Home » The Causes and Risk Factors of Developing an Eating Disorder
Eating disorders may be understood as the external manifestation of internal turmoil on a biological or psychological level.
It may be an attempt to seek security in a body or mind that feels unsafe or foreign; the search for identity in the midst of an unattainable ideal; a way to take up less space and feel as though you exist a little less.
It may be a means of self-erasure or penance for not being quite perfect enough.
Anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), and eating disorders otherwise not specified (EDNOS) are regarded as chronic and multifactorial psychiatric disorders (Zandian, M et al. 2007, p.283). They are primarily characterised by disturbances in eating behaviours/ patterns and a pathological preoccupation with weight regulation and body shape/ body image (Klump, K et al. 2001, p.215).
These disturbances manifest themselves as excessive and/or insufficient food intake and potential pathological compensatory behaviours (e.g. excessive exercise, purging, prolonged fasting etc).
A majority of research posits that eating disorders have multiple, and often interconnected, causes or risk factors – primarily falling under the branches of being biological, psychological, and sociocultural. However, the exact interplay of these contributory factors is yet to be fully understood.
A number of these individual risk factors are defined as being either integral parts of eating disorders (e.g. body image disturbances, perfectionism, etc) or the outcome or result of prolonged disordered eating (e.g. mood disturbances, alterations in brain chemistry, etc) (Rikani, A et al. 2013, p.160)
Brain chemistry may also alter in response to excess or surplus intake, as found within binge eating disorder (BED) and/ or bulimia.
It has been hypothesised that restriction-based eating disorders, as well as associated personality traits (e.g. perfectionism, impulsivity, harm avoidance, etc) are by-products or secondary symptoms which arise as a direct result of starvation (Rikani, A et al. 2013, pp.159 – 160; Zandian, M et al. 2007, p.283).
Observations derived from a six-month study on healthy volunteers undergoing starvation substantiate this theory. Following prolonged malnourishment, the development of psychiatric symptoms, such as depression, anxiety, psychosis, obsessive-compulsive thoughts/ behaviours as well as a reduction in eating rate were noted (Ibid).
In reviewing the impact of starvation on human behaviour, study participants developed an obsessive preoccupation with food so much so that individuals were unable to engage in coherent and creative thought, experienced acute anxiety and demonstrated food-hoarding (Ibid).
Interestingly, all these symptoms/ factors were seen to be reversed by re-feeding.
This causal framework therefore suggests that eating disorders are not only psychiatric disorders, but rather an intake-related disorder in which it is the disordered eating behaviour that gives rise to the psychopathological symptoms of AN, BN, EDNOS and BED and these factors are completely unrelated to the body-weight of the patient (Ibid, p.287).
They are biological reactions to restriction or excess.
These findings suggest that the psychiatric symptoms may be an evolutionary physiological adaptation to food shortages (Ibid).
While physical restriction of dietary intake may propagate further restriction, it may also subsequently, normally increase the drive to eat and result in excessive consumption that may be disturbing for the patient or become pathological. Therefore, it is suggested that starvation may be causation, and comparatively excessive intake may elicit neurobiological (brain chemistry) alterations that propagate the binge-purge or binge cycle.
However, it could be argued that this theory does not account for the impact of individual narratives and the influential factors that initially led the individual to disordered eating behaviours and patters – and therefore may be regarded as a theory of propagation, as within the neurobiological model, as opposed to causation.
A small body of twin studies posit that there is a link between genetic factors and eating disorders. For instance, the study demonstrated that 29-50% of identical twins were congruent for both meeting the categories for anorexia nervosa versus 0% of the fraternal twins within the study (Rikani, A et al. 2013, p.159).
Relatively high heritability estimates for AN and BN of between 48-88% and 28-83% (Hinney, A and Volckmar, AL. 2013, p. 1) respectively suggest that these disorders potentially possess a genetic component that may leave certain individuals more predisposed to developing these psychiatric condition(s).
The remaining variance in the percentages above are often attributed to environmental factors/ familial influence.
Certain research implicates familial spheres in the perpetuation and development of eating disorders. Studies of family interaction, in addition to case reports, suggest that eating disorder patients report either a critical or traumatic familial environment featuring coercive parental control, insecure attachments, and general dysfunction (Polivy, J and Herman, P. 2002, p.194).
Additionally, mothers or primary caregivers of daughters with eating disorders have been shown to have an influence on the development or manifestation of their daughters’ pathology.
Children of primary caregivers, specifically mothers, who themselves suffer(ed) from disordered eating or an eating disorder, or those who were exposed to weight stigma and evaluations from family were more likely to develop eating and/or feeding problems. Statistics demonstrate that approximately 50% of children of mothers with eating disorders suffer from psychiatric disorders (Ibid).
Early exposure to trauma (i.e. sexual abuse, domestic violence, grief etc) is believed to precipitate an increased risk for developing disordered eating (Backholm, K et al. 2013, p. 1), with estimates ranging from 37-100% of trauma history found amongst eating disorder sufferers (Scharff A et al. 2019, p. 1).
Various psychiatric co-morbidities, such as anxiety, depression, obsessive compulsive disorder, personality disorder, substance abuse, self-harm and suicide/ suicide attempts are prominent in patients with eating disorders (Rikani, A et al. 2013, p.158) and may present themselves as precursors to disordered eating or in culmination with.
Body image, or the degree of body satisfaction and dissatisfaction, is understood as being as an integral part of self-esteem and self-worth. Consequently, the assessment or measurement of one’s own body against the culturally idealised body may determine the level of satisfaction or dissatisfaction an individual feels and impact the degree to which someone is susceptible to developing an eating disorder (Rikani, A et al. 2013, p. 159).
Western society’s idealization of thinness and disparagement of “fatness” is intensely focused on constraining the female form, and accounts for the fact that women are 10 times more likely to suffer from a restriction-based eating disorder versus men (Polivy, J and Herman, P. 2002, p. 192).
The internalization of these ideals and consequent distress felt towards a body unable to fulfil this unattainable ideal renders the body a canvas or channel providing an outlet for pathology. Bodily manipulation and may therefore be understood to either attain the thin ideal (restriction-based eating disorders) or a way to refute it/ practice a measure of paradoxical self-rejection by way of excessive consumption.
At Embody Health London, we acknowledge the complexity and uniqueness of every single presentation – irrespective of the cause. If you or someone you know struggles with eating and has a negative association with food please contact us at [email protected] as we would love to support you on your individual recovery journey.
Charlotte Munro, BSc
Blodgett Salafia, E et al. (2015), ‘Perceptions of the causes of eating disorders: a comparison of individuals with and without eating disorders’, Journal of Eating Disorders, 3(32), pp.1-10
Culbert, K et al. (2015), ‘Research Review: What we have learned about the causes of eating disorders – a synthesis of sociocultural, psychological, and biological research’, Journal of Child Psychology and Psychiatry, 56:11, pp. 1141 – 1164. doi:10.1111./jcpp.12441
Hinney, A and Volckmar, AL (2013), ‘Genetics of Eating Disorders’, Current Psychiatry Reports: Eating Disorders, 15(423), pp. 1-9. doi: 10.1007/s11920-013-0423-y
National Eating Disorder Association (2018), Risk Factors. Available at: https://www.nationaleatingdisorders.org/risk-factors (Accessed: 19th November 2020)
Polivy, J and Herman, P (2002), ‘Causes of Eating Disorders’, Annuls Reviews, 53, pp. 187-213.
Rikani, A et al (2013), ‘A critique of the literature on etiology of eating disorders’, Annals of Neuroscience, 20(4), pp.157 – 161. doi: 10.5214/ans.0972.7531.200409
Riva, G and Dakanalis, A (2018), ‘Altered Processing and Integration of Multisensory Bodily Representations and Signals in Eating Disorders: A Possible Path Toward the Understanding of Their Underlying Causes’, Fronteirs in Human Neuroscience. doi: 10.3389/fnhum.2018.00049
Scharff, A et al (2019), ‘Comparing the Clinical Presentation of Eating Disorder Patients with and without Trauma History and/or Comorbid PTSD’, Eating Disorders: The Journal of Treatment and Prevention’, pp. 1-15. doi: 10640266.2019.164203
Trace, S et al. (2013), ‘The Genetics of Eating Disorders’, Annual Review in Clinical Psychology, 9, pp. 589-620. doi: 10.1146/annurev-clinpsy-050212-185546
Zandian, M et al (2007), ‘Cause and treatment of anorexia nervosa’, Physiology & Behaviour, 92, pp.283-290. doi: 10.5214/ans.0972.7531.200409
Embody Health London champions food freedom, positive body image, mental health and emotional wellbeing through a uniquely blended scientific and holistic approach. The EHL team specialises in treating chronic dieting and eating disorders by coaching clients to build confidence and reduce anxiety around their eating habits and food choices.
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