Three Things Nutritionists Need to Know About the Body, Brain, and Eating Disorders

 

Three Things Nutritionists Need to Know About the Body, Brain, and Eating Disorders

By Carolyn Hodges-Chaffee, MS, RDN, CEDRD-S

The Low Carb Craze

There are countless types of diets that influence people in all walks of life.  But despite their proliferation, popular diets are not based on scientific research, but on individuals who have experienced some degree of “success.”  People would think that following a simple diet for a few months would be harmless, and would hopefully result in some weight change, but the problem is that some diets can be very harmful for certain people.  Diets should not be taken lightly – they should come with warnings just as drugs do.  Just as medications can affect individuals differently, so too can diets.  For example, some individuals can go on a low-carbohydrate diet without experiencing any cognitive changes, but those who are susceptible to lower serotonin levels can quickly become obsessed and develop disordered eating or eating disorders.  The newest low-carbohydrate diet that has gotten America’s attention is the “Keto” diet, which allows for less than 20 grams of “net carbs” daily (calculated by subtracting the grams of fiber from the total number of carbohydrates).

The Carbohydrate-Protein Link to Serotonin Levels

When individuals who are sensitive to lower serotonin levels follow a low-carbohydrate diet, their bodies don’t have enough carbohydrates and protein (building blocks for serotonin) to make the neurotransmitter.  If they continue to limit their carbohydrates, their serotonin levels will decrease and this causes a change in brain chemistry that can increase feelings of guilt, which in turn may lead to eating even less – and the cycle repeats.  For those who have bodies (and brains) that are sensitive to changes in serotonin, this cycle can be the beginning phase of an eating disorder.

If the amino acid tryptophan (found in many protein foods) is the building block for serotonin, why is it so important to have carbohydrates?  When individuals follow a high protein, low carbohydrate diet there are many amino acids that are consumed.  The tryptophan must cross the blood brain barrier (BBB) to increase serotonin levels in the brain.  Protein is made up of several amino acids and these are competing to cross the BBB; tryptophan is not a great competitor so very little is able to cross the BBB unless carbohydrate is present.  This results in a gradual decrease of serotonin.  Carbohydrate causes the body to release more insulin which promotes amino acid absorption and leaves tryptophan in the blood.  If protein is consumed with carbohydrates then the carbohydrate will drive the majority of amino acids into the muscle, thus the tryptophan is able to cross the BBB much easier. (Food & Mood, Somer, 1999)

The Brain-Gut Connection

The brain has about 10-20% of the serotonin in the body, the other 80-90% is found in the gut.  This sets up the perfect storm for the development of an eating disorder.  As serotonin levels decrease in the body, the gut function slows down and individuals feel full much sooner and become very uncomfortable with nausea and/or bloating if they try to eat more.  As the gastrointestinal function decreases, constipation often occurs.  Imagine the individual who was simply trying to diet, as serotonin levels decrease they begin to feel more guilty about eating and at the same time because of the low levels of serotonin in the gut they also feel full sooner, as well as feeling bloated and constipated.  It hurts to eat, so they eat less and this leads to further decrease of serotonin in the body.  Clients often describe a noticeable change in their thought process.  Initially, they could control their eating behaviors and it was a choice about what and when to eat.  After restricting their intake, eventually they become a slave to their thoughts and have to follow the food rules or spend the day obsessing about everything they put in their mouth.

What begins as a well-intentioned attempt to lose weight and follow the new trending low carbohydrate diet is not a harmless endeavor.  Low carbohydrate diets should come with a warning that anyone who has a history or family history of an eating disorder, obsessive compulsive traits, depression, and/or anxiety may be at high risk to develop an eating disorder by limiting their carbohydrate intake.  Researchers are now exploring the differences in brain chemistry that may put some individuals at higher risk to develop an eating disorder.  What we do know is that glucose (a byproduct of carbohydrate metabolism) is the sole fuel for the human brain (except in prolonged starvation). The brain lacks fuel stores and requires a continuous supply of glucose.  (Https://www.ncbi.nlm.nih.gov, “Each Organ Has a Unique Metabolic Profile-Biochemistry-=NCBI bookshelf-NIH).   How can the brain be fed if there isn’t an adequate amount of carbohydrate?

Calorie Labeling in Restaurants

 Vol. 26 / No. 6 — Eating Disorders Review

Reprinted from Eating Disorders Review
November/December Volume 26, Number 6
©2015 iaedp

Among the many challenges of recovering from an eating disorder is becoming comfortable eating out in restaurants. At the 2015 International Conference on Eating Disorders, Dr. Christina A Roberto of Harvard School of Public Health, Boston, and Ann Haynas of the University of Nevada, Reno investigated the effects of caloric labels on menus among 633 women (mean age: 22 years). The women had previously completed the Eating Disorder Examination Questionnaire. Using an online survey, the two researchers presented a representative meal, with and without caloric information.Women with more marked eating disorder symptoms ordered less-calorie-dense meals, were more accurate about estimating calories, and were more distressed by eating out and more inclined to avoid restaurants than were women without symptoms of disordered eating. However, labels listing caloric content did not have an adverse effect on either group.

Combatting Bone Loss in Anorexia Nervosa: Nine Reminders

 Vol. 26 / No. 6 — Eating Disorders Review

Reprinted from Eating Disorders Review
November/December Volume 26, Number 6
©2015 iaedp

Bone loss is a common and potentially devastating medical complication of anorexia nervosa (AN). At least half of young women with AN will develop osteoporosis, and their bone loss often occurs relatively early in the disease. It also may not be fully reversible, at least with currently available treatments. It is important to remember that we may not yet appreciate the full impact of osteoporosis in AN. Given the increased prevalence of AN in the last 40 to 50 years, the majority of people who have – or did have – AN may not have yet reached the age when osteoporosis complications are most common and problematic. For this reason, gaining more knowledge about preventing and treating osteoporosis in AN is critically important.

1. Anorexia and Bone Health: A Complex Relationship

In AN patients, bone resorption increases without a corresponding increase in bone formation, leading to a net loss of bone. Levels of bone resorption markers such as N-terminal telopeptide (NTX) and deoxypyridoline may be elevated, but bone formation markers such as osteocalcin are not (Eur J Clin Nutr. 2004:1257. Because significant bone loss can occur so early in AN, even within the first year, early diagnosis and intervention are important.

Baseline screening is recommended for all patients who have had AN or amenorrhea for 6 to 12 months or longer. The Osteoporosis Foundation recommends screening all women under age 65 who have low body weight (Geriatrics. 2000 May; 55:31), and the American College of Sports Medicine recommends screening for osteoporosis in athletes who have a history of low estrogen levels or disordered eating for 6 months or more, or those with a history of stress fracture or any fracture from slight trauma (Med Sci Sports Exerc. 2004;36:1985; Med Sci Sports Exerc. 2007; 39:1867). 

2. Peak Bone Mass Forms between 11 and 14 Years of Age

While peak bone mass is reached by the third decade of life, from 40% to 60% of a woman’s bone mass is gained during the pubertal bone surge from ages 11 through 14, also the time when symptoms of AN often appear. The predictive relationship between bone mineral density (BMD) and short-term fracture incidence is unclear in premenopausal women. For these reasons, the International Society for Clinical Densitometry recommends against the use of T-scores to categorize BMD measurements in premenopausal women. Instead, the Society recommends using Z-scores, which compare women to an age-matched reference population. Young women with BMD Z-scores below — 2.0 should be categorized as having BMD that is “below expected range for age,” and those with Z-scores above — 2.0 should be categorized as having BMD that is “within the expected range for age” (www.iscd.org). 

Drs. Madhusmita Misra and Anne Klibanski at Harvard Medical School point out that as many as 50% of adolescent girls with AN have Z-scores less than -1 recorded at one site and 11% have Z-scores less than -2 recorded at a minimum of one site (Clin Obstet Gynecol. 2013; 56:722). There are no longitudinal prospective studies relating BMD by dual-energy x-ray absorptiometry (DXA) scans to fractures in premenopausal women.

Bone tissue is always in a state of change; old bone is reabsorbed and new bone laid down by osteocytes. During childhood and early adolescence, the osteocytes lay down new bone cells faster than they are being absorbed, leading to peak bone mass. This continues to about age 30, when bone production slows down and bone mass shrinks by about 1% each year afterward.

As Dr. Kathryn Teng of the Cleveland Clinic has written, it is essential to optimize bone mass during these years because even small difference in BMD can have significant implications later. She notes that just a 5% increase in bone density significantly decreases fracture risk, whereas a 10% decrease in adult BMD is associated with twice to three times the risk of fracture (CCJM. 2011; 78:50). After the third decade of life, skeletal mass begins to decrease and is accelerated after the menopause, where the rate of bone loss exceeds that of bone formation. Failure to attain sufficient bone density during adolescence leads to osteopenia, or a bone density between 1 and 2.5 standard deviations below average on Z scores for young adults of the same gender, and is a risk factor for osteoporosis. 

3. Young Patients with Prolonged Amenorrhea Have More Severe and Longer-Lasting Bone Defects

Younger AN patients are at greater risk because often they haven’t reached their peak maximum peak bone mass. Beyond the low DXA measures of BMD, teens with AN have weakened bone microarchitecture. For example, the volume of trabecular (spongy) bone and trabecular thickness are lower and trabecular separation greater in girls with AN than in healthy controls, even when the BMD measurements are the same. This breakdown and weakening of bone microarchitecture is of concern because of the increased risk of fracture risk independent of BMD. 

Young women with amenorrhea should be evaluated to determine if the amenorrhea is primary (absence of menarche by age 16) or secondary (absence of menses for more than 3 cycles or a past history of amenorrhea for more than 6 months). In a study of 73 women with AN, having the illness for 20 months was an important cutoff point: after this, the most severe form of osteopenia was seen (J Endocrinol Metab. 2009; 95:470).Weight gain and resumption of menses led to a 3% annual gain in BMD at the spine and a 2% gain at the hip, compared with a decrease in BMD of about 2.5% at both sites in persons who did not recover. As Drs. Misra and Klibanski point out, however, residual deficits can persist and make it impossible for patients to catch up to normal bone density.

4. Hormonal Changes Also Impact Bone Loss

AN patients also have important endocrine changes in hormonal axes that can affect bone loss. These include the hypothalamic-pituitary-gonadal axis, the growth hormone insulin-like growth factor (IGF-1) axis, and the hypothalamic-pituitary-adrenal axis. (J Clin Endocrinol Metab. 2004; 89: 4920). Many familiar hormones impacted by the patient’s energy status, including peptide YY (PYY), leptin, ghrelin, insulin and adiponectin are affected, and in turn may affect bone health. 

Teens with AN have higher-than-normal serum and urinary cortisol levels, and increased cortisol is associated with a lower body mass index and fat mass and lower glucose levels. According to Drs. Misra and Klibanski, this is an adaptive response to malnutrition, as cortisol is gluconeogenic. But, higher cortisol levels are also associated with lower BMD and inversely with bone turnover markers (J Clin Endocrinol Metab. 2004; 89: 4920). These higher cortisol levels are predictive of lower spine and hip BMD, as well as lower extremity lean mass in AN, which may also impact bone health (J Clin Endocrinol Metab. 2005 95;2580). The hypoestrogenic state noted in AN, a direct result of the effects of hypothalamic amenorrhea, is further worsened by changes in estrogen metabolism.

5. Weight Restoration is the Cornerstone of Treatment

According to Dr. Teng and others, weight restoration is the cornerstone of treatment for low BMD due to AN. All AN patients should be referred to a nutritionist to develop a meal plan. Treatment goals for patients with disordered eating are designed to optimize the patient’s nutritional status, normalize her or his eating behavior, change unhealthy thoughts that maintain the disorder and treat emotional issues that are contributing to the disordered eating.

Restoring weight and with it menses are two of the most important goals of treatment because young women with AN can lose as much as 2% to 6% of their bone mass each year they have AN. While previous studies have shown that BMD increases as the patient recovers, long-term follow-up studies show that loss of bone density may not be completely reversible, even when menses resumes and the patient regains weight. 

6. Estrogen Replacement Is Ineffective

Unlike the positive effects among postmenopausal women, where estrogen therapy maintains or improves BMD and may help reduce the incidence of fractures, the same pattern has not been seen in premenopausal women with osteoporosis. Estrogen Replacement seems to have little independent effect on correcting or preventing osteopenia in AN (Eur J Endocrinol. 2002; 146:45). Some researchers report that this is due to the possibility that the natural cycle of estrogen may be important to bone recovery. In postmenopausal women, estrogen therapy appears to work by impairing osteoclast-mediated bone resorption, but it has only slight effects on bone formation. In premenopausal women with anorexia, in contrast, bone loss appears to be due to a unique “uncoupling” of osteoblastic and osteoclastic functions, according to Dr. Teng and others (Int J Eat Disord. 2001; 29:11). This uncoupling of osteoblastic and osteoclastic functions results in reduced bone formation and increased bone resorption—estrogen may not improve this.

The American College of Sports Medicine recommends considering estrogen therapy if there is evidence of a decline in BMD in an athlete older than 16 years of age who also has persistent functional hypothalamic amenorrhea despite adequate nutritional intake and weight regain (Br J Sports Med. 2014; 48:289). However, the Society also acknowledges that restoring regular menstrual cycles with oral contraceptives will not normalize metabolic factors that impair bone formation, health and performance, and again note that it is unlikely that estrogen will fully reverse low BMD in these patients.

7. Bisphosphonates Are Not Approved for Premenopausal Patients with AN

The FDA has approved use of bisphosphonates only for premenopausal women who are also taking glucocorticoids. The bisphosphonates do increase BMD in young women with AN but at the same time are teratogenic and have a long half-life that enables the drugs to affect bone turnover for up to 2 years after they are stopped (Am J Med. 1997; 103:291). For patients who purge via vomiting, the bisphosphonates also increase the risk of esophageal ulcerations. Thus, for the time being, the bisphosphonates do not represent a major treatment option for osteoporosis in patients with AN.

8. Calcium Supplements Do Not Increase BMD

The National Osteoporosis Association has recently issued a statement in response to the discussion about the need (or not) for calcium supplements. Noting that calcium is needed for strengthening collagen in bone tissue and for many other functions, the organization recommends attempting to get “the recommended daily amount of calcium from food first, and to supplement this as needed to make up for the shortfall.” (For the Association’s full statement, see www.osteoporosis.org .) The organization also mentioned that calcium and vitamin D were recently reaffirmed by the 2015 U.S. Dietary Guidelines Advisory Committee as nutrients of public health concern because their under-consumption has been linked to adverse health outcomes. (http://health.gov/dietaryguidelines/2015-scientific-report/PDFs/Scientific-Report-of-the-2015-Dietary-Guidelines-Advisory-Committee.pdf). 

9. Always Monitor Exercise, Particularly In Patients Who Are Also Athletes

Strenuous exercise is a major factor in maintaining and developing normal bone mass; however, the benefit of exercise on bone loss in anorectic patients is still a topic of debate. The amount of exercise has to be monitored to help limit further weight loss. In addition, abnormal plasma estradiol concentrations may limit the positive effects of exercise on bone density (Calcif Tissue Int. 2000; 67:277). 

— MKS

Turning to the Brain to Explain Lack of Behavioral Inhibition in BN

 Vol. 27 / No. 6 — Eating Disorders Review

 

Two studies add data from adults and teens.

 

Reprinted from Eating Disorders Review
November/December Volume 27, Number 6
©2016 iaedp

There is new evidence for disinhibition of behavior in bulimia nervosa (BN), but it is unclear if this is specific to eating behavior or is more generalized. At University Hospital, Heidelberg, Germany, Dr. Mandy Skunde and colleagues have used functional magnetic resonance imaging (fMRI) to search for possible underlying neural links between impaired general and food-specific behavior inhibition in adult women with BN. Their initial findings suggest that diminished frontostriatal brain activation may underlie disinhibition of eating but that it may also be generalized (J Psychiatry Neurosci. 2016; 41:E69).

Inhibitory control in bulimic-type eating disorders has been analyzed in numerous studies and is not limited to binge eating. It often includes other impulsive behaviors, such as excessive drinking and substance abuse. The final study group included 28 adult women (mean age: 28 years) who met DSM-5 diagnostic criteria for BN and 29 healthy controls (mean age: 27 years).

No greater action noted in the limbic system

Contrary to their original hypothesis, the authors found no significant brain differences during tests of behavioral inhibition to general and food-specific stimuli in the BN group compared with controls. There also was no greater inactivation in the limbic system during exposure to food-specific stimuli. However, significant differences in the frontostriatal networks were noted in a subgroup of patients with more severe symptoms (3 or more binge-eating episodes per week).

The clinical implications of the team’s findings, according to Dr. Skunde, is that better insight into neural mechanisms underlying behavioral inhibition problems among BN patients may help lead to brain-directed treatment, such as neuromodulation with transcranial magnetic stimulation (Eur Eat Disord Rev. 2013;21:436; Neuroimage Clin. 2015; 8:611).

Brain findings in younger patients with BN

In a second study, the first to use fMRI to investigate attentional brain networks in patients with BN, a team at the universities of Aachen, Aachen, Germany, HWTH, Maastricht, the Netherlands, and JARA-BRAIN, Mainz, Germany, demonstrated altered activation of brain regions involved with attention in adolescent and young adult patients with BN (PLOS One, September 8, 2016; doi:10.1371/jurnalk.pone.0161329).

The authors used a modified version of the Attention Network Task to investigate the neural substrates for alerting, reorienting, and executive attention, and correlated brain activation in these areas with symptoms of attention deficit hyperactivity disorder and eating disorders. Some of these symptoms included alterations in activity in parieto-occipital regions, anterior and posterior cingulate regions, and the default mode network.

Dr. Jochen Seitz and colleagues concluded that altered neurotransmission in the sensorimotor frontostriatal network may contribute to behavioral dysfunction in BN patients through increasing attention/preoccupation with eating disorder thoughts, and by increasing the likelihood of inattentive/impulsive behaviors.

Helping Men Recover from an Eating Disorder

 Vol. 27 / No. 6 — Eating Disorders Review

One unfortunate trend: Males waited longer to seek help.

Reprinted from Eating Disorders Review
November/December Volume 27, Number 6
©2016 iaedp

In one of the few studies to examine how men recover from an eating disorder, Drs. Gunn Pettersen, Karin Wallin, and Tabita Björk recently interviewed a small group of Norwegian males from 19 to 52 years of age who had recovered from anorexia nervosa (n=10), bulimia nervosa (n=4), or EDNOS (n=1) (BMJ Open. 2016; 6:e010760).

The researchers wondered whether males with eating disorders might have different recovery rates than female ED patients, perhaps owing to different factors such as feelings of shame at having a ‘female illness,’ or lack of treatment facilities. A majority of the few, and mostly small, studies examining men who have recovered from eating disorders have focused on factors like barriers to seeking help and delay in seeking treatment due to shame or an inability to recognize the signs of an ED.

Participants in the current study were former patients who had completed their treatment for an eating disorder diagnosed with the DSM-IV and who had recovered from the eating disorder. Seventeen males were identified; and 15 gave consent for the study.

Four possible factors linked to recovery

The authors suggest there were four main factors related to recovery in males: (1) a need for change, (2) making a commitment to put the ED behind them, (3) making interpersonal changes, and (4) searching for a new life without an ED.

Many of the men took a long time to understand and admit that they had an ED, and some described having a protracted and very private struggle with their disorder. To these men, admitting to having an ED included admitting that food, weight, and body appearance controlled or dominated all parts of their lives. Some had quit their jobs or dropped out of college because of the effects of living with their eating disorder. Before seeking help, the men recalled their life with an ED as meaningless or chaotic. Few had contacted healthcare professionals, and most reported having been pushed into getting help by a close family member or friend.

A realization they needed help

Some began their recovery process with hospitalization, dieting, or severe weight loss and avoidance of food, leading to hospitalization, while others did contact their primary care physicians for help. No matter how they got help, the primary motivation was the same: realizing they could no longer manage the situation by themselves.

Most of the men acknowledged the importance of stabilizing their eating patterns, seeking better nutrition, and reaching healthier weights during the early phases of recovery. Most also found the structure of in-hospital treatment very helpful. Another common thread in the recovery process was finding a new balance and identifying new coping strategies and leaving their ED behind. Despite the serious effects, most of the men reported that the eating disorder had acted as a functional coping mechanism for many years, and some even described the ED as their ‘best friend.’ Thus, one challenge for the therapists was helping the men let go of the ‘advantages’ their ED seemed to represent.

Recovery similar to that of females, or different?

The authors noted that their findings concur with many of the important themes identified among females recovering from an ED, which might point to a universal nature of change and recovery from an eating disorder. Much of the difference between the course of eating disorders (and treatment seeking) in males may relate to differences in case-finding, perceived stigma, and availability of treatment services for males, rather than to innate gender differences.

Restrictive eating among men

A second study highlights barriers to prompt diagnosis of EDs in males. This retrospective chart review of males with restrictive eating disorders revealed that certain laboratory study results and vital signs had suggested the diagnosis early on (J Adolesc Health. 2016; 59:397) and in some cases had been overlooked.

The men were first seen at an outpatient eating disorder program. The men were from 11 to 25 years of age, had a mean percentage of median body mass index (BMI) of 88.8%, and many had a history of being overweight or obese. Half had a history of a psychiatric disorder; 42% had a history of overweight or obesity; and 12% had a family history of an eating disorder. Studying the patients’ vital signs and results of lab tests revealed that the most prominent abnormality was bradycardia (a heart rate below 60 beats per minute, or bpm). The mean heart rate was 58.7 bpm, and the orthostatic heart rate change was 22 bpm; 51.5% of the men met Society for Adolescent Health and Medicine hospital admission criteria. Nearly a third were anemic.

A lack of treatment options for men

In an accompanying editorial, Mark A. Goldstein, MD of Harvard Medical School and his colleagues noted that a standard vital sign, a lower-than normal pulse rate, could be a “red flag” for males, signifying a need for further evaluation (J Adolesc Health. 2016; 59:371). In their editorial, Dr. Goldstein and colleagues also pointed to another major problem: lack of treatment options. Although 100% of residential-based programs in the US accept females, only about 20% accept males, and a much smaller subset of programs offer male-only treatment (Int J Eat Disord. 2006; 49:434; Eat Disord. 2012; 20:444).

The editorialists also raise another point to ponder: Most successful ED prevention programs have been developed for females, and focus on perceived pressure to be thin, body dissatisfaction, and the cultural thin ideal, which may not be as salient for males. Instead, more helpful approaches for men might focus on body dissatisfaction, size, shape, and muscularity.

Refeeding Hospitalized Adolescents with Restrictive Eating Disorders

 Vol. 27 / No. 6 — Eating Disorders Review

Higher-than-currently-recommended caloric levels were safe.

Reprinted from Eating Disorders Review
November/December Volume 27, Number 6
©2016 iaedp

Correcting malnutrition in adolescents with anorexia nervosa has a special urgency because of impaired growth, loss of menses, and negative effects on bone health. A team of researchers led by nutritionist Elizabeth K. Parker, at the Westmead Hospital, Sydney, Australia, report that higher-caloric refeeding is safe for teens hospitalized with restrictive eating disorders (J Nutr Rehab. 2016; article ID 5168978, published online before print).

Some have recommended a conservative average weekly weight gain of 0.5 kg to 1 kg (for example, following the NICE Guidelines). More recently, others have suggested more rapid weight gains, such as 1 kg to 2 kg per week. The reason for the limited rate of weight gain is, of course, to avoid the refeeding syndrome, which can cause fluid and electrolyte shifts. Low serum phosphate levels, in particular, can lead to complications including cardiac failure and death. However, according to the authors, the recommended slow refeeding may also produce an unintended consequence, the “underfeeding syndrome,” among patients with AN. Thus, standard guidelines for ‘starting low and going slow’ may actually put already malnourished patients at risk for further clinical deterioration and longer hospital stays.

A 3-year retrospective study

To study the benefits of higher initial feeding rates, the authors conducted a 3-year retrospective chart review of 247 consecutive patients with restrictive EDs admitted to an adolescent ED unit between January 2011 and December 2013.

Patients with bradycardia were monitored on a cardiology ward with continuous telemetry measurements for the first 24 to 48 hours or until their resting heart rate was more than 50 bpm. Some patients admitted with bradycardia received continuous nasogastric (NG) feeding with a 1 kcal/mL formula at 100 mL per hour, to provide 2400 kcal per day while restricting oral ingestion to sips of water for 24 to 48 hours. The rationale for continuous NG feeding was to provide medically unstable patients with a constant, controlled supply of carbohydrates for the first 24 to 48 hours.

Phosphate supplementation was started early

Before starting nutritional rehabilitation, all patients were given 1 g of a phosphate supplement and a daily multivitamin, and then a minimum of 500 mg phosphate twice a day during the first week of admission, and supplementation was halted if phosphate levels became abnormally elevated. Blood tests, particularly to measure serum phosphate levels, were done prior to starting nasogastric (NG) feeding, 6 hours after starting NG feeding, and then daily for the first week.

Once hospitalized, all patients received some type of nutrition support within the first 24 hours, including an oral diet only (7.4%); continuing NG tube feeding (54.3%); or a combination of oral diet and a cyclic overnight NG feeding. Slightly more than half of the patients had bradycardia, and were started on an oral diet with overnight NG feeds. Of 7 patients who developed peripheral edema only1 also developed mild hypomagnesemia; the remaining 6 had normal electrolytes.

Once the patients were medically stable, they were treated on an adolescent medical ward, and their NG feeding was decreased to cyclic overnight feeding of 100 mL per hour of a 1 kcal/mL formula over 10 hours. In addition to NG feeds, a meal plan of 1800 kcal was provided during the day, and nursing staff supervised meals. Patients who had not finished the prescribed meal plan were given a nutrition supplement meal replacement. This resulted in a mean caloric intake at admission of 2612 kcal, which rose to 3775 kcal by week 4. Mean weight gain was 2.1 kg per week.

Adequate monitoring and dietary supplements helped avoid the refeeding syndrome

Overall, the findings suggest that with adequate patient monitoring and appropriate supplementation rapid weight regain can be achieved without producing the refeeding syndrome. Among the 52 patients who had overnight NG feeding, only 3.8% received medication to relieve anxiety about the feeding tube. Nearly 12% experienced nose bleeds, and 29% reported nasal irritation. A small number of patients, 3.8%, were discharged before they completed their inpatient treatment.

The authors concluded that a more rapid refeeding protocol with phosphate supplementation can be safely used for teens with restrictive eating disorders, without producing the refeeding syndrome. Parker and colleagues also suggest that prophylactic phosphate supplementation and careful monitoring of electrolytes be stressed more in the guidelines for preventing refeeding syndrome, rather than restricting caloric intake in this already-malnourished patient population.

(Note: Clearly, it will be important to replicate this sort of work before changing guidelines, but this paper adds to our knowledge about rates of refeeding when coupled to prophylactic phosphorus supplementation in adolescents. Also see the article, “Prophylactic Phosphate Supplementation for Anorexic Inpatients,” in the November/December 2016 issue.)

A Relapse Prevention Program for Anorexia Nervosa Patients

 Vol. 27 / No. 6 — Eating Disorders Review

The goal: getting ahead of relapse.

Reprinted from Eating Disorders Review
November/December Volume 27, Number 6
©2016 iaedp

Relapse is common following treatment for AN, and new methods to prevent this are needed. A group in the Netherlands has developed a new program designed to prevent AN relapse, the Guideline Relapse Prevention Anorexia Nervosa (GRP) (BMC Psychiatry. 2016; 16:316).

Tamara Berends and colleagues at Altrecht Eating Disorders Rintveld, the Netherlands, designed a cohort follow-up study of 83 patients successfully treated for AN. The study group included inpatients and outpatients 12 years of age and older who met DSM-IV criteria for a diagnosis of AN or of eating disorder not otherwise specified (EDNOS) that had been “clinically referred to as AN.”

Treatment at the study site addressed three major areas: (1) eating habits, body weight, and body image; (2) psychological aspects of function, such as self-esteem, perfectionism, and trauma; and (3) social functioning. All patients who started the relapse prevention program had completed previous outpatient treatment. Patients were only eligible for the relapse prevention program when remission was reached. Full relapse was defined as a body mass index (BMI, kg/m2) less than 18.5 for adults and SD BMI <-1 for younger patients.

Program content and goals

The primary aim of the GRP program was to enhance cooperation between the professional, the patient, and her relatives, to gain better understanding of each patient’s process of relapse, including triggers and early warning signs. The cooperating parties then formulate actions that they can take in the face of a new and impending relapse. This information is then summarized in a “Relapse Prevention Plan” so that appropriate action can be taken when early warning signs point to relapse.

Once the prevention plan is developed, the aftercare program starts, and continues for at least 18 months. In a series of aftercare visits, the patient, therapist, and family monitor and discuss the patient’s status. Dr. Berends and colleagues described two very common scenarios. In the first, the patient is stable, and thus the focus of the visits is on maintaining stability by promoting good physical health and optimal personal and social function. Real or possible stressful life events in the near future are discussed and anticipated. In the second scenario, the patient has one or more early warning signs of impending relapse. When this happens, the main focus during the aftercare visits is getting a thorough understanding of the actual triggers of relapse and how to deal with these to promote recovery.

The frequency of visits depends on the patient’s condition and the need for treatment and care. Stable patients generally come to the center for a visit 4 to 6 months after initial recovery. If the patient is less stable, visits are planned every 2 months. Working together, patient and therapist can decide whether a longer aftercare period is needed when the patient is vulnerable to relapse. Follow-up lasts for 5 years.

What an aftercare visit looks like

The typical 45-minute visit is attended by the patient and her family. At each visit, there is a weigh-in and the patient’s overall physical condition is evaluated. Two main topics are always on the agenda: psychosocial and social functioning, including discussion of school, friends, sports, and overall moods; and the presence of AN symptoms, such as anorectic cognitions, return of abnormal eating habits or excessive exercise. At the end of each visit, a new appointment is made for the next visit.

How effective was the aftercare program?

Full relapse occurred in 11% of the participants and partial relapse in 19%. Of those who did relapse, about a fifth recovered again during follow-up. Patients were most vulnerable to relapse between months 4 and 16. As intended by the program, contact in case of relapse often occurred within a week.

These results argue for the use of a relapse prevention plan at the end of treatment, together with interval monitoring. Taking this step may be one way to significantly contribute to lowering reduction rates of relapse for AN patients.