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According to Susan J. Noonan, MD, MPH, high nutrient-dense foods, like colorful fruits and vegetables, whole grains, beans, fish, poultry, and a small amount of olive oil and dairy can improve your patient's mood and lower their risk for depressive episodes. 

Keeping glucose levels steady may also help prevent mood swings. 

 is a physician consultant and Certified Peer Specialist in the Department of Psychiatry at McLean Hospital and the Massachusetts General Hospital. She is the author of four books and a blog on managing depression, most recently 

Helping Others With Depression: Words to Say, Things to Do

 (December 2020). Dr Noonan offers peer counseling to fellow patients, including physicians and other professionals, and can be confidentially reached through her website at 

A healthy diet can improve mood and effectiveness of antidepressant medications. Here's why your patients should be eating healthier. 

Food Is the Fuel

 involving 2 million participants, people experiencing depression, anxiety disorder, or bulimia, are at heightened risk of excessive alcohol use.

Unhealthy alcohol use and psychiatric disorders frequently co‐occur, but understanding how the levels of alcohol consumption affect those with psychiatric disorders might provide valuable insight to health care providers. The study sought to learn more about these relationships.

Researchers used alcohol screenings from Kaiser Permanente Northern California (KPNC), an integrated healthcare delivery system, to collect data from a large, population‐based sample. More than 12 million alcohol screenings were conducted, which will help identify subgroups of patients with psychiatric disorders and co‐occurring unhealthy alcohol use.

Medical assistants asked 3 questions. One is a modified version of the National Institute on Alcohol Abuse and Alcoholism single‐item screening question used to determine whether the individual had drinking-heavy days: “How many times in the past 3 months have you had 5 or more drinks in a day?” The second and third are questions used to calculate average alcoholic drinks consumed per week: “On average, how many days per week do you have an alcoholic drink?” and “On a typical drinking day, how many drinks do you have?”

From these questions, patients were classified into 2 groups: low risk of alcohol abuse and unhealthy use. The unhealthy use class was further divided into subgroups: daily, where patients exceeded daily drinking limits; weekly, where patients exceeded weekly drinking limits; and both. Researchers then compared these answers to whether patients had a documented psychiatric disorder diagnosis, focusing on a list of 8 common psychiatric disorders: depression, bipolar disorder, anxiety disorder, obsessive compulsive disorder, schizophrenia, schizoaffective disorder, anorexia nervosa, and bulimia nervosa.

In the final sample of patients, it was found that the daily group was more likely to be male and aged 18 to 34 years old, while the weekly group was more likely to be female and aged 65 or older. The daily and weekly groups were more likely to have higher household incomes, greater than approximately $87,500. Those who reported no alcohol usage were more likely to be Asian, Native Hawaiian, or Pacific Islander. Those diagnosed with bipolar disorder or schizoaffective disorder were more likely to report no drinking, as well.

From this data pool, care management strategies for these patients can be formed, ideally for primary care settings. The findings support a need for screening for unhealthy alcohol use in primary care, which would help clinicians address alcohol problems early and help to prevent the onset of an alcohol use disorder.

1. Palzes VA, Parthasarathy S, Chi FW, Kline-Simon AH, et al. Associations Between Psychiatric Disorders and Alcohol Consumption Levels in an Adult Primary Care Population. 

Alcoholism: Clinical & Experimental Research.

https://onlinelibrary.wiley.com/doi/10.1111/acer.14477

2. Research Society on Alcoholism. Patients with Depression, Anxiety, and Bulimia at Heightened Risk of Unhealthy Drinking and Associated Health Issues. News release. November 2, 2020. 

https://www.newswise.com/articles/patients-with-depression-anxiety-and-bulimia-at-heightened-risk-of-unhealthy-drinking-and-associated-health-issues

A diagnosis of depression, anxiety disorders, or bulimia may also indicate a heightened risk of excessive drinking. 

The Intersection of Excessive Alcohol Use and Psychiatric Disorders 

Carlos M. Grilo, PhD, in his talk at the Annual Psychiatric Times® World CME Conference™, discussed the latest updates in diagnosing, understanding, and treatment options for patients with binge-eating disorder (BED).

“My biggest take home,” Grilo said, “is to avoid stigmatizing. Ask what language your patient would like used when discussing their weight.”

BED is a DSM-5 eating disorder, characterized by the consumption of large amounts of food while experiencing a loss of control. To classify as binge eating disorder, at least 3 of the 5 behavioral indicators must be met: 1) the patient must eat rapidly; 2) the patient must eat large amounts of food even when not hungry; 3) the patient must eat to the point of discomfort; 4) the patient will eat alone due to embarrassment; and 5) the patient will feel disgusted, depressed, or guilty about their eating.

Studies of adults with BED reveal that patients have both elevated psychiatric and medical comorbidity. The most common psychiatric comorbidities include mood disorders, anxiety, and substance use disorders. Medical comorbidities include obesity, chronic pain conditions, and cardiometabolic problems, like diabetes or hypertension.

When discussing pharmacotherapy treatment options for BED, Grilo noted that there is only 1 FDA-approved medication: lisdexamfetamine. Lisdexamfetamine is used for moderate to severe BED, taken once daily in the morning. Patients must be monitored carefully, as it has a black box warning that notes its high potential for abuse. 

Pharmacotherapy for treating BED is an emerging research topic. While several small clinical trials have found medications superior to placebos for reducing binge-eating, those studies only gauged the short-term, limited effects. Next to no data exists regarding long term effects.

A larger variety of psychological and behavioral treatments exist to treat BED. Specific focal psychological treatments, like cognitive behavioral therapy (CBT) and interpersonal psychotherapy (IPT), are well-established, significantly reduce binge eating, and have approximately 50% remission rates. Behavioral weight loss (BWL), a generalist treatment, achieves comparable binge-eating reductions and produces some weight loss.

Grilo concluded his talk with a number of suggestions. First and foremost, be prepared to recognize BED. Once you have assessed the psychiatric and medical comorbidities, consider pharmacological, psychological, and combined therapy options. Let your patient know that treatments exist that may help, often quickly. Discuss options and alternatives, and above all, avoid stigmatizing.

The Annual Psychiatric Times® World CME Conference™ was held October 15 – 17. More information can be found 

. Next year’s conference is scheduled for September 30 – October 2, 2021, in San Diego.

Carlos M. Grilo, PhD, explained symptoms, causes, and treatment for binge-eating disorder in his talk at The Annual Psychiatric Times® World CME Conference™. 

Remove the Stigma Around Binge Eating Disorder 

Orthorexia nervosa (or pathologically “healthy” eating) is distinct from anorexia nervosa, bulimia, and avoidant/restrictive food intake disorder. There are high-risk populations for ON, such as athletes and others who are focused on being healthy However, most of those individuals will only experience social impairment. On the other hand, individuals who view food as medicine are at increased risk for life-threatening medical complications and even death.

In this video, we interview Thomas R. Dunn, PhD, author of a recent CME for 

. Dr Dunn is Professor, School of Psychological Sciences, University of Northern Colorado, Greeley, CO; and Staff Psychologist, Denver Health Medical Center; Dr Hawkins is Chief Executive Officer and Licensed Psychologist, Center for Change, Orem, UT.

Transcript edited for brevity and clarity. For the entire interview, please watch the video. -Ed

About 20 or 30 years ago there was a physician out here in Colorado who recognized that people were very passionate about the quality of food that they were eating, and they were going out of their way to try to find the freshest, most nutritious foods they could.

On the surface this sounds very reasonable, but we want to be careful about what kinds of foods we eat. One of the things he noticed was that there were people who were getting too carried away with this quest to be as healthy as possible. So he developed or coined this term called orthorexia, which is a sort of a straight or rigid diet. Over the years, European researchers especially have been studying this notion that there are people who seem to get pathological about their healthful eating.

So, most of us are aware of anorexia nervosa, a condition where people are worried about being fat; in the case of orthorexia, we are worried about being unhealthy. And so, there's a tipping point. There seem to be people who are overly thoughtful about their diet, when it gets to the point where they restrict to the point of not getting their nutrition. They may start off being vegetarian, then they're vegan, then they're raw, and then they restrict what they can eat. 

There are individuals that have rigid eating habits that have become problematic for them, in their social circles. For example, I dealt with a young woman who was flabbergasted that her fiance would break up with her. After they were engaged, her future mother and father-in-law were coming to celebrate, and they decided to go out to dinner. Sharing meals is a central way of celebrating. He told her, "Please don't be weird about the food," and she got into an argument with the waitress over the croutons. It was this pattern of interacting over diet, that was really disruptive in this case to her social life.

I've seen a couple of people in my practice, in the hospital for severe malnourishment because they believe their diet is going to cure some sort of malady. People who are engaging in food as medicine in that they have a condition, and they're fighting to try to treat that condition. By adopting an overly rigid diet, and they develop a blind spot. They don't see that not only is it not helping, but it's causing additional medical problems.

Sometimes there might be victim blaming for somebody with cancer who "has a terrible diet," eats too much sugar, and so on.

 People are willing to pass judgment on diets, about what people are eating at restaurants. And there has been some who have suggested that maybe orthorexia is really just a flavor of anorexia, and that is certainly a little bit more fashionable to say "I'm on a cleanse," or "I'm doing this diet." And we give people a pass for that. . . There is a lot of pressure out there. I recently evaluated a young man who I was very concerned with having a first break psychosis and his parent was very concerned that he was getting the right vitamins; she has done a lot of research and vitamins were going to help him though his substantial psychiatric emergency.

Although weight loss may be a favorable feature of healthful diets, "clean eating" can be taken to extremes. In this video, we interview Thomas R. Dunn, PhD, author of a recent CME for Psychiatric Times. Orthorexia Nervosa. 

Clean Eating to the Extreme

Scroll below the apple image for the quiz.

B. Complex psychosocial processes that relate to lack of early life deficits

C. Bio-psycho-social interactions that lead to dysregulation of brain circuitry

Based on our current understanding, what is the underlying etiology for anorexia nervosa? Take the quiz.

Mini Quiz: Etiology of Anorexia Nervosa

Anorexia nervosa is the third most common chronic illness among adolescent females. The mortality rate is 12-fold higher than with all other combined causes of death for females aged 15 to 24 years.

 The disorder is associated with severe emaciation from self-driven food refusal and a perception of being overweight despite very low body weight. Anorexia nervosa shows a complex interplay between neurobiological, psychological, and environmental factors, and it is a chronic disorder with frequent relapses, high treatment costs, and severe disease burden. Little is known about the pathophysiology or biomarkers that characterize anorexia nervosa brain function, treatment effectiveness is limited, and there are no FDA-approved medications.

What makes anorexia nervosa so difficult to treat is the seemingly willful food avoidance and self-driven relentless motivation to lose weight. While eating is a very normal behavior for most of us, overcoming the fear of eating and weight gain is extremely difficult for children or adults with anorexia nervosa. Humans have historically evolved to be biologically protected to survive times of food scarcity. The brain circuitry that drives food-seeking has been well defined in basic science models.

Developing neurobiological models for anorexia nervosa and existing mechanisms that disregard or override hunger signals has been much more difficult. Moreover, there are psychological and social factors involved in anorexia nervosa, including anxious traits and the tendency to worry, and their interaction combined with peer pressure and stress in general 

 This has made it difficult to tease apart environmental effects from brain biology that poses a vulnerability for developing or maintaining anorexia nervosa.

Related content: Mini Quiz: Etiology of Anorexia Nervosa

Recent brain research in anorexia nervosa has focused on reward pathways, with the hypothesis that these pathways might disturb food approach mechanism in anorexia nervosa. Food is a salient stimulus or natural reward, and reward pathways similar to those of substance abuse are activated when we desire, approach, or eat food.

 Important regions in this circuitry include the ventral striatum, which receives midbrain dopaminergic input and drives motivation and the reward approach; the orbitofrontal cortex responsible for reward valuation; the insula, which processes our taste sensations and provides input to the striatum; and the hypothalamus, which integrates body homeostasis.

 The circuitry between those brain regions may adapt to weight loss and instead of driving eating may reinforce food restriction in individuals vulnerable to anorexia nervosa.

A variety of studies in the past applied tasks that either showed food pictures or delivered monetary or taste rewards to stimulate the reward system. The studies repeatedly showed that the insula, orbitofrontal cortex, or striatum activated differently in persons with anorexia nervosa during those tasks compared with healthy controls.

In our laboratory, the aim is to identify chemical targets to develop better treatments for anorexia nervosa. To accomplish this, we applied reward tasks that were closely associated with brain dopamine response to find evidence of dopaminergic involvement in the pathophysiology of anorexia nervosa.

The dopamine neurotransmitter system has been intensively studied and well characterized. Its neurons’ cell bodies lie in the brain stem in the ventral tegmental area and substantia nigra and from there distribute to the cortical and subcortical brain. The basal ganglia and especially the ventral striatum that includes the nucleus accumbens receive dopamine input and have been involved in the drive to reward stimuli. The reward stimuli can be unconditioned or conditioned (learned) stimuli.

A central feature of dopamine neuron response is that it is triggered by unexpectancy, ie, a discrepancy between what one expects versus what in fact happens. After receiving an unexpected reward such as food or money, a dopamine surge is elicited in the striatum and midbrain, which is called a 

. When receiving this reward becomes a regular occurrence, the dopamine signal is triggered by the conditioned stimulus that predicts the reward. However, the dopamine system does not respond when the actual reward is received (prediction matches the outcome). If the reward is predicted but not received (there is no food or money after expecting it), there is a dip in dopamine activity in the brain, which reflects the negative prediction error (unexpected omission).

This dynamic can be studied in the living human brain with functional brain imaging during the application of a Pavlovian conditioning paradigm: participants learn to associate sugar-taste or monetary stimuli with pictures of colored shapes that become the conditioned stimulus and appear on the screen before money or sweet solution are delivered (

). Sometimes when the participants expect to get the reward, they will not get it; at other times the reward is delivered unexpectedly.

During these studies, adults and adolescents with anorexia nervosa repeatedly showed elevated response to the unexpected conditions in the insula and striatum, which suggests altered dopamine function.

 Basic science found that in the process of food restriction, the dopamine system in the brain gets sensitized to stimulate food seeking. We interpreted this elevated activation as a normal response.

This brain activation does not drive eating as it would in heathy individuals. In fact, it can often be observed in individuals with anorexia nervosa that despite weight loss, fear of weight gain worsens and there is no limit as to how low the weight will drop. In our most recent study, we propose a model of how this drive to lose weight may be perpetuated and how the elevated prediction error response fits into this behavior.

 Our findings indicate that elevated brain response correlated positively with harm avoidance-a measure of trait anxiety-but negatively with weight gain during treatment.

Harm avoidance was positively correlated with drive for thinness and body dissatisfaction. We propose that when a person who develops anorexia nervosa starts to lose weight, the dopamine system quickly gets faster or more strongly involved, ie, sensitized. Weight loss leads to low blood sugar and changes in hormonal and neuropeptide levels, which signal to the hypothalamus that the organism should eat. However, this biological motivation and drive to eat disagrees with conscious motivation to not eat and lose weight, which leads to high levels of anxiety. To avoid weight gain and driven by extreme anxiety, the person with anorexia eats even less, which further reduces weight and triggers more biological drive to eat and further increases anxiety. Thus, setting off a vicious cycle that is difficult to break (

Clinically, this has been a useful model to discuss the neurobiology of anorexia nervosa with patients or families. I draw and develop this model in a monthly seminar with parents of children with anorexia nervosa, which helps them understand the typically very difficult to comprehend ongoing drive for food restriction.

Understanding a certain mechanism does not cure the illness, but it provides opportunities to support treatment. In psychotherapy it helps to go from something inexplicable to understanding the connection between an anxious temperament with a predisposition to worry and eating problems. This is also relevant for patients who have recovered but who may be at risk for relapse.

Every year in August, around the time when school starts, I see several patients with symptom relapse in my outpatient clinic. This is due to heightened stress over grades that triggers eating problems and food restrictions. The subsequent weight loss may then set in motion the vicious biological cycle as previously described.

As do other biological studies including genetic research, such a model serves another important purpose. Psychiatric diseases are often associated with stigma and personal guilt. The more we understand the underlying neurobiology of psychiatric disorders such as eating disorders, the more we will be able to develop medical models, find more effective treatments, and reduce stigma.

Our research has helped to pose new hypotheses for potential treatment directions. In animal models, fear extinction was aided by dopamine receptor stimulation.

 A main focus of psychotherapy for anorexia nervosa is weight restoration, such as family-based therapy in youth, which requires overcoming the fears of eating. We hypothesized that dopamine receptor stimulation could be helpful in the treatment process for anorexia nervosa. We compared youth treated with the partial dopamine D2 receptor agonist aripiprazole with those who did not receive aripiprazole. The patients who received aripiprazole had better weight outcomes at the end of treatment.

 However, a controlled study is missing, and no firm conclusions can be drawn from these results. Although such a medication alone would probably not cure anorexia nervosa, it could, however, act as a catalyst in concert with psychotherapy.

The conceptualization of the neurobiology of anorexia nervosa in our model poses a dichotomy of frontal cortex cognitive-emotional and subcortical basal ganglia involving circuits. What has been very difficult to model from a biological perspective are the severe eating disorder core behaviors such as body dissatisfaction and drive for thinness. Those thoughts and drives can persist life-long in a person despite having recovered weight-wise from anorexia nervosa. It is possible that the anxious traits commonly found in anorexia nervosa-even before the onset of the disorder-come into play and perpetuate those behaviors, making “letting go” extremely difficult.

Models to test how to target the behaviors pharmacologically still need to be developed. Serotonin reuptake inhibitors can help with anxiety and depression but do not improve the core behaviors of anorexia nervosa.

 A more complex biochemical model may be needed for anorexia nervosa. Such a model would take into account the interaction between neurotransmitter systems such as dopamine and serotonin and signals from the body periphery such as gut hormones and their adaptation to food intake.

Recent data lend themselves to applying a neurobiological model when talking with patients, parents, or families about anorexia nervosa. This can reduce personal burden, shame, or guilt. Weight restoration continues to be a key aspect of treatment, and there is the possibility that this is supported by dopamine receptor agonists, although this is yet uncertain as controlled studies are lacking.

Dr Frank is Professor in Residence, University of California, San Diego, Eating Disorder Program for Treatment and Research, and Rady Children’s Hospital, San Diego, CA. He reports that he has received research funding from the NIMH, is on the Scientific Advisory Board of EDCare, and has provided expect testimony for Senter Goldfarb, & Rice.

1. Golden NH. Eating disorders in adolescence and their sequelae. 

2. Attia E. Anorexia nervosa: current status and future directions. 

3. Kessler RM, Hutson PH, Herman BK, Potenza MN. The neurobiological basis of binge-eating disorder. 

4. Kaye WH, Wierenga CE, Bailer UF, et al. 

Nothing tastes as good as skinny feels: the neurobiology of anorexia nervosa

5. Kelley AE, Berridge KC. The neuroscience of natural rewards: relevance to addictive drugs. J Neurosci. 2002;22:3306-3311.

6. Haber SN, Behrens TE. The neural network underlying incentive-based learning: implications for interpreting circuit disruptions in psychiatric disorders. 

7. DeGuzman M, Shott ME, Yang TT, et al. Association of elevated reward prediction error response with weight gain in adolescent anorexia nervosa. 

8. Frank GK, Reynolds JR, Shott ME, et al. Anorexia nervosa and obesity are associated with opposite brain reward response. 

9. Frank GKW, DeGuzman MC, Shott ME, et al. Association of brain reward learning response with harm avoidance, weight gain, and hypothalamic effective connectivity in adolescent anorexia nervosa. 

10. Abraham AD, Neve KA, Lattal KM. Dopamine and extinction: a convergence of theory with fear and reward circuitry. 

11. Frank GK, Shott ME, Hagman JO, et al. The partial dopamine D2 receptor agonist aripiprazole is associated with weight gain in adolescent anorexia nervosa. 

12. Lock J, La Via MC, and the AACAP Committee on Quality I. Practice parameter for the assessment and treatment of children and adolescents with eating disorders. 

13. Frank GKW, DeGuzman MD, Shott ME. Motivation to eat and not to eat: the psychobiological conflict in anorexia nervosa. 

This article describes a model for anorexia nervosa that is useful when working with patients or families to help them understand the complexity of the illness.

Dysregulation of Brain Processing in Anorexia Nervosa

Eating disorders (ED) are associated with significant comorbid psychopathology and the most extensive medical complications of any psychiatric disorder. Disordered behaviors that present across diagnoses (eg, restriction, binge eating, compensatory behaviors) are linked with acute medical risks that often require careful medical monitoring and clinical intervention. Yet, individuals with EDs frequently express hesitancy towards recovery and have great difficulty controlling their ED symptoms.

EDs are typically chronic and follow a treatment-refractory trajectory. Existing research indicates that even the most effective evidence-based outpatient treatment yields recovery for only around one-half of patients.

 In our clinic, we often encounter patients like “Hayley,” “Georgia,” and “Michael” (see Case Vignettes) for whom outpatient treatment has been unsuccessful. Like many other eating disorder treatment programs, our program seeks to optimize recovery by providing more intensive treatment with stepped levels of care.

Hayley is a 24-year-old graduate student and a competitive runner who competes regularly. She has a diagnosis of anorexia nervosa, restricting type (AN-R), which developed when she was 20 after a period of binging. Two years ago, Hayley began working with a multidisciplinary outpatient team, but she has continued to lose weight. She attributes the weight loss to her unwillingness to eat the large amount of food it would take to offset the calories she burns while running and training. She initially presented to her primary care physician feeling weak then was admitted to an inpatient eating disorders unit for bradycardia. Upon discharge from the hospital she was referred to a partial hospitalization treatment program.

Most research explores the efficacy of treatment at the outpatient level; little is known about the comparative value of the higher levels of care for patients with EDs.

 However, these approaches are important alternatives for treatment-refractory EDs because they provide the more intensive treatment and meal support that many severely ill patients need.

 Common reasons for needing higher levels of care include substantial weight loss that might be life threatening; difficulty eating enough food to gain weight; severe binge/purge behaviors; incapacitating ED symptoms; comorbid substance abuse; and anxiety, depression, obsessive compulsive disorder, or suicidal intent.

It is not unusual that such behaviors result in medical instability with symptoms of cardiovascular compromise, electrolyte disturbances, or hypoglycemia. It is important to note that some individuals have a lack of insight about their behaviors or are not motivated to engage in treatment. Because of these factors, the mortality rate for anorexia nervosa and bulimia nervosa can be 5% or higher.

 Higher levels of care provide a structured and protective environment that can be essential for these serious, life-threatening disorders.

Georgia, aged 17 years, has bulimia nervosa (BN) with comorbid major depressive disorder, panic attacks, and a history of sexual trauma. She has been engaging in polysubstance abuse, including alcohol, marijuana, prescription painkillers, and cocaine, since the age of 12. She has been hospitalized several times for suicide attempts and accidental drug overdoses. She binges and purges daily and states that she is only able to reduce these behaviors when using substances. Her outpatient therapist feels overwhelmed by all of Georgia’s comorbidities and is not sure how to help her reduce these self-destructive behaviors, so she refers Georgia to a PHP program.

Higher levels of care for EDs include various types of programs, with different levels of intensity.

The treatment goals for EDs are similar and include:

• Interrupting binge, purge, and restrictive behaviors;

• Providing psychoeducation regarding regular eating;

Psychotherapy approaches among higher levels of care are typically informed by cognitive behavioral and dialectical behavioral therapies. Family-based treatment is often incorporated for children and adolescents. Patients might transition between levels of care due to variables such as symptom severity, medical status, motivational status, treatment history, and financial limitations.

There are several different levels of care from which to choose:

 is the highest level of care available. This setting can be in a medical hospital and is intended for patients with acute medical instability. Alternatively, this may be in a psychiatric hospital if there are severe behavioral symptoms. In either event, subspecialty medical and behavioral consultation are readily available, meals are supervised, and one-to-one monitoring is available.

 offer full-time treatment in a non-hospital setting. Patients receive multidisciplinary care that includes nutritional support, medication management, and individual and group therapy.

(PHP), or daytreatment, offer treatment in an outpatient setting approximately six to 10 hours a day, between three and seven days per week. Patients typically spend nights and sometimes weekends on their own, allowing them to practice the skills they are learning in social, occupational, and leisure settings outside of treatment.

 (IOPs) offer treatment approximately three hours a day, from three to five days per week. At both the PHP and IOP levels, patients receive meal support, group therapy, individual therapy, dietary sessions, and medication management.

Treatment efficacy for higher levels of care. 

Randomized controlled trials (RCTs) are necessary to avoid the confounding effects of psychopathology severity and evaluate the comparative efficacy of different levels of care. Since patients with more severe symptoms and greater functional impairment are more likely to present to higher levels of care than those with mild ED pathology (and milder ED pathology is associated with better outcomes), reliable findings are dependent on patients matched with controls based on symptom severity or random assignment to level of care.

Unfortunately, RCTs that compare different levels of care are limited given significant costs and ethical considerations related to randomizing acutely ill patients. As such, literature on higher levels of care treatment efficacy is scarce and consists largely of open trials assessing outcome at discharge. A 2015 review of PHP and residential programs identified that duration of treatment was similar between these levels of care, and all but one study reported improvements in outcomes (ie, body mass index [BMI], number of binge/purge episodes) at discharge.

There have been several, more recent naturalistic studies of higher levels of care treatment that also offer support for the effectiveness of care in most patients.

 However, less than half of the open trials identified in the review reported follow-up data after discharge.

 Moreover, follow-up completion rates tend to be low; the average rate of follow-up completion was 66% for PHP and 37% for residential. Although most of the studies reported that positive treatment outcomes at discharge were maintained or improved at follow-up, the missing data at follow-up make long-term results difficult to interpret.

As previously mentioned, the literature on treatment efficacy at higher levels of care is preliminary and consists largely of open trials. Within the context of these trials, researchers have begun to study the predictors of long-term recovery. However, more is known about predictors of recovery from EDs in general, regardless of type of treatment, and no study has looked at how predictors of successful outcome might differ depending on level of care received.

 conducted a metaanalysis of predictors of treatment outcome that included a large number of patients treated at a higher level of care. Their findings indicate that patients with higher BMI, fewer binge/purge behaviors, greater motivation to recover, lower depression, lower shape/weight concern, fewer comorbidities, better interpersonal functioning, and fewer familial problems at baseline had better outcomes both at end-of-treatment and follow-up. The most robust predictor of outcome at both end-of-treatment and follow-up was the meditational mechanism of greater early symptom change.

The literature consistently corroborates that early behavioral change predicts later symptom remission.

 Given that higher levels of care treatment settings typically involve meal supervision and more opportunities to quickly learn skills, these settings may be uniquely well-suited to facilitating early symptom change.

When determining the appropriate level of care, practitioners should consider practice guidelines published by reputable organizations as well as individual variables important in predicting treatment response. The American Psychiatric Association (APA), Royal Australian and New Zealand College of Psychiatrists (RANZCP), and National Institute of Clinical Excellence (NICE) published guidelines for ED treatment that outline factors to consider in making decisions regarding level of care.

Michael is a 12-year-old boy who has avoidant/restrictive food intake disorder (ARFID), generalized anxiety disorder, and panic attacks. He endorses fear of food contamination and reports eating the same foods at the same time every day to avoid illness and/or vomiting. Michael has seen outpatient providers over the past few years for low weight, stunted growth, and gastrointestinal complaints. He was recently admitted to an inpatient eating disorders unit for low weight. Following discharge, he was unable to maintain weight at the outpatient level due to food-related fears resulting in restricted intake. As such, he was readmitted to the inpatient unit; he was later referred to PHP for continued care.

The NICE and RANZCP guidelines recommend first seeking outpatient care and suggest transfering to higher levels of care if there is no improvement of symptoms. Alternatively, the APA advises consideration of various factors when making initial treatment recommendations (

). All guidelines clearly outline criteria for determining medical stability and recommend that patients who do meet these requirements be considered for admission to inpatient hospitalization (

). A recent update on the medical management of EDs offers a list of criteria that indicate medical instability in adolescents that deviates slightly from the APA recommendations.

The RANZCP and APA guidelines suggest that inpatient treatment may be needed if ED symptoms are uncontrolled and require 24-hour supervision. Inpatient care and partial hospitalization also are appropriate when there is significant risk of suicide or self-harm. The NICE and APA guidelines advise considering logistical issues concerning the geographic location of treatment; they recommend that patients first receive care at facilities close to their home. Research indicates that PHPs are more cost-effective than residential or inpatient treatment; therefore, financial factors are important considerations.

 Clinicians might also consider recent scientific developments related to variables that account for significant variance in treatment response.

As any clinician who works with patients who have EDs knows, there are, unfortunately, many patients who are treatment resistant in outpatient care. For patients like Hayley, Georgia, and Michael, specialized higher levels of care facilities can be a relief for the clinician and life-changing for the patient.

Hayley was able to achieve her ideal body weight with PHP and stepped down to IOP. She decided not to return to competitive sports before returning to her outpatient team. Georgia stopped using drugs and alcohol within the structure of PHP, participated in weekly family therapy, and learned skills for coping with emotional dysregulation. Michael restored his weight in PHP through repeated food exposures that helped him increase his food volume and variety and decrease his fears surrounding contamination.

For many of the complex, severely ill patients who present to treatment, intensive treatment with stepped levels of care can offer a cost-effective structure that promotes positive behavioral change.

Dr Anderson is Associate Clinical Professor Director of Training, Ms Simpson is Milieu Therapist, and
	Dr Kaye is Professor and Founder and Executive Director, Eating Disorders Program, Department of Psychiatry, University of California, San Diego, CA. The authors report no conflicts of interest concerning the subject matter of this article.

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16. Golden N, Katzman D, Sawyer S, et al. Update on the medical management of eating disorders in adolescents. 

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19. Vall E, Wade T. Predictors of treatment outcome in individuals with eating disorders: A systematic review and meta-analysis. 

Eating disorders (ED) are associated with significant comorbid psychopathology and the most extensive medical complications of any psychiatric disorder.

Higher Levels of Care for Eating Disorders: A Practical Guide

Avoidant restrictive food intake disorder, or ARFID, is a newly introduced eating disorder in DSM-5. ARFID is characterized by a persistent failure to meet appropriate nutritional and/or energy needs, which can result in at least one of the following: significant weight loss or nutritional deficiency, dependence on enteral feeding or nutritional supplements, and/or a marked interference in psychosocial functioning. ARFID cannot be explained by a lack of food availability, cultural practices, body image concerns, or concurrent medical or mental conditions.

Given that the disorder was introduced in 2013, it remains unclear how prevalent ARFID is in the general population. Early research suggests that compared with anorexia nervosa patients, those with ARFID are typically younger, more likely to be male, more likely to have an anxiety diagnosis, and have a longer duration of illness.

ARFID can present in a variety of ways, making it difficult to describe a typical case.

DSM-5 suggests 3 primary reasons why those with ARFID avoid food

• Fear of negative consequences of eating;

• Avoidance of food based on sensory characteristics.

Our review of 48 children and adolescents (mean age 13.6 years) who presented to a hospital-based eating disorders clinic with ARFID revealed that 13% of cases had a mixed presentation of two or even three of these subtypes.

Most patients with ARFID will avoid food for one or more of the following reasons:

1) Fear of negative consequences of eating.

 Although patients in this category restrict food because they are afraid to eat, they do not have body image concerns and are not afraid of weight gain. The fear of eating may be direct (eg, the patient feels nauseous or experiences abdominal pain when eating so the patient restricts to avoid these symptoms) or indirect (eg, the patient worries that he might vomit or have an allergic reaction if he eats). Other presentations in this cohort may include younger patients who have learned about “bad foods” and avoid these foods out of a fear of being unhealthy. (Although there is debate about whether these patients should be considered as having a form of AN, so further research is required.) Earlier in childhood these patients typically have unremarkable growth histories, and only experience weight loss or insufficient weight gain after an acute event that triggers the eating disorder (eg, fear of eating develops after a choking incident, after an allergic reaction to food, or after doing a school project on healthy eating).

 Parents often describe children in this second AFRID category as being “grazers” or “eating like a bird.” Their histories are characterized by longstanding low appetite, early satiety, and indifference to food. While they may present at any stage of childhood or adolescence, puberty often triggers weight and growth concerns. In these cases, patients’ appetites do not increase sufficiently to meet the increased energy needs of puberty, resulting in a fall off their growth curve. Other examples include children and youth who are active in sports and cannot keep pace with their high energy needs because of low appetite, which is often combined with the stress of busy schedules and lack of family meals (especially for those who eat slowly).

Other examples include patients with comorbid chronic illnesses (which also increase metabolic demands) who also struggle with food indifference and low appetite. It must be noted, however, that in these cases, the comorbid medical condition does not fully account for the feeding disturbance; rather, the feeding issues drive the underlying growth concerns.

Struggles with anxiety or depression may also cause feeding issues that result in impairment and/or medical compromise; some children lose their appetite in response to feeling scared, stressed, or unhappy. Examples of stressors include anxiety associated with going to school; being bullied or rejected by peers; moving or losing a friend; parental conflict, separation or illness; or physical, sexual, or emotional abuse (all of which must be ruled out). Although children with severe school-associated anxiety often eat better on weekends and holidays, their intake does not meet their overall needs.

3) Avoidance of food based on sensory characteristics.

 Patients in this category struggle primarily with food variety; they are often extremely selective (picky) regarding the food that they consume. Their histories of food refusal usually date back to an early age. They often have sensory hypersensitivity that results in profound rigidity involving food (eg, can only eat foods of a certain color or texture). In many cases, the rigidity extends to the manner in which food is served (eg, different foods on a plate cannot touch; the hotdog must be cut up in equal pieces) and to details related to preparation (eg, pasta must be boiled for exactly 11 minutes). These patients often will only accept the same limited number of foods prepared in the exact same manner and served in the exact same way.

These extremely rigid picky eaters are challenging to treat, and treatment will almost always require a multidisciplinary team approach. Often, caregivers are exhausted from years of trying to meet the needs of these children. Although picky eating is common in children, and in most cases improves with age without the need for any intervention, this is not the case for children with this subtype of ARFID. Maybe not surprisingly, early research suggests that children with autism spectrum disorder are more likely to be in this category of ARFID.

It is important that health care professionals not simply dismiss parental concerns around feeding based on weight gain and growth at a rate deemed acceptable. Our early study illustrates that when patients and families with such presentations are treated with an intensive intervention, the child’s weight and growth velocity can supersede that observed before the intervention, and that this weight gain can be associated with improved physical and mental well-being.

 It is also important to recognize that these children may not be simply picky eaters but may have feeding difficulties that severely affect their functioning. For example, one 12-year-old girl would only eat baby food, while one boy with autism would only eat Cheerios and fish crackers.

In children and adolescents, insufficient nutrition that results in weight loss or poor growth is associated with significant medical and psychological complications, and as such should be treated aggressively. This is especially true for a young person who has fallen off his or her growth curve. Using pediatric growth curves and working with families and health care providers to determine a child’s optimal goal weight is an essential step in the assessment and treatment of patients with ARFID.

Limited published evidence exists to guide clinicians in the treatment of ARFID, although trials are presently underway in the US and abroad. Strandjord and colleagues

 undertook an open label trial and concluded that modified family-based therapy was helpful for adolescents with anorexia nervosa or with ARFID, although few adolescent ARFID patients took part in the family-based therapy sessions, thus limiting the study’s conclusions.

Family-based therapy, the gold-standard treatment for adolescent anorexia nervosa, seems well-suited to the treatment of a proportion of underweight youngsters with ARFID, given that family-based therapy focuses on lifting blame, raising the family’s anxiety about the dangers of low weight and malnutrition in young people, and empowering parents to take charge of nutrition and to focus on the goal of weight gain.

We recently published a case series of six young patients with ARFID.6 Two cases had histories of acute events that affected their nutrition (eg, fear of eating after seeing a dog choke on a bone), and the other four were mixed presentations. Although treatment was individualized to meet patient needs, modified family-based therapy was utilized in each case, along with adjunctive pharmacotherapy. For some, individual cognitive behavioral therapy was also added to address anxiety. Each patient reached his or her treatment goal weight (which is essential for reaching optimal physical and mental health), and family therapy played a major role in recovery.

The shared elements in these family therapy sessions included providing education to the families about the negative consequences of insufficient nutrition and low weight, lifting guilt in all family members, empowering parents to take charge of nutrition, providing compassion for the patient, and helping the parents to empathize with their child’s pain, fear, or discomfort while still being firm about the need to take the nutrition. The family was helped to focus on issues relating to intake and weight gain, often using detailed food diaries and the use of weekly weight graphs.

Four of the six patients required admission to hospital to help with weight gain. One 14-year-old girl with autism spectrum disorder plus severe anxiety at school was helped by staying home from school while her mother took time off from work to focus on feeding her; once the patient had gained sufficient weight, she returned to school part-time with additional supports in place.

All six patients were treated with the atypical antipsychotic medication olanzapine for its anti-anxiety properties plus appetite stimulation; four of the patients subsequently transitioned from olanzapine to an SSRI (such as fluoxetine) as they approached their treatment goal weight, and two remained on a low dose of olanzapine at bedtime in addition to an SSRI. These last two patients, who had a combination of chronic low appetite, picky eating, severe anxiety, and acute stressors, also required the appetite stimulant cyproheptadine in addition to olanzapine to help them reach their healthy weight.

The medications were all used off-label because of the lack of evidence for their role in the treatment of ARFID. Currently there is only one case series that explores the utility of olanzapine for treating ARFID. In the Brewerton and D’Agostino’s study,

 it was demonstrated that the use of low-dose adjunctive olanzapine may have improved patients’ appetites and weight gain and helped reduce symptoms of anxiety and depression for nine of the patients.

Some patients with anorexia nervosa may present with low weight, but deny body image concerns. In cases where the diagnosis is unclear, we would recommend proceeding with treatment focused on weight gain as described above. Moreover, the development of eating disorder-specific and ARFID-specific measures and diagnostic instruments should be considered.

 In cases of anorexia nervosa, the fear of weight gain typically becomes apparent during the course of treatment. In our eating disorders clinic, approximately 8% of 77 patients who presented initially with ARFID subsequently received a diagnosis of anorexia nervosa.

Additional research is needed to better understand which treatments or combinations of treatments are most effective for ARFID. There is a lack of evidence to guide clinicians, and in many cases, consultation with a feeding or eating disorder specialist is helpful. Moving forward, it will be important for researchers to conduct treatment outcome studies that investigate the effectiveness of various therapies and medications, alone and in combination, for the various subtypes of ARFID in both children and adults. Helping underweight patients reach their treatment goal weight is often an essential first step in address their physical and mental well-being.

Dr Spettigue is Associate Professor, Department of Psychiatry, University of Ottawa, Children’s Hospital of Ontario, Canada; Dr Norris is Associate Professor of Pediatrics, Adolescent Health Physician, Division of Adolescent Medicine, University of Ottawa, Children’s Hospital of Eastern Ontario. The authors report no conflicts of interest concerning the subject matter of this article.

1. Norris ML, Robinson A, Obeid N, et al. Exploring avoidant/restrictive food intake disorder in eating disordered patients: a descriptive study. 

Avoidant restrictive food intake disorder, or ARFID, is a newly introduced eating disorder in DSM-5. Given that the disorder was introduced in 2013, it remains unclear how prevalent ARFID is in the general population.

Eating Disorders