Palliative Care

Orthorexia Nervosa: An Obsession With Healthy Eating

Fed Pract. 2017 June;34(6):36-39

References

1. Bratman S. Health food junkie. Yoga J. 1997;136:42-50.

2. American Psychiatric Association. Feeding and eating disorders. In: Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Publishing; 2013:329-354.

3. Varga M, Dukay-Szabó S, Túry F, van Furth EF. Evidence and gaps in the literature on orthorexia nervosa. Eat Weight Disord. 2013;18(2):103-111.

4. Donini LM, Marsili D, Graziani MP, Imbriale M, Cannella C. Orthorexia nervosa: validation of a diagnosis questionnaire. Eat Weight Disord. 2005;10(2):e28-e32.

5. Dunn TM, Gibbs J, Whitney N, Starosta A. Prevalence of orthorexia nervosa is less than 1 %: data from a US sample. Eat Weight Disord. 2016;22(1):185-192.

6. Bundros J, Clifford D, Silliman K, Neyman Morris M. Prevalence of orthorexia nervosa among college students based on Bratman’s test and associated tendencies. Appetite. 2016;101:86-94.

7. Vandereycken W. Media hype, diagnostic fad or genuine disorder? Professionals’ opinions about night eating syndrome, orthorexia, muscle dysmorphia, and emetophobia. Eat Disord. 2011;19(2):145-155.

8. Dell’Osso L, Abelli M, Carpita B, et al. Historical evolution of the concept of anorexia nervosa and relationships with orthorexia nervosa, autism, and obsessive-compulsive spectrum. Neuropsychiatr Dis Treat. 2016;12:1651-1660.

9. Bratman S. Orthorexia: an update. http://www.orthorexia.com/orthorexia-an-update. Updated October 5, 2015. Accessed April 18, 2017.

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17. Barnes MA, Caltabiano ML. The interrelationship between orthorexia nervosa, perfectionism, body image and attachment style. Eat Weight Disord. 2017;22(1):177-184.

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Pathophysiology

The exact cause of ON is unknown, though it is likely multifactorial. Individuals with ON have neurocognitive deficits similar to those seen in patients with AN and OCD, including impairments in set-shifting (flexible problem solving), external attention, and working memory.^11,13 Given these cognitive deficits as well as similar symptomatology, there may be analogous brain dysfunction in patients with ON and AN or OCD. Neuroimaging studies of patients with AN have revealed dysregulation of dopamine transmission in the reward circuitry of the ventral striatum and the food regulatory mechanism in the hypothalamus.¹⁴

Dysmorphology of and dysfunction in neural circuitry, particularly the cortico-striato-thalamo-cortical pathway, have been implicated in OCD.¹⁵ Neuroimaging studies have revealed increased volume and activation of the orbitofrontal cortex, which may be associated with obsessions and difficulty with extinction recall.^14,15 In contrast, decreased volume and activity of the thalamus may impair its ability to inhibit the orbitofrontal cortex.^15,16 Decreased volume and activity of the cingulate gyrus may be associated with difficulty in error monitoring and fear conditioning, while overactivation of the parietal lobe and cerebellum may be associated with compulsive behaviors.^15,16

Risk Factors

Factors that contribute to the development of AN and possibly ON include development of food preferences, inherited differences in taste perception, food neophobia or pickiness, being premorbidly overweight or obese, parental feeding practices, and a history of parental eating disorders.¹⁴ One survey associated orthorexic tendencies with perfectionism, appearance orientation, overweight preoccupation, self-classified weight, and fearful and dismissing attachment styles.¹⁷ Significant predictors of ON included overweight preoccupation, appearance orientation, and a history of an eating disorder.¹⁷

Treatment

In contrast to patients with AN, patients with ON may be easily amenable to treatment, given their pursuit of and emphasis on wellness.¹⁸ Experts recommend a multidisciplinary team approach that includes physicians, psychotherapists, and dieticians.¹¹Treatment may be undertaken in an outpatient setting, but hospitalization for refeeding is recommended in cases with significant weight loss or malnourishment.¹¹Physical examination and laboratory studies are warranted, as excessive dietary restrictions can lead to weight loss and medical complications similar to those seen in AN, including osteopenia, anemia, hyponatremia, pancytopenia, bradycardia, and even pneumothorax and pneumomediastinum.^19-21

There are no reported studies exploring the efficacy of psychotherapy or psychotropic medications for patients with ON. However, several treatments have been proposed given the symptom overlap with AN. Serotonin reuptake inhibitors may be beneficial for anxiety and obsessive-compulsive traits.¹⁸However, patients with ON may refuse medications as unnatural substances.¹⁸

Cognitive behavioral therapy may be beneficial to address perfectionism and cognitive distortions, and exposure and response prevention may reduce obsessive-compulsive behaviors.¹¹ Relaxation therapy may reduce mealtime anxiety. Psychoeducation may correct inaccurate beliefs about food groups, purity, and preparation, but it may induce emotional stress for the patient with ON.¹¹

Conclusion

Orthorexia nervosa is perhaps best summarized as an obsession with healthy eating with associated restrictive behaviors. However, the attempt to attain optimum health through attention to diet may lead to malnourishment, loss of relationships, and poor quality of life.¹¹ It is a little-understood disorder with uncertain etiology, imprecise assessment tools, and no formal diagnostic criteria or classification. Orthorexic characteristics vary from normal to pathologic in degree, and making a diagnosis remains a clinical judgment.²²Further research is needed to develop valid diagnostic tools and determining whether ON should be classified as a unique illness or a variation of other eating or anxiety disorders. Further research also may identify the etiology of ON, thus enabling targeted multidisciplinary treatment.