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.
SIGNIFICANCE FOR THE PRACTICING PSYCHIATRIST
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.1,2
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;
• Low appetite or disinterest in food;
• 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.3
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).
2) Low appetite or disinterest in food. 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.1 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.4
Limited published evidence exists to guide clinicians in the treatment of ARFID, although trials are presently underway in the US and abroad. Strandjord and colleagues5 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,7 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.8,9 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.
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