Psychology, Treatment & Care
A common misconception about eating disorders is that they’re a disease of vanity. This is a myth perpetuated by laypersons who haven’t taken the time to understand their complexity. Eating disorders can be quite diverse in nature. They are just as complicated as each individual they affect.
Furthermore, diets and eating disorders are not interchangeable concepts. Eating disorders are not necessarily "a diet gone wrong" and by the time restricting food becomes pathological, it is not about vanity, even if a diet's origins had been to "look better in a bathing suit" or to fit in with one’s peer group. Once individuals begin to starve themselves, binge eat, or purge, those behaviors in and of themselves can alter brain chemistry and exacerbate the eating disorder.
The impetus behind eating disorders isn’t as straightforward as you may imagine. They are brain-based, biological illnesses. In addition to the biological, there can also be social, psychological, and interpersonal factors at play.
DNA, upbringing, home environment, history of trauma or abuse, self-esteem, peer pressure, mental health, even athletics and academics can have an impact on whether someone might develop an eating disorder at some point in their life. So far, no singular cause or trigger has been teased out by researchers, doctors, and psychologists collectively as the root cause for any given person struggling with the illness. It’s far more complicated than that. What we do know is it’s a complex puzzle that’s as unique as the sufferer’s own genetic makeup.
The risk of developing an eating disorder is 50-80% determined by genetics making it common for eating disorders to run in families. Some recent, tentatively hopeful progress is being made in the research field of epigenetics that points to more specific biological evidence. Researchers at Columbia University Medical Center recently investigated key components behind anorexia and, although they are myriad, focused on two biological factors and one environmental factor. One biological factor was the specific gene (BDNF-Val66Met variant), another biological factor was the state of calorie deprivation (dieting may alter brain chemistry), and the environmental factor was their theory of “peer-pressure causation.” In the study, they were actually able to mimic all of these conditions in the environment of the test subjects and the mice did, in fact, exhibit anorexic behavior. The study’s ultimate goal was to pinpoint the appropriate corrective measures for those suffering from this disease or preventative measures for those predisposed, as the case may be.
From a very early age, we learn that in order to be accepted, we must emulate the messages we were taught via mass communication.
It is my opinion that a disproportionate amount of blame for causing eating disorders is attributed to the impossibility of maintaining body image standards set by the media to the exclusion of other issues equally or more causative such as trauma, family of origin, or epigenetics. However, with unrealistic pressures to obtain the "perfect" body, the constant influx of images of perfection and narrow definitions of beauty, society can definitely influence our self-esteem and self-worth to some degree, but it’s all relative. That is, we learn what is “attractive” or “acceptable” as a comparative term, measuring ourselves against others and basing our value on what we derive from that.
At the beginning of my twenty year battle with anorexia and bulimia, and 14 years old, I had a conscious desire to be thin. But to be clear, my desire was to be thin in the way that my friends were thin, the way that those in my peer group were thin. I wanted to fit in – not with the unrealistic media images, but in my real adolescent life.
Interestingly, this is precisely the aforementioned “peer-pressure causation” environmental factor of the anorexia study recently conducted at Columbia University Medical Center involving mice and the emergence of anorectic traits when a particular set of environmental and genetic risk factors were involved. "Our findings show that having the at-risk genotype alone is not sufficient to cause anorexia-like behavior, but it confers susceptibility to social stress and dieting, especially during adolescence," said Dr. Zeltser. "You need all of these variables in place to see this robust effect on eating behavior."
So, essentially, the genetic predisposition must exist, combined with peer pressure to diet and the dieting itself.
Eating disorders have substantial co-morbidity with other mental health disorders including depression, anxiety, obsessive-compulsive disorder, post-traumatic stress disorder, and personality disorders.
Studies have shown that there are a high number of people suffering with eating disorders who have been subjected to some form of emotional, physical, or sexual abuse. Many of these people have found that their eating disorders help to protect them, repress or block out the memories, or numb their feelings. Additionally, if an individual was constantly teased or bullied while growing up, they might be inclined toward disordered food behaviors as a coping mechanism. "One driver of anorexia in humans is peer pressure, specifically, the desire to be thin," says Dr. Lori Zeltser of Columbia University Medical Center.
Personal trauma plays a role, too. Disordered eating may arise as a way of coping with a death, loss, or emotional or physical abandonment. About 20-50% is due to unique environmental factors like abuse while a comparatively smaller bit is due to shared environmental influences like the media.
There is great significance and validity in the results of the mice model study as one who has experienced body image disturbance from the get-go, perceived peer pressure concerning weight, self-induced calorie deprivation, and the diagnostic criteria for anorexia nervosa on and off for two decades. My own anorexia and bulimia have strong roots in heritability, a need for control, comorbid mood disorders, bipolar I disorder, and chronic generalized anxiety manifested as obsessive compulsive diet and exercise. The good news is that researchers are getting closer to decreasing the incidence of the number one killer amongst all mental disorders for others.
Just like genetic makeup, eating disorders themselves have the ability to change or adapt over time. Far more perplexing than the other factors, is the genetic fountainhead – more complex than our own DNA, bigger than the beauty industry, and more involved than Columbia University’s mouse model.
“Anorexia-like condition in mice triggered by combination of genetic risk, stress, dieting.” Medical Xpress. Science x Network. 11 April 2016. Accessed 11 Nov 2016. http://medicalxpress.com/news/2016-04-anorexia-like-condition-mice-triggered-combination.html
“Eating Disorder Statistics. How Many People Have Eating Disorders?” Mirasol. 2016. Accessed 11 Nov 2016. http://www.mirasol.net/learning-center/eating-disorder-statistics.php
“Media, Body Image, and Eating Disorders.” PROUD 2B ME Campaign. National Eating Disorder Association (NEDA). 2016. Accessed 14 Nov 2016. http://www.nationaleatingdisorders.org/media-body-image-and-eating-disorders
Nybo, Kristie, PhD. “Exploring the Biology of Eating Disorders”, Biotechniques, The International Journal of Life Science Methods. 11 Nov 2015. Accessed 18 Nov 2016. http://www.biotechniques.com/news/Exploring-the-Biology-of-Eating-Disorders/biotechniques-361`522.html#.WC5-oPkrLgw
Pjetri, Eneda. Ulrike Schmidt, Martien J. Kas, Ian C. Campbell. “Epigenetics and Eating Disorders”. Research Gate. Accessed 14 Nov 2016. https://www.researchgate.net/publication/225056288_Epigenetics_and_eating_disorders
Sansone, Randy, M.D. Lori Sansone, M.D. “Personality Pathology and Its Influence on Eating Disorders”. Innovations In Clinical Neuroscience. Mar 2011. Accessed 18 Nov 2016. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3074200/
“What Causes Eating Disorders.” The Alliance For Eating Disorder Awareness. Donor Community. 2016. Accessed 16 Nov 2016. https://www.allianceforeatingdisorders.com/portal/what-causes-eating-disorders
Zerwas, S., & Bulik, C. (2011). Genetics and Epigenetics of Eating Disorders Psychiatric Annals, 41 (11), 532-538 Cross-referenced: DOI:http://www.healio.com/psychiatry/journals/psycann/2011-11-41-11/%7Bfd02e407-8457-48f0-b49a-f002f4921594%7D/genetics-and-epigenetics-of-eating-disorders
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