Eating Disorders: Anorexia Nervosa, Bulimia Nervosa, Binge Eating Disorder, and also, Food Addiction?

Eating Disorders: Anorexia and Bulimia Nervosa 

There has been some debate over the diagnostic groups, characterization, and relevance to therapy for patients with disordered eating. However, Eating Disorders are important and common. Estimates suggest that the prevalence of Anorexia Nervosa (AN) is 0.6%, 1.0% for Bulimia Nervosa (BN), and 2.8% for Binge Eating Disorder (BED).

Anorexia, Bulimia & Binge Eating Disorder remain major causes of morbidity and mortality, among the top causes of death among young women who are more at risk. Individuals with eating disorders have significantly elevated mortality rates, with the highest rates occurring in those with Anorexia Nervosa.

The mortality rates for BN and BED are similar. A metanalysis found age at assessment to be a significant predictor of mortality for patients with AN [1]. In a recent study, U.S. adults with a history of eating disorders were five to six times more likely to also have a history of suicidal behavior, compared with adults who did not have an eating disorder [2].

History of suicide attempts was significantly higher among those with a DSM-5-defined eating disorder—25% for those with anorexia nervosa, 31% for bulimia nervosa, and 23% for binge-eating disorder—versus 5% for those without an eating disorder. Among those with anorexia, 44% of those with the binge/purge subtype and 16% of those with the restricting subtype reported a previous suicide attempt.

The three established eating disorders have been clinically defined and diagnosed with the DSM 5 [3]—Anorexia Nervosa, Bulimia Nervosa, and Binge Eating Disorder [4]. Anorexia nervosa and bulimia nervosa are two distinct eating disorders, but they do share many common symptoms.

Both disorders can be fatal and include behavior directed at controlling weight, body image distortions, and inability to estimate body weight and shape. Both AN and BN can include binge eating and purging. Anorexia and bulimia nervosa can also involve restrictive eating behaviors and excessive exercising. Many experts have also discussed diagnostic crossover.

One patient may meet the criteria for AN or BN and then seemingly switch. A pure form of AN or BN does exist. In terms of treatment, most treatment applies to both AN or BN. So-called, cross-diagnostic therapies such as CBT-cognitive behavioral therapy are associated with favorable outcomes in both anorexia nervosa and bulimia nervosa.

No pharmacological treatment has really been shown to be effective in AN [5]. For BN, Fluoxetine [6] and CBT is preferred to other SSRIs. Fluoxetine is effective for treating BN and can improve relapse outcomes in patients. Fluoxetine was approved for acute treatment and maintenance of BN in 1994, and randomized placebo-controlled studies have supported its efficacy in the treatment of BN.

Co-occurring illnesses and complications of these diseases are well known, and there are effective treatments for the medical complications of both anorexia nervosa and bulimia nervosa [7]. Experts debate whether they are one illness or two or if we cannot figure out which is which without blood or similar test.

Family history is also relevant, and they also overlap. Relatives of individuals with anorexia nervosa have increased risk (over four times) of bulimia nervosa compared to the same types of relatives of individuals without anorexia nervosa, and vice versa.

In a recent study of the heritability of clinically diagnosed anorexia nervosa and bulimia nervosa, it was estimated at 43% and 41%, respectively. Significant genetic overlaps exist between AN and BN. This recent study [8] supports the idea that many patients with AN and BN have the same disease or at the least share many common features and can manifest one or the other and switch between them.

Binge Eating Disorder

Binge-eating disorder (BED) is the most common eating disorder [9]. The addition of the eating disorder, binge eating disorder, to the DSM is welcomed as this is a distinct diagnostic category. Having such a diagnosis also led to therapeutic trials.

BED diagnosis suggests specific evidence-based and defined treatments. The concept of binge eating as “overeating without compensatory behaviors” was introduced by Stunkard in 1959, described in DSM-IV-TR.

At least 3.5 percent of adult women and 2 percent of adult men have binge eating disorder. For men, binge eating disorder is most common in midlife, between the ages of 45 to 59.

For women, binge eating disorder most commonly starts in early adulthood, between the ages of 18 and 29. About 1.6 percent of teenagers are affected.

A much larger number of adults and children have episodes of binge eating or loss-of-control eating, but the episodes do not occur frequently enough to meet the criteria for binge eating disorder. This is a group that is yet to be defined but might be what Gearhardt [10] and Avena describe as food addicts or hedonic overeating [11] disorder.

Due to intense research activity, the DSM-5 has recently recognized BED as an autonomous disease. BED diagnosis is relevant for treatment planning and outcome. Psychological, CBT, and behavioral interventions are a treatment for BED, while the stimulant prodrug lisdexamfetamine-is the FDA approved treatment of BED.

Numerous classes of medications, including antidepressants, anticonvulsants, and anti-obesity drugs, have been explored as off-label treatments for BED such as second-generation antidepressants and topiramate. [12] BED seems to be quite separate and distinct from AN and BN. 

Food Addiction (or Sugar Addiction)

We have studied the effects of highly palatable food on eating in laboratory animals and people for many years [13]. If this is a fourth possible diagnosis to consider, it is a big and unsettled question. In truth, it is true that some highly processed food is not easily resisted.

Bet you can’t eat one…was a famous Lays Potato Chip commercial [14]. They were correct. Some foods are made to be irresistible [15]. You probably cannot eat just one as they engineered this “food” to be more like a drug, stimulating its own taking and causing along the way, loss of control.

Food science gone wild produces manufactured food that has drug-like properties [16]. Not all people have the same neurobiology or life experiences, but also, not everything that you eat is food. All are not created equal.

Some of the manufactured foods that we are attracted to and eat are better at producing a drug of abuse-like dopamine release in our reward systems. These tend to be designer foods or what is called ultra-processed foods combining sugar, fat, salt, and refined carbs in a way that isn’t found in naturally occurring food sources.

Our dopamine pleasure system isn’t prepared by evolution to say not to these manufactured foods. We evolved our tastes and appetite to help us through harvesting and scarcity, making these sorts of high-calorie designer foods almost irresistible.

Our ancestors found sugar in some seasons, but not all seasons, usually by looking for honey or berries. Sugar, when added to neutral foods or drinks, has such an effect as well. Large amounts of sugar are added to soft drinks or foods, making them more palatable and reinforcing.

We have even gone so far as to compare cigarettes to soft drinks in this analogy cigarettes: nicotine then the way that soft drinks: sugar. A study by Paul Kenny [17], a former Florida colleague, showed that when rats were fed a diet of junk food, they became so hooked that when it was taken away and replaced with a healthy meal, the rodents chose to starve.

The scientists fed groups of rats different types of food. One group was given a healthy diet. Another group was given a healthy diet with unlimited access to junk food. “We bought all of the stuff that people like — Ding-Dongs, cheesecake, bacon, sausage, the stuff that you enjoy, but you really shouldn’t eat too often,” researcher Paul Kenny told Reuters.

However, those rats were driven to eat cheesecake, bacon, and sausage even when they knew doing so would result in them being given an electric shock to their feet. The rats were given the junk food option consumed twice as many calories. They became inactive.

Even after the light went off, warning them of a coming electrical shock, if they ate more, they continued to gorge. The rats eating a healthy diet stopped eating at the light rather than get a shock. Of course, all people are not the same, and homo sapiens are not the same, nor do they have the same dopamine or pleasure systems as rodents or even non-human primates [18]. 

Work by my former mentees and current colleagues, Nicole Avena [19] and Ashley Gearhardt, have led in this research. Gearhardt has worked on adding food addiction questions to the assessment of patients with eating disorders, especially binge eating disorder.

The marked overlap between positive scores for food addiction (as measured on a dedicated scale—the Yale Food Addiction Scale (YFAS; see below)) and binge eating disorder. Also, the overlap between food addiction and binge-eating disorder is obvious and striking.

Positive scores for the Yale food addiction scale (see the YFAS below) and binge eating in the context of bulimia nervosa and binge-eating disorder is striking. In the most recent study, they are using the revised YFAS -YFAS2.0. The results shown are similar to the previous version of the YFAS.

There is a very strong overlap between bulimic symptomatology and addiction-like eating. In this study, almost all participants with bulimia (96%) received a YFAS2.0 diagnosis.

This result is in line with studies in which the previous version of the YFAS was used, which similarly found that prevalence rates of ‘food addiction’ range between 80% and 100% in individuals with bulimia.

In the controls without eating disorders, 14% received a YFAS2.0 diagnosis, which is similar to the prevalence rates found with the English version of the YFAS2.0 (approximately 15%). Thus, although there is a high overlap between eating disorders, particularly bulimia, and ‘food addiction,’ there is also a substantial subset of individuals without eating disorders who receive a YFAS2.0 diagnosis. [20]

One conclusion from this might be that food addiction is not a distinct eating disorder. Food addiction is an important concept with public health, obesity, and intervention implications. Some practical implications derived from the food addiction concept provide promising avenues for future research, especially in animal models and new pharmacological treatment inventions. [21, 22]

TABLE 1- The Yale Food Addiction Scale [23] asks how frequently you have experienced any of the following in the past year:

1. 1. I ate to the point where I felt physically ill.
   2. I spent a lot of time feeling sluggish or tired of overeating.
   3. I avoided work, school, or social activities because I was afraid I would overeat there.
   4. If I had emotional problems because I hadn’t eaten certain foods, I would eat those foods to feel better.
   5. My eating behavior caused me a lot of distress.
   6. I had significant problems in my life because of food and eating. These may have been problems with my daily routine, work, school, friends, family, or health.
   7. I was so distracted by eating that I could have been hurt (for example, when driving the car, crossing the street, operating machinery).
   8. My overeating got in the way of me taking care of my family or doing household chores.
   9. I kept eating in the same way, even though it caused me emotional problems.
   10. Eating the same amount of food did not give me as much enjoyment as it used to.
   11. I had such strong urges to eat certain foods that I couldn’t think of anything else.
   12. I tried and failed to cut down on or stop eating certain foods.

The dopamine reward pathways in the brain can be easily overstimulated by sugar or junk food, and the system turns off. Like other addictions, you need more junk food just to break even.

The D2 receptor responds to dopamine, a neurotransmitter that is released in the brain by pleasurable experiences like food or sex or drugs like cocaine. In cocaine abuse, for example, the drug alters the flow of dopamine by blocking its retrieval, flooding the brain, and overstimulating the receptors, something that eventually leads to physical changes in the way the brain responds to the drug.

The animal gets stuck in a vicious cycle and requires constant stimulation from palatable food to avoid entering a persistent state of anhedonia, depression, or negative reward. Johnson and Kenny [24] extended the earlier work making sense out of the concept of food addiction.

“These findings confirm what we and many others have suspected,” Kenny said, “that overconsumption of highly pleasurable food triggers addiction-like neuroadaptive responses in brain reward circuitries, driving the development of compulsive eating. Common mechanisms may, therefore, underlie obesity and drug addiction.”

How the food is made or engineered really matters. Basic science studies convincingly demonstrate that intermittent availability of high-sugar, high-fat, or high-sugar plus high-fat diets provokes both compulsive patterns of eating in rats and a state similar in many ways to drug addictions– reduced dopamine receptor function, increased self-stimulation thresholds, and, in the case of sugar, anxious behaviors that may be relatable to withdrawal symptoms.

Such studies constitute the most compelling evidence that highly palatable foods administered intermittently can produce changes in brain and behavior that replicate substance addiction. Gearhardt has even done new work on binge trigger and hyperpalatable foods [25], which is quite useful to patients with EDs and their therapists.

Still, the evidence food or sugar addiction data while interesting and useful for clinicians but does not meet the DSM threshold until the diagnosis is confirmed by either common genes or prediction of new pharmacological therapies. 

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References:

1. Arcelus J, Mitchell AJ, Wales J, Nielsen S. Mortality Rates in Patients With Anorexia Nervosa and Other Eating Disorders: A Meta-analysis of 36 Studies. Arch Gen Psychiatry. 2011;68(7):724–731. doi:https://doi.org/10.1001/archgenpsychiatry.2011.74

2. Udo, T., Bitley, S. & Grilo, C.M. Suicide attempts in US adults with lifetime DSM-5 eating disorders. BMC Med 17, 120 (2019) doi:10.1186/s12916-019-1352-3

3. https://doi.org/10.1176/appi.ajp.2013.13030326

4. Sysko R, Glasofer DR, Hildebrandt T, Klimek P, Mitchell JE, Berg KC, Peterson CB, Wonderlich SA, Walsh BT. The eating disorder assessment for DSM-5 (EDA-5): Development and validation of a structured interview for feeding and eating disorders. Int J Eat Disord. 2015 Jul;48(5):452-63. doi: 10.1002/eat.22388. Epub 2015 Jan 30. PMID: 25639562; PMCID: PMC4721239.

5. Corinne Blanchet, Sébastien Guillaume, Flora Bat-Pitault, Marie-Emilie Carles, Julia Clarke, Vincent Dodin, Philibert Duriez, Priscille Gerardin, Mouna Hanachi-Guidoum, Sylvain Iceta, Juliane Leger, Bérénice Segrestin, Chantal Stheneur, Nathalie Godart Medication in AN: A Multidisciplinary Overview of Meta-Analyses and Systematic Reviews. J Clin Med. 2019 Feb; 8(2): 278.

6. Aigner M, Treasure J, Kaye W, Kasper S, World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for the pharmacological treatment of eating disorders. WFSBP Task Force On Eating Disorders. World J Biol Psychiatry. 2011 Sep; 12(6):400-43.

7. Mehler, P. S., Krantz, M. J., & Sachs, K. V. (2015). Treatments of medical complications of anorexia nervosa and bulimia nervosa. Journal of eating disorders, 3, 15. doi:10.1186/s40337-015-0041-7

8. Yao S, Larsson H, Norring C, Birgegård A, Lichtenstein P, DʼOnofrio BM, Almqvist C, Thornton LM, Bulik CM, Kuja-Halkola R.Genetic and environmental contributions to diagnostic fluctuation in anorexia nervosa and bulimia nervosa. Psychol Med. 2019 Oct 29:1-8

9. Swanson SA, Crow SJ, Le Grange D, Swendsen J, Merikangas KR. Prevalence and correlates of eating disorders in adolescents. Results from the National Comorbidity Survey Replication Adolescent Supplement. Archives of General Psychiatry. 2011;68(7):714–23.

10. Schulte EM, Sonneville KR, Gearhardt AN. Subjective experiences of highly processed food consumption in individuals with food addiction.Psychol Addict Behav. 2019 Mar;33(2):144-153

11. Avena NM1, Gold MS. Food and addiction – sugars, fats, and hedonic overeating. Addiction. 2011 Jul;106(7):1214-5;

12. Amodeo G1, Cuomo A1, Bolognesi S1, Goracci A1, Trusso MA1, Piccinni A2, Neal SM3, Baldini I1, Federico E1, Taddeucci C1, Fagiolini A1. Pharmacotherapeutic strategies for treating binge eating disorder. Evidence from clinical trials and implications for clinical practice. Expert Opin Pharmacother. 2019 Apr;20(6):679-690. doi: 10.1080/14656566.2019.1571041. Epub 2019 Jan 29.

13. Avena NM, Bocarsly ME, Hoebel BG, Gold MS. Overlaps in the nosology of substance abuse and overeating: the translational implications of “food addiction.” Curr Drug Abuse Rev. 2011; 4:133-9.

14. https://bigthink.com/world-in-mind/bet-you-cant-eat-just-one

15. https://theconversation.com/why-it-can-be-hard-to-stop-eating-even-when-youre-full-some-foods-may-be-designed-that-way-126729

16. https://www.nytimes.com/2013/02/24/magazine/the-extraordinary-science-of-junk-food.html

17. https://www.nature.com/articles/464652c

18. Kenneth Blum, Marjorie Gondré-Lewis, Bruce Steinberg1, Igor Elman, David Baron, Edward J Modestino, Rajendra D Badgaiyan, Mark S Gold Our evolved unique pleasure circuit makes humans different from apes: Reconsideration of data derived from animal studies. J Syst Integr Neurosci. 2018 Jun; 4(1): 10.15761/JSIN.1000191. 

19. 10.1371/journal.pone.0117959

20. Meule A A Critical Examination of the Practical Implications Derived from the Food Addiction Concept. Curr Obes Rep. 2019 Mar;8(1):11-17

21. Fletcher, P. C., & Kenny, P. J. (2018). Food addiction: a valid concept?. Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology, 43(13), 2506–2513. doi:10.1038/s41386-018-0203-9

22. Yarnell S, Oscar-Berman M, Avena NM, Blum K, Gold MS. Pharmacotherapies for Overeating and Obesity. J Genet Syndr Gene Ther. 2013 April 1; 4(3):131-. doi: 10.4172/2157-7412.1000131.; Avena NM, Murray S, Gold MS. The next generation of obesity treatments: beyond suppressing appetite. Frontiers in Psychology. 2013; 4(721): 1-3

23. https://www.ncbi.nlm.nih.gov/pubmed/26866783

24. https://www.nature.com/articles/464652c

25. https://wfpc.sanford.duke.edu/podcasts/ashley-gearhardt-food-addiction

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About the Author:

Mark S. Gold, M.D.  served as Professor, the Donald Dizney Eminent Scholar, Distinguished Professor and Chair of Psychiatry from 1990-2014.

Dr. Gold was the first Faculty from the College of Medicine to be selected as a University-wide Distinguished Alumni Professor and served as the 17th University of Florida’s Distinguished Alumni Professor.
Learn more about Mark S. Gold, MD

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The opinions and views of our guest contributors are shared to provide a broad perspective of eating disorders. These are not necessarily the views of Eating Disorder Hope, but an effort to offer a discussion of various issues by different concerned individuals.

We at Eating Disorder Hope understand that eating disorders result from a combination of environmental and genetic factors. If you or a loved one are suffering from an eating disorder, please know that there is hope for you, and seek immediate professional help.

Published on December 16, 2019.
Reviewed & Approved on December 16, 2019, by Jacquelyn Ekern MS, LPC

Published on EatingDisorderHope.com