What Caused My (or My Loved One's) Eating Disorder?

Environmental, Genetic, and Interactive Risk Factors

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Overview

When we get sick, we typically want to understand why. This search for explanations pertains generally to any illness, from diabetes to cancer to the flu. When applied to eating disorders, which are associated with many negative stereotypes, the question of causation is especially confusing.

The culture at large, and even some health professionals, commonly blame eating disorders on oversimplified explanations, such as the media’s promotion of unrealistically slender models or on bad parenting.

Based on recent research, we know that families—longtime scapegoats—do not cause eating disorders, at least not in any simple, straightforward manner. For example, while growing up in a dysfunctional home could increase the risk for a number of psychological problems, including eating disorders, it does not condemn a child to a psychological disorder, let alone an eating disorder.

In fact, we can’t say for sure what exactly causes an eating disorder in an individual, and we can’t predict who will go on to develop an eating disorder. In general, most experts agree that:

  • eating disorders are complicated illnesses that stem not from a single cause but from a complex interaction of biological, psychological, and environmental factors; and
  • there are many different pathways to what is essentially the same outcome (e.g., anorexia nervosa or bulimia nervosa or binge eating disorder).

Let’s look at some of the areas of research on the causes of eating disorders.

Risk Factors

Risk factor research focuses on identifying traits or experiences that precede the development of a disorder. For a risk factor to be shown as a causal factor for an eating disorder, that risk factor must be shown to come before the development of the eating disorder. It also must be capable of being manipulated, and it must be demonstrated that manipulating it actually prevents the occurrence the disorder.

For example, smoking is a causal risk factor for lung cancer because it comes before the development of the disease, and not smoking reduces one’s risk of developing lung cancer.

Because eating disorders are relatively rare and diverse disorders, it is both difficult and expensive to perform the kinds of large and long-term studies needed to better assess risk factors. To date, there is limited risk factor research that has successfully demonstrated causality. According to a 2015 paper by Stice, only the following risk factors have been shown to be causal factors for eating disorders.

Anorexia nervosa

  • Low body mass index (BMI)

Bulimia nervosa

  • Thin-ideal internalization – the degree to which a person believes that thinness is equivalent to attractiveness
  • Perceived pressure to be thin – what a person believes to be preference for thinness among others around them
  • Body dissatisfaction – negative body image
  • Dieting
  • Negative affect – unpleasant feelings (e.g., fear, anger, and sadness and varieties thereof)

Binge eating disorder

  • None identified at this time

Purging disorder

  • Dieting

However, these are likely not the only factors that may contribute to the development of an eating disorder. These are merely the ones that have met a higher burden of proof in research.

For instance, there is not yet enough evidence to support that dieting behavior is a causal factor for anorexia nervosa, but future studies may show that it is (and as noted above, it is already known that low BMI, one result of extreme dieting, is a causal factor for anorexia nervosa). In addition, others might criticize this list because these risk factors are so closely similar to the actual symptoms of these illnesses.

Many other factors have been, or are being, studied as possible contributors to the development of eating disorders:

  • Weight-related teasing and critical comments about weight
  • Bullying
  • Fixation with a thin body
  • Peer pressure
  • Early childhood feeding and eating problems and gastrointestinal problems
  • Low self-esteem
  • Body dissatisfaction
  • Anxiety and depression
  • Childhood sexual abuse

You can see that identifying actual causal factors for an eating disorder is complicated. As well, determining whether these factors are present in an individual can be difficult. Furthermore, the presence of these factors, each of which predicts higher risk, does not guarantee the development of an eating disorder.

Genetics

Genetic explanations have received increased focus in the last 10 years. The primary reason that eating disorders run in families appears to be genetics. Coming from a family with a history of eating disorders can increase one’s risk of developing an eating disorder. A portion of this increased risk could potentially be due to the modeling of eating disorder-linked behaviors within a family (e.g., observing a family member dieting). However, twin study research, which can isolate the role of genetics, has confirmed that approximately 40-60% of the risk for anorexia nervosa, bulimia nervosa, and binge eating disorder arises from genetic influence.

This finding does not imply that there exists a single eating disorder gene, or even that genes cause eating disorders. It is more likely that for some people, variations in several different genes contribute in various degrees to traits that in turn increase or decrease their risk for these disorders. Some individuals may inherit traits such as anxiety, fear, perfectionism, or moodiness that have been associated with the development of an eating disorder. It is worth noting, however, that these aspects of temperament have been linked to a number of other disorders, too.

Some individuals with eating disorders are able to identify several other family members who also had eating disorders. There are certain families in which the risk of eating disorders is much higher than in the general population, but such families are relatively rare. Even a high-risk family history indicating an increased genetic risk does not mean that one is destined to develop an eating disorder.

Conversely, not everyone who has an eating disorder can identify another family member with one. Though genetics does play a role in the development of eating disorders, it is important to note that the occurrence of eating disorders is low enough that many – in fact, a clear majority of – cases are sporadic, with no family history. Given the smaller size of today’s families, there is often not enough data to determine whether a specific individual has a genetic tendency. In addition, eating disorders are stigmatized diseases, and family members often do not share their struggles with their disorder, with extended or even immediate family members.

Previous genetic studies have not found specific genes associated with risk likely partly because the studies were not big enough to detect such genes. However, convincing evidence has been found that genes contribute to the development of eating disorders. The largest and most rigorous genetic investigation of eating disorders ever conducted, the Anorexia Nervosa Genetics Initiative (ANGI), has just completed blood collection and shown some initial results. This project is being conducted by researchers in the United States, Sweden, Australia, United Kingdom, and Denmark. Hopefully, soon researchers will be able to provide more information about the genetic profile that contributes to eating disorders.

Environmental Factors

Much of the earlier research on eating disorders examined environmental risk factors. As a result, they are frequently blamed for causing eating disorders. Environmental factors include events and influences in an individual’s life, such as diet culture, the media, trauma, and weight teasing.

One environmental factor commonly implicated in eating disorders is media exposure. Dr. Ann Becker’s research assessed two cohorts of school children in Fiji in 1995 and 1998, before and after the arrival of Western television. She found a significant increase in disordered eating behaviors and specifically purging to lose weight following the arrival of Western television in Fiji.

Of course, society and culture do influence eating behavior as well as our ideal of body shape. However, such environmental factors cannot fully account for the presence of eating disorders. If they did, 100 percent of the people exposed to the environmental factor(s) would develop an eating disorder, which we know is not the case.

Indeed, it is likely more complex than that. One model for understanding some of the sociocultural risk factors for eating disorders is the tripartite model. This model proposes that exposure to media, peer, and parent messages all contribute to whether an individual buys into the thin ideal and engages in social comparison. These two factors, in turn, may potentially lead to poor body image and various forms of disordered eating. Additionally, sociocultural models suggest that other influences, such as gender, ethnicity, or certain athletic settings, can strengthen or lessen other factors. This further explains why specific groups, such as dancers, may be at greater risk of developing eating disorders.

Gene and Environment Interplay

Since neither genes nor environment causes an eating disorder on their own, it is now recognized that eating disorders are likely the result of a more complicated interplay of these factors. Even when patients or family members can cite a precipitating factor, there is almost always a combination of contributing factors. The one event cited as the cause is most likely the trigger that tripped a cascade of events.

A genetic susceptibility may influence the types of situations to which a person exposes oneself, or it may influence their response to certain stressors. Examples may include the following:

  • A person who is genetically vulnerable to an eating disorder might select activities such as reading fashion magazines or taking ballet classes, which reinforce negative body image and in turn lead to an increase in exercise and weight loss.
  • A person who is genetically susceptible to an eating disorder may be more sensitive to weight-related teasing and have a heightened reaction – for instance, initiating a diet that snowballs into a full disorder.
  • A teenager who is genetically vulnerable may continue dieting much longer than peers who diet and then stop.
  • A person who has the temperament that commonly underlies anorexia nervosa (anxious and perfectionistic) may seek out the types of social environments that contribute to the onset of dieting.

Epigenetics

The emerging field of epigenetics, the study of whether, how, and when genes are expressed, offers further complexity. Epigenetics explains that certain environmental factors determine the expression of genes or even turn certain genes on or off in the next generation. Thus, stress to a parent alters not only their behavior but can actually turn genes on and off in their later offspring who were not even exposed to that stressor. In terms of eating disorders, there is evidence that the longer patients have anorexia nervosa, the greater the chance they will have alterations in how their genes are expressed. It appears that malnourishment could turn on or off certain genes, which influence the course of the disorder. However, epigenetic studies of eating disorders are in their infancy.

In summary, genes influence temperament and behavior while environmental factors influence biology through complex feedback loops and vice versa.

Summary

THERE IS HOPE. We can help to create protective factors for those who might be vulnerable.

While the inability to determine precisely what caused an eating disorder may seem depressing, the silver lining is that just as environmental factors can increase one’s susceptibility to an eating disorder, the converse is true: by changing the environment, you can help create the conditions and contingencies that will facilitate prevention and recovery. For example, growing up in a home characterized by parental warmth could mitigate genes that otherwise promote anxiety.

Some of the potential protective environmental factors that have been investigated are family meals, eating breakfast, emotional regulation skills, and mindfulness techniques. Other potential protections include various techniques that help groups and individuals to question and challenge unrealistic ideals of beauty, including the glorification of thinness and the stigmatization of fat people. Many of these environmental changes, such as improving the status and power of women, reducing the objectification of females and males, and increasing respect for all sizes and shapes, will benefit all people and help create kinder and safer—and likely more protective—communities.

However, keep in mind that chance and bad luck play a role, and individuals vary in their genetic risk. Even in the face of every preventative measure in the book, some people with extremely high genetic risks may still go on to develop an eating disorder after just one or two triggering events that are outside of anyone’s control. Others who have low genetic risk may show resilience to developing an eating disorder even in the face of many potential environmental risk factors.

In conclusion, when someone—including you—gets an eating disorder, it’s no one’s fault. The cause of eating disorders has been found, thus far, to be complex.

Sources:

Bulik CM, Sullivan PF, Tozzi F, Furberg H, Lichtenstein P, Pedersen NL. PRevalence, heritability, and prospective risk factors for anorexia nervosa. Arch Gen Psychiatry [Internet]. 2006 Mar 1 ; 63(3):305–12. http://jamanetwork.com/journals/jamapsychiatry/fullarticle/209373.

Klump KL, Burt S, McGue M, Iacono WG. Changes in genetic and environmental influences on disordered eating across adolescence: A longitudinal twin study. Arch Gen Psychiatry [Internet]. 2007 64(12):1409–15: http://jamanetwork.com/journals/jamapsychiatry/fullarticle/482517

Mazzeo SE, Bulik CM. Environmental and genetic risk factors for eating disorders: What the clinician needs to know. Child Adolesc Psychiatr Clin N Am [Internet]. 2009 Jan [cited 2016 Aug 17];18(1):67–82. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719561/

Striegel-Moore RH, Bulik CM. Risk factors for eating disorders. American Psychologist. 2007;62(3):181–98

Stice E. Interactive and Mediational Etiologic Models of Eating Disorder Onset: Evidence from Prospective Studies. Annual Review of Clinical Psychology, 2016 12:359-381, http://www.annualreviews.org/doi/abs/10.1146/annurev-clinpsy-021815-093317

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