What are the causes of eating disorders? The most recent research on eating disorders has been, and continues to be very progressive. Theories that regard eating disorders as a result of over controlling parents or a desire to be thin are steadily taking a back seat to genetic studies that prove otherwise. An eating disorder in any individual will have been caused by a complex mixture of biological, behavioral, psychological and social factors.
Research has established that there is a genetic basis for eating disorders in the same manner that there is for other prominent psychiatric disorders such as schizophrenia, bipolar disorder, and autism (11). For example, individuals who have an immediate family member (e.g., mother, father, sibling) with an eating disorder are up to 11-times more likely to develop an eating disorder themselves. (12)
Twin studies, which allow us to determine the heritability of a trait—the proportion of variation in a trait that is attributable to genes—have shown that approximately 40-60% of the risk for anorexia nervosa, bulimia nervosa, and binge-eating disorder are accounted for by genetic factors (11). However, we have yet to identify which specific genes may be involved in the risk for eating disorders.
Early molecular genetic studies aimed at identifying the specific genes involved in eating disorder risk suggested that genes involved in mood, appetite regulation, reward, food intake, and weight regulation may play a role in eating disorder development (11,13). From this work, the most promising candidate genes seemed to be within the serotonin system, which is involved in mood, anxiety, and weight regulation. However, these early studies showed inconsistent findings such that some studies would observe a significant association between a specific gene and eating disorder risk while others would show no significant association.
The challenge with identifying the genes involved in eating disorder risk is the sample sizes needed in order to be able to find meaningful results. From the work of other psychiatric disorders like schizophrenia we know that at least 10,000 individuals are needed for genetic studies! This is because the genetic risk for eating disorders is not inherited through a single gene, but transmitted through a polygenetic pattern of inheritance, which means that several genes, each of which only have a small effect, come together to increase risk. It is because each of these genes only plays a small role that such large sample sizes are necessary.
It is also important to note that, while research has established that eating disorders have a genetic component that is not to say that there is not an environmental effect. For example, not everyone with a family history of an eating disorder develops an eating disorder. And people with no family history can also develop an eating disorder. In fact, genetic factors likely work in combination with environmental effects to increase risk.
One way in which genes and environment interact is that an individual’s genetic predisposition might influence how they respond to a stressor or the environment. For example, although adolescents may diet, only those who are more genetically predisposed may slip into an eating disorder.
A second way that genes and environment can interact is that individuals’ genetic predispositions may influence what types of environments they expose themselves to. An individual’s genetically influenced trait (e.g., personality) may influence whether or not s/he participates in sports and whether s/he is attracted to a sport that is highly weight and performance focused.
In sum, research tells us that genes and environment work together in combination to influence risk for an eating disorder. Genes are not destiny; however, genetic and environmental factors can also buffer against the development of an eating disorder.
External influences can trigger an eating disorder, that is not to say that they can cause one unless the individual is predisposed to having one. The vast majority of people have dieted at some point in their life without developing an eating disorder. The reasons behind wanting to diet in the first place are questions for society that should be kept separate from questions around eating disorders. However, in some individuals, the restriction in calories can spark the eating disorder in their brain.
It is true that most eating disorders typically onset during adolescence, however there are plenty of cases of onset being in early childhood before puberty or in later life. It may be the case that the majority of cases will onset during puberty due to the vast changes that are occurring in the body and the brain at this time. It is likely to be a complicated matrix of genetic, biological, psychological and sociocultural effects(3). There has not been one single factor that has been shown to cause an eating disorder.
The ratio of females to males in anorexia is reported to be higher, however more recently it is considered that statistical values here are inaccurate due to the lack of adequate diagnosis in males. In fact recent data from the NHS has shown a 66% rise in the number of males diagnosed with eating disorders. It is certainly not true that men and boys cannot develop an eating disorder. A 2013 study(4) estimated that 10-15% of bulimia sufferers are male, this has implications for treatment centers to look to gear their approaches in a more unisex manner.
A Brain Based Disorder
Neuroimaging studies have been helpful in identifying the difference here in the brain of a person with an eating disorder. They appear to be able to ignore the hunger signals that most other people in the population cannot. There is also research into the role of dopamine and the reward signals that are usually given when one eats food that suggests this system is changed in anorexia(5).
For the majority of the population, appetite is simple, one gets hungry and then one eats. In the brain, appetite is a very complicated system of excitatory and inhibitory chemical reactions that involve different hormones, senses and a constant analysis of the levels of different nutrients in the bloodstream. When person has an eating disorder, elements of this appetite system can be compromised or not functioning as they did before. Anxiety may take the place of hunger, or feeling full may take the place of feeling empty. Eating less can begin to feel soothing and pleasant. Eating disorders present differently in sufferers due to the complexity of the neurological and biological system that eating is, and for this reason cause and effect cannot be generalized.
However, there are some things that we do know for sure about the causes of Eating Disorders:
- Parents do not cause eating disorders(6).
- Eating disorders are not a choice. They are a serious mental disorder.
- A persons external appearance is not something that should be used as an indication of their potential to develop an eating disorder.
- There is research that is investigating anorexia to be relevant on the autism scale(7).
- Eating disorders often, but not always occur alongside other mental conditions such as OCD, depression and anxiety disorders.
- Studies like The Minnesota Starvation Experiment show that the effects of malnutrition mean that a person’s personality can be distorted(8).
- Eating disorders do not discriminate. Both genders can be affected and all ages groups.
- Malnutrition can lead to severe physical and psychological problems(9) (Garner 1997). For this reason treatment should be sought as soon as an eating disorder is suspected.
- Malnutrition puts the sufferers brain in an altered state, for this reason they may be unable to make rational decisions about food.
- In some individuals malnutrition can fuel a desire to exercise excessively(10).
Causes of Relapse
The relapse rate for people that have been treated for anorexia nervosa or bulimia nervosa is particularly high. Individuals being treated in an inpatient facility for eating disorders often regain some weight but then lose it again when they return home. This is why it is crucial to work with families, parents and caregivers in order to make sure that the sufferer has continued support outside of their inpatient facility. Here is more on the relapse warning signs.
The good news is that there are programs in operation that are designed to tackle the potential of relapse by working with families. Treatments that have been developed from evidence based methods and scientific literature are beginning to show very positive results in terms of lessening the relapse rate of eating disorders.
The bottom line is that eating disorders are complicated, and spending too much energy trying to figure out the cause has proven to be largely ineffective in terms of recovery and treatment. That is not to say that environmental factors such as body image and past trauma/abuse do not need to be addressed if they were indeed present as a triggering factor, they do. But they should be addressed and treated separately from the eating disorder.
Read more about Treatment options here. To learn about the links between food allergies and eating disorders, eating disorders and the media, or celebrities with eating disorders, just follow the links provided. We also have information on pregnancy and eating disorders and why dieting doesn’t work.
Updated 2015 by Dr. Jessica Baker, PhD from the Center of Excellence for Eating Disorders in the Department of Psychiatry at the University of North Carolina (UNC).
Written by Tabitha Farrar – April, 2014
The Genetic Risk For Eating Disorders And The Anorexia Nervosa Genetics Initiative (ANGI)
Restrictive Eating Disorders Study at the Mass. Gen. Hospital Research Program
Should Schools Have Eating Disorder Prevention Programs?
Puzzling Symptoms – A family guide to the Neurobiology of Eating Disorders.
Eating Disorders 101 – University of California.
3. Lilenfeld L, Wonderlich S, Riso LP, Crosby R, Mitchell J. Eating disorders and
personality: a methodological and empirical review. Clin Psychol Rev. 2006;26(3):299-320
4. Carlat, D.J., Camargo. Review of Bulimia Nervosa in Males. American Journal of Psychiatry, 154, 1997.
5. Kontis, D., & Theochari, E. (2012). Dopamine in anorexia nervosa; A systematic review Behavioural Pharmacology, 23 (5 and 6), 496-515
10. Hillebrand, J.J., Kas, M.J., van Elburg, A.A., Hoek, H.W., & Adan, R.A. (2008). Leptin’s effect on hyperactivity: potential downstream effector mechanisms. Physiology & Behavior, 94 (5), 689-95 PMID: 18495181 – See more at: http://www.scienceofeds.org/2014/02/15/models-of-anorexia-nervosa-a-few-insights-from-our-animal-cousins/
11. Trace, S.E., et al., The genetics of eating disorders. Annu Rev Clin Psychol, 2013. 9: p. 589-620.
12. Strober, M., et al., Controlled family study of anorexia nervosa and bulimia nervosa: evidence of shared liability and transmission of partial syndromes. Am J Psychiatry, 2000. 157(3): p. 393-401.
13. Baker, J.H., et al., Genetics of Anorexia Nervosa. September 2013. In: eLS. John Wiley & Sons, Ltd: Chichester.