What is ARFID?
It’s been a while since the last installment of this series. The initial goal was to upload one of these in-depth reviews everyday over the course of National Eating Disorders Awareness week, but life hits you hard sometimes and plans change. With that said, the last four are still coming (this being one of them), and I will do my best to get them all finished in a timely manner without sacrificing quality (or abundance of research!).
If you haven’t read the other three, you can find those here:
Today’s review discusses ARFID, one of the new disorders mentioned in the DSM 5. Read on to learn more about what this disorder actually entails, how it compares and contrasts to anorexia, which treatments are currently available, and more!
Definition and Diagnosis
Avoidant/Restrictive Food Intake Disorder (ARFID) is a trickier condition to define and diagnose. Though it often crosses into anorexia or bulimia territory (due to its signature restrictive behaviors), it is distinct from them in its emphasis on sensory qualities and types of food. Put crudely, ARFID is “pathological picky eating.” But of course, there is much more to it than a simple dislike of certain foods.
For an ARFID diagnosis, four criteria must be met:
Disturbance in eating or feeding, as evidenced by one or more of the following:
Substantial weight loss (or, in children, absence of expected weight gain)
Dependence on a feeding tube or dietary supplements
Significant psychosocial interference
Disturbance not due to unavailability of food, or to observation of cultural norms
Disturbance not due to anorexia nervosa or bulimia nervosa, and no evidence of disturbance in experience of body shape or weight
Disturbance not better explained by another medical condition or mental disorder, or when occurring concurrently with another condition, the disturbance exceeds what is normally caused by that condition
For further clarification, the current edition of the DSM provides three examples of ARFID presentation. These behaviors (and those similar to them) can occur independently or in combination:
Sensory sensitivity leads to avoidance of certain foods due to specific taste, smell, or texture aversions.
Lack of interest in eating, or lack of appetite, leads to restricting food intake.
A traumatic eating-related experience (i.e. choking, vomiting, eating molded or infectious food, etc.) leads to avoidance of specific foods or cessation of eating entirely.
Those with ARFID, especially children and young adolescents, often exhibit specific fears of what will happen when they eat (either a specific food/food type or any food at all). This could mean a fear of choking, vomiting, GI upset, infection, or defecation.
Finally, for the official ARFID diagnosis, these behaviors and beliefs must lead to some sort of serious medical or psychosocial impairment, such that medical attention is required. Examples of such conditions include stunted growth, frank nutrient deficiencies, or failure to move from feed tube nutrition to whole foods.
While distinguishing ARFID symptoms from AN can be difficult for medical providers, recent studies suggest those with ARFID score lower on a self-report measure of purposeful dieting but score higher on a self-report measure of actual deficits in calorie intake (Thomas et al., 2017b).
Misdiagnosis remains a large issue with ARFID. For example, body image distortion is specifically contraindicated as diagnostic criteria, yet almost a quarter of youth diagnosed with ARFID were found to exhibit body image issues in one study (Nicely et al., 2014).
The DSM-IV introduced Feeding Disorder of Infancy and Early Childhood, a disorder functionally identical to what the DSM 5 now calls ARFID. The major difference, as the name change insinuates, is the expansion of age range, as studies have increasingly shown this is not an age-specific disorder and can affect anyone, young or old.
Though incidence rates of ARFID are hard to gather, due to the limited research on this disorder, some available studies give us epidemiological insight. Prevalence of ARFID patients as a percentage of those in eating disorder treatment centers is somewhere between 7 and 17% (Ornstein et al., 2013; Fisher et al., 2014). This varies greatly, depending on study length and course of the disorder; one study that looked at patients over a four-year period of treatment admission (rather than the standard one-year period) found prevalence of ARFID to be as high as 23% (Nicely et al., 2014).
Etiology and Pathophysiology
Autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) are both some of the most common comorbidities to ARFID (Nicely et al., 2014). This makes sense because of the hallmark sensory sensitivity issues seen in both disorders.
It is important to note that body image and diet-related concerns cannot be present for an ARFID diagnosis. In fact, most children suffering from ARFID have a strong desire to gain weight (Strandjord, Sieke, Richmond & Rome, 2015).
Thomas et al. (2017b) have proposed a “three-dimensional model” of the neurobiology of ARFID, which is currently the most empirically comprehensive look at this available. The three dimensions of this model include sensory sensitivity, fear of aversive consequences, and lack of interest in eating or food (taken directly from the DSM’s three listed examples of ARFID symptomatology).
With this model, the authors posit that an individual’s experience with ARFID can be plotted somewhere along the three possible presentations, as illustrated below.
Though the common clinical understanding of this ARFID presentation is that it is only an issue of limited exposure to these foods, there is evidence that there is a true, objectively real difference in taste perception of these foods in anyone with sensory sensitivity issues (Kauer et al., 2015).
Fear of aversive consequences
It’s unlikely that food-related trauma alone has a causative role in development of ARFID. Many individuals will choke on, vomit up, or be made sick from something eaten at some point in early to late childhood, yet very few will go on to develop clinical ARFID. As such, there is thought to be a degree of predisposition for this disorder.
The authors hypothesize a hyperactive role of the brain’s phobia-related defense system in ARFID pathophysiology. This includes the amygdala, anterior cingulate (ACC), and the ventral prefrontal cortex (vPFC) (Lang & McTeague, 2009).
As mentioned in the review of bulimia nervosa, the ACC has limbic connections that could implicate its role in tying perceived emotion to external stimuli in the environment. Its connection to the amygdala, as well as the amygdala’s independent role in ARFID, makes sense, because this largely influences the fear element of this disorder. The vPFC also functions in reward and fear processing, albeit through different pathways. Hyperactivation of all three of these brain regions gives us promising leads into the pathology and etiology of ARFID.
Lack of interest in eating/food
This lack of interest is likely a direct result of hypothalamic dysregulation and feedback issues (Holsen et al., 2012). There is currently no indication that this at all deviates from the hypothalamic problems in the pathophysiology of AN.
The dangers present in ARFID are most pronounced in children and young adults affected by the disorder, as avoiding entire food groups (or food entirely) can have profound implications for growth metrics (physically and mentally) (Zucker et al., 2015).
Among other possible health risks, ARFID disproportionately predisposes individuals to amenorrhea, bradycardia (slow heart rate), electrolyte imbalances, and deficits with bone mass accrual (Strandjord et al., 2015). The nutritional deficiencies seen in ARFID can, and often do, occur even when there is no significant weight loss to explain it (Chandran et al., 2015).
There are no current FDA-approved drugs for the treatment of ARFID, just as there are none for AN (Kelly et al., 2014). By extension, limited research exists on pharmacological treatment of the disorder. At least one study looked at the effects of low-dose, supplemental olanzapine (i.e. not used as the sole treatment variable), an atypical antipsychotic drug prescribed to treat schizophrenia and bipolar disorder. While it was found to help facilitate increased feeding and weight gain, much more research (and more robust research, at that) is needed before this can be officially recommended anywhere (Brewerton & D’Agostino, 2017).
The singling out of olanzapine is not accidental; this is a drug with an extensive history of usage in the attempted pharmacological management of AN symptoms. Most of these studies found it to be at least somewhat effective in facilitating feeding and weight restoration, but only so far as it augments other more established methods of therapy and refeeding (Bosanac, Burrows & Norman, 2003; Powers, Santana & Bannon, 2002; Bissada, Tasca, Barber & Bradwejn, 2008).
Buspirone administration has also been documented but only so far as it treats the anxiety component of ARFID (Okereke, 2018). The anxiety component is more traditionally treated with conventional therapy modes.
As is thematic with therapeutic eating disorder interventions, cognitive-behavioral therapy (CBT) is primarily recommended for the medical management of ARFID. In fact, an ARFID-specific form of CBT (called CBT-AR) has been formulated and tested. This approach takes the standard CBT model and applies skill-teaching for the ability to approach novel food types that the sufferer may have aversions toward (Thomas, Wons & Eddy, 2018). A detailed case study following an 11-year-old girl with severe ARFID symptoms found this approach to be exceptionally effective (Thomas et al., 2017a). Its introduction into formal treatment settings is still pending, but further research should go on to show its utility long-term.
Family-based therapy (FBT) has also been implicated as a potentially useful therapeutic model for ARFID patients, especially due to the conventionally young age of those suffering from the disorder (Strandjord et al., 2016). Reviews and trials have found FBT to be beneficial, but they have also highlighted some plausible hiccups, including complacency in long-term behavioral accommodations, a lack of parental alignment and understanding, and psychiatric comorbidities (Lock et al., 2018).
Just as with AN, refeeding strategies become the primary area of interest here, as it is ultimately weight restoration that predicts long-term remission of symptoms.
When it comes to medical refeeding methods, there are at least four commonly used. Whole food refeeding is usually the first option, if possible, so that patients can relearn normal eating patterns and not have important salivary enzymes downregulated. Then there is enteral feeding, otherwise known as “complete nutrition supplementation.” This comes in the form of high-calorie drinks like Boost or Ensure, though in my podcast appearance discussing refeeding I explain why these might be issues when it comes to the refeeding syndrome.
The third option is nasogastric feed tubes. These tubes are inserted through the nose and bring supplemental nutrition directly down to the small intestine; this is commonly resorted to in cases of severe food refusal (especially when weight is critically low) or gastrointestinal insufficiencies anywhere from the mouth to the stomach, such that these need to be bypassed. Finally, there is total parenteral nutrition (TPN), which refers to intravenous feeding. This is clearly the last resort in all cases, as it carries a risk of infection, there is a smaller margin for error, and the experience can be traumatizing for patients.
With ARFID patients, nasogastric feeding is more common than it is with AN (Peebles et al., 2017). It’s thought that this is due to the common trait of pseudodysphagia (fear of choking on food) in those with ARFID, rendering oral routes of calorie consumption less viable options (Ornstein et al., 2017).
One major barrier to recovery from ARFID is its self-fulfilling prophecy nature. In other words, those with ARFID, especially those afraid that some negative consequence will come of their consumption of a certain food [type], will restrict said foods and consequently end up with actual gastrointestinal issues, which render it even harder (and often scarier) to consume those foods. This is a vicious cycle that especially threatens younger sufferers, whose undeveloped brain regions involved in executive decision making bar them from mustering the motivation to recover and break out of this cycle.
More than half of individuals diagnosed with ARFID are admitted to inpatient hospitalization, again highlighting the paramount role of refeeding in the recovery process (Cooney, Lieberman, Guimond & Katzman, 2018). Part of the current worry with admission protocols is that, at the time of this writing, there exists no official set of criteria for admission to inpatient (or any level of care) for patients with ARFID, leaving medical providers to either make a purely subjective decision or rely on AN-specific criteria (Guss, Richmond & Forman, 2018). Importantly, this ill-recommended transference of AN-specific protocols extends into how inpatient practitioners exercise refeeding protocols as well.
Compared to other restrictive EDs, ARFID patients have the longest hospital stays (Pitt & Middleman, 2018). This is possibly because of their comparatively more severe comorbidities and medical outcomes, as well as a need for a more nuanced refeeding approach (since AN patients, for example, do not have to clear the basic hurdle of food sensitivity issues or physiological food/feeding aversion).
Extremely limited data is available on the average course or outcome of treatment for ARFID. However, patterns indicate ARFID patients are followed for less time and are less likely to reach a healthy body weight than those with AN (Forman et al., 2014). This could be due to the fact that those diagnosed with ARFID have dealt with the disorder for longer, on average, than those with AN.
Significantly more research is needed so that medical practitioners can have more official diagnostic criteria available and the literature can have more prognostic markers available. In all hope, the 6th edition of the DSM will continue to expand upon the progress in ARFID symptom classification that was made from DSM-IV to DSM 5.
NEDA - The largest national eating disorder advocacy forum, which regularly hosts outreach events, funds important research, and directly helps those affected via their helpline.
ANAD (National Association of Anorexia and Related Disorders) - Non-profit corporation that advocates for and seeks to spread awareness of eating disorders, especially anorexia nervosa and bulimia nervosa.
AED (Academy for Eating Disorders) - Organization that specializes in ensuring the professional standards of eating disorder research, treatment, and information.
NEDA’s Helpline number is: 1-800-931-2237
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