This last semester I took a Research Methods class where we to put together an entire research proposal. I am refraining from putting my final, 40 page proposal however, I wanted to share a bit of my work for those of you interested. So here is my final literature review:
Nutritional Intervention in Eating Disorder Treatment: Review of Literature
Melinda L. Schneider
University of Missouri- Kansas City
ABSTRACT: As relapse rates continue to be a prevalent occurrence amongst those suffering from an eating disorder it is imperative that research continues to seek new techniques that could improve outcomes for traditional psychotherapy. One area that is frequently missed in this population are they physiological affects of their disorder and how those might impact recovery. This paper aims to review the current literature around the effectiveness of current therapy options and the need for research address the nutritional status of individuals with an eating disorder.
There are two main pathways used when studying nutrition in those with an eating disorder (ED): deprivation theory and serotonin uptake. As those with eating disorders become more malnourished due to restriction ability to control food intake decreases, resulting in a binge. The most common deficiencies seen in those with disordered eating are known to result in depression, anxiety and suppression of appetite. Therefore, my hypothesis is that if the nutritional status of those with an ED can be reestablished and maintained, the frequency and duration of relapse will lessen. According to Maslow’s hierarchy of needs, it will also allow the individual to be able to move past meeting physical needs and focus more on behavioral and/or cognitive changes in psychotherapy.
What About Current Treatment Options?
Psychotherapy alone as a means to treat individuals with various eating disorders does not present with adequate success rates. Approximately 5.9% of women and 1.5% of men revealed having eating disturbances in a survey using EDE-Q (Hilbert, A., de Zwaan, M., & Braehler, E., 2012). Current studies have found that nearly 50% of individuals who reach partial remission and 30% of those who reach full remission will relapse (Richard, M., Bauer, S., & Kordy, H. 2005). Remission is defined when a maximum of two symptom episodes per month for two consecutive months occurs. The risk for relapse, meeting diagnostic criteria for three consecutive months, has been reported highest in the first six to seven months after achieving remission (Olmsted, M. P., Kaplan, A. S., & Rockert, W. 2005).
Some of the predicted factors of relapse in individuals with AN that have been published include desired weight, duration of illness, EDI scores, specialization of the clinic used and additional treatment following remission. Predicting factors of relapse for individuals with BN are symptomatic status, continued treatment after remission and motivation for treatment (Richard et al. 2005). Other published predictors of relapse include previous suicide attempts, severity of obsessive-compulsive symptoms, excessive exercise after treatment, residual concern about shape and weight and severe pretreatment caloric restriction (J. C., C., E., B., K., S., & D. B., W., 2004; McFarlane, T., Olmsted, M. P., & Trottier, K., 2008).
The Physiological Aspect
The problem with treating an eating disorder by providing only psychotherapy is that an eating disorder affects more than just an individuals mental or psychological state; it also affects them physiologically. There are two physiological pathways frequently examined within the eating disorder community: deprivation theory and serotonin uptake.
Deprivation theory utilizes the starvation response pathway. Starvation response assumes that once an individual has reached a state of starvation or malnutrition they will be unable to control their eating when food is available. This response could result in a binge episode for individuals diagnosed with BN or AN-B. Individuals with BN would respond to the binge behavior by purging in order to maintain body weight thereby reinforcing the pathological cycle (Rock, 1987). A study done in 2000 examined the effects of acute food deprivation during a 19 hour fast on eating behaviors with individuals diagnosed with AN-B and BN. Results should that individuals diagnosed with BN receiving inpatient treatment consumed significantly more food than BN individuals in outpatient treatment or individuals diagnosed with AN-B. The study found acute food deprivation did not result in significant food consumption pathology however; the chronic food restriction typically seen within the ED community is not accurately addressed.
The second pathway frequently discussed involves the neurotransmitter serotonin. Often times severe dieting and food restriction seen in individuals with AN leads to malnutrition. Tryptophan, a common deficiency seen in AN, is only available through food intake. It is also a precursor to the serotonin neurotransmitter. Food restriction and malnutrition, therefore, cause a decrease in brain serotonin stores as tryptophan becomes less available. The decrease in serotonin leads to hyperactivity, depression, behavioral impulsivity, anxiety and suppression of appetite. This suppression reinforces AN restricting behaviors. (Haleem, 2012).
Reported deficiencies in those diagnosed with AN include zinc, iron, riboflavin, B-6 and thiamin (Bakan, 1993; Chu, E., Gaudiani, J., Mascolo, M., Statland, B., Sabel, A., Carroll, K., & Mehler, P. 2012; Rock, C., Vasantharajan, S. 1995; Winston, A. P., Jamieson, C. P., Madira, W. W., Gatward, N. M., & Palmer, R. L., 2000).
Approximately half of individuals diagnosed with AN are also vegetarians. Vegetarian AN individuals consume significantly lower zinc than non-vegetarian AN individuals. Bakan therefore suggested that zinc supplementation should be indicated for those diagnosed with AN who are also vegetarians (1993). One of the problems facing those diagnosed with a zinc deficiency is that a zinc deficiency promotes changes in taste and reduces appetite (Rock, 1987). The reduced appetite caused by a zinc deficiency reinforces AN restriction which is similar to the deprivation theory.
Reported deficiencies in those diagnosed with BN include potassium, calcium, magnesium and phosphorus (Judge, B., Eisenga, B. 2005). Deficiencies in these vitamins are depression and anxiety, both of which are common co-morbid diagnosis in individuals with an ED. Phosphorus deficiency, like zinc, can result in loss of appetite, whi
Current Research on Nutrition Intervention
A study by Hart and Abraham (2011) found that the use of protein supplementation with women diagnosed with BN or BED reduces food intake and binge eating over a 2-week period. A study by McAleavey (2010) provided a nutritional intervention to girls aged 12-18 that resulted in an increase awareness of nutritional knowledge but no change in attitudes toward eating healthy which would support the need to combine both nutrition interventions and psychological/behavioral counseling.
Future Research Implications
More research involving nutritional supplementation and education combined with psychotherapy is needed. It could also be beneficial to look at the use of nutrition with the male population because current treatment outcomes are even less as effective for them than for females. Further research regarding what supplements or nutrition interventions/education result in the greatest impact would also be beneficial.
Bakan, R. A. (1993). Dietary Zinc Intake of Vegetarian and Nonvegetarian
Patients with Anorexia Nervosa. International Journal Of Eating
Chu, E., Gaudiani, J., Mascolo, M., Statland, B., Sabel, A., Carroll, K., & Mehler,
P. (2012). ACUTE center for eating disorders. Journal Of Hospital Medicine:
An Official Publication Of The Society Of Hospital Medicine, 7(4), 340-344.
Haleem, D. (2012). Serotonin neurotransmission in anorexia nervosa.
Behavioural Pharmacology, 23(5-6), 478-495.
Hart, S. S., Russell, J. J., & Abraham, S. S. (2011). Nutrition and dietetic practice
in eating disorder management. Journal Of Human Nutrition And Dietetics,
24(2), 144-153. doi:10.1111/j.1365-277X.2010.01140.x
Hilbert, A., de Zwaan, M., & Braehler, E. (2012). How frequent are eating
disturbances in the population? Norms of the Eating Disorder Examination-
Questionnaire. Plos ONE, 7(1), doi:10.1371/journal.pone.0029125
J. C., C., E., B., K., S., & D. B., W. (2004). Relapse in anorexia nervosa: a
survival analysis. Psychological Medicine, 34(4), 671-679.
Judge, B., & Eisenga, B. (2005). Disorders of fuel metabolism: medical
complications associated with starvation, eating disorders, dietary fads, and
supplements. Emergency Medicine Clinics Of North America, 23(3), 789.
McAleavey, K. (2010). Nutritional Intervention in Young Women with Eating
Disorders: A Brief Report. Journal Of Child & Family Studies, 19(5), 669-673.
McFarlane, T., Olmsted, M. P., & Trottier, K. (2008). Timing and prediction of
relapse in a transdiagnostic eating disorder sample. International Journal Of
Eating Disorders, 41(7), 587-593. doi:10.1002/eat.20550
Olmsted, M. P., Kaplan, A. S., & Rockert, W. (2005). Defining Remission and
Relapse in Bulimia Nervosa. International Journal Of Eating Disorders, 38(1),
Richard, M., Bauer, S., & Kordy, H. (2005). Relapse in Anorexia and Bulimia
Nervosa–A 2.5-Year Follow-Up Study. European Eating Disorders Review,
13(3), 180-190. doi:10.1002/erv.638
Rock, C. (1987). Nutrition and Eating Disorders: A Primer for
Clinicians.International Journal Of Eating Disorders, 6(2), 267-280.
Rock, C. L., & Vasantharajan, S. (1995). Vitamin status of eating disorder
patients: Relationship to clinical indices and effect of treatment. International
Journal Of Eating Disorders, 18(3), 257-262. doi:10.1002/1098-
Winston, A. P., Jamieson, C. P., Madira, W. W., Gatward, N. M., & Palmer, R. L.
(2000). Prevalence of thiamin deficiency in anorexia nervosa. International
Journal Of Eating Disorders, 28(4), 451-454. doi:10.1002/1098-