinal problems
• Intestinal distress and irritation from laxative abuse
• Severe dehydration from purging
• Electrolyte imbalance (too low or too high levels of sodium, calcium, potassium, and other minerals), which can lead to stroke or heart attack

What is binge-eating disorder?

Binge-eating disorder is a condition where people lose control of their eating and have reoccurring episodes of eating unusually large amounts of food. Unlike bulimia nervosa, periods of binge eating are not followed by purging, excessive exercise, or fasting. As a result, people with binge-eating disorder are often overweight or obese.

Symptoms of binge-eating disorder include:

• Eating unusually large amounts of food in a short amount of time, for example, within two hours
• Eating rapidly during binge episodes
• Eating even when full or not hungry
• Eating until uncomfortably full
• Eating alone or in secret to avoid embarrassment
• Feeling distressed, ashamed, or guilty about eating
• Frequently dieting, possibly without weight loss

What is avoidant restrictive food intake disorder?

Avoidant restrictive food intake disorder (ARFID), previously known as selective eating disorder, is a condition where people limit the amount or type of food eaten. Unlike anorexia nervosa, people with ARFID do not have a distorted body image or extreme fear of gaining weight. ARFID is most common in middle childhood and usually has an earlier onset than other eating disorders. Many children go through phases of picky eating, but a child with ARFID does not eat enough calories to grow and develop properly, and an adult with ARFID does not eat enough calories to maintain basic body function.

Symptoms of ARFID include:

• Dramatic restriction of types or amount of food eaten
• Lack of appetite or interest in food
• Dramatic weight loss
• Upset stomach, abdominal pain, or other gastrointestinal issues with no other known cause
• Limited range of preferred foods that becomes even more limited (“picky eating” that gets progressively worse)

How are eating disorders treated?

Eating disorders can be treated successfully. Early detection and treatment are important for a full recovery. People with eating disorders are at higher risk for suicide and medical complications.

A person’s family can play a crucial role in treatment. Family members can encourage the person with eating or body image issues to seek help. They also can provide support during treatment and can be a great ally to both the individual and the health care provider. Research suggests that incorporating the family into treatment for eating disorders can improve treatment outcomes, particularly for adolescents.

Treatment plans for eating disorders include psychotherapy, medical care and monitoring, nutritional counseling, medications, or a combination of these approaches. Typical treatment goals include:

• Restoring adequate nutrition
• Bringing weight to a healthy level
• Reducing excessive exercise
• Stopping binge-purge and binge-eating behaviors

People with eating disorders also may have other mental disorders (such as depression or anxiety) or problems with substance use. It’s critical to treat any co-occurring conditions as part of the treatment plan.

Specific forms of psychotherapy (“talk therapy”) and cognitive-behavioral approaches can treat certain eating disorders effectively. For general information about psychotherapies, visit the National Institute of Mental Health (NIMH) psychotherapies webpage .

Research also suggests that medications may help treat some eating disorders and co-occurring anxiety or depression related to eating disorders. Information about medications changes frequently, so talk to your health care provider. Visit the U.S. Food and Drug Administration (FDA) website  for the latest warnings, patient medication guides, and FDA-approved medications.

Where can I find help?

If you're unsure where to get help, your health care provider is a good place to start. Your health care provider can refer you to a qualified mental health professional, such as a psychiatrist or psychologist, who has experience treating eating disorders.

You can learn more about getting help and finding a health care provider on NIMH's Help for Mental Illnesses webpage . If you need help identifying a provider in your area, call the Substance Abuse and Mental Health Services Administration (SAMHSA) Treatment Referral Helpline at 1-800-662-HELP (4357). You also can search SAMHSA’s online Behavioral Health Treatment Services Locator  , which lists facilities and programs that provide mental health services.

For tips on talking with your health care provider about your mental health, read NIMH’s fact sheet, Taking Control of Your Mental Health: Tips for Talking With Your Health Care Provider .

For additional resources, visit the Agency for Healthcare Research and Quality website  .

Are there clinical trials studying eating disorders?

NIMH supports a wide range of research, including clinical trials that look at new ways to prevent, detect, or treat diseases and conditions, including eating disorders. Although individuals may benefit from being part of a clinical trial, participants should be aware that the primary purpose of a clinical trial is to gain new scientific knowledge so that others may be better helped in the future.

Researchers at NIMH and around the country conduct clinical trials with patients and healthy volunteers. Talk to your health care provider about clinical trials, their benefits and risks, and whether one is right for you. For more information about clinical research and how to find clinical trials being conducted around the country, visit NIMH's clinical trials webpage .

The information in this publication is in the public domain and may be reused or copied without permission. However, you may not reuse or copy images. Please cite the National Institute of Mental Health as the source. Read our copyright policy to learn more about our guidelines for reusing NIMH content.

For More Information

MedlinePlus  (National Library of Medicine) ( en español  ) ClinicalTrials.gov  ( en español  )

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health NIH Publication No. 21-MH-4901 Revised 2021

Cris E. Haltom Ph.D., CEDS

Cris E. Haltom, Ph.D., CEDS is a Certified Eating Disorders Specialist and clinical psychologist who has treated eating disorders for over 35 years. She has presented and published research and clinical work at national, state, and local conferences and organizations. She is past Education and Prevention Liaison of the Western New York Comprehensive Care Centers for Eating Disorders and the author of A Stranger at the Table: Dealing with Your Child’s Eating Disorder (2004) and co-author of Understanding Teen Eating Disorders by Haltom (2018).

• Find a Therapist
• Find a Treatment Center
• Find a Psychiatrist
• Find a Support Group
• Find Online Therapy
• United States
• Brooklyn, NY
• Chicago, IL
• Houston, TX
• Los Angeles, CA
• New York, NY
• Portland, OR
• San Diego, CA
• San Francisco, CA
• Seattle, WA
• Washington, DC
• Asperger's
• Bipolar Disorder
• Chronic Pain
• Eating Disorders
• Passive Aggression
• Personality
• Goal Setting
• Positive Psychology
• Stopping Smoking
• Low Sexual Desire
• Relationships
• Child Development
• Self Tests NEW
• Therapy Center
• Diagnosis Dictionary
• Types of Therapy

At any moment, someone’s aggravating behavior or our own bad luck can set us off on an emotional spiral that threatens to derail our entire day. Here’s how we can face our triggers with less reactivity so that we can get on with our lives.

• Emotional Intelligence
• Gaslighting
• Affective Forecasting
• Neuroscience

Cookie Acceptance Needed

This website would like to use cookies to collect information to improve your browsing experience. Please review our Privacy Statement for more information. Do you accept?

Accept Deny

• News |  
• Articles |  
• Body image research to practice

Customized care: Auburn University body image research sets new standard for person-centered treatment

From research to treatment, students and faculty at Auburn University are leading the charge to dispel stereotypes about eating disorders. Their work lays a foundation for a new clinical model, one that understands that eating disorders can happen to anyone, and through that understanding, prepares clinicians to better help everyone.

Assistant Professor of Psychological Sciences Tiffany Brown leads the Appearance Concerns, Eating, Prevention and Treatment (ACCEPT) Lab and co-directs the Auburn Eating Disorders Clinic (AEDC). Through both, she leads a cyclical effort to investigate, test and improve eating disorders treatment.

"The really exciting thing for me as both a clinician and then also a researcher, an academic, is being able to integrate what we're finding out in research about risk for eating disorder behaviors within diverse groups," Brown said. "We can then actually apply that or target some of those factors in treatment."

Culturally informed research

The ACCEPT Lab researches the factors behind negative body image and eating disorders across traditionally underserved populations. Recent psychology graduate and research assistant Minh Le's '24 work focused on how identity-related stress affects body dissatisfaction, including in populations across racial groups and the LGBTQ+ community.

Le said Brown helped him translate his hope for positive change into deliverable results that will benefit future researchers and clinicians. For example, Le's study revealed that stress around hiding sexual identity can predict body dissatisfaction in Asian individuals.

"My initial process of wanting to do this project was me being a part of a minority group and also the LGBTQ+ community. I really saw a difference between individuals that I have met in my life, and I wanted to see if there was an impact on body dissatisfaction," Le said. "I saw in my experiences that there is a sense of shame and dishonor whenever you are seen outside of the 'normal' group within Asian cultures. So, I see why it makes sense that sexual orientation concealment would be the highest predictor for it."

Graduate research assistant and clinical psychology student Marley Billman Miller also studies body dissatisfaction with an intersectional lens. Her latest work studied how race, gender and sexuality interacts with body image and eating disorders.

She found that while BIPOC (Black, Indigenous or other people of color) men have low rates of body dissatisfaction, they reported higher rates of eating disorder behavior. Those behaviors included purging and excessive exercise, which may be considered atypical if research is only limited to body dissatisfaction as the driving force behind eating disorders.

Billman Miller said these findings are important because while stereotypes around eating disorders are changing, treatment is slower to develop.

"My hope for the future is that more representation is seen in clinical trials and better adaptations are made to the existing, evidence-based treatments," Billman Miller said. "What we know is even our best treatments are only meeting the needs of about 50% of our patients, so if we incorporate more representation within our clinical trials or adapt our existing evidence-based treatments for those groups, we'll see better outcomes for everybody."

Evidence backed treatment

Research from the ACCEPT Lab applies directly to developing informed treatments for AEDC patients. The AEDC, co-directed by Brown and Associate Professor April Smith , treats a variety of eating disorders across the lifespan.

Billman Miller, who came to Auburn after serving as a clinical research coordinator at the Penn State College of Medicine, said that direct link between research and treatment drew her to Auburn's doctoral program.

"Knowing that we had an in-house training clinic, where I could work directly with individuals who were struggling with eating disorders, was a huge draw, as well as the ample opportunities to get involved with both research and clinical work," Billman Miller said. "Auburn does a great job of balancing the two, so I knew I'd come out a very well-rounded researcher and clinician at the end of my training."

Graduate students both conduct research and serve as clinicians in the AEDC. They also help undergraduate researchers address the gap between body image literature and treatment.

Brown said undergraduate and graduate students bring a variety of perspectives to challenging the one-size-fits-all approach to eating disorder treatment.

"One of the things we're trying to do with both the ACCEPT Lab and then also the AEDC is to help provide affirmative care for LGBTQ folks. Specifically, our research is currently focused on developing more specific treatments that target unique risk factors for LGBTQ individuals with an eating disorder," Brown said. "For men, both in the ACCEPT Lab and at the AEDC, we're really trying to develop and deliver prevention and treatment programs that focus on both traditional and male-specific body image and eating disorder concerns."

Lifesaving results

Research and treatment for eating disorders, which are the deadliest among mental health conditions, is underfunded compared to other psychological disorders. While Auburn faculty and students treat as many people as possible, their efforts also contribute to preventative measures.

Through the research collected in the ACCEPT Lab and the AEDC, Auburn has developed and delivered programs to prevent body dissatisfaction and eating disorders before they start. One of those interventions focused on improving body image concerns for young men.

Le served as an interventionist during the program and said his work around body image has completely changed the trajectory of his psychology career.

"Initially I didn't really know where I wanted to go or what I had to do for it, but joining this lab has set so many foundations for me to know what my path is, what my goal is at the end," Le said. "I really hope to see a bigger understanding of how to accommodate each person's need, depending on their backgrounds, depending on their identities, that we do focus on what is the most important part of helping these individuals rather than just finding out what's wrong."

The demand for high-quality, research-informed eating disorders treatment in Alabama is high. The AEDC is uniquely positioned to deliver specialized care, but currently has a waitlist to manage its patient load. Further, it follows a sliding scale model for treatment cost, meaning patients can receive treatment at a more affordable rate than other clinics.

Brown said the self-funded clinic hopes to expand services to care for even more patients in the future.

"We had a waitlist basically within a week of opening, which both shows a huge need in the community here for eating disorder treatment, but also shows that we weren't able to fully care for everybody who was coming in and needing treatment," Brown said. "One of the really great things with having increased support from the university and donors is we've been able to expand our services further."

Since the AEDC opened in 2022, support from the Auburn Family has helped the clinic double its patient capacity by hiring two full-time graduate clinicians and assisting its low-income patients by covering treatment costs.

To give or learn more about how your support makes a difference, visit the AEDC website .

Tags: Students Faculty Research Community and Outreach Psychological Sciences

Related Articles

Health services administration senior Megan Watkins wins national essay competition

Benson featured in Voice and Speech Review for new article on practicing equity in voice studio

Auburn’s Marshall Scholarship winner working to find solutions

Auburn senior Williams-Cole sworn in as mayor of Camp Hill

Auburn University, The Election Center partnership professionalizes elections work

Auburn Art junior Collin Crowder unfolds passions through origami

Newsletter signup.

• Open access
• Published: 17 May 2024

Dismantling the myth of “all foods fit” in eating disorder treatment

• Timothy D. Brewerton 1 ,
• Kim Dennis 2 , 3 &
• David A. Wiss 4  

Journal of Eating Disorders volume  12 , Article number:  60 ( 2024 ) Cite this article

2517 Accesses

26 Altmetric

Metrics details

We call for a reevaluation of the long-standing dogmatic nutritional principle that “all foods fit” for all cases of eating disorders (EDs) and its corollary, “there are no bad foods” (for anyone ever) during ED treatment. Based on accumulated scientific research, we challenge these ideologies as outdated, confusing, and potentially harmful to many patients. We review the evidence that indicates the folly of these assumptions and show there are a variety of exceptions to these rules, including (1) food allergies, sensitivities, and intolerances, (2) religious and spiritual preferences or doctrines, and (3) the ubiquitous emergence and widespread availability of ultra-processed foods leading to the potential development of addiction-like eating and a higher prevalence of various medical and psychiatric comorbidities, as well as higher mortality. This evidence supports a nutritional psychiatry approach that should be integrated into (rather than dissociated from) ED treatment research and practice.

The adage, “all foods fit,” has been an eating disorder (ED) treatment dogma for decades. In other words, there is an almost monolithic belief or proclamation within the ED field that “there are no bad foods” when it comes to the nutritional rehabilitation of all patients with all forms of EDs. Decades of clinical experience have demonstrated that this approach is helpful in addressing the restrictive dimension of ED pathology across phenotypes. However, for many individuals with EDs, eating symptoms extend beyond the domain of dietary restraint. The well-intentioned assertion that “all foods fit” persists in the anti-diet culture movement despite mounting evidence substantiating the association of ultra-processed foods with negative physical and mental health outcomes.

This essay calls into question these suppositions and proclaims that for many patients, they, at best, represent an incomplete truth and, at worst, stand to cause harm. When uniformly and rigidly applied to all patients, the age-old adage that “all foods fit” no longer serves the entire ED treatment community. This is most pressingly true for patients with EDs from communities historically marginalized and underrepresented in ED research, advocacy groups, training programs, and treatment settings. We will discuss why assumptions associated with “all foods fit” are outdated and incomplete concepts for some patients with EDs. These strong assumptions no longer align with the evidence base that has emerged over the last decade, which we as clinical scientists strive to translate to good clinical care.

“Food is medicine,” a shortened version of “Let thy food be thy medicine, and thy medicine be thy food,” has also been a related ED dogma for decades. This saying (often misattributed to Hippocrates), carries a lot of truth and heuristic value [ 1 ]. However, are all foods medicinal? Are there any “bad” or harmful medicines for any given patient? Of course, there are. Medicines are neither “good” nor “bad” unto themselves. It’s how they’re used or prescribed, for which problems, in which persons, at what times, and in what doses. The same medicine may help or harm an individual depending on many factors, and biopsychosocial-spiritual context is paramount.

The scientific literature clearly indicates that some foods “don’t fit” and are harmful, at least to some people under specific circumstances. An obvious example is a food allergy, which can cause various problems, including anaphylaxis, which has been increasing in prevalence and affects up to 20% of individuals in the population [ 2 , 3 ]. There are 14 identified food allergens: celery, cereals containing gluten (such as barley and oats), crustaceans (such as prawns, crabs, and lobsters), eggs, fish, lupin, milk, mollusks (such as mussels and oysters), mustard, peanuts, sesame, soybeans, sulfur dioxide and sulfites (at concentrations > ten parts per million) [ 4 ]. Food allergies are associated with high degrees of psychological distress and significantly reduced health-related quality of life [ 5 ]. In addition, recent studies suggest positive associations between EDs and food allergies, so this is an important area of inquiry in clinical evaluation and subsequent dietary management [ 6 ].

A related problem is food sensitivity, in which certain individuals develop various adverse effects, both acute and chronic, including neurobehavioral, gastrointestinal, metabolic, or teratogenic consequences, upon exposure to certain substances, such as gluten, food additives, Fermentable Oligo-, Di- and Mono-saccharides And Polyols (FODMAPs), and non-nutritive sweeteners [ 7 , 8 , 9 , 10 , 11 , 12 , 13 ]. There are several examples of these phenomena relevant to the treatment of patients with EDs, including comorbid migraine headaches, irritable bowel syndrome, attention deficit hyperactivity disorder (ADHD), major depressive disorder, and anxiety disorders [ 12 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ], in which a nutritional psychiatry perspective can be highly influential [ 26 , 27 , 28 ].

While not eating can be a trigger for acute migraine headache, so can the ingestion of certain foods, such as those containing monosodium glutamate, sugar, alcohol, nitrites, gluten, cheese, chocolate, caffeine, and fermented, processed, and pickled foods [ 29 , 30 , 31 ]. However, not all foods will trigger migraine in every individual with migraines, and there is tremendous variation that needs to be individually evaluated [ 32 ]. For a patient with an ED, restrictive or not, and comorbid migraine, who routinely gets migraine headaches after consuming certain food types, they may need a meal plan that explicitly does not include or includes very little of those foods. Often, in ED treatment, patients expressing preferences to avoid these foods are assumed to be related to restrictive pathology rather than intuitive eating and adaptive dietary restraint. Nevertheless, dietary interventions have been successfully employed in the treatment of this common comorbidity that needs to be routinely considered in the comprehensive treatment of ED patients [ 13 , 30 , 33 ].

Attention deficit hyperactivity disorder (ADHD) is another disorder commonly associated with EDs that may be affected by nutritional intake of specific substances, such as food color additives [ 34 , 35 , 36 , 37 ]. Of particular interest are several studies showing that a diet high in refined sugar and saturated fat can increase the risk of ADHD, whereas a diet characterized by higher consumption of whole fruits and vegetables may be protective against ADHD [ 38 ].

Apart from allergies and sensitivities, some individuals have food intolerances (e.g., lactose, gluten, onions, shallots, leeks, bell peppers, etc.), all of which can cause gastrointestinal distress and which have been associated with anxiety and depression [ 39 , 40 , 41 , 42 , 43 ].

Then, there are individual food preferences for religious, spiritual, and/or ethical reasons, such as those who are vegan, vegetarian, pescatarian, Kosher, etc [ 44 , 45 , 46 ]. . . These proclivities have only sometimes been respected by ED therapists and programs, and practices have evolved over time as it has been realized that more research is needed to decipher their effects on clinical course and outcomes [ 46 , 47 , 48 , 49 ].

What is particularly controversial of late is the issue of food addiction (FA) or ultra-processed food addiction (UPFA), which, despite its strong scientific foundation [ 50 , 51 ], remains highly controversial in ED circles [ 52 ]. Unfortunately, UPFA and its treatment often get conflated with caloric restriction and diet culture, which are not equivalent. In fact, there are studies currently examining flexible, calorically robust, and weight-neutral dietary interventions for patients with FA [ 53 ]. Ultra-processed foods (UPFs), which are now identified as NOVA-4 in the NOVA classification system [ 54 ], have been associated with a host of adverse health effects and increased mortality [ 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 ]. The NOVA classification system categorizes foods according to their degree of processing, and the NOVA-4 group includes foods with the highest degree of processing. Specifically, they include packaged formulations of industrial ingredients and substances derived from foods or else created in laboratories, and typically contain little or even no whole foods [ 66 ]. UPFs have been shown to promote binge eating [ 67 , 68 ] and higher body weights [ 69 , 70 , 71 , 72 ], as well as worsen depression [ 73 , 74 , 75 , 76 , 77 ], type-2 diabetes [ 78 , 79 ], cardiovascular disease [ 80 , 81 , 82 , 83 , 84 ], and chronic kidney disease [ 85 ]. In terms of mechanisms for this multitude of adverse effects, UPFs have been associated with stimulating inflammation, altering multiple neurobiological and endocrine pathways (e.g., insulin), and disrupting the microbiome [ 86 , 87 , 88 ]. The presence of UPFA has also been associated with a poorer treatment outcome for binge eating disorder [ 89 ], which is known to be highly comorbid with addiction-like eating [ 90 , 91 , 92 ].

The intake of UPFs accounts for the great majority of calories ingested in Westernized countries and is only increasing in availability and popularity as time goes on [ 93 ]. Estimates of the worldwide prevalence of FA/UPFA using the Yale Food Addiction Scale are on the order of 14% in non-clinical samples [ 94 ]. In addition to having high concentrations of refined sugars and oils, UPFs also contain potentially obesogenic endocrine-disrupting chemicals that have been added (or neo-formed during high heat processes) to foods and food packaging by the food industry for the last several decades [ 95 , 96 , 97 , 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 , 106 ]. Many have called out the crisis in food quality as a major public health problem [ 65 , 107 ], and its contribution to the ED field is substantial, albeit mostly unrecognized. Up to 80% of food advertising promotes UPF and drink products, with food companies often targeting communities of color [ 108 ]. The ED community disregarding the role of the food supply chain and systemic racism in food access further compounds the racial inequities marginalized communities face with regard to accessing culturally attuned, comprehensive ED care [ 109 ].

We contend that inattention to and outright avoidance of the adverse effects of the Western diet has been a gaping blind spot of ED research and practice and, therefore, draw attention to the dire need to address this [ 86 ]. Evidence-based treatment of EDs is a work in progress, and much research remains to be done to establish best practices, particularly for patients of color and for newer diagnostic categories like atypical anorexia nervosa. Outcomes are less than ideal, particularly in complex patients with multimorbidity, such as those with addiction-like eating [ 110 , 111 ].

We understand the resistance to any departure from an “all foods fit” philosophy. The toxic impact of diet culture, intensified by social media, and its impact on people with restrictive EDs of all body sizes is an important factor. A “one size fits all” mentality is simple and easy to implement, particularly in treatment centers where services are scaled, staff turnover may be high, and individualized nutritional approaches may be challenging to implement and manage in a therapeutic milieu. Maintaining the status quo self-serves ED programs, which then don’t have to individualize nutritional approaches and can avoid the clinical work of supporting patients who may be triggered by peers with different nourishment plans. This stance may avoid potential conflicts among patients with various types of EDs who have different nutritional needs. Patients with ED (and their care teams) are often competitive, prefer rigid rules, and have strong tendencies to compare treatment approaches, including meal plans, with each other or across programs.

We posit that another major reason for the anti-FA stance of many in the ED field is that FA/UPFA is associated with obesity. This topic has become taboo in the ED field largely as a result of weight-based stigma that has harmed (and continues to harm) many patients with ED living in larger bodies navigating medical and mental health treatment settings [ 112 , 113 , 114 , 115 , 116 ]. Any suggestion of reducing or eliminating UPFs is often equated with caloric restriction or attempts to lose weight, which is viewed as anathema to a traditional ED treatment philosophy [ 117 ]. All too often, ED professionals do not acknowledge that there may be times when a patient’s desire to lose weight is not necessarily reflective of restrictive ED pathologies, such as when there is comorbid type II diabetes, pseudotumor cerebri, hypertension, heart disease, or severe osteoarthritis. In fact, there are definitely times when weight loss occurs as a result of improved eating behaviors and normalized eating in the course of ED treatment. There may be times when it is indicated and appropriate, even in patients who may have or have had EDs, to support rather than pathologize a patient’s desire to lose weight, for example, when the benefits of weight loss can reasonably be expected to outweigh the risks. Care must be taken to mitigate the risk of worsening disordered eating behaviors and cognitions and to ensure that patients are fully nourished. The importance of advocacy for body neutrality and weight-inclusive care is essential, especially for ED patients in larger bodies who have suffered great harm from implicit bias related to weight stigma. Ongoing advocacy is undoubtedly of critical importance, but we maintain that a balanced, culturally attuned, individualized, and scientifically sound approach is needed, given how highly contentious these issues are and the limitations of these data. For example, recent studies illustrate that weight loss can be achieved in patients in higher weight categories who are receiving appropriate medical supervision without exacerbating ED symptoms and behaviors [ 118 , 119 , 120 , 121 , 122 , 123 ]. In fact, in a recent systematic review of ED risk during behavioral weight management in adults with overweight or obesity, out of 14 studies that reported the prevalence of binge eating, all 14 studies reported a reduction in binge frequency [ 121 ]. In addition, in those studies that measured global ED symptoms, the majority of studies reported reductions in ED risk. As stated in the new guidelines for treating EDs in patients living in larger bodies, “The presence of an eating disorder should not delay and does not preclude treatment for other medical/psychological conditions” [ 117 ]. Nevertheless, future research on better meeting the needs of the increasing population of ED patients with higher weights will hopefully continue to open up more avenues of effective, weight-inclusive, comprehensive care [ 124 ].

Notwithstanding, if the ED treatment community doesn’t acknowledge the evolving nutritional science, the role of the food environment, and medical multimorbidity and integrate this biopsychosocial perspective into our practices, there is a great risk of inflicting harm on our patients, as well as losing our credibility as a field [ 86 ]. In our opinion, it is imperative that ED clinicians challenge any all-or-nothing thinking that they may have when it comes to the dogmatic nutritional approaches like “all foods fit” and instead make way for a more nuanced, scientifically sound approach that accounts for the myriad of complex comorbidities that ED patients may present with that may necessitate more fine-tuned nutritional prescriptions. We owe it to the 30–40% of patients who do not fully recover with current evidence-based, standard ED treatment approaches, not to mention the countless patients who have no access to clinical trials or treatment settings and of course, those who avoid ED care altogether for fear of being pathologized and poorly served by paternalistic ED treatment delivery models.

Data availability

No datasets were generated or analysed during the current study.

Witkamp RF, van Norren K. Let thy food be thy medicine… when possible. Eur J Pharmacol. 2018;836:102–14. https://doi.org/10.1016/j.ejphar.2018.06.026 .

Article   PubMed   Google Scholar  

Warren CM, Jiang J, Gupta RS. Epidemiology and Burden of Food Allergy. Curr Allergy Asthma Rep. 2020;20(2):6. https://doi.org/10.1007/s11882-020-0898-7 .

Article   PubMed   PubMed Central   Google Scholar  

Spolidoro GCI, Amera YT, Ali MM, Nyassi S, Lisik D, Ioannidou A, et al. Frequency of food allergy in Europe: an updated systematic review and meta-analysis. Allergy. 2023;78(2):351–68. https://doi.org/10.1111/all.15560 .

Houben GF, Baumert JL, Blom WM, Kruizinga AG, Meima MY, Remington BC, et al. Full range of population eliciting dose values for 14 priority allergenic foods and recommendations for use in risk characterization. Food Chem Toxicol. 2020;146:111831. https://doi.org/10.1016/j.fct.2020.111831 .

Golding MA, Batac ALR, Gunnarsson NV, Ahlstedt S, Middelveld R, Protudjer JLP. The burden of food allergy on children and teens: a systematic review. Pediatr Allergy Immunol. 2022;33(3):e13743. https://doi.org/10.1111/pai.13743 .

Jafri S, Frykas TL, Bingemann T, Phipatanakul W, Bartnikas LM, Protudjer JLP. Food Allergy, eating disorders and Body Image. J Affect Disord Rep. 2021;6. https://doi.org/10.1016/j.jadr.2021.100197 .

Pepino MY. Metabolic effects of non-nutritive sweeteners. Physiol Behav. 2015;152(Pt B):450–5. https://doi.org/10.1016/j.physbeh.2015.06.024 .

Shaher SAA, Mihailescu DF, Amuzescu B. Aspartame Safety as a Food Sweetener and Related Health hazards. Nutrients. 2023;15(16). https://doi.org/10.3390/nu15163627 .

Sambu S, Hemaram U, Murugan R, Alsofi AA. Toxicological and teratogenic effect of various food additives: an updated review. Biomed Res Int. 2022;2022:6829409. https://doi.org/10.1155/2022/6829409 .

Miller MD, Steinmaus C, Golub MS, Castorina R, Thilakartne R, Bradman A, et al. Potential impacts of synthetic food dyes on activity and attention in children: a review of the human and animal evidence. Environ Health. 2022;21(1):45. https://doi.org/10.1186/s12940-022-00849-9 .

Gibson PR, Halmos EP, So D, Yao CK, Varney JE, Muir JG. Diet as a therapeutic tool in chronic gastrointestinal disorders: lessons from the FODMAP journey. J Gastroenterol Hepatol. 2022;37(4):644–52. https://doi.org/10.1111/jgh.15772 .

Spiller R. Impact of Diet on symptoms of the irritable bowel syndrome. Nutrients. 2021;13(2). https://doi.org/10.3390/nu13020575 .

Taheri S. Effect of exclusion of frequently consumed dietary triggers in a cohort of children with chronic primary headache. Nutr Health. 2017;23(1):47–50. https://doi.org/10.1177/0260106016688699 .

de Oliveira-Souza AIS, da Silva Freitas D, Ximenes RCC, Raposo MCF, de Oliveira DA. The presence of migraine symptoms was associated with a higher likelihood to present eating disorders symptoms among teenage students. Eat Weight Disord. 2022;27(5):1661–7. https://doi.org/10.1007/s40519-021-01302-5 .

D’Andrea G, Ostuzzi R, Bolner A, Colavito D, Leon A. Is migraine a risk factor for the occurrence of eating disorders? Prevalence and biochemical evidences. Neurol Sci. 2012;33(Suppl 1):S71–6. https://doi.org/10.1007/s10072-012-1045-6 .

Seidel S, Karwautz A, Wagner G, Zormann A, Eder H, Huemer J, et al. Migraine in patients with eating disorders: a study using a sister-pair comparison design. Headache. 2011;51(2):220–5. https://doi.org/10.1111/j.1526-4610.2010.01822.x .

D’Andrea G, Ostuzzi R, Francesconi F, Musco F, Bolner A, d’Onofrio F, et al. Migraine prevalence in eating disorders and pathophysiological correlations. Neurol Sci. 2009;30(Suppl 1):S55–9. https://doi.org/10.1007/s10072-009-0070-6 .

Ostuzzi R, D’Andrea G, Francesconi F, Musco F. Eating disorders and headache: coincidence or consequence? Neurol Sci. 2008;29(Suppl 1):S83–7. https://doi.org/10.1007/s10072-008-0894-5 .

Brewerton TD, George MS. Is migraine related to the eating disorders? Int J Eat Disord. 1993;14(1):75–. https://doi.org/10.1002/1098-108x(199307)14:1<75::aid-eat2260140110>3.0.co;2-d .  9.

Brewerton TD, Gavidia I, Suro G, Perlman MM. Associations between major depressive and bipolar disorders and eating disorder, PTSD, and comorbid symptom severity in eating disorder patients. Eur Eat Disord Rev. 2024;32(2):188–200. https://doi.org/10.1002/erv.3035 .

Brewerton TD, Perlman MM, Gavidia I, Suro G, Jahraus J. Headache, eating disorders, PTSD, and comorbidity: implications for assessment and treatment. Eat Weight Disord. 2022;27(7):2693–700. https://doi.org/10.1007/s40519-022-01414-6 .

Wiklund CA, Rania M, Kuja-Halkola R, Thornton LM, Bulik CM. Evaluating disorders of gut-brain interaction in eating disorders. Int J Eat Disord. 2021;54(6):925–35. https://doi.org/10.1002/eat.23527 .

Peters JE, Basnayake C, Hebbard GS, Salzberg MR, Kamm MA. Prevalence of disordered eating in adults with gastrointestinal disorders: a systematic review. Neurogastroenterol Motil. 2022;34(8):e14278. https://doi.org/10.1111/nmo.14278 .

Ziobrowski H, Brewerton TD, Duncan AE. Associations between ADHD and eating disorders in relation to comorbid psychiatric disorders in a nationally representative sample. Psychiatry Res. 2018;260:53–9. https://doi.org/10.1016/j.psychres.2017.11.026 .

Brewerton TD, Duncan AE. Associations between attention deficit hyperactivity disorder and eating disorders by gender: results from the National Comorbidity Survey Replication. Eur Eat Disord Rev. 2016;24(6):536–40. https://doi.org/10.1002/erv.2468 .

Adan RAH, van der Beek EM, Buitelaar JK, Cryan JF, Hebebrand J, Higgs S, et al. Nutritional psychiatry: towards improving mental health by what you eat. Eur Neuropsychopharmacol. 2019;29(12):1321–32. https://doi.org/10.1016/j.euroneuro.2019.10.011 .

Sarris J. Nutritional Psychiatry: from Concept to the clinic. Drugs. 2019;79(9):929–34. https://doi.org/10.1007/s40265-019-01134-9 .

Marx W, Moseley G, Berk M, Jacka F. Nutritional psychiatry: the present state of the evidence. Proc Nutr Soc. 2017;76(4):427–36. https://doi.org/10.1017/S0029665117002026 .

Kelman L. The triggers or precipitants of the acute migraine attack. Cephalalgia. 2007;27(5):394–402. https://doi.org/10.1111/j.1468-2982.2007.01303.x .

Kokavec A. Dietary therapy could be an important factor in the prevention of headache symptoms in migraine - a case study. Food Public Health. 2014;4(2):15–22. https://doi.org/10.5923/j.fph.20140402.01 .

Article   Google Scholar  

Hajjarzadeh S, Mahdavi R, Shalilahmadi D, Nikniaz Z. The association of dietary patterns with migraine attack frequency in migrainous women. Nutr Neurosci. 2020;23(9):724–30. https://doi.org/10.1080/1028415X.2018.1550890 .

Papetti L, Moavero R, Ferilli MAN, Sforza G, Tarantino S, Ursitti F, et al. Truths and myths in Pediatric Migraine and Nutrition. Nutrients. 2021;13(8). https://doi.org/10.3390/nu13082714 .

Perzia BM, Dunaief JL, Dunaief DM. Chronic migraine reversal and prevention with the LIFE diet: a nutrient dense whole food plant-based diet (WFPBD). BMJ Case Rep. 2021;14(12). https://doi.org/10.1136/bcr-2021-243987 .

Nigg JT, Lewis K, Edinger T, Falk M. Meta-analysis of attention-deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms, restriction diet, and synthetic food color additives. J Am Acad Child Adolesc Psychiatry. 2012;51(1):86–e978. https://doi.org/10.1016/j.jaac.2011.10.015 .

Sonuga-Barke EJ, Brandeis D, Cortese S, Daley D, Ferrin M, Holtmann M, et al. Nonpharmacological interventions for ADHD: systematic review and meta-analyses of randomized controlled trials of dietary and psychological treatments. Am J Psychiatry. 2013;170(3):275–89. https://doi.org/10.1176/appi.ajp.2012.12070991 .

Rambler RM, Rinehart E, Boehmler W, Gait P, Moore J, Schlenker M, et al. A review of the Association of Blue Food Coloring with attention deficit hyperactivity disorder symptoms in children. Cureus. 2022;14(9):e29241. https://doi.org/10.7759/cureus.29241 .

Millichap JG, Yee MM. The diet factor in attention-deficit/hyperactivity disorder. Pediatrics. 2012;129(2):330–7. https://doi.org/10.1542/peds.2011-2199 .

Del-Ponte B, Quinte GC, Cruz S, Grellert M, Santos IS. Dietary patterns and attention deficit/hyperactivity disorder (ADHD): a systematic review and meta-analysis. J Affect Disord. 2019;252:160–73. https://doi.org/10.1016/j.jad.2019.04.061 .

De Petrillo A, Hughes LD, McGuinness S, Roberts D, Godfrey E. A systematic review of psychological, clinical and psychosocial correlates of perceived food intolerance. J Psychosom Res. 2021;141:110344. https://doi.org/10.1016/j.jpsychores.2020.110344 .

Nasr IH, Wahshi HA. Food Intolerance versus Food Allergy. J Integr Food Sci Nutr. 2017;1(1):1–3.

Google Scholar  

Nettleton S, Woods B, Burrows R, Kerr A. Experiencing Food Allergy and Food Intolerance. Sociology. 2010;44(2):289–305. https://doi.org/10.1177/0038038509357208 .

Nettleton S, Woods B, Burrows R, Kerr A. Food allergy and food intolerance: towards a sociological agenda. Health (London). 2009;13(6):647–64. https://doi.org/10.1177/1363459308341433 .

Chen J, Spleen A, Adkins AE, Dick DM, Warren CM, Mountcastle SB, et al. Self-reported Food Allergy and Intolerance among College undergraduates: associations with anxiety and depressive symptoms. J Coll Student Psychother. 2020;36(1):1–22. https://doi.org/10.1080/87568225.2020.1753610 .

Barthels F, Meyer F, Pietrowsky R. Orthorexic and restrained eating behaviour in vegans, vegetarians, and individuals on a diet. Eat Weight Disord. 2018;23(2):159–66. https://doi.org/10.1007/s40519-018-0479-0 .

Timko CA, Hormes JM, Chubski J. Will the real vegetarian please stand up? An investigation of dietary restraint and eating disorder symptoms in vegetarians versus non-vegetarians. Appetite. 2012;58(3):982–90. https://doi.org/10.1016/j.appet.2012.02.005 .

McLean CP, Moeck EK, Sharp G, Thomas NA. Characteristics and clinical implications of the relationship between veganism and pathological eating behaviours. Eat Weight Disord. 2022;27(5):1881–6. https://doi.org/10.1007/s40519-021-01330-1 .

Mathieu S, Hanras E, Dorard G. Associations between vegetarianism, body mass index, and eating disorders/disordered eating behaviours: a systematic review of literature. Int J Food Sci Nutr. 2023;74(4):424–62. https://doi.org/10.1080/09637486.2023.2232953 .

McLean CP, Kulkarni J, Sharp G. Disordered eating and the meat-avoidance spectrum: a systematic review and clinical implications. Eat Weight Disord. 2022;27(7):2347–75. https://doi.org/10.1007/s40519-022-01428-0 .

McLean CP, Chen Z, Fielding J, Sharp G. Preliminary identification of clinical cut-off of the vegetarian vegan eating disorder screener (V-EDS) in a community and self-reported clinical sample of vegetarians and vegans. J Eat Disord. 2024;12(1):17. https://doi.org/10.1186/s40337-024-00969-2 .

Gearhardt AN, DiFeliceantonio AG. Highly processed foods can be considered addictive substances based on established scientific criteria. Addiction. 2023;118(4):589–98. https://doi.org/10.1111/add.16065 .

Gearhardt AN, Schulte EM. Is Food Addictive? A review of the Science. Annu Rev Nutr. 2021;41:387–410. https://doi.org/10.1146/annurev-nutr-110420-111710 .

Mestre-Bach G, Jiménez-Murcia S, Fernández-Aranda F, Potenza MN. Addressing controversies surrounding food addiction. Compulsive Eating Behavior and Food Addiction2019. pp. 419 – 48.

Skinner JA, Leary M, Whatnall M, Collins RA, Pursey KM, Verdejo-Garcia A, et al. A three-arm randomised controlled trial of a telehealth intervention targeting improvement in addictive eating for Australian adults (the TRACE program). Appetite. 2024;195:107211. https://doi.org/10.1016/j.appet.2024.107211 .

Monteiro CA, Cannon G, Moubarac JC, Levy RB, Louzada MLC, Jaime PC. The UN Decade of Nutrition, the NOVA food classification and the trouble with ultra-processing. Public Health Nutr. 2018;21(1):5–17. https://doi.org/10.1017/S1368980017000234 .

Chen X, Zhang Z, Yang H, Qiu P, Wang H, Wang F, et al. Consumption of ultra-processed foods and health outcomes: a systematic review of epidemiological studies. Nutr J. 2020;19(1):86. https://doi.org/10.1186/s12937-020-00604-1 .

Blanco-Rojo R, Sandoval-Insausti H, Lopez-Garcia E, Graciani A, Ordovas JM, Banegas JR, et al. Consumption of Ultra-processed Foods and Mortality: a national prospective cohort in Spain. Mayo Clin Proc. 2019;94(11):2178–88. https://doi.org/10.1016/j.mayocp.2019.03.035 .

Romero Ferreiro C, Martin-Arriscado Arroba C, Cancelas Navia P, Lora Pablos D, de la Gomez A. Ultra-processed food intake and all-cause mortality: DRECE cohort study. Public Health Nutr. 2021;1–10. https://doi.org/10.1017/S1368980021003256 .

Elizabeth L, Machado P, Zinocker M, Baker P, Lawrence M. Ultra-processed Foods and Health outcomes: a narrative review. Nutrients. 2020;12(7). https://doi.org/10.3390/nu12071955 .

Suksatan W, Moradi S, Naeini F, Bagheri R, Mohammadi H, Talebi S, et al. Ultra-processed Food Consumption and adult mortality risk: a systematic review and dose-response Meta-analysis of 207,291 participants. Nutrients. 2021;14(1). https://doi.org/10.3390/nu14010174 .

Rico-Campa A, Martinez-Gonzalez MA, Alvarez-Alvarez I, Mendonca RD, de la Fuente-Arrillaga C, Gomez-Donoso C et al. Association between consumption of ultra-processed foods and all cause mortality: SUN prospective cohort study. BMJ. 2019;365:l1949. https://doi.org/10.1136/bmj.l 1949.

Bonaccio M, Costanzo S, Di Castelnuovo A, Persichillo M, Magnacca S, De Curtis A, et al. Ultra-processed food intake and all-cause and cause-specific mortality in individuals with cardiovascular disease: the Moli-Sani Study. Eur Heart J. 2022;43(3):213–24. https://doi.org/10.1093/eurheartj/ehab783 .

Taneri PE, Wehrli F, Roa-Diaz ZM, Itodo OA, Salvador D, Raeisi-Dehkordi H, et al. Association between Ultra-processed Food Intake and all-cause mortality: a systematic review and Meta-analysis. Am J Epidemiol. 2022;191(7):1323–35. https://doi.org/10.1093/aje/kwac039 .

Orlich MJ, Sabate J, Mashchak A, Fresan U, Jaceldo-Siegl K, Miles F, et al. Ultra-processed food intake and animal-based food intake and mortality in the Adventist Health Study-2. Am J Clin Nutr. 2022;115(6):1589–601. https://doi.org/10.1093/ajcn/nqac043 .

Dehghan M, Mente A, Rangarajan S, Mohan V, Swaminathan S, Avezum A, et al. Ultra-processed foods and mortality: analysis from the Prospective Urban and Rural Epidemiology study. Am J Clin Nutr. 2023;117(1):55–63. https://doi.org/10.1016/j.ajcnut.2022.10.014 .

Prescott SL, Logan AC, D’Adamo CR, Holton KF, Lowry CA, Marks J, et al. Nutritional criminology: why the Emerging Research on Ultra-processed Food Matters to Health and Justice. Int J Environ Res Public Health. 2024;21(2). https://doi.org/10.3390/ijerph21020120 .

de Araujo TP, de Moraes MM, Afonso C, Santos C, Rodrigues SSP. Food Processing: comparison of different food classification systems. Nutrients. 2022;14(4). https://doi.org/10.3390/nu14040729 .

Ayton A, Ibrahim A, Dugan J, Galvin E, Wright OW. Ultra-processed foods and binge eating: a retrospective observational study. Nutrition. 2021;84:111023. https://doi.org/10.1016/j.nut.2020.111023 .

Figueiredo N, Kose J, Srour B, Julia C, Kesse-Guyot E, Peneau S, et al. Ultra-processed food intake and eating disorders: cross-sectional associations among French adults. J Behav Addict. 2022. https://doi.org/10.1556/2006.2022.00009 .

Askari M, Heshmati J, Shahinfar H, Tripathi N, Daneshzad E. Ultra-processed food and the risk of overweight and obesity: a systematic review and meta-analysis of observational studies. Int J Obes (Lond). 2020;44(10):2080–91. https://doi.org/10.1038/s41366-020-00650-z .

Beslay M, Srour B, Mejean C, Alles B, Fiolet T, Debras C, et al. Ultra-processed food intake in association with BMI change and risk of overweight and obesity: a prospective analysis of the French NutriNet-Sante cohort. PLoS Med. 2020;17(8):e1003256. https://doi.org/10.1371/journal.pmed.1003256 .

Hall KD, Ayuketah A, Brychta R, Cai H, Cassimatis T, Chen KY, et al. Ultra-processed diets cause excess calorie intake and weight gain: an Inpatient Randomized Controlled Trial of Ad Libitum Food Intake. Cell Metab. 2019;30(1):67–e773. https://doi.org/10.1016/j.cmet.2019.05.008 .

Machado PP, Steele EM, Levy RB, da Costa Louzada ML, Rangan A, Woods J, et al. Ultra-processed food consumption and obesity in the Australian adult population. Nutr Diabetes. 2020;10(1):39. https://doi.org/10.1038/s41387-020-00141-0 .

Gomez-Donoso C, Sanchez-Villegas A, Martinez-Gonzalez MA, Gea A, Mendonca RD, Lahortiga-Ramos F, et al. Ultra-processed food consumption and the incidence of depression in a Mediterranean cohort: the SUN Project. Eur J Nutr. 2020;59(3):1093–103. https://doi.org/10.1007/s00394-019-01970-1 .

Gangwisch JE, Hale L, Garcia L, Malaspina D, Opler MG, Payne ME, et al. High glycemic index diet as a risk factor for depression: analyses from the women’s Health Initiative. Am J Clin Nutr. 2015;102(2):454–63. https://doi.org/10.3945/ajcn.114.103846 .

Samuthpongtorn C, Nguyen LH, Okereke OI, Wang DD, Song M, Chan AT, et al. Consumption of Ultraprocessed Food and Risk of Depression. JAMA Netw Open. 2023;6(9):e2334770. https://doi.org/10.1001/jamanetworkopen.2023.34770 .

Lane MM, Gamage E, Travica N, Dissanayaka T, Ashtree DN, Gauci S, et al. Ultra-processed Food Consumption and Mental Health: a systematic review and Meta-analysis of Observational studies. Nutrients. 2022;14(13). https://doi.org/10.3390/nu14132568 .

Mazloomi SN, Talebi S, Mehrabani S, Bagheri R, Ghavami A, Zarpoosh M, et al. The association of ultra-processed food consumption with adult mental health disorders: a systematic review and dose-response meta-analysis of 260,385 participants. Nutr Neurosci. 2023;26(10):913–31. https://doi.org/10.1080/1028415X.2022.2110188 .

Srour B, Fezeu LK, Kesse-Guyot E, Alles B, Debras C, Druesne-Pecollo N, et al. Ultraprocessed Food Consumption and Risk of type 2 diabetes among participants of the NutriNet-Sante prospective cohort. JAMA Intern Med. 2020;180(2):283–91. https://doi.org/10.1001/jamainternmed.2019.5942 .

Lane MM, Gamage E, Du S, Ashtree DN, McGuinness AJ, Gauci S, et al. Ultra-processed food exposure and adverse health outcomes: umbrella review of epidemiological meta-analyses. BMJ. 2024;384:e077310. https://doi.org/10.1136/bmj-2023-077310 .

Zhong GC, Gu HT, Peng Y, Wang K, Wu YQ, Hu TY, et al. Association of ultra-processed food consumption with cardiovascular mortality in the US population: long-term results from a large prospective multicenter study. Int J Behav Nutr Phys Act. 2021;18(1):21. https://doi.org/10.1186/s12966-021-01081-3 .

Srour B, Fezeu LK, Kesse-Guyot E, Alles B, Mejean C, Andrianasolo RM, et al. Ultra-processed food intake and risk of cardiovascular disease: prospective cohort study (NutriNet-Sante). BMJ. 2019;365:l1451. https://doi.org/10.1136/bmj.l1451 .

Juul F, Vaidean G, Lin Y, Deierlein AL, Parekh N. Ultra-processed Foods and Incident Cardiovascular Disease in the Framingham offspring study. J Am Coll Cardiol. 2021;77(12):1520–31. https://doi.org/10.1016/j.jacc.2021.01.047 .

Montero-Salazar H, Donat-Vargas C, Moreno-Franco B, Sandoval-Insausti H, Civeira F, Laclaustra M, et al. High consumption of ultra-processed food may double the risk of subclinical coronary atherosclerosis: the Aragon workers’ Health Study (AWHS). BMC Med. 2020;18(1):235. https://doi.org/10.1186/s12916-020-01678-8 .

Du S, Kim H, Rebholz CM. Higher Ultra-processed Food Consumption is Associated with increased risk of Incident Coronary Artery Disease in the atherosclerosis risk in communities Study. J Nutr. 2021;151(12):3746–54. https://doi.org/10.1093/jn/nxab285 .

Du S, Kim H, Crews DC, White K, Rebholz CM. Association between Ultraprocessed Food Consumption and Risk of Incident CKD: a prospective cohort study. Am J Kidney Dis. 2022;80(5):589–. https://doi.org/10.1053/j.ajkd.2022.03.016 . 98 e1.

Ayton A, Ibrahim A. The Western diet: a blind spot of eating disorder research?-a narrative review and recommendations for treatment and research. Nutr Rev. 2020;78(7):579–96. https://doi.org/10.1093/nutrit/nuz089 .

Juul F, Vaidean G, Parekh N. Ultra-processed Foods and Cardiovascular diseases: potential mechanisms of action. Adv Nutr. 2021;12(5):1673–80. https://doi.org/10.1093/advances/nmab049 .

Srour B, Kordahi MC, Bonazzi E, Deschasaux-Tanguy M, Touvier M, Chassaing B. Ultra-processed foods and human health: from epidemiological evidence to mechanistic insights. Lancet Gastroenterol Hepatol. 2022;7(12):1128–40. https://doi.org/10.1016/S2468-1253(22)00169-8 .

Romero X, Aguera Z, Granero R, Sanchez I, Riesco N, Jimenez-Murcia S, et al. Is food addiction a predictor of treatment outcome among patients with eating disorder? Eur Eat Disord Rev. 2019;27(6):700–11. https://doi.org/10.1002/erv.2705 .

Carbone EA, Aloi M, Rania M, de Filippis R, Quirino D, Fiorentino TV, et al. The relationship of food addiction with binge eating disorder and obesity: a network analysis study. Appetite. 2023;190:107037. https://doi.org/10.1016/j.appet.2023.107037 .

Carter JC, Van Wijk M, Rowsell M. Symptoms of ‘food addiction’ in binge eating disorder using the Yale Food Addiction Scale version 2.0. Appetite. 2019;133:362–9. https://doi.org/10.1016/j.appet.2018.11.032 .

Jimenez-Murcia S, Aguera Z, Paslakis G, Munguia L, Granero R, Sanchez-Gonzalez J, et al. Food Addiction in Eating Disorders and Obesity: analysis of clusters and implications for treatment. Nutrients. 2019;11(11). https://doi.org/10.3390/nu11112633 .

Lee JH, Duster M, Roberts T, Devinsky O. United States Dietary trends since 1800: lack of Association between saturated fatty acid consumption and non-communicable diseases. Front Nutr. 2021;8:748847. https://doi.org/10.3389/fnut.2021.748847 .

Praxedes DRS, Silva-Junior AE, Macena ML, Oliveira AD, Cardoso KS, Nunes LO, et al. Prevalence of food addiction determined by the Yale Food Addiction Scale and associated factors: a systematic review with meta-analysis. Eur Eat Disord Rev. 2022;30(2):85–95. https://doi.org/10.1002/erv.2878 .

Kladnicka I, Bludovska M, Plavinova I, Muller L, Mullerova D. Obesogens in Foods. Biomolecules. 2022;12(5). https://doi.org/10.3390/biom12050680 .

Heindel JJ, Lustig RH, Howard S, Corkey BE. Obesogens: a unifying theory for the global rise in obesity. Int J Obes (Lond). 2024. https://doi.org/10.1038/s41366-024-01460-3 .

Di Pietro G, Forcucci F, Chiarelli F. Endocrine Disruptor Chemicals and Children’s Health. Int J Mol Sci. 2023;24(3). https://doi.org/10.3390/ijms24032671 .

Heindel JJ, Howard S, Agay-Shay K, Arrebola JP, Audouze K, Babin PJ, et al. Obesity II: establishing causal links between chemical exposures and obesity. Biochem Pharmacol. 2022;199:115015. https://doi.org/10.1016/j.bcp.2022.115015 .

Shahnazaryan U, Wojcik M, Bednarczuk T, Kurylowicz A. Role of Obesogens in the pathogenesis of obesity. Med (Kaunas). 2019;55(9). https://doi.org/10.3390/medicina55090515 .

Maqbool F, Mostafalou S, Bahadar H, Abdollahi M. Review of endocrine disorders associated with environmental toxicants and possible involved mechanisms. Life Sci. 2016;145:265–73. https://doi.org/10.1016/j.lfs.2015.10.022 .

Janesick AS, Blumberg B. Obesogens: an emerging threat to public health. Am J Obstet Gynecol. 2016;214(5):559–65. https://doi.org/10.1016/j.ajog.2016.01.182 .

Amato AA, Wheeler HB, Blumberg B. Obesity and endocrine-disrupting chemicals. Endocr Connect. 2021;10(2):R87–105. https://doi.org/10.1530/EC-20-0578 .

Gupta R, Kumar P, Fahmi N, Garg B, Dutta S, Sachar S, et al. Endocrine disruption and obesity: a current review on environmental obesogens. Curr Res Green Sustainable Chem. 2020;3. https://doi.org/10.1016/j.crgsc.2020.06.002 .

Kim JT, Lee HK. Childhood obesity and endocrine disrupting chemicals. Ann Pediatr Endocrinol Metab. 2017;22(4):219–25. https://doi.org/10.6065/apem.2017.22.4.219 .

Petrakis D, Vassilopoulou L, Mamoulakis C, Psycharakis C, Anifantaki A, Sifakis S, et al. Endocrine disruptors leading to obesity and related diseases. Int J Environ Res Public Health. 2017;14(10). https://doi.org/10.3390/ijerph14101282 .

Darbre PD. Endocrine disruptors and obesity. Curr Obes Rep. 2017;6(1):18–27. https://doi.org/10.1007/s13679-017-0240-4 .

Cassin SE, Buchman DZ, Leung SE, Kantarovich K, Hawa A, Carter A, et al. Ethical, Stigma, and Policy Implications of Food Addiction: a scoping review. Nutrients. 2019;11(4). https://doi.org/10.3390/nu11040710 .

Harris JL. Targeted marketing report. Increasing disparities in unhealthy food advertising targeted to Hispanic and Black youth: The Rudd Center for Food Policy & Obesity; 2019 [ https://media.ruddcenter.uconn.edu/PDFs/TargetedMarketingReport2019.pdf .

Nguyen KH, Glantz SA, Palmer CN, Schmidt LA. Transferring Racial/Ethnic Marketing Strategies from Tobacco to Food Corporations: Philip Morris and Kraft General Foods. Am J Public Health. 2020;110(3):329–36. https://doi.org/10.2105/AJPH.2019.305482 .

Brewerton TD. Food Addiction and its associations to Trauma, Severity of Illness and Comorbidity. In: Cottone P, Sabino V, Moore C, Koob GF, editors. Compulsive eating behavior and food addiction: emerging pathological constructs. First ed. Philadelphia: Elsevier; 2019. pp. 449–68.

Chapter   Google Scholar  

Brewerton TD. Food addiction as a proxy for eating disorder and obesity severity, trauma history, PTSD symptoms, and comorbidity. Eat Weight Disord. 2017;22(2):241–7. https://doi.org/10.1007/s40519-016-0355-8 .

Hay P, Mitchison D. Eating disorders and obesity: the challenge for our Times. Nutrients. 2019;11(5). https://doi.org/10.3390/nu11051055 .

Bristow C, Allen KA, Simmonds J, Snell T, McLean L. Anti-obesity public health advertisements increase risk factors for the development of eating disorders. Health Promot Int. 2022;37(2). https://doi.org/10.1093/heapro/daab107 .

Bristow C, Meurer C, Simmonds J, Snell T. Anti-obesity public health messages and risk factors for disordered eating: a systematic review. Health Promot Int. 2020;35(6):1551–69. https://doi.org/10.1093/heapro/daaa018 .

Sanchez-Carracedo D, Neumark-Sztainer D, Lopez-Guimera G. Integrated prevention of obesity and eating disorders: barriers, developments and opportunities. Public Health Nutr. 2012;15(12):2295–309. https://doi.org/10.1017/S1368980012000705 .

Macpherson-Sanchez AE. Integrating fundamental concepts of obesity and eating disorders: implications for the obesity epidemic. Am J Public Health. 2015;105(4):e71–85. https://doi.org/10.2105/AJPH.2014.302507 .

Ralph AF, Brennan L, Byrne S, Caldwell B, Farmer J, Hart LM, et al. Management of eating disorders for people with higher weight: clinical practice guideline. J Eat Disord. 2022;10(1):121. https://doi.org/10.1186/s40337-022-00622-w .

Hay P, Palavras MA, da Luz FQ, Dos Anjos Garnes S, Sainsbury A, Touyz S, et al. Physical and mental health outcomes of an integrated cognitive behavioural and weight management therapy for people with an eating disorder characterized by binge eating and a high body mass index: a randomized controlled trial. BMC Psychiatry. 2022;22(1):355. https://doi.org/10.1186/s12888-022-04005-y .

Palavras MA, Hay P, Mannan H, da Luz FQ, Sainsbury A, Touyz S, et al. Integrated weight loss and cognitive behavioural therapy (CBT) for the treatment of recurrent binge eating and high body mass index: a randomized controlled trial. Eat Weight Disord. 2021;26(1):249–62. https://doi.org/10.1007/s40519-020-00846-2 .

Eichen DM, Strong DR, Rhee KE, Rock CL, Crow SJ, Epstein LH, et al. Change in eating disorder symptoms following pediatric obesity treatment. Int J Eat Disord. 2019. https://doi.org/10.1002/eat.23015 .

Jebeile H, Libesman S, Melville H, Low-Wah T, Dammery G, Seidler AL, et al. Eating disorder risk during behavioral weight management in adults with overweight or obesity: a systematic review with meta-analysis. Obes Rev. 2023;24(6):e13561. https://doi.org/10.1111/obr.13561 .

Jebeile H, Gow ML, Baur LA, Garnett SP, Paxton SJ, Lister NB. Treatment of obesity, with a dietary component, and eating disorder risk in children and adolescents: a systematic review with meta-analysis. Obes Rev. 2019. https://doi.org/10.1111/obr.12866 .

Jebeile H, Gow ML, Baur LA, Garnett SP, Paxton SJ, Lister NB. Association of Pediatric Obesity Treatment, including a Dietary Component, with change in depression and anxiety: a systematic review and Meta-analysis. JAMA Pediatr. 2019;173(11):e192841. https://doi.org/10.1001/jamapediatrics.2019.2841 .

McMaster CM, Paxton SJ, Maguire S, Hill AJ, Braet C, Seidler AL, et al. The need for future research into the assessment and monitoring of eating disorder risk in the context of obesity treatment. Int J Eat Disord. 2023. https://doi.org/10.1002/eat.23898 .

Download references

Acknowledgements

Not applicable.

Author information

Authors and affiliations.

Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, SC, USA

Timothy D. Brewerton

SunCloud Health, Chicago, IL, USA

Department of Psychiatry, University of Illinois Chicago College of Medicine, Chicago, IL, USA

Nutrition in Recovery, Los Angeles, CA, USA

David A. Wiss

You can also search for this author in PubMed   Google Scholar

Contributions

T.B. wrote the initial draft, and all authors participated in the creation, preparation, and editing of the manuscript.

Corresponding author

Correspondence to Timothy D. Brewerton .

Ethics declarations

Ethics approval and consent to participate, consent for publication.

All authors consent to publication.

Clinical implications

The ED dogma that “all foods fit” is outdated and potentially harmful to many. Evidence indicates several exceptions to this rule, including the following: (a) food allergies, sensitivities, intolerances, (b) religious/spiritual preferences (c) ultra-processed foods, which promote addiction-like eating, higher morbidity/mortality. This evidence should be integrated into (rather than dissociated from) ED treatment.

Competing interests

The authors declare no competing interests.

Additional information

Publisher’s note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ . The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/ ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Cite this article.

Brewerton, T.D., Dennis, K. & Wiss, D.A. Dismantling the myth of “all foods fit” in eating disorder treatment. J Eat Disord 12 , 60 (2024). https://doi.org/10.1186/s40337-024-01017-9

Download citation

Received : 09 March 2024

Accepted : 09 May 2024

Published : 17 May 2024

DOI : https://doi.org/10.1186/s40337-024-01017-9

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

• Eating disorders
• Nutritional rehabilitation
• Food allergies
• Food addiction
• Ultra-processed food

Journal of Eating Disorders

ISSN: 2050-2974

• General enquiries: [email protected]

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

• Advanced Search
• Journal List
• J Eat Disord

Risk factors for eating disorders: findings from a rapid review

Sarah barakat.

1 InsideOut Institute for Eating Disorders, University of Sydney, Sydney Local Health District, Sydney, Australia

4 Faculty of Medicine and Health, Charles Perkins Centre (D17), InsideOut Institute, University of Sydney, Level 2, Sydney, NSW 2006 Australia

Siân A. McLean

2 School of Psychology and Public Health, La Trobe University, Melbourne, Australia

Emma Bryant

3 Healthcare Management Advisors, Melbourne, Australia

Stephen Touyz

Sarah maguire, associated data.

Not applicable—all citations provided.

Risk factors represent a range of complex variables associated with the onset, development, and course of eating disorders. Understanding these risk factors is vital for the refinement of aetiological models, which may inform the development of targeted, evidence-based prevention, early intervention, and treatment programs. This Rapid Review aimed to identify and summarise research studies conducted within the last 12 years, focusing on risk factors associated with eating disorders.

The current review forms part of a series of Rapid Reviews to be published in a special issue in the Journal of Eating Disorders, funded by the Australian Government to inform the development of the National Eating Disorder Research and Translation Strategy 2021–2031. Three databases were searched for studies published between 2009 and 2021, published in English, and comprising high-level evidence studies (meta-analyses, systematic reviews, moderately sized randomised controlled studies, moderately sized controlled-cohort studies, or population studies). Data pertaining to risk factors for eating disorders were synthesised and outlined in the current paper.

A total of 284 studies were included. The findings were divided into nine main categories: (1) genetics, (2) gastrointestinal microbiota and autoimmune reactions, (3) childhood and early adolescent exposures, (4) personality traits and comorbid mental health conditions, (5) gender, (6) socio-economic status, (7) ethnic minority, (8) body image and social influence, and (9) elite sports. A substantial amount of research exists supporting the role of inherited genetic risk in the development of eating disorders, with biological risk factors, such as the role of gut microbiota in dysregulation of appetite, an area of emerging evidence. Abuse, trauma and childhood obesity are strongly linked to eating disorders, however less conclusive evidence exists regarding developmental factors such as role of in-utero exposure to hormones. Comorbidities between eating disorders and mental health disorders, including personality and mood disorders, have been found to increase the severity of eating disorder symptomatology. Higher education attainment, body image-related factors, and use of appearance-focused social media are also associated with increased risk of eating disorder symptoms.

Eating disorders are associated with multiple risk factors. An extensive amount of research has been conducted in the field; however, further studies are required to assess the causal nature of the risk factors identified in the current review. This will assist in understanding the sequelae of eating disorder development and in turn allow for enhancement of existing interventions and ultimately improved outcomes for individuals.

Supplementary Information

The online version contains supplementary material available at 10.1186/s40337-022-00717-4.

Plain English summary

Research into the risk factors associated with eating disorders (EDs) is necessary in order to better understand the reasons why people develop EDs and to inform programs which aim to reduce these risk factors. In the current study we reviewed studies published between 2009 and 2021 which had researched risk factors associated with EDs. This study is one review of a wider Rapid Review series conducted as part the development of Australia’s National Eating Disorders Research and Translation Strategy 2021–2031. The findings from this review are grouped into nine main risk factor categories. These include (1) genetics, (2) gastrointestinal microbiota and autoimmune reactions, (3) childhood and early adolescent exposures, (4) personality traits and comorbid mental health conditions, (5) gender, (6) socio-economic status, (7) ethnic minority, (8) body image and social influence, and (9) elite sports. Further research is needed to better understand the relationship between the risk factors, in particular the ways in which they may interact with each other and whether they cause the ED or are just associated with the ED.

Introduction

Eating disorders (ED) are complex psychiatric conditions associated with significant psychological and physical impairment. Individuals with EDs are at greater risk of suicide attempts, mortality, and poorer quality of life relative to both the general population and individuals with other psychiatric conditions [ 1 – 3 ]. Central to addressing the pervasive nature of EDs is understanding the circumstances which make individuals more vulnerable to developing these psychiatric conditions. The development of an ED is dependent on a myriad of variables ranging from sociocultural, to biological and genetic, and psychological factors. Despite the variation and complexity present in the aetiology of EDs, efforts have been made by researchers to identify risk factors which commonly predict onset [ 4 – 6 ]. Understanding the range of risk factors and their potential contribution to onset of an ED is crucial to identifying at risk groups and providing effective screening and prevention programs, as well as targeted interventions [ 7 , 8 ].

EDs can be severe and are often chronic in nature, particularly if not addressed in a timely manner. A recent study of ED patients identified an average delay of 5.28 years between ED symptom onset and treatment-seeking [ 9 ]. A factor considered to contribute to this delay is health professionals’ lack of awareness of indicators of disordered eating behaviours, meaning EDs often go unrecognised by treating clinicians [ 10 ]. Identification of risk factors for EDs offers an opportunity for targeted education of health professionals to assist in distinguishing patterns of psychosocial, biological, and genetic vulnerabilities for disordered eating even in the absence of any overt weight or dietary concerns [ 11 ].

Knowledge of the risk factors for EDs offers the opportunity for early identification of high-risk groups and in turn a timely and tailored response via avenues such as public policy development or initiation of targeted prevention programs [ 12 ]. Prevention and early intervention programs based upon aetiological models may help to prevent movement along the spectrum from at-risk to full threshold disorder [ 13 ]. Additionally, EDs are complex psychiatric conditions with a somewhat limited range of efficacious evidence-based interventions [ 14 , 15 ]. In addition, a significant number of patients with EDs do not respond to current evidence-based treatments [ 16 – 20 ]. As such, attempts to better understand the role of risk factors in aetiological and causal pathways of EDs are necessary in order to form more nuanced conceptualisations of these illnesses. This may inform the development of more effective treatments, especially for those with persistent and chronic course [ 21 ].

The current Rapid Review paper forms part of a series of reviews commissioned by the Australian Federal Government to inform the Australian National Eating Disorders Research and Translation Strategy 2021–2031[ 22 ]. This paper aims to identify and explore the risk factors associated with EDs by summarising the existing evidence related to aetiological underpinnings. Importantly, the review is inclusive of research which considers risk factors to be either causal in nature or associated with the onset of ED.

The Australian Government Commonwealth Department of Health funded the InsideOut Institute for Eating Disorders (IOI) to develop the Australian Eating Disorders Research and Translation Strategy 2021–2031 [ 1 ] under the Psych Services for Hard to Reach Groups initiative (ID 4-8MSSLE). The strategy was developed in partnership with state and national stakeholders including clinicians, service providers, researchers, and experts by lived experience (including consumers and families/carers). Developed through a two-year national consultation and collaboration process, the strategy provides the roadmap to establishing EDs as a national research priority and is the first disorder-specific strategy to be developed in consultation with the National Mental Health Commission. To inform the strategy, IOI commissioned Healthcare Management Advisors (HMA) to conduct a series of RRs to broadly assess all available peer-reviewed literature on the six DSM-5 listed EDs.

A RR Protocol [ 23 ] was utilised to swiftly synthesise evidence in order to guide public policy and decision-making [ 24 ]. This approach has been adopted by several leading health organisations including the World Health Organisation [ 25 ] and the Canadian Agency for Drugs and Technologies in Health Rapid Response Service [ 26 ], to build a strong evidence base in a timely and accelerated manner, without compromising quality. A RR is not designed to be as comprehensive as a systematic review – it is purposive rather than exhaustive and provides actionable evidence to guide health policy [ 27 ].

The RR is a narrative synthesis and sought to adhere to the PRISMA guidelines [ 28 ]. It is divided by topic area and presented as a series of papers. Three research databases were searched: ScienceDirect, PubMed and Ovid/Medline. To establish a broad understanding of the progress made in the field of EDs, and to capture the largest evidence base from the past 12 years (originally 2009–2019, but expanded to include the preceding two years), the eligibility criteria for included studies into the rapid review were kept broad. Therefore, included studies were published between 2009 and 2021, in English, and conducted within Western healthcare systems or health systems comparable to Australia in terms of structure and resourcing. The initial search and review process was conducted by three reviewers between 5 December 2019 and 16 January 2020. The re-run for the years 2020–2021 was conducted by two reviewers at the end of May 2021.

The RR had a translational research focus with the objective of identifying evidence relevant to developing optimal care pathways. Searches therefore used a Population, Exposure, Outcome (PEO) approach [ 29 ] whereby search terms are specified to identify literature relating to the population or group of interest (i.e., individuals of any age or background with the propensity to develop and eating disorder), exposure to the risk factors that are associated with the development of an eating disorder, and the outcome of interest (i.e., the development of an eating disorder). By using the three PEO components to guide the search strategy, the PEO approach aims to facilitate a thorough and systematic examination of existing literature. Purposive sampling focused on high-level evidence studies such as: meta-analyses; systematic reviews; moderately sized randomised controlled studies (RCTs) ( n  > 50); moderately sized controlled-cohort studies ( n  > 50), or population studies ( n  > 500). However, the diagnoses ARFID and UFED necessitated a less stringent eligibility criterion due to a paucity of published articles. As these diagnoses are newly captured in the DSM-5 (released in 2013, within the allocated search timeframe), the evidence base is emerging and fewer studies have been conducted. Thus, smaller studies (n =  < 20) and narrative reviews were also considered and included. Grey literature, such as clinical or practice guidelines, protocol papers (without results) and Masters’ theses or dissertations, was excluded. Other sources (which may not be replicable when applying the current methodology) included the personal libraries of authors, yielding four additional studies (see Additional File 1 ). This extra step was conducted in line with the PRISMA-S: an extension to the PRISMA Statement for Reporting Literature Searches in Systematic Reviews [ 30 ].

Full methodological details including eligibility criteria, search strategy and terms and data analysis are published in a separate protocol paper [ 31 ]. The full RR included a total of 1320 studies (see Additional File 1 for PRISMA flow diagram). Data from included studies relating to risk factors for EDs were synthesised and are presented in the current review.

The Rapid Review identified 284 studies for inclusion in the ‘Risk Factors’ category. When referring to ‘risk factors’ in this review, we are not always referring to causal risk factors. Accordingly, some of the risk factors included in this review are correlated or associated with increased risk of an ED, without evidence of causation. As the aim of a Rapid Review is to broadly synthesise findings, we did not narrow to studies only providing evidence regarding the causal relationship of risk factors. Rather, the current review focused on a range of research including prospective, experimental and correlational studies to identify a large number of potential correlates which have risk capacity for EDs. According to the Kraemer et al. (2001) criteria, this review covers research related to the following technical terms: “correlate” (a measure associated with the outcome), “risk factor” (a measure which precedes the outcome), and “causal risk factor” (a risk factor, which when manipulated, causes a change in the outcome) [ 32 ]. Therefore, the factors identified in this review are associated or predictive factors, unless in cases where a causative link has been demonstrated. A summary of the key risk factors associated with EDs is provided in Table ​ Table1 1 and are discussed in this section. Results are subdivided into nine categories: (1) genetics, (2) gastrointestinal microbiota and autoimmune reactions, (3) childhood and early adolescent exposures, (4) personality traits and comorbid mental health conditions, (5) gender, (6) socio-economic status, (7) ethnic minority, (8) body image and social influence, and (9) elite sports. A full list of included studies for this topic, including population, aims, design, and outcome measures is available in Additional File 1 .

Risk factors associated with EDs

ED eating disorder; AN anorexia nervosa; BN bulimia nervosa; BED binge eating disorder; EDNOS eating disorder not otherwise specified; BMI body mass index; AN-BP anorexia nervosa (binge-purge subtype); PD personality disorder; ARFID avoidant restrictive food intake disorder; AN-R anorexia nervosa (restrictive subtype); A-AN atypical AN

1. Genetics: endocrines and neurotransmitters

Genetic risk factors and polymorphisms (variations in gene expression), relating to core EDs have been widely studied. Research conducted within twins and family groups as well as large-scale genomic studies have indicated a genetic component to risk of Anorexia Nervosa (AN), Bulimia Nervosa (BN) and Binge Eating Disorder (BED) [ 33 ]. Incidence rates in individuals with a parent with a history of ED have been found to be over twice as high compared to individuals with parents with no history of an ED [ 34 ]. Familial studies have demonstrated a strong genetic association for AN in particular. An individual is 11 times more likely to develop AN if they have a relative with the disorder as compared to someone with no family history. Similarly, an individual is 9.6 times more likely to develop BN, and 2.2 times more likely to develop BED if they have a relative with the disorder [ 33 ]. Evidence of genetic risk factors for other EDs is growing [ 33 ], although there have been no genetic studies to date conducted with Avoidant Restrictive Food Intake Disorder (ARFID) [ 35 ].

Anorexia nervosa and bulimia nervosa

Genetic factors have been shown to strongly contribute to both AN and BN [ 36 ]. There is evidence to suggest approximately half of the genetic factors implicated in AN and BN are shared between the disorders, with the remaining 50% being unique to one or the other [ 36 ]. An older study of Norwegian twins found some support for different features of AN being more heritable than others; having found weight/shape concern to have greater genetic association than low BMI and amenorrhea [ 37 ]. In contrast the landmark 2019 study by two international genome-wide association consortiums found that both metabolic and anthropometric related genetic loci associated with BMI lowering alleles have strong correlations with AN [ 38 ].

Hereditary patterns of EDs have been shown to disproportionately affect females [ 34 ]. In a sample of adolescent twins aged 15 to 17, Baker et al. (2009) found females were at greater genetic risk for disordered eating than males [ 39 ]. This is consistent with earlier evidence suggesting drive for thinness and body dissatisfaction showed lower heritability in males [ 40 ]. Baker et al. [ 39 ] found that only half of the genetic risk factors predicting drive for thinness and body dissatisfaction in females predicted the same traits in males. A possible explanation for this difference was offered in a study of French and German cohorts whereby inherited variations in an estrogen receptor gene (ESR1) significantly increased risk of restrictive eating and subsequently development of AN restrictive subtype (AN-R) [ 41 ].

Comorbidities

Genetic risk has been implicated in co-occurrence of EDs and other psychiatric diagnoses. Genetic associations have been found between Attention-Deficit/Hyperactivity Disorder (ADHD) and all EDs, with the strongest correlation to binge/purge-type ED behaviours [ 42 , 43 ]. Strong positive genetic associations have also been identified between AN and other psychiatric comorbidities, including Obsessive Compulsive Disorder (OCD), major depressive disorder, suicidality, schizophrenia, neuroticism, autism, and neurodevelopmental delay [ 44 – 48 ]. Genetic risk for comorbid AN and Generalised Anxiety Disorder (GAD) has also been identified [ 46 , 47 ].

The contribution of comorbid mental health disorders to ED risk and outcomes are further discussed in Sect.  Results and in another topic paper of the Rapid Review, ‘Psychiatric Comorbidities and Medical Complications.’

Genes and polymorphisms

Several genomic studies have attempted to locate specific gene loci implicated in the development of EDs. See Table ​ Table2 2 for a summary of genes and polymorphisms identified in ED genomic studies. A recent genome-wide association study published in 2021 has suggested that there is a distinct difference in the underlying biology between binge-type EDs (BN and BED) and AN. The study reported that both BN and BED shared genomic variant with overweight and obesity, whereas the directions of these associations were reversed for AN [ 49 ].

Genes and polymorphisms identified in the development of EDs

ED eating disorder; AN anorexia nervosa; BN bulimia nervosa, BED binge eating disorder

Genetic susceptibility to AN was explored in a landmark meta-analysis of 33 datasets from international genome-wide association studies. Watson et al. [ 38 ] compared the DNA of almost 17,000 individuals with AN to the DNA of 55,000 people without AN around the world. Eight loci associated with significant risk of developing AN were identified [ 38 , 50 ], including genetic correlations with certain psychiatric, anthropometric, and metabolic traits, as well as physical activity. Positive associations were found for physical activity, anxiety and schizophrenia disorders, and HDL cholesterol. Negative associations were found for metabolic (including glycemic), lipid, and anthropometric traits including fat mass, fat-free mass, BMI, obesity, type 2 diabetes, fasting insulin, insulin resistance, and leptin [ 48 ]. Analysis of causality revealed a bi-directional relationship between potential AN genes and risk for low body mass index (BMI). However, there is stronger evidence that low-BMI-causing alleles increase risk of AN than there is for AN-risk genes leading to low BMI [ 38 ].

A study of Norwegian adolescents found an association between poor appetite and undereating, and the COMT gene, which is responsible for regulating dopamine levels through the production of the COMT enzyme [ 51 ]. Brain studies of patients with AN have indicated that, due to disturbances in regular serotonin and dopamine reward pathways, individuals with AN may use restricted eating as a mechanism to reduce anxiety [ 52 ]. In one study of patients with AN and BN, mutations in genes with heightened expression in brain tissue (CNTF, NTRK) were associated with a higher minimum lifetime BMI and earlier ED onset [ 53 ].

Six genetic polymorphisms have been associated with the development of BN in people with obesity [ 54 ]. Of the six genetic polymorphisms, three are thought to be related to the neuroendocrine receptors of dopamine, serotonin, and cannabinoid. This association is supported by evidence that genetic variations which lead to low dopamine production and neurotransmission are associated with an increased risk of binge/purge type EDs [ 55 ]. The remaining three polymorphisms identified in BN aetiology were associated with an estrogen receptor, the production of an enzyme expressed in brain tissue, and the FTO gene (which has a role in BMI regulation) [ 54 ]. While dopamine and serotonin receptor genes (DRD2 and SLC6A4, respectively) are implicated in the development of both BN and BED, differing polymorphisms in these genes appear to be associated with increased risk of developing one disorder over the other [ 54 ]. Further, triallelic 1 variations in a serotonin receptor allele (5-HTTLPR) have also been observed to contribute to compulsive personality traits and the development of AN, BN, and eating disorder not otherwise specified (EDNOS) [ 56 , 57 ]. A polymorphism of the oxytocin receptor gene (OXT-R) was also found to distinguish between risk of onset for restricting type EDs or binge/purge type EDs, indicating the potential role of oxytocin in the development and maintenance of EDs [ 58 ]. Additional research has identified an association between a polymorphism in a neurotransmitter inhibition gene (HTR1B) and an increased risk of developing BN as well as greater severity of AN symptoms, including low BMI [ 59 ].

Expression of genes associated with the production of appetite and weight control endocrines (leptin, melanocortin, and neurotrophin) are thought to have a role in ED development and severity [ 45 ]. A case–control study by Zeeland et al. [ 60 ] found a significant number of AN participants with a polymorphism in a cholesterol metabolism gene (EPHX2), which was also associated with lower BMI (see Table ​ Table2). 2 ). Yilmaz et al. (2014) examined 20 single-nucleotide polymorphisms 2 (SNPs) in the endocrine system genes in a sample of individuals with BN (n = 745) and AN (n = 245). Although no significant differences were observed between either ED diagnosis or control participants, two SNPs associated with regulation of BMI were found to have an impact on disease severity (See Table ​ Table2) 2 ) [ 61 ].

Consequences of variations in endocrine signalling in individuals with ED also include reduced capacity for interoception 3 particularly relating to gastric interoception. A systematic review of interoception in individuals with ED found the strongest correlations were observed in individuals with AN who consistently had lower gastric interoception relating to satiety and self-reported fullness, while individuals with BN were found to have lower pain interoception resulting in higher pain thresholds. However, researchers were unable to ascertain whether lack of gastric interoception in individuals with AN was a result of conscious processing of satiety cues or disruptions in endocrine signalling [ 62 ].

Non-shared vs. shared environments

A Swedish study of female monozygotic (identical) and dizygotic (fraternal) twins aged between 20 and 47 found that nonshared environmental factors between twins had a greater impact on ED risk than shared environmental factors [ 36 ]. This finding was further supported by a study of an Australian twin sample, which concluded that nonshared environmental factors contributed to the genetic factors associated with weight loss behaviours and overeating behaviours in AN and BN, respectively [ 63 ]. Shared environmental factors were not observed to have an impact on disordered eating behaviours [ 63 ].

Exposure to childhood trauma has been linked to polymorphisms in genes expressed in the glucocorticoid receptor pathway which are associated with increased risk of developing BN, binge eating, and loss of control over eating [ 51 , 64 – 66 ]. This finding is supported by research conducted by Monteleone et al. [ 67 ], who found significantly lower levels of cortisol in individuals with AN and BN with a history of childhood maltreatment than healthy controls and those ED patients with no history of childhood trauma. Exposure to childhood trauma was also found to interact with gene expression through creating higher levels of DNA methylation 4 in women with BN [ 68 ]. Analysis of evidence from seven studies found a strong additive effect for serotonin transporter 5-HTTLPR polymorphism combined with childhood experiences of physical and sexual abuse in the development of BN [ 69 ]. Childhood trauma and abuse as a risk factor for EDs, particularly related to environmental influence, will be further discussed in Sect.  Results .

Binge eating disorder

Variation in genes linked to appetite and satiety modulating hormones such as ghrelin are often implicated in the development of BED, as well as several genes related to regulation of BMI and fat storage. A study of 4,360 adolescents aged 14 or 16 found that frequency of binge eating was associated with expression of a polymorphism in the FTO gene, thought to play a role in BMI and obesity [ 70 ]. Further, mutations of the MC4R gene, involved in metabolism and feeding, is also associated with BED and obesity [ 71 , 72 ].

As previously discussed, polymorphisms in genes responsible for the production of neuroendocrine receptors such as dopamine and serotonin are also commonly associated with BN and BED [ 54 ]. Reward responses to food have long been implicated in the development and perpetuation of BED. The expression of two alleles in the dopamine D2 receptor has been found to be positively associated with BED in a sample of 230 individuals with obesity [ 73 ]. The authors concluded that expressions of these alleles was associated with hypersensitivity to reward, likely having a causal relationship with BED [ 73 ]. In a study of female twins in the US, increased binge eating frequency was also found to be associated with genetic factors related to the personality traits neuroticism and conscientiousness [ 74 ].

Night eating syndrome

Genetic research relating to Night Eating Syndrome (NES) is less developed than the primary EDs. Work in animal models has implicated variants of the VGF, a gene responsible for production of a neuropeptide precursor in NES aetiology [ 75 , 76 ]. One familial study was identified assessing the heritability of NES involving families where at least one parent had obesity. Night eating symptoms in mothers were strongly associated with similar behaviours in their sons and daughters, while no such correlation was observed for fathers [ 77 ]. Interestingly, the association was slightly stronger in sons (r = 0.19) than in daughters (r = 0.15), whereas heritability relationships are typically stronger in female offspring in other ED diagnoses [ 34 , 77 ]. This finding was further supported by evidence from a Swedish twin registry study where males were more likely to endorse night eating traits associated with genetic factors, while females were more likely to endorse binge eating [ 76 ]. Further research is required to understand any potential genetic risk factors associated with NES.

There is considerable evidence pointing to genetic risk in the development of EDs, with the highest heritability conferred for AN [ 33 , 34 ]. Females are also at greater genetic risk for disordered eating in comparison to males [ 39 ]. When considering the specific genetic variations thought to contribute to increased ED risk, genetic associations have been found between EDs and other psychiatric comorbidities, however the type of comorbidity differs according to the ED diagnosis. For binge-type EDs (BN and BED) strongest genetic correlations are observed with ADHD [ 42 , 43 ] whilst AN has strong correlations with OCD, MDD, suicidality, schizophrenia, neuroticism, autism, and neurodevelopmental delay [ 44 – 48 ]. In a similar manner, genetic correlations with metabolic traits appear to differ between ED diagnoses, such that BN and BED have been found to share genomic variants with overweight and obesity [ 49 ] whereas potential AN genes uphold a bi-directional relationship with low BMI [ 38 ]. Genes associated with other metabolic functions, including appetite and weight control endocrines (leptin, melanocortin, neurotrophin) have also been implicated in ED development and severity, however fewer differences between ED diagnoses are apparent. Polymorphisms in the genetic loci responsible for neurotransmitters associated with reward processing and appetite regulation hormones, including dopamine, serotonin, and cannabinoid have been identified as a risk factor across several ED diagnoses including AN, BN, and EDNOS [ 45 , 50 – 62 ]. Additionally, genetic polymorphisms in the glucocorticoid receptor pathway responsible for the stress response have been linked to individuals who have experienced trauma and are associated with increased risk for BN [ 51 , 65 , 66 ].

2. Gastrointestinal microbiota and autoimmune reactions

Gastrointestinal microbiota.

The role of gut microbiota and immune system reactions in the development and perpetuation of EDs is an emerging field, however is receiving growing attention. Endocrines produced in the gastrointestinal (GI) tract communicate with the brain to regulate functions of appetite and satiety. Given the role of these functions in EDs, it is thought that dysregulation of the gut microbiome may be partially responsible for ED psychopathology [ 78 – 80 ]. A review of evidence on the gut microbiome suggests that the growth cycle of gut bacteria and their metabolites 5 may contribute to patterns of accelerated and/or prolonged satiety in AN and periodic lack of satiation in BN [ 78 ]. In a study of 33 AN patients undergoing refeeding, Hanachi et al. [ 81 ] found the AN patients to have significant gut microbial dysbiosis compared with 22 healthy controls.

Several studies of AN have investigated the role of a protein (CIpB) produced by the Escherichia Coli ( E. Coli ) bacteria. The CIpB protein has a similar structure to the human hormone responsible for simulating secretion of satiation peptide YY. The peptide YY has been detected in high levels in the blood plasma of individuals with AN compared to healthy controls [ 78 , 82 , 83 ]. Peptide YY levels have also been found to be elevated among individuals with AN-R as compared to those with AN-BP and healthy controls [ 84 ]. Intestinal infections and chronic inflammation can lead to large increases in the number of E. coli bacteria in the GI tract, therefore increasing the levels of peptide YY and potentially increasing risk of ED [ 83 ]. The CIpB protein produced by E. Coli also prompts an immune reaction whereby autoantibodies are created. The position on the receptor for this autoantibody has been shown to differentiate between risk for BN and BED or AN [ 78 ]. Despite such emerging evidence indicating a role for gut microbiome dysregulation in EDs, researchers consider much of the evidence to be in an observational phase or using murine models 6 and lacking the capacity to explain aspects of ED pathology [ 79 , 85 ].

Autoimmune and autoinflammatory diseases

Gut microbiota are also known to interact with autoimmune responses, which have been investigated as a potential risk factor for EDs. In a large population-based cohort study, autoimmune and autoinflammatory diseases were identified as a significant predictor in the development of EDs and were associated with a 36% increased chance of developing AN. Interestingly, risk of BN and EDNOS was much higher at 73% and 72%, respectively [ 86 ]. Among a sample of patients hospitalised for EDs in Finland, higher prevalence of type 1 diabetes and Crohn’s disease was observed compared with healthy controls [ 87 ]. A recent meta-analysis has also identified a bidirectional association between coeliac disease and EDs. In particular, patients with AN are at a significantly greater risk of coeliac disease than healthy adults without AN [ 88 ]. Further, researchers argue that symptoms of ED commonly mimic those of chronic inflammatory GI and endocrine disease, including inflammatory bowel disease and diabetes type 1 and 2, emphasising the importance of screening for possible co-occurrence [ 89 ]. Unlike the vast majority of other risk factors associated with EDs, autoimmune and autoinflammatory diseases represented a greater risk for male participants as compared to females [ 86 ].

As a type of autoimmune disease, diabetes is commonly associated with EDs. There is a substantial evidence base indicating an increased prevalence of disordered eating behaviours among individuals with both type 1 and type 2 diabetes [ 90 , 91 ]. However, much of the evidence is observational and there are limitations in distinguishing between avoidance of certain food groups due to presence of an ED versus a feature of diabetes management [ 92 , 93 ]. Nevertheless, high rates of ED behaviours not related to food restriction (e.g., excessive exercise, vomiting, and laxative abuse) have been observed in adolescents and adults with diabetes [ 94 , 95 ]. Insulin manipulation or restriction has also been observed in adolescents with diabetes resulting in poor glycaemic control and poorer outcomes [ 89 , 90 , 94 – 96 ]. Interestingly, a study of adults has revealed that weight/shape overvaluation was lower in participants with diabetes (31.5%) compared to those who did not have diabetes (41.2%). The authors suggest that this may indicate that BED, as an ED for which weight/shape overvaluation is not a diagnostic criteria, may be of particular concern among adults with diabetes [ 97 ].

In terms of biological risk factors, evidence has largely focused upon proteins produced by gut bacteria, which have been implicated in dysregulation of appetite and satiety in individuals with EDs. The metabolites of gut bacteria are thought to play a role in disordered eating patterns, including prolonged satiety in AN and periodic absence of satiety in BN [ 78 – 80 ]. For example, a protein produced by E. Coli bacteria has been found to mimic the structure of the satiation peptide YY, a protein that is higher in individuals with AN as compared to healthy controls [ 83 , 84 ]. Findings such as these have led researchers to consider intestinal infections and chronic inflammation as a potential risk factor for EDs. However, research in this field is emerging, with further studies needed to better understand the association between gut microbiome dysregulation and EDs. Large studies have indicated that having an autoimmune or autoinflammatory disease, such as Crohn’s disease, inflammatory bowel disease, diabetes type 1 and 2, and coeliac disease, is also significantly associated with increased risk of BN and EDNOS, and to a lesser extent, AN [ 90 – 95 ].

3. Childhood and early adolescent experiences

A range of childhood experiences have been linked to the development of EDs later in life, including in-utero exposures, family dynamics and parental characteristics, childhood weight, and experiences of abuse and trauma.

In utero exposures

There is evidence to suggest that exposure to certain levels of hormones during foetal development could increase risk of ED development later in life. In a large cohort study of women in the UK, daughters whose mothers had a lifetime diagnosis of BN were found to have been exposed to high levels of prenatal testosterone in the womb, which was implicated in an increased risk of BN and binge eating [ 98 ]. However, a large multinational twin study was unable to find any link to in utero exposure to sex hormones and ED onset later in life [ 99 ].

Research has indicated that in-utero exposure to high levels of cortisol through maternal stress is associated with later development of ED [ 100 , 101 ]. A further study in the UK found that individuals who were born preterm had an increased risk of ED associated with structural brain alterations linked to underdevelopment [ 102 ]. Additional risk factors include the use of substances during pregnancy (e.g., nicotine) and maternal illness leading to malnutrition (e.g., anaemia), which have also been linked to an increased risk of AN and BN in the child later in life [ 103 ].

Risk factors conferred during foetal development are further supported by findings that risk of BED is associated with high weight at birth or being large for gestational age, while AN was associated with low weight at birth. No significant foetal developmental risk factors have been identified for BN [ 104 ]. Moreover, stressful events experienced by mothers in the year prior or during pregnancy, in particular the death of a close relative in the six months preceding pregnancy, have been shown to have an impact on the development of feeding or EDs in infants and toddlers [ 105 ]. Feeding issues in babies of mothers who had an ED diagnosis during pregnancy were also noted in this cohort [ 106 ].

A recent systematic review identified an association between AN and older maternal age, preterm birth (< 32 weeks), lower birth size, and maternal health complications (e.g., preeclampsia, eclampsia). The review also reported an association between BN and maternal stress during pregnancy [ 107 ].

There appears to be an impact of pregnancy upon the eating behaviours of women with an ED diagnosis. One study has found that ED behaviours across diagnoses tended to improve significantly during the pregnancy period, although this may not be maintained after [ 108 ]. It has also been reported that pregnancy is associated with remission of BN but an increased risk of BED onset [ 109 , 110 ]. Women with a history of psychosocial adversities have been found to possess a significantly greater risk for BN during pregnancy [ 111 ].

Family dynamics and parental characteristics

Research has shown that children are more likely to develop an ED if their parents display characteristics commonly associated with ED psychopathology, such as drive for thinness and perfectionism [ 112 ]. Specifically, maternal history of an ED has been shown to be associated with higher rates of emotional eating in children as young as four years old [ 113 ]. The children of women with lifetime AN have also been found to exhibit deficits in cognitive functioning, including social understanding, visual-motor function, planning, and abstract reasoning [ 114 ].

Additionally, Larsen et al. [ 115 ] reported that general parental psychiatric illness is associated with increased risk of BN and EDNOS. The authors also identified the experience of childhood adversity and significant family disruption as significant risk factors for development of BN and EDNOS. Interestingly, no associations between childhood adversities and risk of AN could be identified by authors, although a separate study identified maternal depressive symptoms as a predictor of AN [ 116 ].

Adopted individuals have also been identified as having a greater risk of binge eating and extreme weight loss behaviours, as well as increased risk of a lifetime diagnosis of an ED [ 117 ]. Other parental characteristics which have been associated with ED behaviours include high maternal BMI at 16 weeks’ gestation and when their child is eight years old, high maternal education attainment, and low parental self-esteem [ 118 – 120 ].

Individuals’ perceptions of the quality and nature of their parental relationship has been investigated as a potential risk factor for development of an ED. Research has found that female individuals diagnosed with AN or BN report significantly lower perceived emotional connectedness prior to disorder onset than their healthy sisters. In a family-based study of 332 female individuals, low emotional connectedness conferred a greater risk of developing BN over AN-R [ 121 ]. Further, females who report low maternal warmth have a higher risk of developing binge/purge type EDs [ 122 ]. Low parental warmth appears to be a risk factor for ED development in females but not males [ 123 ]. A study of AN patients and their healthy siblings found that both siblings in these families perceived low maternal care and high maternal overprotection. Siblings affected by AN developed insecure attachment compared with their siblings and had higher preoccupation with relationships, while healthy siblings were able to develop secure attachment and low need for approval and high self-transcendence [ 124 ]. Other risk factors include an oppressive parental relationship and childhood unhappiness [ 122 ].

Parents’ communication about food, as well as parental eating behaviours, have been shown to be a significant risk factor for EDs in their children. Several studies have found that exposure to disordered eating behaviours such as dietary restriction in parents is likely to have an impact on the early development on EDs in children, beyond the influence of genetics [ 125 , 126 ]. One study identified maternal distress as a mediating factor in the relationship between maternal ED and infant feeding difficulties [ 127 ]. Maternal dieting and poor communication among family members have also been associated with long-term risk for restrictive disordered eating [ 128 ]. Conversely, parental conversations regarding healthy eating, rather than dieting or weight, and regular family meals were found to be protective against development of EDs among child and adolescent samples in Europe and the US [ 129 , 130 ]. Parental pressure to eat, early negative experiences with food, and high disgust sensitivity were found to predict picky eating behaviours associated with ARFID. Parental encouragement around food in childhood was observed as a protective factor. Being male was also found to be a significant risk factor for adult picky eating behaviour and potential ARFID [ 131 ].

The experience of stressful life events, including bereavement, separation from family members, or involvement in an accident have been found to have an impact on ED development, in particular BN and BED. The occurrence of three or more events in combination with external criticism of weight or shape has been shown to be significant predictors in the year prior to BN onset [ 132 ]. No significant differences were observed between BN and BED in terms of the number or types of events experienced prior to onset [ 133 ].

Childhood weight

Research on the association between childhood weight and risk of eating pathology in later years is ambiguous. Several studies have reported that higher weight during childhood poses an increased risk of developing an ED in later years, including among culturally and linguistically diverse (CALD) individuals, as well as males [ 134 – 138 ]. Analysis of specific ED behaviours among adolescents in the US between 1999 and 2010 found that ED symptomatology and weight/shape concern persisted beyond adolescence for individuals who were overweight. Contrastingly, for non-overweight individuals, unhealthy weight control behaviours and body dissatisfaction decreased over time [ 139 ]. Other studies have found that adolescents with a weight history in the overweight range experience a significantly greater drop in BMI, higher levels of ED psychopathology and comorbid mental health difficulties, and take much longer to be identified than adolescents without a history of overweight [ 140 ], 141 .

Contrastingly, explorations of the association between weight history and AN specifically have found that low baseline BMI is a significant risk factor for development of both atypical AN and AN [ 38 , 142 , 143 ].

It has been suggested that parental perception of their child as being overweight may be a more powerful predictor of ED development than the child’s weight itself [ 118 , 144 , 145 ]. The significant impact of parental behaviours on ED risk has been supported by a study comparing individuals with BN to healthy controls and individuals with other psychiatric conditions. While being overweight or obese in childhood was identified as a risk factor, high maternal expectations and negative parental attitudes about weight and obesity in childhood were more strongly associated with the onset of BN among participants [ 146 , 147 ]. These risk factors are also associated with onset of BED [ 148 ]. Negative parental attitude towards childhood weight, including parental teasing about weight, has been shown to have a strong positive association with ED behaviours in both males and females, in particular binge eating behaviours [ 146 , 149 , 150 ]. Parental comments about their child’s weight and eating behaviours are also significantly associated with increased drive for thinness and body dissatisfaction [ 151 , 152 ].

Abuse and trauma

Experience of childhood trauma and abuse has been consistently identified as a non-specific risk factor for the development of EDs, although these experiences are more strongly associated with binge-purge type disorders such as BN, BED, and AN-BP [ 153 – 157 ]. Evidence from several studies suggests that emotional abuse is a significant predictor of binge/purge symptomology in women, while sexual abuse and physical neglect were associated with symptoms in men [ 158 – 160 ]. Sexual harassment has also been identified as a risk factor for EDs however little is known about the causal relationship or the role of mediating factors [ 161 ]. Attempts to investigate the association between types of childhood trauma and specific ED diagnoses have found that emotional abuse is a risk factor for all core ED symptoms [ 162 ]. A large-scale study of young adults in the US found that participants who reported multiple types of maltreatment in childhood were almost twice as likely to report binge eating and skipping meals as compared to those who reported no or low maltreatment [ 163 ]. Verbally abusive fathers have been shown to be strongly associated with AN-BP and BN, and verbally abusive mothers influence the development of BN [ 164 ].

Studies conducted in groups of women with obesity have found relationships between binge eating and childhood abuse and neglect. The severity of the abuse, rather than the type of abuse, appears to have a role in the development of BED and severity of food addiction [ 165 , 166 ]. A recent study has found that childhood food neglect is associated with increased risk for BN and BED even after adjusting for other adverse experiences and financial difficulties experienced during childhood [ 167 ]. A study on the impact of childhood emotional abuse and ED risk found that low self-perception and self-esteem caused by the abuse contributed to an increased risk of BED and NES [ 168 ]. Further, individuals with both an ED diagnosis and a history of childhood trauma and abuse have been found to have increased risk of lifetime suicide attempts [ 169 , 170 ].

The experience of childhood bullying has been found to increase risk of AN, and to a lesser extent BN, in children and adolescents [ 171 – 173 ]. However, increased risk of EDs was not found to carry on into early adulthood [ 171 ]. Weight-based teasing has also been associated with emotional eating, eating in the absence of hunger, and disordered eating attitudes and behaviours [ 174 ]. Consistent with existing evidence, an observational study of 182 adolescents receiving treatment for EDs found bullying was the most common form of trauma experienced by patients [ 175 ]. Assessment of the impact of cyberbullying also found the experience predicted onset of AN, BN, and EDNOS in a group of individuals with an ED diagnosis and increased ED symptomology and depression among a group of high-risk individuals [ 176 ]. Exposure to online content and risk of ED development is discussed further in Sect.  Gender .

An overview of the evidence regarding the impact of early experiences in terms of ED risk has identified a range of factors starting from the in-utero environment through to adolescence. In-utero exposure to high levels of testosterone, cortisol, or substances have been associated with increased risk of EDs [ 98 – 100 , 102 , 103 ]. There is also evidence to linking high birth weight to BED and low birth weight to AN [ 104 ]. Weight persists as a risk factor throughout childhood and adolescence, with research findings that high maternal expectations and negative parental attitudes about weight are also associated with ED risk. The quality and nature of one’s parental relationship is considered another risk factor for EDs, such that lower ratings of parental warmth or emotional connectedness have been reported by individuals with AN and BN as compared to their healthy siblings [ 121 – 124 ]. Experiences of childhood adversity, significant family disruption, childhood trauma (including neglect and emotional or sexual abuse) are well-documented risk factors, with evidence suggesting that they are most likely to contribute to the development of binge/purge type disorders (AN-BP, BN, BED, PD) [ 115 , 153 – 156 ]. Researchers have also suggested that the link between EDs and trauma is likely to be underestimated due to non-disclosure [ 207 ].

4. Personality traits and comorbid mental health conditions

Traits such as anxiety, perfectionism and obsessive-compulsivity are frequently associated with increased risk of EDs and may play a substantial role in the severity of symptoms, response to treatment, and risk of relapse [ 178 ].

Perfectionism, impulsivity, compulsiveness, and avoidance motivation

Rather than being linked to diagnostic type, a meta-analysis of personality traits (Farstad et al., 2016) found a more robust association with specific behaviours and symptomatology. Studies have shown that relative to controls, individuals with ED have elevated levels of perfectionism (setting of excessively high standards for performance, accompanied by overly critical self-evaluation); neuroticism (tendency to experience negative effects such as anger, anxiety, self-consciousness, irritability, emotional instability, and depression); impulsivity, particularly negative urgency (tendency to engage in impulsive behaviour when experiencing strong negative emotion); compulsivity (tendency toward overcontrolled behaviour); avoidance motivation (tendency to move away from or avoid situations associated with punishment); sensitivity to social rewards; introversion; and self-directedness (goal-oriented behaviour) [ 178 – 186 ].

Perfectionistic traits are common in both AN and BN. A systematic review and meta-analysis concluded that individuals with AN tended to place greater emphasis on high personal standards, while individuals with BN were more likely to perceive high levels of parental criticism [ 178 ]. The contribution of perfectionism to ED symptomatology (including dietary restriction and shape and weight overvaluation) was further supported by Joyce et al. [ 180 ] in a community-based sample of women. The study was inconclusive as to whether perfectionism was the cause of the ED symptoms. However, a significant positive association between perfectionism and weight and shape overvaluation was observed [ 180 ].

Among a sample of adolescent females recruited from an ED service in Australia, researchers found both a direct relationship between perfectionism and AN symptoms as well as an indirect relationship when mediated by depression [ 187 ]. The two different relationships were found to be equally viable, further supporting the notion of a reciprocity of symptoms between anxiety, depression, and AN, which are preceded by perfectionism.

In a 10-year follow-up study of university-aged adults in the US perfectionism was associated with the onset of AN, BN, and EDNOS and found to contribute significantly to disorder maintenance [ 188 ]. The tendency toward perfectionism in AN has been linked to a trait of vulnerable narcissism, ‘hiding the self,’ described as an unwillingness to show one’s faults or needs to others. The ability to exhibit control over emotional needs and relationships was correlated with AN-R in a comparison study involving individuals with AN and BN. However, the cross-sectional design was unable to determine whether this trait preceded AN-R and the sample size was relatively small [ 189 ].

Obsessiveness has also been found to be strongly associated with AN. Among a clinical sample of patients with AN and atypical AN, obsessiveness was positively correlated with a drive for thinness, a key aspect of AN symptomatology. The study did not find any significant differences between AN and atypical AN in terms of obsessive behaviours [ 190 ].

Studies seeking to assess personality traits contributing to differences in clinical presentation between restricting and binge/purge ED subtypes conclude that alexithymia – the inability to identify or verbally describe feelings or emotions – plays a role in the emotional dysregulation displayed by both AN-R and BN patients [ 191 , 192 ]. Higher levels of alexithymia have been associated with greater risk of re-hospitalisation in a three-year follow-up study of women with both AN and BN [ 193 ]. Prefit et al.’s [ 194 ] meta-analysis of studies into EDs and associated personality traits found lack of emotional awareness and inability to regulate emotions leading to maladaptive ED symptomology was not diagnosis specific [ 194 ]. Findings from the meta-analysis support Brown et al. (2018), suggesting a need for emotion-focused treatment approaches such as dialectical behaviour therapy (DBT) [ 192 , 195 ].

While binge/purge presentations are consistently associated with impulsivity and greater emotional dysregulation [ 196 , 197 ], one study demonstrated no significant differences in ability to regulate emotions between AN-R and BN patients with high levels of alexithymia [ 192 ]. However, in another study involving clinical samples of AN-R, AN-BP and BN patients, individuals with AN-R were found to have fewer fluctuations in mood than individuals with AN-BP and BN. Only in groups exhibiting binge/purge symptomology were these behaviours observed as a method for alleviating negative affect [ 198 ]. Similarly, among a group of 139 female college students, lower impulsivity in addition to lower self-esteem was found to be associated with AN risk [ 199 ]. A recent systemic review has warned that due to methodological limitations in the studies conducted to date, there is insufficient evidence to support the characterisation of AN and BN as being low and high in impulsivity, respectively [ 200 ].

Individuals with binge/purge subtypes EDs, including AN-BP, BN, BED and various OSFEDs, have been found to have higher levels of avoidance motivation, impulsivity, emotional dysregulation, anxiety, depression, and paranoia than healthy controls [ 178 ]. Within a clinical sample of AN patients, individuals displaying binge/purge symptoms were more likely to engage in non-suicidal self-injurious behaviour and have lower self-directedness and co-operation than individuals with AN only [ 201 ]. However, the literature is inconclusive as to whether these traits contribute to ED onset or are symptoms of it.

Several studies have observed high levels of impulsivity in individuals with BN, with these individuals commonly displaying negative urgency, lack of planning and sensation seeking. Farstadt et al. (2016) in their meta-analysis also argue a role for compulsiveness (i.e., the tendency towards overcontrolled behaviour), suggesting that the interaction of personality traits such as impulsiveness and compulsiveness can have implications for ED symptomology and disorder severity [ 161 , 180 , 183 , 184 ]. In this manner, impulsivity was found to have a significant impact on the types of ED symptomatology displayed by the individual and clinical presentation [ 178 , 195 ]. In contrast, Waxman [ 195 ] found no significant differences in impulsivity between ED diagnoses. Waxman [ 195 ] suggested that while there is a lack of evidence from longitudinal studies to determine conclusively that impulsivity is a risk factor in the development of ED, evidence from studies using proxy measures such as delinquency found these behaviours preceded BN onset. One further study has reported an association between NES and impulse control disorder [ 202 ]. It has also been suggested that impulsivity and addiction-like mechanisms may explain the association between ED psychopathology and both high-risk sexual behaviours and substance misuse [ 203 , 204 ].

A study of 83 sister pairs found participants with a lifetime ED diagnosis displayed higher levels of internalising behavioural issues (social withdrawal, anxiety, depression) and/or externalising behavioural problems (aggression and delinquency) than their healthy sisters [ 205 ]. Internalising behaviours were found to be a strong predictor for AN-R, while externalising behaviours were strongly associated with later onset of bulimic symptoms and BN [ 205 ].

Two models illustrating risk of bulimic behaviours among young females have attempted to account for both the role of personality traits and traditional ED concepts of the ‘thin ideal’ [ 206 ]. Pearson’s integrated model of risk combines the ‘state-based’ pathway, which shows binge eating as an impulsive lack of control behaviour and purging as a compulsive correction, and the ‘trait-based’ pathway, which emphasises negative urgency as a consistent tendency toward impulsivity and stress alleviation through binge eating. The ‘trait-based’ pathway also considers the role of inherited ED risk and predisposing childhood exposures [ 206 ]. Pearson et al. argue that integration of the ‘trait-based’ model considers the important role of heritability and negative urgency that is absent from the Stice model [ 207 ]. Further investigation of disease models of bulimic behaviour by Dakanalis et al. [ 208 ] indicate that risk factors are more complex than can be mapped by the dual pathway model, citing bi-directional relationship between dietary restriction and negative affect.

Negative urgency has also been found to be an independent predictor of food addiction among individuals displaying binge-eating symptomology [ 209 ]. A further study by Utschig et al. [ 210 ] indicated that fear of negative evaluation from others is a predictor for body dissatisfaction and pressure to be thin, contributing to an internalised ‘thin ideal’ in individuals with BN and feeding into the state-based model. Fear of negative evaluation is considered an aspect of social anxiety and relates to heightened sensitivity to social rewards, a trait found to be elevated across ED diagnoses [ 178 , 210 ].

Personality disorders

The central role of certain personality traits in the perpetuation and potential development of ED symptomology reflects established relationships between some personality disorders and EDs [ 211 – 213 ]. Comorbidity studies have found borderline personality disorder (BPD) to most commonly occur with BN and other binge/purge ED subtypes [ 212 ]. This finding is supported by research on personality traits in EDs where avoidant behaviours and low emotion regulation flexibility are elevated in bulimic-type disorders and also a core feature of BPD [ 178 , 212 , 214 ]. However, some researchers argue that the co-occurrence of EDs and personality disorders may have been inflated in previous studies [ 215 ]. In a sample of 132 females with ED, prevalence of any personality disorder was 21%, lower than in other studies where reported figures were between 27 and 95% [ 215 ]. However, findings from von Lojewski et al. [ 215 ] were consistent with existing evidence that BPD traits were significantly associated with binge/purge EDs compared with AN-R. Individuals with comorbid BPD and ED were also more likely to report self-induced vomiting as compared to any other personality disorder. Co-occurrence of EDs and BPD has also been associated with increased risk of engaging in non-suicidal, self-injurious behaviours within a clinical sample [ 212 ]. Meta-analysis of 20 studies published between 1987 and 2010 found comorbidity of BPD with EDNOS (now OSFED) to be 38%, and 29% with BED. Researchers indicated that ED and personality disorder comorbidity are more common among individuals with AN and BN than BED and EDNOS [ 216 ]. However, among patients with BED or EDNOS, avoidant personality disorders were found to be the most common, followed by BPD [ 216 ]. It should however be noted that two of three studies identified by the Rapid Review concerning ED and personality disorders were restricted to relatively small clinical samples without control groups. They were also limited by their cross-sectional design in their capacity to investigate the temporal relationships between disorders.

Anxiety, mood disorders and psychiatric comorbidities

Co-occurring and preceding mental health conditions, particularly those with shared genetic and experiential influences such as anxiety and mood disorders, are also risk factors for EDs. While it is difficult to assess which condition precedes the other without use of prospective study designs [ 217 ] these relationships have been widely studied in AN and BN, and there is some evidence for anxiety and mood disorders including depression and bipolar disorder preceding ED symptomatology. Evidence from a three-year prospective study of 615 pairs of twins in the US suggests elevated risk for AN is associated with higher levels of depression and anxiety in combination with a high drive for thinness, rather than either risk factor alone [ 218 ]. There is less conclusive evidence on the relationship between BN, anxiety, and depression although some preliminary research was identified indicating several key symptoms were shared between the three disorders [ 219 ].

Mood disorders

In clinical ED populations, prevalence of mood disorders is frequently high [ 220 ]. In one study, major depressive disorder (MDD) was found to affect 64% of individuals with AN-R and over 75% of binge/purge ED subtypes (AN-BP, BN). Sequencing of disorder onset found that mood disorders preceded ED onset in a third of the AN-R cases and 40% of the AN-BP/BN cases. The remaining comorbid cases were either co-occurring or onset following ED diagnosis. These findings from Godart et al. [ 220 ] indicate that depressive disorders can be both a predictor and consequence of ED, as well as a comorbidity caused by malnutrition further complicating management and treatment of EDs.

Assessment of the temporal relationship between depression and disordered eating in an eight-year longitudinal study found depressive symptoms predicted increases in BN behaviours, which in turn predicted increases in depressive symptoms [ 221 ]. These findings indicate there may be a reciprocal relationship between the two conditions. A reciprocal relationship was also identified in a larger cohort of adolescent females where individuals who reported depressive symptoms were twice as likely to engage in overeating and binge eating at four-year follow-up, and individuals reporting overeating and binge eating were also more likely to report depressive symptoms at follow-up [ 222 ].

Anxiety disorders

There is evidence to suggest that anxiety is the most commonly occurring comorbidity with ED [ 223 ]. Childhood anxiety disorders have repeatedly been found to precede the onset of an ED, particularly AN [ 224 – 228 ]. Studies have identified a greater incidence of childhood obsessive–compulsive traits in individuals diagnosed with AN in comparison to control groups without an ED [ 177 ]. Micali et al. [ 211 ] conducted a longitudinal study of 231 young people diagnosed with OCD over a nine year period. Of the 126 participants who completed the follow up assessment, 12.7% had a diagnosis of an ED. Such findings highlight predictive value of childhood anxiety disorders in the later development of EDs, especially AN.

A reciprocal relationship between GAD and AN was indicated in a large twin study by Thornton et al. [ 229 ] whereby having GAD significantly increased likelihood of AN and having AN significantly increased likelihood of GAD. The group with AN and GAD had the lower mean adult BMI than both AN only and GAD only groups and healthy controls. These findings indicate the presence of comorbid mental health conditions may exacrerbate EDs and increases severity of symptoms. Sihvola et al. (2009) found co-occurrence of MDD and GAD at age 14 was strongly associated with onset of ED at follow-up (age 17). Weaker associations were observed for both MDD and GAD alone [ 230 ].

Ciarma and Mathew [ 231 ] investigated the relationship between social anxiety disorder (SAD) and disordered eating among adults aged between 18 and 35 living in the community. This study found self-esteem and stress reactivity resulting from interpersonal conflict to be partial mediators, indicating that ED symptoms can be elicited by heightened responses to stress from social conflict and negative self-view. However, the partial mediation effect observed indicated that other unidentified factors may also have a role in the relationship. A further study of adolescents found evidence of a bidirectional relationship whereby depression and anxiety were risk factors for disordered eating behaviours, which in turn led to increased depression and anxiety [ 232 ].

Prevalence of social anxiety was also found to be high among a separate clinical sample of Australian adults with an ED, where 42% were found to have social phobia. It was also the most commonly diagnosed anxiety disorder within each of the ED subtypes, including 33% of those diagnosed with BN, 26% for AN and 25% for EDNOS. Investigations into the temporal relationship between ED diagnosis and anxiety disorder have found many individuals have anxiety prior to their ED diagnosis [ 225 – 227 ]. However, in one systematic review, this was supported only by the included retrospective case–control and cohort studies, and was not supported by evidence from prospective studies included in the review [ 227 ]. This discrepancy highlights the potential role of recall bias that may be present across studies relating to anxiety and EDs [ 227 ]. OCD and SAD also tend to precede onset of ED, and BN in adolescence may increase risk of SAD and panic disorders in adulthood [ 233 ].

In some individuals, shame has been found to predict later onset of BN and social anxiety, indicating a shared risk factor for both conditions [ 234 ]. Impaired psychosocial functioning and capacity to maintain interpersonal relationships associated with shame or shyness was also found to predict ED onset among adolescents in the US [ 235 ].

Psychiatric comorbidities of ED diagnoses other than AN/BN

Evidence relating to mental health comorbidities for EDs other than AN and BN is less developed. Studies conducted investigating BED and NES are confined to clinical samples with cross-sectional designs, highlighting a need for further work in this area, especially considering the high prevalence of psychiatric comorbidities detected in individuals with these diagnoses. Among patients receiving treatment for BED, 74% had a lifetime psychiatric disorder diagnosis, and 43% had a current diagnosis [ 236 ]. In a population of overweight and obese patients with severe mental illness, 25% were diagnosed with NES and 6% with BED [ 237 ]. Other studies measuring NES in patient samples with depression and bipolar disorder (BD) found the prevalence to be 32.5% and 8.8% respectively [ 238 , 239 ]. Higher prevalence of NES was detected in both depression and BD groups compared with healthy controls, indicating increased risk among these individuals.

ED and BD comorbidities are also commonly reported in research, with association between BD and BN/BED considered particularly significant, although the casual and temporal relationships between the disorders are not well understood [ 240 – 242 ]. While it is likely that some risk factors are shared, lack of data regarding disorder onset limits commentary on the relative risk BD confers to the development of ED [ 241 ]. One review found incidence of BD to be 4.7 times higher in individuals with BN, 3.6 times higher in individuals with BED and 3.5 times higher for binge/purge ED subtypes overall. Due to the low prevalence of AN and BD in the general population, an accurate estimation of this comorbidity is difficult to obtain [ 241 , 243 ]. BD in individuals with ED is associated with increased severity of core symptoms including body dissatisfaction, weight/shape concern, eating concern, impulse regulation, interoceptive awareness and perfectionism [ 244 ]. Mood instability is also significantly higher in individuals with a BD/ED comorbidity compared to those with BD alone. Systematic review of BD and its clinical correlates by McDonald et al. [ 245 ] suggests this finding indicates shared aetiology between ED and BD through emotional dysregulation.

ADHD and autism spectrum disorders

There is an emerging body of literature exploring associations between EDs and attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorders (ASDs), however few have examined the conditions as risk factors in the development of ED. A 2016 meta-analysis of twelve studies found a three-fold increased risk of ED among individuals with ADHD [ 246 ]. Similarly, a 2020 matched cohort screening study found the same three-fold increase—almost one third of children and adolescents with ADHD were at risk of ED, compared to 12% of healthy controls. Here, BMI was a statistically significant predictor of risk [ 247 ]. Impulsivity and inattention symptoms of childhood ADHD have been positively associated with the development of overeating and bulimic-type behaviours in adolescence [ 248 ]. A longitudinal study of a large sample of adolescents reported that the onset of emotional and behavioural issues, including those associated with ADHD and conduct disorder, was observed to occur prior to the onset of disordered eating behaviours [ 249 ].

A 2013 systematic review found elevated rates of ASDs in ED populations compared with healthy controls, however, six of the eight studies in this review were based on longitudinal research using the same community sample [ 250 ]. The authors suggested a need to integrate appropriate, well-structured ASD assessment tools into routine care of ED service users, with the prevalence of ASD traits potentially contributing to ‘high treatment resistance to conventional therapies’ [ 250 ]. Dell’ Osso et al. [ 251 ] tested such an instrument in a sample of 138 individuals meeting DSM-5 criteria for an ED and 160 controls. They found significantly higher autism spectrum traits in participants with EDs, particularly verbal and non-verbal communication, inflexibility and adherence to routine, and restricted interest and rumination. Individuals with restrictive EDs were more likely to display ASD traits. Similarly, as part of a large, population-based prospective study of women and their children, Schaumberg et al. (2021) found autistic-like social communication difficulties during middle childhood were associated with BN symptoms during adolescence in both males and females [ 252 ]. They also discovered that misattribution of faces as sad or angry at 8.5 years of age was associated with a diagnosis of AN and purging behaviours at age 14. Contrarily, Dinkler et al. [ 253 ] in their prospective twin cohort study found no association between traits of autism in nine-year-old children and a later AN diagnosis, as well as noting a marked elevation in restricted/repetitive behaviour and interests only in the subgroup of individuals with acute AN. They questioned previous reports of elevated prevalence of ASD in AN and instead wondered if autistic traits may be best conceptualised as an epiphenomenon of the acute phase of AN.

Post-traumatic stress disorder

Although there is a large body of evidence relating to childhood trauma and abuse as a risk factor for the development of ED, few studies were identified investigating the role of post-traumatic stress disorder (PTSD) specifically as a risk factor. No distinction was made in the search methodology for this review between complex trauma and early childhood adverse events, with all studies captured under the search term ‘risk factors.’ Studies presented in this section, focused on the link between diagnosed PTSD and development of ED.

Results from two cohort studies observed an association between PTSD and severity of ED symptoms as well as relatively high prevalence rates within sample populations [ 254 , 255 ]. Among a patient sample in Sweden who had experienced trauma either prior to ED onset, after onset or within a year of onset, lifetime prevalence of PTSD was observed to be 24.1% [ 255 ]. An almost identical PTSD prevalence was found within a smaller ethnically diverse sample of obese women with BED in the US, at 24% [ 254 ]. Analysis of the impact of timing of trauma exposure on ED symptom severity in the Swedish sample found the association was only significant in the group who had experienced trauma in the same year of their ED diagnosis [ 255 ]. This analysis was not undertaken in the US study. Brewerton et al. [ 256 ] assessed adults entering ED treatment at seven US sites and found 49.3% had PTSD. It was found that individuals who were significantly more symptomatic had a higher propensity towards binge-type disorders and reported worse quality of life than those without PTSD. Co-occurrence of PTSD and AN was reported by Reyes-Rodriguez et al. (2011) as part of their cross-sectional study of 753 women with AN. They found 13.7% of the sample of AN patients also met criteria for PTSD with childhood sexual traumas being the most common traumatic event associated with the diagnosis [ 257 ].

Evidence from three studies relating to EDs in veteran populations—a meta-analysis (Barlett and Mitchell [ 259 ]); a retrospective chart review (Forman-Hoffman et al. [ 258 ]); and a retrospective cohort study of female veterans (Mitchell et al. [ 260 ])—found an association between increased ED prevalence and PTSD and trauma. Through a telephone interview with 1004 veterans, Formann-Hoffman et al. [ 258 ] determined that 16% of their sample had a lifetime ED with many of the cases also experiencing comorbid PTSD or lifetime sexual trauma. However, increased risk for ED among the veteran population could not be solely attributed to trauma, as unhealthy weight control behaviours are also common in this population due to strict weight and fitness requirements within the military [ 259 – 261 ].

The prevalence of personality traits appear to differ according to the ED diagnostic category. Elevated levels of perfectionism are common amongst AN and BN, obsessiveness strongly associated with AN, and binge/purge presentations consistently associated with impulsivity and greater emotional dysregulation, whereas lack of emotional awareness is not ED specific and common amongst most ED diagnoses [ 178 – 183 , 196 ]. Although co-occurrence of ED and personality disorders has been consistently identified in studies of comorbidity (e.g., BPD and binge/purge EDs), mood and anxiety disorders represent the most common psychiatric comorbidities in individuals with EDs (e.g., MDD affects over 75% of binge/purge EDs, SAD affects 42% of adults with an ED) [ 212 , 220 , 223 , 225 – 227 ]. There is also good evidence to suggest that the presence of a diagnosable childhood anxiety disorder (e.g., OCD) precedes the onset of an ED later in life [ 177 , 211 ]. Other psychological factors which appear to contribute to the risk of EDs include diagnoses of PTSD, ADHD, or ASD [ 246 , 250 , 254 ].

5. Gender differences

EDs impact a higher number of females with greater symptom severity. While common risk factors are shared across genders, such as low self-esteem and high shape/weight concern, males have been identified as less likely to engage in severe dieting behaviours compared with their female counterparts [ 262 , 263 ].

Puberty is a period of significant risk for ED development in both males and females. Research has implicated increased production of sex hormones during puberty, in particular estrogen, in the onset of EDs [ 264 ]. Evidence has consistently demonstrated that early onset of puberty is strongly associated with increased risk for ED development in both young males and females. Favaro et al. [ 265 ] linked earlier age of menarche with a younger mean age of onset of AN and BN. It has been suggested that if an individual experiences changes to their body shape, associated with menarche, at an earlier time than their peers, this may lead to heightened body dissatisfaction and which in turn may contribute to early the onset of EDs.

Despite the commonality between males and females in terms of the risk of ED development posed by puberty, it had been suggested that bodily changes experienced during this time possess a stronger impact for females as compared to males. It is thought that changes to one’s body shape move females further away from the thin ideal, whereas the changes for males move them closer to ideals around muscularity [ 266 ]. These findings have been supported by a cohort study, which found that bulimic symptoms and body dissatisfaction were associated with early puberty in females and late puberty in males [ 267 ]. Similarly, having a higher BMI comparative to peers has been associated with ED risk among teenage girls but not boys in a US school cohort [ 265 ].

Comorbidity

Research into gender differences has found that an equal proportion of male and female adolescents with an ED experience comorbid anxiety or depression [ 268 ]. A further four-year retrospective study in male adolescents with a diagnosed ED supported the assertion that comorbid anxiety and depression posed considerable ED risk to males [ 269 ]. Research has also identified increased prevalence of compulsive disorders, including gambling and substance use, among males as compared to females in a cohort of individuals at risk of ED [ 270 ]. While male ED risk has been associated with compulsive and depressive symptoms in these studies, evidence presented in a longitudinal study of adolescents found depression to be associated with higher ED symptomology in 12-year-old girls but not in boys [ 271 ]. Further research into EDs and depression in males is required to clarify the impact of this association.

Gender roles

Gender roles have been investigated as a potential contributor to ED risk. Exposure to media ideals has been found to be associated with increased body dissatisfaction and ED symptomology in university-aged males [ 272 ]. Research has also indicated that increased femininity in heterosexual males is negatively associated with muscle dissatisfaction [ 273 ]. Weak associations have also been found between femininity in women and eating pathology and body satisfaction. Among both sexes, masculinity was found to have a significant negative relationship with eating pathology, also conferring modest protection to body dissatisfaction [ 273 ].

Interactions between societal gender roles and sexual orientation is also known to play a role in ED risk with researchers suggesting that greater social body image pressures are present among gay males. A systematic review of disordered eating among sexual minority individuals has reported that elevated ED symptomology exists across all LGBTQI + groups as compared to heterosexual males and females [ 274 ]. A further study of men aged 18 to 35 found that disordered eating and body dissatisfaction was higher in gay and bisexual men compared to heterosexual men, as was susceptibility to social messaging around body image [ 275 ]. The occurrence of body image disorders has also been found to be higher among sexual minorities as compared to heterosexual samples [ 276 ]. A recent study involving a sample of transgender and gender non-binary individuals reported that increased internalised transphobia was associated with increased likelihood of disordered eating symptoms [ 277 ]. There is insufficient evidence currently available to separate risk of engagement in specific types of ED behaviours according on sexual identity [ 274 ].

The literature indicates that whilst both males and females are susceptible to risk factors for EDs such as early puberty onset and elevated weight/shape concerns, it appears that these factors have a stronger impact upon females as compared to males in terms of risk of developing disordered eating behaviours and psychopathology (e.g., severe dieting, bulimic symptoms and body dissatisfaction) [ 292 , 294 , 297 – 300 ]. Recent findings also indicate that LGBTQI + groups are at a higher risk of ED symptomology and body image disorders as compared to heterosexual individuals [ 305 – 307 ].

6. Socio-economic status

Despite the pervasive view that EDs disproportionately affect more affluent groups, evidence suggests that disordered eating behaviours occur at similar rates across all income levels and regardless of employment status [ 278 ]. Differences between socio-economic status (SES) seem to emerge in the types of disordered eating. Specifically, a positive correlation has been reported between non-fulltime workers and binge eating and purging behaviours. Also, a trade or certificate qualification has been shown to be positively associated with strict dieting as compared to groups with no higher education [ 278 ]. In contrast, a large study conducted in Sweden failed to find a relationship between social class and household income and incidence of EDs in females. However, in males, lower household income was associated with increased risk of BN and EDNOS, although the study observed a very low rate of BN in males [ 279 ].

Recent studies in the US have found low food security to be a predictor for disordered eating behaviours [ 280 ]. Among higher SES adolescents, binge eating behaviours were associated with weight-related teasing by family members [ 281 ]. In an adult sample, experience of low food security was more common among individuals with BN and BED as compared to healthy weight controls [ 282 ]. Lower food security in these individuals was associated with more frequent binge eating episodes and, in individuals with BN, unhealthy compensatory behaviours [ 282 ].

High levels of parental education have also been identified as a predictor of EDs [ 119 , 283 ]. Higher educational attainment by both parents as well as maternal grandparents has been associated with higher incidence of AN, BN, and EDNOS equally across diagnoses in females [ 279 , 284 ]. In males a positive association was found between parental education and AN, but not for BN or EDNOS [ 279 ].

Research into sociocultural risk factors for EDs suggests that income has little impact on overall ED risk although available evidence points to specific indicators that have an influence [ 278 ]. Higher education attainment is associated with restrictive ED behaviours, while experience of food insecurity is associated with binge-type behaviours and EDs [ 279 , 282 , 284 ].

7. Ethnic minority

Although there is no evidenced association between ethnic background and the risk of ED onset, specific aspects of ED psychopathology do appear to differ between ethnic groups [ 285 , 286 ]. A cohort study of females aged between nine and 22 years old found those with an ED were more likely to be non-Hispanic White, come from well-educated households, and be well-educated themselves [ 287 ]. A recent study of a treatment-seeking community sample in US found that Black individuals displayed higher rates of BED as compared to other ethnic groups, however overall Asian and Black individuals were less likely to report ED symptoms than White individuals [ 288 ]. Significantly higher thin ideal internalisation has been observed among Asian-American participants as compared with other groups [ 285 ]. Additionally, the association between fear of losing control of eating and depressive symptoms has been found to be stronger in Asian and Pacific Islander minorities than other ethnic groups [ 289 ]. In a study comparing thin-ideal internalisation among young Australian and Malaysian women, a stronger association between body dissatisfaction and restrained eating practices was observed in the Australian sample [ 286 ].

Further investigation of ethnic minority status has implicated perceived ethnic discrimination as a risk factor in ED development. In a cohort of college students, perceived discrimination based upon one’s ethnicity was associated with increased prevalence of key ED symptoms including restraint, weight/shape concern, body dissatisfaction and bulimia [ 290 ]. Perceived discrimination was also found to increase drive for muscularity among males in the sample but not drive for thinness among females. These findings indicate a potentially growing risk for ED in CALD individuals [ 290 ].

A small body of evidence was identified in the current RR regarding the association between ethnic minority status and ED risk. Of the studies reviewed, unique associations have been found between particular ethnic groups and specific aspects of ED psychopathology. For example, in comparison to other ethnic groups, higher rates of BED have been observed in Black-Americans and greater thin ideal internalisation in Asian-Americans [ 286 , 289 ]. Given that a significant proportion of ED research has been conducted using White/Caucasian participants, greater research efforts are needed to better understand the features of EDs in ethnically diverse groups.

8. Body image and social influence

Weight/shape concern, overvaluation of weight/shape and drive for thinness, referred to here using the term body image concerns, are key concepts in ED [ 291 , 292 ]. Along with the social and cultural factors that contribute to body image concerns, these concerns have been extensively investigated as risk factors for the development of EDs. Research in this area has been concentrated among women and girls whose body image concerns are characterised by a focus on low body weight and the thin-ideal [ 293 ], but greater recent focus on men and boys with regard to the muscular/lean ideal has been seen due to increasing recognition of muscle orientated EDs in males. Engagement with particular environments that shape social norms for appearance and promote pursuit of the ideal body shape or weight, or involvement in certain activities with a culture of strict dieting and excessive exercise is encouraged, such as college level or professional sports, are also well studied risk factors in ED literature.

Body image and appearance ideals

Studies using prospective designs have found evidence for body image concerns predicting development of EDs and ED behaviours. In an eight-year longitudinal study of adolescent girls, higher levels of perceived pressure to be thin, thin-ideal internalisation, and body dissatisfaction were significant predictors of later onset ED (BN, BED, and purging disorder) [ 294 ]. Among an adolescent sample, dissatisfaction with weight and shape, but not overvaluation or preoccupation, was a predictor of onset of an ED after 12 months [ 295 ]. The authors suggest that while body dissatisfaction may impart risk for ED development, the other body image-related constructs of overvaluation and preoccupation, may indicate presence of ED psychopathology. A systematic review of the impact of anti-obesity public health messages has found that endorsement of thin ideals and drive for thinness are exacerbated in response to exposure to messages which are stigmatising towards individuals who are overweight or obese [ 296 ]. In a large longitudinal sample of adolescent boys and girls, body image concerns predicted binge eating over 5 years to young adulthood [ 297 ] and persistent disordered eating 10 years later among both males and females [ 298 ], and body dissatisfaction, preoccupation with body weight and shape, and overvaluation predicted increases in disordered eating 15 years later, particularly in females [ 299 ]. Similarly, in a cohort of this sample characterised as having BMI in the overweight category, higher body image concerns predicted prevalence and onset of disordered eating (binge eating and extreme weight control behaviours) over five years [ 300 ]. Findings for body image concern as a risk factor for development of AN are mixed. In this regard, a systematic review of 46 longitudinal studies by Glashouwer et al. [ 301 ] with a pooled sample of 4,928 patients with AN was unable to definitively determine whether body dissatisfaction was a causal factor in disorder onset.

Media, social media, and the internet

The impact of media depictions of appearance ideals on ED symptoms have been examined with studies of varying methodologies. A meta-analysis of laboratory-based experimental studies found that viewing idealised images resulted in a small but non-significant increase in body dissatisfaction. However, exposure to these images was found to have a greater impact on groups considered at high-risk for developing EDs [ 302 ]. Of note, there were no differences observed in the impact of these images based on gender, indicating that men and women are equally affected by media portrayals of idealised bodies [ 302 ].

Among 574 women aged between 14 and 36, social expectations to be thin were found to mediate the relationship between protective self-presentation and disordered eating [ 303 ]. This finding aligns with research on exposure to negative parental attitudes regarding weight to be a risk factor in the later development of ED, discussed previously [ 118 , 303 ].

As with traditional media, the effects of portrayal of idealised bodies on the internet and on social media has been explored. Among young women, use of social media was found to impact weight and shape concerns [ 304 ] and among a predominantly female sample of participants with AN, use of appearance-focused social media was found to be associated with higher levels of ED symptoms [ 305 ]. A systematic review found that general internet use was associated with body image and eating concerns [ 306 ]. Further exploration of problematic internet use suggested excessive use of social media was associated with increased risk of AN and BN, while video gaming was associated with risk of BED [ 307 ]. However, recent proliferation of pro-AN or pro-ED websites and social media networks may create online environments that are more detrimental to the health of individuals at risk of ED than other forms of media. Even among females with normal BMI and no history of ED, one week of exposure to pro-ED website content resulted in a significant reduction (20%) in calorie intake among participants compared to groups who were exposed to other website content including health and fitness websites [ 308 ]. Dangers associated with pro-ED websites is not restricted to females, with a content analysis study finding that up to 25% of participants on pro-AN forums are male, suggesting that these sites may have a substantive negative impact with males engaged with these sites expressing negative experiences including body dissatisfaction [ 309 ].

Body image concerns are a well-known risk factor for EDs. High levels of body dissatisfaction and internalisation of the thin ideal have been found to be predictors of ED onset, whereas related constructs of overvaluation and preoccupation with weight and shape are considered to reflect current ED psychopathology [ 270 – 277 ]. Exposure to the thin ideal via either traditional media or social media is associated with greater risk of an ED, with evidence suggesting that both males and females are equally impacted by this content [ 278 – 283 ].

9. Elite sports, female athlete triad, and excessive exercise

Engagement in activities that accept or promote strict dieting practices and endorsement of low body fat has the potential to contribute to development and maintenance of ED symptoms [ 310 ]. Consistent with this, EDs among elite and college/university level athletes were observed at higher rates than in non-athlete comparison groups [ 311 ], although no difference in prevalence of EDs was found between athletes engaged in sports with an emphasis on aesthetics and/or weight and athletes engaged in sports without this focus. The female athlete triad (FAT), characterised by low energy availability (through increased physical activity or dietary restriction), amenorrhea and low mineral bone density, is considered a consequence of training for elite level sports and pursuit of lean physiques [ 312 ]. Features of FAT have also been observed in elite para-athletes (n = 260) with no difference in risk between genders or sport type [ 313 ].

In relation to ED behaviours, among elite athletes (n = 224), high prevalence of clinically significant ED symptomology (22.8%) has also been found [ 314 ].Similarly, in a sample of college level female gymnasts and swimmers (n = 325), 4.6% (n = 15) engaged in intentional vomiting, 1.5% (n = 5) used laxatives and 2.5% (n = 8) used diuretics for weight control. Additionally, 10.5% (n = 3.4) engaged in binge eating two or more times a week, while almost all participants engaged in binge eating once a week, 96.6% (n = 314) [ 315 ]. However, in a smaller UK sample of male and female gymnasts (n = 51) no purging behaviours were observed, although 31% of male gymnasts in this group scored highly on ED self-report questionnaires [ 316 ].

However, other studies have not found these differences between athlete and non-athlete groups. For example, a cohort study comparing elite and non-elite athletes to controls (n = 725) was also unable to find any differences between the three groups in terms of ED behaviours. However, it did highlight distinct differences associated with social pressures and influences on body image and weight in athletes versus non-athletes. There is some evidence to suggest that unlike female athletes, male athletes are not at greater risk of developing EDs than non-athletes [ 317 ]. Evidence from a meta-analysis of 31 studies of ED athletes indicated that, with the exception of wrestling, male athletes were not at greater risk of disordered eating than non-athletes. Although, researchers noted that studies were heterogenous and measurements were impacted by the potential inappropriateness of ED assessment tools for male populations [ 318 ].

Among non-elite populations, recognising excessive physical activity or exercise levels among women in the community is particularly important in risk assessment of ED, as these individuals were found to be 2.5 times as likely to have an ED diagnosis than non-excessively exercising individuals [ 319 ]. Furthermore, participation in activities promoting lean body types such as yoga and pilates has also been highlighted as a potential risk factor for ED development. However, in a large cohort study (n = 2,287) of young adults no association was found between participating in yoga and pilates and ED symptomology among female subjects but increased risk of unhealthy and extreme weight control behaviours as well as binge eating was observed in males [ 320 ]. Further research is required to understand the unique associations identified in this study.

Similar to athletic settings, other physical activity pursuits take place in environments that may promote ED symptoms. A systematic review and meta-analysis observed higher rates of ED among dancers, where dancers were found to have three times greater risk of having AN or EDNOS but not BN, than the general population and risk was particularly heightened among ballet dancers [ 321 ].

Involvement in elite sports is a potential risk factor for disordered eating behaviours among both male and female athletes [ 311 – 317 ]. Increased attention should be paid towards excessive exercise by non-elite populations in the community as risk factor for EDs and to support screening and early intervention activities [ 318 – 320 ].

This review to aimed to summarise recent peer-reviewed evidence relating to risk factors associated with EDs. An extensive number of research studies were identified, exploring a multitude of risk factors. For the purposes of this review, the research findings were broadly characterised into nine primary categories: (1) genetics, (2) gastrointestinal microbiota and autoimmune reactions, (3) childhood and early adolescent experiences, (4) personality traits and comorbid mental health conditions, (5) gender, (6) socio-economic status, (7) ethnic minority, (8) body image and social influence, (9) and elite sports.

Identification of the recent evidence relating to key risk factors offers valuable knowledge to researchers, clinicians, and policy makers, such that it may inform the development of evidence-based approaches for the care and treatment of individuals with EDs. An understanding of risk factors is essential for the development and refinement of aetiological models [ 8 ]. In a recent review of existing models of disordered eating, Pennesi and Wade [ 21 ] reported that very few of the existing theoretical models (18.5%) have informed the development of effective interventions. The authors call upon researchers to use empirically supported risk-factors to modify existing theories, which then can inform prevention and treatment interventions [ 21 ].

The findings of the current review can be used to determine which risk factors are differentially appropriate targets for prevention, early intervention, and/or treatment efforts [ 322 ]. For example, modifiable risk factors such as negative parental comments towards weight and eating behaviours may be best approached using targeted prevention parenting programs to assist with modelling of healthy eating patterns and family dialogue. There is evidence to suggest targeted prevention programs addressing early signs of disordered eating in adolescents (e.g., the Body Project, StudentBodies2-BED ) are effective in significantly reducing future onset of EDs [ 323 , 324 ]. They represent a targeted, efficient way of addressing modifiable risk factors rather than approaching the population as a whole in a largely non-specific manner.

Identifying risk factors which are less amenable to modification, such as genetic risk factors and autoimmune conditions, may represent an opportunity for enhanced screening measures to recognise early signs of disordered eating prior to onset of full ED diagnosis. Research has identified low levels of screening and poor detection rates of EDs by health practitioners, in particular non-stereotypical presentations of EDs in primary care settings [ 325 – 327 ]. A noteworthy outcome of the current review pertains to the growing field of evidence supporting increased risk of EDs within the sexual minority groups as compared to heterosexual samples. Given the high levels stigma surrounding both LGBTQI and EDs, particularly for young males, it is of particular importance that clinicians thoroughly assess for disordered eating behaviours within sexual minority groups [ 328 , 329 ]. Accordingly, the findings of this review may offer an opportunity for advances in the development of resources (e.g., screening instruments) to assist practitioners in recognising evidenced risk factors for EDs.

Finally, awareness of comorbid psychiatric illnesses or personality traits may inform targets for treatment interventions, including as specific programs for individuals with comorbid personality disorders and ED. Enhanced Cognitive Behaviour Therapy (CBT-e) offers an example of the way in which comorbid psychological traits, considered to be “external” to the ED itself, can be addressed to create a more efficacious, tailored treatment for patients [ 330 ]. The inclusion of additional treatment targets to address comorbid psychological mechanisms (clinical perfectionism, core low self-esteem, and interpersonal problems) allows for cognitive behaviour therapy treatment to meet the needs of non-responders for whom comorbid psychopathology may have interfered with their treatment response [ 331 ].

Additionally, given the search strategy of the review adopted a timeline which overlaps between two versions of the Diagnostic and Statistical Manual of Mental Disorders [ 332 ], namely Version 4 and 5 (i.e., DSM-IV and DSM-5), our findings were able to highlight inconsistences in the degree of research conducted across various ED diagnoses. In particular, the findings demonstrate that considerably less is known about the risk factors associated with EDs which were recently included as formal diagnoses in the DSM-5, including ARFID, BED, rumination disorder, and pica, highlighting the need for more focused research efforts to be put towards these diagnoses.

In this review, gaps in the existing literature were identified. Many of the research studies included in the review adopted a cross-sectional study design and therefore focused upon associations and correlations between EDs and potential risk factors. Consequently, some studies were limited in their capacity to delineate temporal or causal relationships, or how in fact the associations connect the factor with the illnesses. For example, although an understanding of psychiatric comorbidities of EDs (e.g., perfectionism, impulsivity etc.) provides value, without longitudinal research it is difficult to disentangle whether these traits contribute to ED onset or are symptoms of it. Similarly, identification of trauma and abuse as a risk factor for eating disorders needs further clarification as this association has been described for many other mental health conditions such as anxiety and depression [ 333 ], and is not likely a specific association to eating disorders. Additionally, several of the studies included in the current review were not able to distinguish between factors related to onset and factors related to maintenance in EDs, which represents an important differentiation of different classes of risk factors and their influence [ 207 ]. It is possible that some of the constructs reviewed in the present paper have a role as maintenance factors, even if they may not have a role as a causal risk factor. An understanding of whether one psychiatric condition precedes another can assist clinicians in treatment planning and inform sequencing of treatment targets. Taken together, these considerations represent a limitation in our ability to understand the implications of these identified risk factors. For risk factors which have relied heavily upon cross-sectional studies, future research is encouraged to adopt experimental or prospective study designs to better capture the nature of the variable being examined.

Several of the studies included in the review examined risk factors in isolation from one another and thus assessment of their association with EDs occurred as though they were independent contributors of risk. This is markedly distinct from real world environments in which EDs develop in response to a multitude of risk factors and consequently, weakens the ecological validity of the reported findings. An understanding of the ways in which various risk factors interact with each other (e.g., whether they are cumulative in nature), is necessary to form a detailed conceptualisation of illness profiles for both clinicians and researchers, which can in turn inform the development of targeted interventions. Conversely, in the absence of this information, the mechanisms of change are less clear. Future research would benefit from adopting an approach towards risk factors as co-occurring, interactional variables as opposed to a siloed view.

Given the attempt to summarise peer-reviewed ED literature in a broad-reaching and prompt manner, there are some limitations of the review. First broad search terms, required to fulfil the purpose of the large series of rapid reviews, of which this paper forms part, were used to collate evidence, which may have compromised the specificity of the included studies for individual ED diagnoses and/or phenotypes and individual risk factors. Additionally, research studies were excluded if they reported on unpublished data, implementation research, or if they were observational studies; and included studies were mostly limited to those conducted in Western cultures with high-resource health systems. Finally, having a specified time period for the review meant that seminal studies conducted prior to the start date were not included.

Conclusions

This review has identified risk factors for which a substantial evidence-base exists as well as emerging areas requiring further investigation (e.g., ADHD) and ED diagnoses where there is less available evidence (e.g., BED, ARFID). A broad review of the literature has been provided, however future studies are required which critique the strength of evidence of the causal nature of these risk factors.

Acknowledgements

The authors would like to thank and acknowledge the hard work of Healthcare Management Advisors (HMA) who were commissioned to undertake the Rapid Review. Additionally, the authors would like to thank all members of the consortium and consultation committees for their advice, input, and considerations during the development process. Further, a special thank you to the carers, consumers and lived experience consultants that provided input to the development of the Rapid Review and wider national Eating Disorders Research & Translation Strategy. Finally, thank you to the Australian Government—Department of Health for their support of the current project.

Abbreviations

Author contributions.

PM, ST and SM oversaw the Rapid Review process; AL carried out and wrote the initial review; SB, SMC and EB wrote the first manuscript; all authors edited and approved the final manuscript.

The RAPID REVIEW was in-part funded by the Australian Government Department of Health in partnership with other national and jurisdictional stakeholders. As the organisation responsible for overseeing the National Eating Disorder Research & Translation Strategy, InsideOut Institute commissioned Healthcare Management Advisors to undertake the RAPID REVIEW as part of a larger, ongoing, project. Role of Funder: The funder was not directly involved in informing the development of the current review.

Availability of data and materials

Declarations.

Not applicable.

ST receives royalties from Hogrefe and Huber, McGraw Hill and Taylor and Francis for published books/book chapters. He has received honoraria from the Takeda Group of Companies for consultative work, public speaking engagements and commissioned reports. He has chaired their Clinical Advisory Committee for Binge Eating Disorder. He is the Editor in Chief of the Journal of Eating Disorders. ST is a committee member of the National Eating Disorders Collaboration as well as the Technical Advisory Group for Eating Disorders. AL undertook work on this RAPID REVIEW while employed by HMA. A/Prof Sarah Maguire is a guest editor of the special issue “Improving the future by understanding the present: evidence reviews for the field of eating disorders.”

1 having three different alleles at the same locus.

2 Polymorphism is a DNA sequence variation.

3 perception or awareness of sensations inside the body.

4 DNA methylation is a process that controls the expression/suppression of a gene without changing the genetic sequence.

5 Small molecules formed in or necessary for metabolism.

6 Models using rates and mice.

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Contributor Information

Phillip aouad, robert boakes.

5 School of Psychology, Faculty of Science, University of Sydney, Sydney, NSW Australia

Leah Brennan

6 School of Psychology and Public Health, La Trobe University, Melbourne, VIC Australia

Susan Byrne

7 School of Psychology, Western Australia, Perth, Australia

Belinda Caldwell

8 Eating Disorders Victoria, Melbourne, VIC Australia

Shannon Calvert

9 Perth, WA Australia

Bronny Carroll

David castle.

10 Medicine, Dentistry and Health Sciences, University of Melbourne, Melbourne, VIC Australia

Ian Caterson

11 School of Life and Environmental Sciences, University of Sydney, Sydney, NSW Australia

Belinda Chelius

12 Eating Disorders Queensland, Brisbane, QLD Australia

13 Sydney Local Health District, New South Wales Health, Sydney, Australia

Simon Clarke

14 Westmead Hospital, Sydney, NSW Australia

Janet Conti

15 Translational Health Research Institute, Western Sydney University, Sydney, NSW Australia

Lexi Crouch

16 Brisbane, QLD Australia

Genevieve Dammery

Natasha dzajkovski, jasmine fardouly.

17 School of Psychology, University of New South Wales, Sydney, NSW Australia

Carmen Felicia

18 University of Sydney, Sydney, NSW Australia

John Feneley

19 New South Wales Health, Sydney, NSW Australia

Amber-Marie Firriolo

Nasim foroughi, mathew fuller-tyszkiewicz.

20 School of Psychology, Faculty of Health, Deakin University, Geelong, VIC Australia

Anthea Fursland

21 School of Population Health, Faculty of Health Sciences, Curtain University, Perth, Australia

Veronica Gonzalez-Arce

Bethanie gouldthorp.

22 Hollywood Clinic, Ramsay Health Care, Perth, Australia

Kelly Griffin

Scott griffiths.

23 Melbourne School of Psychological Sciences, University of Melbourne, Victoria, Australia

Ashlea Hambleton

Amy hannigan.

24 Queensland Eating Disorder Service, Brisbane, QLD Australia

25 Hunter New England Local Health District, Sydney, NSW Australia

26 St Vincent’s Hospital Network Local Health District, Sydney, NSW Australia

Phillipa Hay

27 Brain and Mind Centre, University of Sydney, Sydney, Australia

Francis Kay-Lambkin

28 School of Medicine and Public Health, University of Newcastle, Sydney, NSW Australia

Michael Kohn

29 Westmead Hospital, Sydney, Australia

Eyza Koreshe

Isabel krug.

30 Healthcare Management Advisors, Victoria, Australia

Jake Linardon

Randall long.

31 College of Medicine and Public Health, Flinders University, Adelaide, SA Australia

Amanda Long

32 Exchange Consultancy, Redlynch, NSW Australia

Sloane Madden

33 Eating Disorders Service, Children’s Hospital at Westmead, Sydney, NSW Australia

Danielle Maloney

Sian mclean.

34 The Bouverie Centre, School of Psychology and Public Health, La Trobe University, Victoria, Australia

Thy Meddick

35 Clinical Excellence Queensland, Mental Health Alcohol and Other Drugs Branch, Brisbane, QLD Australia

Jane Miskovic-Wheatley

Deborah mitchison, richard o’kearney.

36 College of Health and Medicine, Australian National University, Canberra, ACT Australia

Shu Hwa Ong

Roger paterson.

37 ADHD and BED Integrated Clinic, Melbourne, VIC Australia

Susan Paxton

38 Department of Psychology and Counselling, La Trobe University, Melbourne, VIC Australia

Melissa Pehlivan

Genevieve pepin.

39 School of Health and Social Development, Faculty of Health, Deakin University, Geelong, VIC Australia

Andrea Phillipou

40 Swinburne Anorexia Nervosa (SWAN) Research Group, Centre for Mental Health, School of Health Sciences, Swinburne University, Melbourne, VIC Australia

Judith Piccone

41 Children’s Health Queensland Hospital and Health Service, Brisbane, QLD Australia

Rebecca Pinkus

Bronwyn raykos.

42 Centre for Clinical Interventions, Western Australia Health, Perth, WA Australia

Paul Rhodes

Elizabeth rieger, sarah rodan, karen rockett, janice russell.

43 Central Clinical School Brain and Mind Research Institute, University of Sydney, Sydney, NSW Australia

Haley Russell

Fiona salter.

44 Ramsay Health Care, Perth, Australia

Susan Sawyer

45 Department of Paediatrics, The University of Melbourne, Melbourne, Australia

Beth Shelton

46 National Eating Disorders Collaboration, Melbourne, VIC Australia

Urvashnee Singh

47 The Hollywood Clinic Hollywood Private Hospital, Ramsey Health, Perth, Australia

Sophie Smith

48 Sydney, NSW Australia

Evelyn Smith

Karen spielman, sarah squire.

49 The Butterfly Foundation, Sydney, Australia

Juliette Thomson

Marika tiggemann.

50 College of Education, Psychology and Social Work, Flinders University, Adelaide, SA Australia

Ranjani Utpala

Lenny vartanian, andrew wallis.

51 Eating Disorder Service, The Sydney Children’s Hospital Network, Westmead Campus, Sydney, Australia

Warren Ward

52 Department of Psychiatry, University of Queensland, Brisbane, Australia

Sarah Wells

53 University of Tasmania, Hobart, TAS Australia

Eleanor Wertheim

Simon wilksch, michelle williams.

54 Royal Hobart, Tasmanian Health Service, Hobart, TAS Australia

Mental disorders may spread in young people's social networks

Using population-wide registry data, researchers from the University of Helsinki, the Finnish Institute for Health and Welfare, the University of Jyväskylä and the University of Manchester investigated whether mental disorders can be transmitted within social networks formed by school classes.

The study is the largest and most comprehensive so far on the spread of mental disorders in social networks, with more than 700,000 ninth-grade pupils from 860 Finnish schools participating. The adolescents were followed from the end of ninth grade for a median of 11 years.

The researchers demonstrated that the number of classmates diagnosed with a mental disorder was associated with a higher risk of receiving a mental disorder diagnosis later in life.

"The observed link was the strongest during the first year of follow-up in the study. This was not explained by a number of factors related to parents, school and residential area. The link was most pronounced in the case of mood, anxiety and eating disorders," says Associate Professor Christian Hakulinen of the University of Helsinki.

Research enabled by comprehensive Finnish registers

According to Hakulinen, prior studies have yielded similar results: for example, American researchers have observed indications of depressive symptoms potentially being transmitted from one individual to another in social networks.

In prior research, however, social networks have typically been chosen independently by the research subjects, which may result in bias in the data. Hakulinen points out that school classes are social networks well suited to research, as people are usually not able to choose their classmates.

"Defining the social networks and following adolescents were made possible by extensive Finnish registers. The findings significantly deepen our understanding of how mental health problems develop and affect other people in our social networks," he says.

Hakulinen nevertheless notes that the connection observed in the study is not necessarily causal. Furthermore, the study did not investigate how mental disorders can potentially be transmitted between individuals.

"It may be possible, for instance, that the threshold for seeking help for mental health issues is lowered when there are one or more people in your social network who have already sought help for their problems. In fact, this kind of normalisation of diagnosis and treatment can be considered beneficial contagion of mental disorders," Hakulinen says.

More preventive measures?

Mental disorders are a significant global challenge, adversely affecting individuals, society and the economy. According to Hakulinen, anxiety and mood symptoms in particular have in recent years increased among young people.

Previous studies have shown that, in roughly half of all cases, the onset of mental disorders in adulthood occurs when people are under 18. In fact, Hakulinen emphasises the importance of preventive measures and early intervention.

"When taking preventive measures, it's worthwhile considering that mental disorders can spread from one adolescent to another," Hakulinen says.

The study involved a total of 713,809 Finnish citizens born between 1985 and 1997. The adolescents were investigated from the end of comprehensive school until they received their first mental disorder diagnosis, relocated from the country or died. At the latest, the follow-up was discontinued at the end of 2019, resulting in a median follow-up period of 11.4 years.

The study received funding from the European Research Council (ERC) and the Research Council of Finland.

• Mental Health Research
• Down Syndrome
• Chronic Illness
• Children's Health
• Mental Health
• Disorders and Syndromes
• Mental illness
• Personality disorder
• Psychopathology
• Eating disorder
• Social cognition
• Controversy about ADHD
• Sleep disorder

Story Source:

Materials provided by University of Helsinki . Note: Content may be edited for style and length.

Journal Reference :

• Jussi Alho, Mai Gutvilig, Ripsa Niemi, Kaisla Komulainen, Petri Böckerman, Roger T. Webb, Marko Elovainio, Christian Hakulinen. Transmission of Mental Disorders in Adolescent Peer Networks . JAMA Psychiatry , 2024; DOI: 10.1001/jamapsychiatry.2024.1126

Cite This Page :

Explore More

• Caterpillars Detect Predators by Electricity
• 'Electronic Spider Silk' Printed On Human Skin
• Engineered Surfaces Made to Shed Heat
• Innovative Material for Sustainable Building
• Human Brain: New Gene Transcripts
• Epstein-Barr Virus and Resulting Diseases
• Origins of the Proton's Spin
• Symbiotic Bacteria Communicate With Plants
• Birdsong and Human Voice: Same Genetic Blueprint
• Molecular Dysregulations in PTSD and Depression

Trending Topics

Strange & offbeat.