[En español]

Warning: potential trigger

Anorexia nervosa.  A disease for the privileged?  Shallow white girls trying to look like fashion models? Women on a vanity-driven quest to be skinny and popular? Self-centered, “basic” girls aspiring to be the #thinspiration models of their social media circles?

Dispelling the Stereotypes

The stereotypes attached to anorexia add to the devastating reality of a serious brain disorder.  Anorexia nervosa (AN) is defined by three characteristics according to the DSM-V: restrictive energy intake relative to requirement, intense fear of gaining weight, and disturbance in the way in which one’s body weight or shape is experienced.  Fear.  And an alteration of perception.  Not vanity or shallowness.  If you enter the dark world of pro-ana (encouraging anorexia) websites or instagram accounts, you will find red flags of depression and anxiety, not arrogance. #depressed and #suicidal make frequent appearances in the sea of hashtags.

And anorexia is not a #whitegirlproblem. It affects women of every race and socioeconomic background (and men too, although less frequently). In a piece called “Eating Disorders Do Not Discriminate,” Michelle Konstantinovsky passionately tackles the stereotypes associated with anorexia by sharing stories of women who were not only suffering from AN but also not receiving the attention and care that they needed because of the preconceived racial and cultural notions blinding their families, schools, and doctors.  While the specific triggers for sufferers across various cultures might be different, the biological changes that accompany the development of AN are a common denominator.

So, let’s begin again.

Anorexia nervosa. Dry and brittle bones prone to breaking, hair loss, anemia, drop in internal body temperature, dehydration, fatigue, slowed circulation, serious structural and functional damage to the heart caused by decreased muscle mass.  That is the stark reality of AN, which claims the lives of 5-20% of those who suffer from it, often from heart failure, malnutrition, or suicide.

Despite the seriousness of the disorder, anorexia research is miserably underfunded.  In 2014, the NIH spent only $11 million on anorexia research (compared to, for example, $562 million on Alzheimer’s disease, $253 on schizophrenia, $396 million on depression, and $1,011 million on diabetes [1]), even though the lifetime prevalence of AN in the U.S. is astonishingly high.  If you were to delve deeper into the funding report from the NIH, you would notice that this $11 million was used to fund just 32 research projects.  Given these demoralizing statistics, it is not surprising that the neurobiological mechanisms underlying AD remain poorly understood.

Research Falls Short

Earlier this year, pop-science media outlets such as Science of Us and IFL Science were all abuzz reporting a new anorexia study from researchers at Columbia University and the New York State Psychiatric Institute.  The original article [2], however, is underwhelming in both its explanation of neural underpinnings and in its relevance to treatment.

The researchers designed a task to compare brain activity related to food choice between a group of women newly hospitalized for anorexia nervosa and a group of healthy female subjects.  The researchers found that, when making food choices, those with AN displayed more activity in the dorsal striatum, an area that has long been linked to habit learning [3].  AN patients also showed stronger connections between the striatum and the prefrontal cortex—a structure known for its role in executive function and decision-making—when shown images of low-fat foods.  This pattern was opposite for healthy control subjects, who showed stronger connectivity between the striatum and cortex when viewing high-fat fod items.  These findings suggest that, in AN, automatic habits are strongly driving food decisions and the brain’s response to high and low fat foods has somehow become altered.

Screen Shot 2015-12-03 at 8.03.03 PM

Screen Shot 2015-12-03 at 5.01.02 PM

Foerde et al., 2015

Although this study was published in a high-profile journal, it is not exactly groundbreaking. Given that the lives of those with AN are completely overtaken by ensuring minimal calories, it is unsurprising that they rely strongly on the striatum for food decisions.  And while the second finding is slightly more interesting, it is impossible to know from this study whether these connectivity differences made the participants more vulnerable to AN in the first place or whether the changes occurred as a result of living with the disorder.  To answer this question, researchers would need to image a large sample of young children and follow them through young adulthood. Assuming that some of these children would eventually develop AN, those subjects’ original brain scans could then be investigated for predictive features. Without a study like this—without any clues regarding cause and effect—the results do not do much to help those suffering from AN.

Not only do imaging studies present a problem in terms of deciphering cause and effect, they also do not allow scientists to delve into the basic biology.  To answer questions about what changes are happening inside and between the brain cells in affected brain regions, scientists must turn to genetic information or to animal models of the disease.  Can certain inherited genes make a person more vulnerable to the disorder?  If so, what do those genes code for?  What molecular pathways might be involved?

While environment and circumstance certainly come into play in AN (and will be discussed later), there does seem to be a strong genetic component to the disorder; a particular study suggests that female relatives of AN patients are about eleven times more likely to develop AN themselves [4].  But which genes might be involved remains unclear.  While some genes such as those coding for cannabinoid and opioid receptors (both associated with the reward system and habit learning) have been implicated, results have been mixed.  Large-scale genome-wide association studies have not found any significant differences in the AN population, but it is likely that differences do exist and these studies simply did not have the statistical power to detect them [5].

Usually, scientists have a number of ways (genetic, pharmacological, etc.) to model a psychiatric disorder in rodents so that they can reach a better understanding of the underlying neurobiological dysfunction via experiments impossible to do in humans.  Unfortunately, absence of a good rodent model of AN has long plagued the AN research community.  There is a mouse strain with a particular mutation (dubbed anx/anx mice) that for a while seemed promising.  Mice with this genetic alteration have significantly lower body mass due to reduced food intake, appear emaciated, and die prematurely [6]. However, recent studies have suggested that the mutation causes mitochondrial dysfunction [7], which then leads to symptoms that look like anorexia but may have no physiological relevance to the disorder.

There is, however, a phenomenon that occurs in rodents that might hold promise for scientists studying anorexia.

A New Hope: Running Rodents

Despite shortcomings in our ability to probe the biological underpinnings of anorexia nervosa, there is a newly re-discovered rodent model with exciting potential.  It is based on a phenomenon that was observed decades ago.  In the 1950s and 60s, a couple groups of scientists noticed that if rats were given a running wheel and were switched from having constant access to food to a restricted diet (fed once a day), the restricted rats would run more than those with constant access to food and would eventually barely eat despite increased physical activity [8,9].  Somehow, these rats’ brains become wired for self-starvation and addicted to exercise.  What is happening?!  Investigating this phenomenon will hopefully lead to new clues about the neural basis of AN.

What makes this model especially rare and exciting?  Often, rodent models of disease involve either a drug or a genetic manipulation—removing a gene that makes a certain receptor or causing certain brain cells to produce extra amounts of a particular molecule.  For example, in most mouse models of Alzheimer’s disease, all brain cells are made to create mutated forms of the protein that misfolds and aggregates in the human disease.  The mice develop the “plaques” characteristic of Alzheimer’s and have memory deficits, but the pathology and symptoms were induced—they did not occur naturally—which limits how much the models can tell us about the sporadic, age-related Alzheimer’s that afflicts humans.  The activity-based model of anorexia, however, involves no drugs or gene changes; the alarming behavior change in the rodents occurs with just a change in feeding schedule and the opportunity for unlimited exercise.  This not only provides a model with which to study the very basic biology of affected neural circuits, but it also means that the tendencies underlying AN might somehow have been incredibly conserved through evolution if they can develop in the rat brain with minimal researcher manipulation.

Environmental Triggers

As mentioned previously, even if scientists were to identify some of the genes that might make people more vulnerable to developing anorexia, genetics would not explain everything; environmental pressures play a crucial role as well.  These triggers take countless forms, from chronic abuse to traumatic events to a desire to portray self-discipline.  In some cases the pressure might come from an elite sports team where competitiveness and repetitive workouts act as stressors.  Or perhaps a death or a divorce in the family leads to a feeling that life has spiraled out of control; tight control over what one eats might paradoxically appear as a way to regain some of this control.  For Joanna Kay, it was the latter.

Earlier this year, I heard Joanna interviewed on NPR for a piece on eating disorders and the dark, addicting network of websites where girls share tips on how to be successful anorexics.  I reached out to her when I decided to write this post so that I could begin to understand the disorder from the perspective of someone who knows it all too well.  Joanna’s story begins when she was just barely in her teens:

The illness developed just before I turned 14, while my parents were going through a very acrimonious divorce. I don’t know why I began to skip meals to make myself feel better, or what even gave me that idea, but that’s what happened. I couldn’t control what was happening at home, but I could control what I was doing to my body (I also self-harmed and eventually began to abuse alcohol). For the next decade I bounced between remission and relapse. I would lose weight, and then get scared by how sick I became. So I would tell myself that I had to stop with all the self-destruction, and I’d try to eat more. But gaining weight scared the hell out of me, so I would ultimately drop it all and then some. Every time I tried to relax my restrictive attitude toward food, I panicked and ran back into anorexia. Because I was chronically underweight, everyone believed that my body type was naturally thin, which is partly why no one noticed something was wrong. Even I believed that lie after a while.  

Joanna is now well into the recovery process, but still struggles with losing the tight control over her weight that she became habituated to.  She is not allowed to know her weight and still does not perceive her appearance accurately.  After so many years of agonizing over each fraction of a pound, the inability to even gauge weight gain engenders an anxiety that she must continuously fight to keep at bay.

Women of all races are vulnerable to body dissatisfaction; studies have shown that Asian, Hispanic, and African American girls harbor greater body image dissatisfaction than Caucasian girls [10,11], possibly increasing their susceptibility to eating disorder development.  There is also evidence that minorities endure additional stress in terms of a culture dissonance between body image/beauty in their cultures and in dominant American culture [12].  Another factor that comes into play in the development of eating disorders is the perception of parental control; studies have shown that Asian adolescents tend to have high levels of perceived maternal control which exacerbates unhealthy eating habits and leads to higher incidence of bulimia [13,14].

Attacking Anorexia from All Angles

In addition to circumstantial and cultural complications, there is an incontrovertible link between anorexia and mood disorders, especially depression.  In a publication earlier this year, doctors reviewed the evidence for an association between AN and a dysfunction in a series of brain regions associated with the generation and regulation of mood and emotion (including the anterior cingulate cortex, amygdala, and nucleus accumbens), arguing that it is this dysregulation that drives AN behavior [15].   However, it is not straightforward whether mood disorders lead to anorexia or vice versa.  A study published earlier this year examined 271 patients with anorexia or bulimia and found that among each eating disorder group, there was about 80% prevalence of a mood disorder.  In some cases the eating disorder had preceded the mood disorder, and in others the mood disorder appeared first [16].

Given this undisputed overlap between mood disorders and AN, it is essential to address comorbid mood dysregulation when treating patients.  This means thoroughly individualized treatment. Joanna relates from personal experience that the most effective approach is multidisciplinary, with a treatment team of a therapist, nutritionist, physician, and sometimes a psychiatrist.  This team must arrange a different treatment plan depending on the patient’s strongest needs.  And after this plan has been implemented, it must be very gradually decreased in terms of intensity level–abruptly stopping treatment leads to certain relapse.

Although it seems logical that therapy might put an AN patient in a better frame of mind to concentration on recovery, therapy is simply not possible without a bit of recovery first, which creates a bit of a catch-22.  Imagine how you feel when you’ve had to work way too late and haven’t eaten in hours.  When you finally escape your desk and stumble home, a therapy session would be the last place you’d want to go–you’re past the “hangry” phase, you can barely form simple thoughts much less engage in an in-depth self-reflection.  Imagine feeling like that all the time.   Joanna confirms that “weight restoration has to be prioritized. You cannot do the hard work of recovery if you are sick, weak, and malnourished. You need stamina, both physical and mental.”

Above all, though, according to Joanna, is the aspect of community; meeting and sharing stories with others who have endured similar struggling helps to normalize the experience. Not only is this support necessary during the initial stages of treatment, but it is also essential to maintain recovery.

Fighting a National Unhealthy Health Obsession

Regardless of whether we can personally relate to Joanna’s experiences, we can all make an effort to have a healthier relationship with food.  In an interesting and quite entertaining article, Michael Pcavemanollan goes so far as to diagnose “Our National Eating Disorder.  Our country’s strange cultural relationship with food—as well as prevalent deep-seated stigmas against those who are obese—unfortunately creates an atmosphere ripe for the development of AN.  So, fight back.  Don’t make so many rules and restrictions with regards to food. Avoid the ridiculous roller coasters of fad diets (Eat like cavemen did! Sugar is the enemy! Actually, consume ONLY sugar—in the form of overpriced juice!).  Eat more slowly.  Eat at a table instead of in front of a television.  But perhaps most importantly, eat with family or a friend or a significant other.  Make food a celebration and a means for personal connection.

And if someone you know and love is suffering from AN, remember that her brain reacts differently to food, and processes food-related decisions in an altered manner–she cannot just “snap out of it” and gain weight.  Be her emotional support. Help her realize that no one should have to live with the burden of constant anxiety over food and body weight.  She deserves peace of mind.  She needs treatment, as difficult as that road may be.  Tell her you’ll be with her on that road.


I would like to thank Joanna for her incredible willingness to share her experiences with me for this piece, and I am happy to report that she is currently the healthiest she has ever been, both emotionally and physically.  Her inspiring recovery blog can be found at  Joanna, you are amazingly strong and we here at NeuWriteSD are wholeheartedly rooting for you ♥



  1. National Institutes of Health. (2015). Estimates of Funding for Various Research, Condition, and Disease Categories (RCDC).
  2. Foerde K, Steinglass JE, Shohamy D, Walsh BT. Neural mechanisms supporting maladaptive food choices in anorexia nervosa. Nat Neurosci. 2015 Nov;18(11):1571-3. doi: 10.1038/nn.4136. Epub 2015 Oct 12. PubMed PMID: 26457555
  3. Wise RA. Neurobiology of addiction. Curr Opin Neurobiol. 1996 Apr;6(2):243-51. Review. PubMed PMID: 8725967.
  4. Strober M, Freeman R, Lampert C, Diamond J, Kaye W. Controlled family study of anorexia nervosa and bulimia nervosa: evidence of shared liability and transmission of partial syndromes. Am J Psychiatry. 2000 Mar;157(3):393-401. PubMed PMID: 10698815.
  5. Boraska V et al.  A genome-wide association study of anorexia nervosa. Mol Psychiatry. 2014 Oct;19(10):1085-94. doi: 10.1038/mp.2013.187. Epub 2014 Feb 11. PubMed PMID: 24514567
  6. Son JH, Baker H, Park DH, Joh TH. Drastic and selective hyperinnervation of central serotonergic neurons in a lethal neurodevelopmental mouse mutant, Anorexia (anx). Brain Res Mol Brain Res. 1994 Aug;25(1-2):129-34. PubMed PMID:7984037.
  7. Lindfors C, Nilsson IA, Garcia-Roves PM, Zuberi AR, Karimi M, Donahue LR, Roopenian DC, Mulder J, Uhlén M, Ekström TJ, Davisson MT, Hökfelt TG, Schalling M, Johansen JE. Hypothalamic mitochondrial dysfunction associated with anorexia in the anx/anx mouse. Proc Natl Acad Sci U S A. 2011 Nov 1;108(44):18108-13. doi:10.1073/pnas.1114863108. Epub 2011 Oct 24. PubMed PMID: 22025706
  8. Hall JF, Hanford PV. Activity as a function of a restricted feeding schedule. J Comp Physiol Psychol. 1954 Oct;47(5):362-3. PubMed PMID: 13221681.
  9. Routtenberg A, Kuznesof AW. Self-starvation of rats living in activity wheels on a restricted feeding schedule. J Comp Physiol Psychol. 1967 Dec;64(3):414-21. PubMed PMID: 6082873.
  10. Vander Wal JS, Thomas N. Predictors of body image dissatisfaction and disturbed eating attitudes and behaviors in African American and Hispanic girls. Eat Behav. 2004 Nov;5(4):291-301. PubMed PMID: 15488444.
  11. Robinson TN, Killen JD, Litt IF, Hammer LD, Wilson DM, Haydel KF, Hayward C,Taylor CB. Ethnicity and body dissatisfaction: are Hispanic and Asian girls at increased risk for eating disorders? J Adolesc Health. 1996 Dec;19(6):384-93.PubMed PMID: 8969369.
  12. Lake AJ, Staiger PK, Glowinski H. Effect of Western culture on women’s attitudes to eating and perceptions of body shape. Int J Eat Disord. 2000 Jan;27(1):83-9. PubMed PMID: 10590452.
  13. Ahmad S, Waller G, Verduyn C. Eating attitudes among Asian schoolgirls: the role of perceived parental control. Int J Eat Disord. 1994 Jan;15(1):91-7. PubMed PMID: 8124331.
  14. McCourt J, Waller G. Developmental role of perceived parental control in the eating psychopathology of Asian and Caucasian schoolgirls. Int J Eat Disord. 1995 Apr;17(3):277-82. PubMed PMID: 7773264.
  15. Lipsman N, Woodside DB, Lozano AM. Neurocircuitry of limbic dysfunction in anorexia nervosa. Cortex. 2015 Jan;62:109-18. doi: 10.1016/j.cortex.2014.02.020. Epub 2014 Mar 12. Review. PubMed PMID: 24703713.
  16. Godart N, Radon L, Curt F, Duclos J, Perdereau F, Lang F, Venisse JL, Halfon O, Bizouard P, Loas G, Corcos M, Jeammet P, Flament MF. Mood disorders in eating disorder patients: Prevalence and chronology of ONSET. J Affect Disord. 2015 Oct 1;185:115-22. doi: 10.1016/j.jad.2015.06.039. Epub 2015 Jun 25. PubMed PMID: 26162282.