research on eating disorders

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Anx indicates anxiety; depr, depression; ICD-10 , International Statistical Classification of Diseases and Related Health Problems, Tenth Revision ; suic, suicide. Claims reflect anorexia nervosa ( ICD-10 : F50.0), bulimia nervosa ( ICD-10 : F50.2), other ( ICD-10 : F50.8), and unspecified eating disorders ( ICD-10 : F50.9).

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Asch DA , Buresh J , Allison KC, et al. Trends in US Patients Receiving Care for Eating Disorders and Other Common Behavioral Health Conditions Before and During the COVID-19 Pandemic. JAMA Netw Open. 2021;4(11):e2134913. doi:10.1001/jamanetworkopen.2021.34913

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Trends in US Patients Receiving Care for Eating Disorders and Other Common Behavioral Health Conditions Before and During the COVID-19 Pandemic

1 Division of General Internal Medicine, the University of Pennsylvania, Philadelphia
2 Leonard Davis Institute of Health Economics, the University of Pennsylvania, Philadelphia
3 OptumLabs, Minnetonka, Minnesota
4 Department of Psychiatry, the University of Pennsylvania, Philadelphia
5 The Corporal Michael J. Crescenz VA Medical Center, Philadelphia, Pennsylvania

The lay press has reported an increase in eating disorders during the COVID-19 pandemic. 1 We examined trends in health care for eating disorders from January 1, 2018, to December 31, 2020, alongside other common behavioral health conditions among a large cohort of commercially insured individuals in the US.

This cohort study used deidentified data and was deemed exempt by the institutional review board group of UnitedHealth Group. We followed the Strengthening the Reporting of Observational Studies in Epidemiology ( STROBE ) reporting guidelines.

We counted the unique individuals per 100 000 members per month with outpatient or inpatient care and a primary diagnosis code ( International Statistical Classification of Diseases and Related Health Problems, Tenth Revision [ ICD-10 ]) for eating disorders ( ICD-10 : F50); alcohol use disorders ( ICD-10 : F10); depression, anxiety, and suicidality ( ICD-10 : F33, F34, F40, F41, T14); or opioid use disorders ( ICD-10 : F11). We excluded outpatient claims from members with inpatient claims in the same condition-month and emergency department claims.

This study included 3 281 366 individuals (2 053 432 females [62.6%]) with a mean (SD) age of 37.7 (16.2) years. Patient characteristics were similar across years, except that the age of patients with eating disorders decreased over time ( Table ). The number of patients with inpatient care for eating disorders remained approximately 0.3 per 100 000 members per month until May 2020 when it more than doubled to 0.6. This increase was seen across anorexia nervosa, bulimia nervosa, and other and unspecified eating disorders. The median (IQR) length of inpatient stays also increased from 9 (5-17) days and 8 (3-14) days in June to December of 2018 and 2019, respectively, to 12 (5-27) days in the same period in 2020. The number of patients with outpatient care for eating disorders increased from approximately 25 patients per 100 000 per month to 29 patients per 100 000 per month. Similar increases were not seen for the 3 comparison behavioral health conditions ( Figure ).

In this cohort study, we found that inpatient stays for eating disorders rose during the pandemic. Many aspects of the pandemic plausibly intensified eating disorders and their ascertainment. The pandemic may have promoted disordered eating behaviors among susceptible individuals. For example, obesity was frequently cited as a risk factor for COVID severity 2 , 3 ; grocery shopping became more fraught in the early pandemic because of contagion concerns, new rules, and rituals; and many bought large quantities of foods to minimize shopping frequency or fear of shortage. 4 , 5 Additionally, exercise may have become a focus of control or a compensatory mechanism for eating. 6 Furthermore, the closing of schools and colleges may have helped families identify unhealthy eating or recognize its effects, and outpatient care may have been delayed until symptoms required hospitalization. This study was limited because the data was based on the commercial claims of a single insurer.

Accepted for Publication: September 22, 2021.

Published: November 16, 2021. doi:10.1001/jamanetworkopen.2021.34913

Corresponding Author: David A. Asch, MD, Center for Health Care Innovation, University of Pennsylvania, 3400 Civic Center Blvd, 14-171 PCAM South Tower, Philadelphia, PA 19104 ( [email protected] ).

Author Contributions : Mr Buresh had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Asch, Islam, Sheils, Doshi, Werner.

Acquisition, analysis, or interpretation of data: Buresh, Allison, Sheils, Doshi, Werner.

Drafting of the manuscript: Asch, Allison, Sheils.

Critical revision of the manuscript for important intellectual content: All authors.

Statistical analysis: Islam, Doshi, Werner.

Administrative, technical, or material support: Sheils.

Supervision: Sheils, Werner.

Conflict of Interest Disclosures: Dr Allison reported receiving grants from Novo Nordisk Investigator Initiated Study outside the submitted work. Dr Sheils, Dr Islam, and Mr. Buresh own stock in UnitedHealth Group, which is the parent company of their employer Optum Labs, outside the submitted work. No other disclosures were reported.

Additional Contributions: We thank Yong Chen, PhD (University of Pennsylvania), for useful comments made on the manuscript. Dr Chen was not compensated for his time.

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New insights on eating disorders

Scientists are uncovering the faulty neurobiology behind anorexia and bulimia, debunking the myth that such eating disorders are solely driven by culture and environment.

By Kirsten Weir

April 2016, Vol 47, No. 4

Print version: page 36

10 min read

Public misunderstanding of mental health disorders is nothing new. But for eating disorders in particular, misinformation abounds.

"You still read more about anorexia in the celebrity section of publications than in health sections," says Nancy Zucker, PhD, a professor of psychology and neuroscience at Duke University. "The emphasis is on it being a culturally guided phenomenon."

Even medical definitions of eating disorders have often focused on external factors, including cultural pressures, parents' attitudes toward weight and diet, and stressful or traumatic events that might trigger disordered eating habits.

While the environment certainly plays a part in shaping the behaviors, evidence is mounting that eating disorders begin in the brain.

"Lots of people diet or want to lose weight, but relatively few of them end up with anorexia nervosa or bulimia nervosa," says Walter Kaye, MD, director of the Eating Disorders Treatment and Research Program at the University of California, San Diego (UCSD) School of Medicine.

In fact, fewer than 1 percent of women develop anorexia, the more severe of those two diseases. "Culture plays some role — but maybe less so than we thought in the past," Kaye says.

Now, researchers including Kaye are beginning to sort out the brain regions and neural circuits that underlie the illnesses. For the millions of Americans who suffer from anorexia and bulimia, it's a welcome step toward better interventions for the notoriously hard-to-treat illnesses.

"People die from these disorders," Kaye says. "It's critical that we understand the contributing factors and develop new treatment approaches."

Circuits gone awry

Broadly speaking, eating disorders are any illnesses that cause serious disturbances to one's diet. These disorders include the relatively well-known anorexia, characterized by extreme food restriction and emaciation, and bulimia, marked by episodes of binge eating followed by purging, fasting or excessive exercise. At the opposite end of the spectrum from anorexia is binge-eating disorder, in which people experience insatiable cravings that cause them to eat large amounts of food beyond mere "overeating." Still other eating disorders fall into a catchall category known as "eating disorders not otherwise specified."

What all of these disorders share is a dangerously maladaptive approach to food.

Unsurprisingly, binge-eating disorder is often associated with obesity. People with anorexia and bulimia, on the other hand, fear gaining weight. Anorexia and bulimia often arise during the teen or early adult years, and are more common among women than men. According to a study by James Hudson, MD, ScD, and colleagues, 0.9 percent of women and 0.3 percent of U.S. men develop anorexia during their lifetime, while 1.5 percent of women and 0.5 percent of men develop bulimia ( Biological Psychology , 2007).

Untreated, bulimia can lead to serious illnesses including gastrointestinal problems, electrolyte imbalance and cardiovascular disease. Anorexia can cause muscle wasting, heart and brain damage, and multiorgan failure. Indeed, anorexia has been reported to have one of the highest mortality rates of any psychiatric disorder.

"There are many disorders that are maladaptive, but in anorexia, individuals are basically starving themselves to death," Zucker says. "You don't have to be a scientist to step back and say there's something horribly wrong here."

While anorexia and bulimia both have distinct features, the disorders appear to share some biological underpinnings. Both are highly heritable, for example. But while one family member might develop anorexia, another will experience bulimia. And it's not uncommon for someone with one of the disorders to later develop the other. "That points to some common vulnerability — possibly neurological vulnerabilities," Zucker says.

People with anorexia and bulimia also tend to have relatively similar temperaments.

"When they're children, before the onset of an eating disorder, these tend to be kids [who] are anxious, obsessive, perfectionistic and achievement-oriented," Kaye says.

Yet eating disorders are more complicated than a perfectionist temperament gone awry. A faulty reward-processing system seems to be an important feature of the diseases. Learning from rewards is an ancient ability across the animal kingdom, and the process is particularly potent in guiding eating behaviors. When we eat a bite of chocolate cake, we're rewarded with the pleasure of its taste, and want to take another.

That basic process breaks down in anorexia, Kaye says. "There's an altered balance in people with anorexia where they have difficulty coding reward, and they're oversensitive to punishment."

In one demonstration of this breakdown, Kaye and colleagues scanned the brains of healthy women and women with anorexia as they played a monetary betting game. In women with anorexia, brain circuits involved in reward processing were less active when they won, but more active when they lost ( Psychiatry Research: Neuroimaging , 2013).

An important piece of the altered reward system seems to be dopamine, the neurotransmitter that motivates us to cut a second helping of that chocolate cake. Dopamine activity is altered in both bulimia and anorexia — but in opposite ways, according to research by Guido Frank, MD, a professor of psychiatry at the University of Colorado Anschutz Medical Campus.

Women with bulimia have a weaker-than-normal response in brain regions that are part of the dopamine-related reward circuitry, while the reward circuits in women with anorexia are overly sensitive to food-related stimuli, as Frank described in a recent review ( CNS Spectrums , 2015).

For most people, eating is an enjoyable activity. People with anorexia, though, often report that sitting down to a meal makes them feel worried — and there appears to be a biological reason for that reaction. Kaye and colleagues have found that in people with anorexia, the release of dopamine in the dorsal striatum triggers anxiety rather than pleasure ( International Journal of Eating Disorders , 2012).

Body signals

As scientists delve into the faulty reward system, they've identified several brain regions that are possible perpetrators. One is the orbitofrontal cortex, which is involved in signaling us when to stop eating. Research has found that people with anorexia and bulimia have structural and functional differences in this area, Frank says.

Women with anorexia also appear to have more activity in the dorsal striatum, the brain area linked to habitual behavior, according to New York University psychologist Karin Foerde, PhD, and colleagues who scanned the brains of anorexic and healthy women as they decided what to eat. (Because anorexia is much less common in men, most research focuses on women.)

Traditionally, people with anorexia have often been thought of as having formidable willpower, allowing them to avoid food even when they're starving. Foerde's study suggests maladaptive eating behaviors may have more to do with habit than with willpower, the authors say ( Nature Neuroscience , 2015).

The brain region known as the right insula also seems to be altered in people with anorexia. That bit of brain helps to process taste sensations, but it's also involved in interoception, the ability to sense one's own bodily signals.

Those skewed body signals are the subjects of Zucker's research at Duke. Most people only notice their bodies' clicks and rumbles when something's amiss, she says — when their stomachs rumble with hunger or their hearts skip a beat. But according to a concept known as visceral hypersensitivity, people with anorexia might pick up on bodily "noise" that the rest of us tune out.

"The theory is that they are hypersensitive to changing body sensations," Zucker says. "The input from their physiology is constantly interfering with their ability to focus."

Extreme food restriction might be a coping response to that hypersensitivity, Zucker believes. In response to starvation, the body slows down. Heart rate declines, menstrual cycles stop. "The whole body becomes muted," Zucker says.

Recently, she tested this idea as part of a team led by W. Kyle Simmons, PhD, at the Laureat Institute for Brain Research. The scientists scanned the brains of healthy women and women who had been treated for anorexia as they focused on sensations in their hearts, stomachs or bladders. They found abnormal insula activity in the women with anorexia. Interestingly, a particular subregion of the insula also showed increased activity when the women with anorexia were asked to think about situations that worried them. That finding suggests that altered interoception might contribute to their anxious temperament, Zucker says ( Neuropsychopharmacology , 2016).

Traits and scars

While researchers are beginning to see patterns of brain abnormalities in eating disorders, the literature has been inconsistent, Frank says. Being severely malnourished can cause changes to the brain — many of which return to normal after a person begins eating again. Study results can vary dramatically depending on whether participants are actively restricting food, undergoing treatment or have recovered to a normal weight. For that reason, Frank favors studying women in highly controlled treatment programs so that he knows exactly how long, and how much, they have been eating.

Still, it can be difficult to know whether certain brain differences are the cause or the consequence of an eating disorder — in neurobiology terms, a "trait" or a "scar." Most likely, says Frank, some pre-existing features of the brain put a person at risk for developing an eating disorder, while other changes develop in response to one's eating habits.

Yet neurobiology can inform treatments even before it answers the question of trait-versus-scar. "If we can go in and directly and precisely intervene on a circuit that seems to be associated with illness severity, the chicken-or-the-egg question doesn't have to forestall intervening immediately," she says.

And better interventions are sorely needed. Approximately half of people with anorexia have the illness for five years or more, yet there is no FDA-approved medication nor a go-to psychotherapeutic approach proven to reverse the symptoms.

"Treatments for eating disorders are not very effective," says Christina Wierenga, PhD, a clinical neuropsychologist and associate professor of psychiatry at UCSD who works closely with Kaye. "Relapse rates are high, and that's because treatments have not been guided by an understanding of the etiology of the disorder."

Wierenga and other researchers are optimistic that neuroscience will point the way to new medications and therapeutic tools. She and Kaye have already begun testing new treatment programs that stem from neurobiology. Presenting brain-based findings can be helpful for motivating patients in recovery, Wierenga says. "One thing that makes these patients very difficult to treat is that they often lack an awareness of the severity of the disorder, and many times they lack a motivation to change," she says.

In light of the findings implicating defective reward circuits in eating disorders, Kaye and Wierenga are developing a treatment model that emphasizes negative consequences over rewards. Those consequences aren't intended to punish patients, Wierenga says, but rather to help guide patients toward positive behavior. A patient who refuses to drink her nutritional supplement might be moved into a more controlled level of inpatient care, for instance.

"Sometimes [the negative consequences we use are] as basic as not being allowed to wear makeup or your favorite pair of jeans," Wierenga says. "Those are privileges that you have to earn back."

Emphasizing the neurobiology of the disorders also reduces stigma, Zucker says, and helps parents better understand how to support their children during treatment.

"Eating disorders seem very behavioral. Sometimes it even seems oppositional when a child refuses to eat," she says. "Showing there are brain circuits that are not functioning effectively gives parents some pause, and helps them understand their child's illness."

There's a lot left to learn about the neurobiology of eating disorders, including whether the neurobiological risk factors are similar across racial and ethnic groups, and how those physical factors might interact with cultural messages about weight and body image. In the meantime, using neuroscience insights to motivate and educate patients and their families is a great place to start in treating eating disorders, Zucker says. Hopefully, that's just the beginning. She and her colleagues in the field are beginning to develop potential new interventions, ranging from deep brain stimulation to cognitive training exercises, that could reformat a faulty brain circuit.

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Binge eating appears more widespread, persistent than thought

New research takes broader, deeper look at common, but poorly understood, disorder

Alvin Powell

Harvard Staff Writer

Binge eating is one of the world’s most common eating disorders but is poorly understood. Kristin Javaras , assistant professor of psychology at Harvard Medical School’s Department of Psychiatry and instructor in epidemiology at Harvard T.H. Chan School of Public Health , recently shed light on the subject in a study, published in the journal Psychological Medicine. The findings showed that earlier research, which focused on younger women, underestimated how chronic the problem can be for many in the broader population, lasting for years or even decades. Javaras, who is also associated psychologist at McLean Hospital’s Division of Women’s Mental Health, spoke to the Gazette about her recent research.

What is binge eating?

Binge-eating disorder is characterized by binge eating episodes, which have two components, according to the DSM — the reference manual for diagnoses. One is an objectively large amount of food. Second — and most importantly — there’s a sense of loss of control, a feeling that you can’t stop or you can’t avoid starting. Some people feel like they’re driven by a motor, and they can’t stop until either they feel so sick that they have to or the food is gone.

These episodes are often characterized by eating quickly and eating alone and accompanied by a feeling of shame. People have recurrent episodes. So, if the person experiences marked distress around binge eating and isn’t engaged in compensatory behaviors that you see in bulimia nervosa — purging regularly, using laxatives or diuretics, extreme dieting or fasting, or engaging in excessive or compulsive exercise — there would be a diagnosis of binge-eating disorder.

“When people diet and think, ‘I’m going to try to eat as little as possible,’ that sets them up to engage in binge eating.”

When you say “an objectively large amount,” we’re not talking about Thanksgiving dinner or another holiday where we’re socialized to overeat? How do we know the difference?

If it is typical for a circumstance, it is not binge eating. Likewise, if there’s no loss of control it’s not binge eating. For instance, if I want to run a marathon tomorrow and I eat a large amount of pasta intentionally, with a sense of control, that wouldn’t be binge eating.

It can be tricky to evaluate, but the question is whether it’s an objectively large amount for that person in that context. So Thanksgiving typically wouldn’t count unless it was far beyond what other people are eating, and accompanied by a sense of loss of control.

Does it have to be every day? Once a month?

The diagnostic guidelines have changed recently. In DSM-4, it was two days a week, while in DSM-5 it is one episode a week. But there are people for whom it doesn’t happen as frequently, but the binges are very upsetting. They technically don’t meet DSM-5’s definition of binge-eating disorder, but it could still be very clinically significant, even if it’s not happening once a week. It’s important to note that the study we’re talking about was done under DSM-4.

What is the harm if you binge once a week and eat normally the rest of the week? Weight gain? Poor nutrition?

We know that binge eating does have metabolic consequences. There is a study that shows if you eat the same amount of food in a very short period of time, it’s metabolically worse for you than if you ate it over a whole day, particularly the types of foods that are consumed in a binge, which tend to be highly palatable and have metabolic consequences.

But what’s more important are the psychological effects. People are often restricting to some degree: not eating enough, not allowing themselves to eat certain types of foods. They hold beliefs like, “I should never eat X” or “This food is bad.” There’s a lot of binary thinking and people often feel extremely negatively about their bodies.

The binge eating is in the DSM, but for those of us in practice, we see it as one symptom among many in the eating disorder. Addressing restriction — getting people to eat regularly — is one of the most potent interventions. Often people feel that, because they are at a higher weight, they should be dieting all the time. And when people diet and think, “I’m going to try to eat as little as possible,” that sets them up to engage in binge eating.

“A lot of the initial studies on eating disorders were based on treatment-seeking samples, which are, by definition, not representative. Anyone can get an eating disorder.”

What’s the prevalence of binge eating in society?

That’s a tricky question because the research doesn’t entirely agree. The National Comorbidity Survey Replication, which was done in 2007 by my mentor, Jim Hudson, and Ron Kessler, suggested that the prevalence of DSM-4 binge-eating disorder was around 2.6 percent [chance over a] lifetime in the U.S.

DSM-5, because it’s a broader category, would be higher than that. A more recent study by Udo and Grilo in 2018 was just under 1 percent lifetime. There are some methodological reasons why they may differ, so it’s hard to get a clear estimate, but I’d say somewhere between 1 and 3 percent lifetime in the U.S.

So millions of people. Is it the most common eating disorder?

Yes, it is — in the U.S. and globally — though we don’t have good data from some regions of the world.

Let’s talk about your study. You were trying to settle differences in earlier studies about how long binge-eating disorder takes to resolve on its own. What did you find?

My mentors, Jim Hudson and [Harrison] Skip Pope, did a family study of binge-eating disorder in the early aughts. They subsequently followed the study participants forward for five years, re-interviewing them every 2.5 years.

They thus had really unique, valuable data on the disorder’s duration, and I suggested we look at both remission and relapse, and also use machine learning to see if we can predict whether somebody will go into remission. Our analyses showed that although there is improvement over time, the disorder doesn’t just vanish after a few months for most people in our sample.

And the key finding was focused on it resolving naturally, not with treatment?

That’s why this study is so important. We already have very good data on how people respond to treatment. But because they’re getting treatment, it’s not a representative sample of what happens in the real world.

We found that, at 2.5 years, about 15 percent of people had moved into remission, with no binge-eating episodes for three months. At five years, that was a little over 20 percent. And a little less than two-thirds of people still had full DSM-4 binge-eating disorder at 2.5 years. A little under half still had the disorder at five years. The rest were somewhere in the middle: They didn’t meet the DSM-4 criteria for binge-eating disorder, but they weren’t fully in remission.

I should also mention that this was snapshot data at 2.5 and 5 years, but people move around in between. When we looked at the in-between data, based on people’s retrospective report of what had happened over the 2.5 years, we see some people are experiencing remission, but relapse is fairly common, and the median time to remission is over 60 months.

And that is different from the other studies you looked at?

There were a couple of levels. The older prospective studies were small, under 50 people, excluded males, and the participants tended to be younger.

We know that, for younger people with eating disorders, presentations can change more rapidly than someone who’s had binge-eating disorder for 20 years. Those studies suggest that only a minority of people still had a full threshold of binge-eating disorder at two to five years of follow-up.

But also we knew that the individuals in those studies were young, were mostly at lower BMI, and there were no men. Our sample had a much wider age range, was primarily high BMI, as well as being a bigger sample.

Were the samples in these older studies representative of outdated societal perceptions about who is affected by binge-eating disorder?

A lot of the initial studies on eating disorders were based on treatment-seeking samples, which are, by definition, not representative. Anyone can get an eating disorder.

Does this work say anything about treatment?

It does, although it requires making a few assumptions. If you look at the longer-term outcomes seen in high-quality, randomized controlled trials of psychotherapy for binge-eating disorder, the percent of people experiencing remission is higher than in our study. That suggests that people would get better faster with treatment than they would under natural circumstances.

I don’t want people to feel hopeless after seeing our study. There are effective treatments for binge-eating disorder, including one FDA-approved medication, lisdexamfetamine, and multiple evidence-based psychotherapies. Although our treatments are not perfect, they do help many people.

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Recent Advances in Developmental and Risk Factor Research on Eating Disorders

Affiliation.

1 Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, DoD, 4301 Jones Bridge Road, Bethesda, MD, 20814, USA, [email protected].
PMID: 25894358
DOI: 10.1007/s11920-015-0585-x

The Diagnostic and Statistical Manual of Mental Disorders (i.e., DSM-5) currently recognizes three primary eating disorders: anorexia nervosa, bulimia nervosa, and binge eating disorder. The origins of eating disorders are complex and remain poorly understood. However, emerging research highlights a dimensional approach to understanding the multifactorial etiology of eating disorders as a means to inform assessment, prevention, and treatment efforts. Guided by research published since 2011, this review summarizes recent findings elucidating risk factors for the development of eating disorders across the lifespan in three primary domains: (1) genetic/biological, (2) psychological, and (3) socio-environmental. Prospective empirical research in clinical samples with full-syndrome eating disorders is emphasized with added support from cross-sectional studies, where relevant. The developmental stages of puberty and the transition from adolescence to young adulthood are discussed as crucial periods for the identification and prevention of eating disorders. The importance of continuing to elucidate the mechanisms underlying gene by environmental interactions in eating disorder risk is also discussed. Finally, controversial topics in the field of eating disorder research and the clinical implications of this research are summarized.

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Special Report: Youth With Eating Disorders—Time Is of the Essence in Achieving Remission

Brittany Matheson , Ph.D. ,
Nandini Datta , Ph.D. ,
James Lock , M.D., Ph.D.

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Given that the symptoms of eating disorders may emerge over time and stay undetected even by loved ones and friends, early identification and treatment of children and adolescents are imperative.

Trivia time: imagine you are on a popular game show—you know, the one with the catchy theme song we can’t name due to copyright issues. The category “Psychiatric Disorders” comes up and you start to feel pretty confident you’ll get this one right. Suddenly, the clue is revealed: “This disorder has one of the highest mortality rates in all of psychiatry, with 12 times higher death rates in 15- to 24-year olds than any other cause.”

The theme show music starts as you rack your brain for the name of the disorder. The most deadly? By 12 times more? Your mind begins to race back through your coursework, trainings, clinical rotations, readings, and patient interactions, which leaves you with a number of potential answers. Perhaps major depressive disorder, or psychosis with command hallucinations, or substance use? Anything else? Aahh—time is running out. Quick, quick—what’s your final answer?

Did eating disorders come to mind? Because if they did, you would be correct (and hopefully win big in this fictional game show!). Eating disorders—in particular, anorexia nervosa—have one of the highest mortality rates of any psychiatric disorder, due in part to associated medical complications as well as an increased risk of suicide. Research suggests that 1 in 5 deaths from anorexia nervosa is the result of suicide. For children and adolescents, eating disorders are the third most common chronic health condition, behind only asthma and obesity in numbers. An estimated 1 in 30 people will develop an eating disorder at some point in life.

Eating Disorders Can Be Life Threatening Yet Underresearched

Eating disorders can severely impact just about every organ system in the body, including the cardiovascular system; cause diminished muscles, growth potential, and bone density; disrupt the endocrine and gastrointestinal systems; and can affect the brain. (Did you know the brain is the fattiest organ in the body?) While most of the medical complications of eating disorders resolve with improved nutrition and resolution of the eating disorder, not all damage is reversible, depending on the severity of symptoms and length of illness. Importantly, research suggests that after about three years of an eating disorder such as anorexia nervosa, for example, chances of full recovery diminish greatly. That’s three years from the onset of symptoms. Given that symptoms may emerge slowly over time and can stay undetected even by loved ones and friends, time is of the essence to identify and treat children and adolescents for eating disorders.

Despite these shocking statistics, eating disorder research has historically been significantly underfunded. For example, recent estimates of U.S. federal funding amounted to just $.73 per person impacted with an eating disorder, compared with almost $87 per person for schizophrenia and $59 per person for autism spectrum disorder. In Canada, estimates ranged from $0.11 to $0.61 per person impacted with an eating disorder, compared with nearly $47 for schizophrenia research and $54 for autism spectrum disorder. In addition, it can be challenging for patients and families to access expert medical and psychological care, which is often uniquely available in large, urban areas or in connection to academic medical centers. Access to telehealth options, videoconferencing platforms, and online treatments has helped alleviate this burden and broaden access to care, though finding qualified providers or programs with availability continues to be difficult. Obtaining training and certification in evidence-based treatment modalities also poses challenges for private practice or community-based providers who may not have convenient access to trainings and supervision needed to learn these treatments.

Our research team is currently exploring solutions to this hurdle by testing the effectiveness of online asynchronous clinical trainings in family-based treatment (FBT) for clinicians in private practice (NCT04428580; study still recruiting). Results of this implementation study as well as further work in this area will inform intervention training practices with the goal of improving access to expert, high-quality, and effective treatments for youth with eating disorders.

Fighting Myths and Misconceptions

Eating disorders represent a heterogenous category of diagnostic criteria, from restrictive undereating to disinhibited, overeating behaviors. And not all eating disorders are driven by concerns over shape and weight. In fact, avoidant restrictive food intake disorder (ARFID)—characterized by difficulty with maintaining adequate nutritional intake resulting in physical and psychosocial impairment—is not related to body image or weight concerns at all and can begin in much younger children. One shared trait that all eating disorders have in common? They are incredibly disruptive, distressing, and dangerous to the person suffering from one.

Although not every psychiatrist will be directly involved in providing eating disorder treatment, we all play an important role in recognizing the signs and symptoms of disordered eating while also disrupting myths about eating disorders that have become pervasive in today’s society. For example, it is not possible to look at someone and know the person has an eating disorder. A person’s outward physical appearance communicates little to no data about overall health. Moreover, eating disorders may impact anyone. Outdated myths that eating disorders affect only cis-gender, White, affluent females fuel harmful stereotypes and impede care for individuals who are suffering. Eating disorders are prevalent among gender-diverse youth and individuals who are from diverse racial and ethnic backgrounds. A 2011 study by Daniel Eisenberg, Ph.D., and colleagues in the Journal of American College Health found that 1 out of every 4 college students with an eating disorder identified as male. Another study by Michelle Goeree, Ph.D., and colleagues reported in a 2012 paper from the University of Zurich that female youth from low-income families were more than 150% more likely to have bulimia nervosa than female youth from high-income families.

Most important, eating disorders are not choices; they are not volitional. This is one of the biggest misconceptions about eating disorders. A teenager cannot simply wake up one morning and choose to have an eating disorder. Rather, there are strong biological and genetic influences that interact with individual differences, personality traits, neurobiological processes, and environmental contexts to result in an eating disorder. In our clinical care of adolescents with eating disorders, the number one question we get asked over and over is, “How did my child develop this? Where did it come from?”

Psychosocial treatments for youth with eating disorders

The truth is that we don’t know. Research is underway to examine this very question, and perhaps one day, we’ll be able to posit a solution to this perplexing question. The good news is that we don’t need to know the “why” to treat patients with the disorder. And until we know more about the “why,” we encourage families to act quickly to help their young person overcome this terrible illness. Hemming and hawing over the “why” often delays families from focusing on the task at hand—and recovery from an eating disorder is a monumental task.

Sometimes we use the following analogy to help families better understand our “agnostic” stance. We might say, “Imagine you were just diagnosed with cancer. You are meeting with your oncologist and have just learned this devastating news. Would you ask your oncologist to hold off on talking about treatment options and therapeutic approaches until everyone figures out exactly how or why you got cancer?” Of course not. Instead, the conversation would immediately turn to treatment planning and next steps. An eating disorder diagnosis should be no different; the conversation must focus on how someone is going to start the recovery process. Although we may never truly understand the “why” for each individual patient, we do have effective treatment options for eating disorders in youth. And we need to get started right away.

Our team is composed of experts in the assessment and treatment of children and adolescents with eating disorders, and thus the information we present below is curated for this population. Importantly, there are key distinctions in the presentation and treatment options for youth compared with adults with eating disorders. For example, eating disorders in youth are more likely to be non-chronic and more responsive to intervention, and they rely heavily on family support in recovery efforts. We provide a brief overview of anorexia nervosa, bulimia nervosa, binge eating disorder, and avoidant restrictive food intake disorder with a tailored focus on the current evidence-based interventions as well as promising future research directions. These are also outlined for you in Table 1.

Anorexia Nervosa (AN)

Diagnostic criteria for AN includes restriction of energy intake driven by an intense fear of weight gain and shape/weight concerns. Individuals may be diagnosed with AN, restricting subtype (F50.01), or AN, binge-eating/purging subtype (F50.02). Common comorbidities include mood disorders, anxiety disorders, and obsessive-compulsive disorder. AN occurs across genders; socioeconomic statuses; and racial, ethnic, and cultural backgrounds, and it presents with the same preoccupations with weight, thinness, dieting, and overexercise that, if left untreated, results in significant medical consequences. Youth with AN require ongoing medical monitoring to ensure vital sign stability. With food restriction and malnutrition, all systems of the body are impacted, including the heart and brain. Common medical complications of AN include bradycardia—slowed heart rate, orthostatic changes in blood pressure from lying to standing, and electrolyte imbalances. At times, an inpatient hospitalization may be warranted for medical stabilization. AN has significant psychosocial implications for youth as well. Frequently, adolescents with AN withdraw from family and friends, becoming less social and engaged with their life outside of AN preoccupations.

Individuals who meet criteria for atypical AN report the same preoccupations with thinness, body image, and weight and engage in restriction, yet are not underweight by body mass index or growth chart standards. Not uncommonly, patients with atypical AN may also need to restore lost weight to promote vital sign stability and cognitive recovery from the eating disorder. The use of the word “atypical” is hotly debated and perhaps does not communicate the appropriate graveness and severity to families and clinicians.

For youth with AN, family-based treatment (FBT) is a well-established Level I treatment. It is the first-line treatment recommended by international guidelines and practice standards. In FBT, all family members who eat together in the home—parents/guardians, patient, siblings, even grandparents if applicable—attend hour-long outpatient treatment sessions with a certified therapist. FBT consists of three phases:

Phase 1, which consists of weekly sessions focused on parental involvement in renourishment, disrupting eating disorder behaviors, and establishing regular nonrestricting eating patterns.

Weight gain is often a target early in treatment, as research studies suggest that adolescents who gain 2.3 kg by session 4 of FBT have a 70% to 90% chance of achieving symptom remission by the end of treatment. Given that research trials of FBT typically achieve 40% to 50% remission rates, this marker of early response is critical for therapists, families, and patients to all work toward to promote improved outcomes.

Phase 2, which consists of biweekly sessions focused on transitioning independence with eating back to the adolescent while also working on social eating goals.

Phase 3, which consists of monthly sessions focused on an adolescent development task that the family has identified to work on together. The second session of FBT during this phase includes a family meal during which the family eats together with the therapist to learn new strategies to help the child overcome AN at mealtimes.

Adaptations and augmentations of FBT have been developed, including separate parent-only FBT and adding extra intensive parental coaching sessions for adolescents who do not respond to FBT within the first month of treatment. Based on clinical experience and supervision, virtual delivery of FBT looks quite similar to in-person treatment, though research studies have yet to directly compare outcomes across these two delivery formats. Guided self-help (GSH) adaptations for FBT are also in development, which, if found to be effective in adequately powered clinical trials, could significantly improve efficacy of treatment and reduce further barriers to accessing evidence-based care. Other evidence-based treatment modalities for AN are explored and briefly described in Table 1. More information about these treatment modalities can be found in our team’s evidence-based update for children and adolescents with eating disorders , published in the Journal of Clinical Child and Adolescent Psychology on August 11, 2022.

Bulimia Nervosa (BN)

The diagnostic criteria for BN include binge-eating episodes (loss of control eating plus consuming an objectively large amount of food within a discrete period of time) as well as use of compensatory behaviors at a frequency of approximately once a week for three months. Common comorbidities including mood disorders, obsessive-compulsive disorder, posttraumatic stress disorder, substance use disorders, and emotion regulation difficulties. Oftentimes, adolescents with BN report distress over their eating disorder symptoms and are typically more motivated to engage in care compared with adolescents with AN, given the egodystonic nature of BN.

FBT is a well-established outpatient treatment for adolescents with BN. Early response markers suggesting reduction in purging behaviors by session 2 and binge eating by session 4 may predict abstinence rates at the end of treatment. However, to date, there have been only four randomized clinical treatment trials for adolescent BN, with a total of 376 participants across the trials. As such, significantly more research is needed to replicate previous study outcomes as well as include a greater number of diverse individuals to improve generalizability.

Binge Eating Disorder (BED)

BED is the most commonly diagnosed eating disorder in adult populations, with a mean age of onset estimated to be about 23 years old. Individuals with BED report experiencing a sense of loss of control eating (LOC eating) while consuming an objectively large amount of food in a discrete period of time, often within two hours. Additionally, to meet diagnostic criteria, these eating episodes must be accompanied by marked distress and at least three of the following: eating rapidly; eating until uncomfortably full; eating when not feeling hungry; eating alone due to shame or embarrassment about how much one is consuming; and feeling disgusted with oneself, depressed, or guilty about the eating episode. Among children and adolescents, research has suggested that the experience of LOC eating correlates with anxiety, depression, marked distress, and poorer quality of life, independent of the amount of food consumed during these eating episodes. Prevalence estimates of LOC eating vary widely, from 8% to 30%, and may be greater among youth with obesity. LOC eating in childhood or adolescence may be a risk factor for the development of BED and/or BN.

To date, there are no Level I well-established treatments or Level II possibly efficacious treatments for binge eating in youth. Research studies have examined a range of treatment approaches within randomized clinical trials and small case series, including dialectical behavioral therapy, interpersonal psychotherapy, cognitive-behavioral therapy, and guided self-help cognitive-behavioral therapy. Evidence-based treatments for binge eating in adults may not directly translate to youth, given age and developmental differences as well as the child’s embedment within the family system. Thus, additional research into this area is needed.

Avoidant Restrictive Food Intake Disorder (ARFID)

A recently recognized eating disorder that was added to DSM in its fifth edition, ARFID is a selective eating disorder characterized by difficulties in maintaining adequate nutritional intake resulting in medical and/or psychosocial impairments. Individuals with ARFID do not express body image concerns despite engaging in restrictive eating behaviors, which uniquely separates this disorder from the others in the same category. Rather, eating behavior in ARFID is driven by three noninclusive subtypes: a lack of interest in eating/pervasively low appetite, sensory sensitivity (these kids know the difference between two seemingly identical boxes of Cheerios), and/or fear of aversive consequences such as vomiting or choking.

Individuals with lack of interest/low appetite presentation often present with longstanding histories of undereating and difficulties maintaining adequate intake, typically from very early on in life. It is not uncommon for youth with this presentation to forget to eat, be easily distracted by other activities, and report not feeling hungry. They may have difficulty receiving and interpreting internal hunger cues. Youth with the sensory sensitivity profile of ARFID report restrictive eating patterns based on sensory aspects of food and eating, which may include texture, temperature, smell, taste, color, or other aspects of appearance.

Children with ARFID may eat only a very narrow range of foods and often have strong preferences for specific brands or styles of food preparation. Varying from a preferred, known brand or preparation style may result in refusal to eat; for example, a child may eat chicken nuggets from McDonald’s without difficulty but will not eat chicken nuggets from other restaurants or those made at home. Children with this presentation may miss certain key nutritional elements due to their restrictive food range or may miss out on engaging in social events, such as birthday parties, traveling, sleepovers, family gatherings, or celebrations involving food.

General Characteristics Associated with Eating Disorders

For youth with fear of aversion consequences, their ARFID typically onsets after an event, such as choking on a hotdog, throwing up repeatedly due to food poisoning, or even experiencing pain while eating after orthodontic work. Children then become concerned about eating foods and may even go as far as to restrict all solid foods in an effort to avoid whatever unpleasant outcome they are afraid may happen after eating. This presentation often has a more rapid onset than the other subtypes and usually occurs later in childhood or early adolescence, though not always. Children with ARFID often don’t fall neatly into one of these categories, instead falling into two or even all three categories.

With any presentation of ARFID, families often feel significant pressure and stress regarding feeding their child. Parents can easily fall into the role of short-order cook. Also the adage “Your child will eat if hungry enough” simply does not hold true for many families’ experiences of a child with ARFID, particularly those within the low appetite subtype who will happily forgo eating. Parents report feeling frustrated, isolated, and guilty, fearful they have done something that caused their child’s eating difficulties. Parents may feel additional stress and worry if their child is not growing as expected or experiences medical complications stemming from their difficulties with eating, necessitating the consideration of enteral feeding. Although the recognition of ARFID as a psychological disorder is growing, it can still be missed or misdiagnosed by physicians who may assume it is a form of “picky eating” that the child will eventually outgrow without intervention.

Treatments for youth with ARFID are in development; the research is still in its infancy. To date, cognitive-behavioral therapy, FBT, and interoceptive-based exposure approaches have been explored in case series and small clinical trials. Our team is currently comparing FBT for ARFID with a psychoeducational and motivational treatment (PMT) in an adequately powered randomized clinical trial for children 6 to 12 years old (NCT04450771). This study is actively recruiting from a nationwide sample, with data collection underway; if you have patients interested in participating, please send an email to [email protected] .

Key Takeaways and Next Steps

Eating disorders in children and adolescents represent a broad range of symptoms with various medical and psychological sequalae. It is important to act quickly and aggressively to treat these disorders before they become chronic or intractable. In youth particularly, eating disorders may threaten to disrupt windows for growth and opportunities for adolescent development and individuation. While many advances have been made in the past decade in treatment development and implementation, there is definite room for growth. There is an active effort to increase the diversity of youth in study samples to ensure cultural sensitivity and efficacy across diverse populations. We aspire to continue learning, developing, implementing, and disseminating treatment efforts to increase access to care and help treat youth with this dangerous category of illnesses. ■

References for Further Reading

Nandini Datta, Ph.D., Brittany E. Matheson, Ph.D., et al. Evidence Based Update on Psychosocial Treatments for Eating Disorders i3n Children and Adolescents . Journal of Clinical Child & Adolescent Psychology . August 11, 2022.

Daniel Eisenberg, Ph.D., et al. Eating Disorder Symptoms Among College Students: Prevalence, Persistence, Correlates, and Treatment-Seeking . Journal of American College Health . September 27, 2011.

Michelle Goeree, Ph.D., John Ham, Ph.D., Daniela Iorio, Ph.D. Race, Social Class, and Bulimia Nervosa . Working Paper, No. 86, University of Zurich, Department of Economics, Zurich, 2012.

(left to right) Brittany Matheson, Ph.D., Nandini Datta, Ph.D., and James Lock, M.D., Ph.D.

All three authors work in the Department of Psychiatry and Behavioral Sciences at Stanford University School of Medicine.

Brittany Matheson, Ph.D., is a licensed clinical psychologist and faculty scholar.

Nandini Datta, Ph.D., is a postdoctoral fellow on the Eating Disorders Research Team.

James Lock, M.D., Ph.D., is the Eric Rothenberg Professor and senior associate chair of the department and has conducted seminal research on eating disorders for over two decades. He is the editor of Pocket Guide for the Assessment and Treatment of Eating Disorders from APA Publishing from APA Publishing. APA members may purchase the book at a discount.

Open access
Published: 18 June 2024

Overlap of eating disorders and neurodivergence: the role of inhibitory control

Bethany Norton 1 ,
Jade Sheen 1 ,
Lewis Burns 1 ,
Peter G Enticott 1 ,
Matthew Fuller-Tyszkiewicz 1 &
Melissa Kirkovski 1 , 2

BMC Psychiatry volume 24 , Article number: 454 ( 2024 ) Cite this article

Metrics details

Difficulties with inhibitory control have been identified in eating disorders (EDs) and neurodevelopmental disorders (NDs; including attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder), and there appear to be parallels between the expression of these impairments. It is theorised that impairments in inhibitory control within NDs may represent a unique vulnerability for eating disorders (EDs), and this same mechanism may contribute to poorer treatment outcomes. This review seeks to determine the state of the literature concerning the role of inhibitory control in the overlap of EDs and neurodivergence.

A scoping review was conducted to summarise extant research, and to identify gaps in the existing knowledge base. Scopus, Medline, PsycInfo, Embase, and ProQuest were systematically searched. Studies were included if the study measured traits of ADHD or autism, and symptoms of ED, and required participants to complete a performance task measure of inhibitory control. Where studies included a cohort with both an ND and ED, these results had to be reported separately from cohorts with a singular diagnosis. Studies were required to be published in English, within the last 10 years.

No studies explored the relationship between autism and EDs using behavioural measures of inhibitory control. Four studies exploring the relationship between ADHD and EDs using behavioural measures of inhibitory control met selection criteria. These studies showed a multifaceted relationship between these conditions, with differences emerging between domains of inhibitory control. ADHD symptoms predicted poorer performance on measures of response inhibition in a non-clinical sample; this was not replicated in clinical samples, nor was there a significant association with EDs. Both ADHD and ED symptoms are associated with poor performance on attentional control measures; where these diagnoses were combined, performance was worse than for those with a singular diagnosis of ADHD. This was not replicated when compared to those with only ED diagnoses.

Impairments in attentional control may represent a unique vulnerability for the development of an ED and contribute to poor treatment outcomes. Further research is needed to explore the role of inhibitory control in EDs, ADHD and autism, including the use of both self-report and behavioural measures to capture the domains of inhibitory control.

Peer Review reports

Introduction

Neurodivergence and eating disorders: the role of inhibitory control.

Eating disorders (EDs) are complex mental illnesses that typically emerge in childhood and adolescence, although they can impact individuals across the lifespan [ 1 ]. EDs are estimated to impact 2.2% of the population in a given year, with a lifetime prevalence of 11.1% [ 2 , 3 ]. When subthreshold diagnoses are considered, however, these estimates increase to up to 15% of the population affected in any given year [ 4 ]. Among the most prevalent of these disorders are binge-eating disorder (BED), bulimia nervosa (BN), and anorexia nervosa (AN) [ 5 ]. These disorders can be differentiated by their behaviours with food; those with AN utilise primarily restrictive behaviours, whereas BED and BN include episodes of binge eating. Those with BN, and the binge-purge subtype of AN (AN-BP), also engage in purging behaviours [ 6 ].

The outcomes for EDs are poor, and recovery rates vary by disorder. After ten years, up to 70% will still meet criteria for diagnosis, and between 10 and 25% will develop a chronic condition [ 7 , 8 , 9 , 10 ]. Despite a range of evidence-based treatments, these disorders carry one of the highest mortality rates in mental health; it is estimated that, globally, 3.3 million years of healthy life are lost each year due to EDs [ 11 ]. Some of the most significant predictors of treatment outcomes include illness duration, severity, and the presence of comorbid psychiatric difficulties [ 8 , 9 ], including neurodevelopmental disorders (ND; neurodivergence Footnote 1 ).

Two NDs, autism spectrum disorder (ASD; hereafter, ‘autism’) and attention-deficit hyperactivity disorder (ADHD) have been identified as contributing to an increased risk of developing an ED. A study by Karjalainen et al. [ 4 ] examined the presence of EDs and subthreshold ED psychopathology in adults diagnosed with ADHD, autism or both. This study identified that 7.9% of the total participants had a lifetime history of ED. Of the subset who completed ED screening during the study, 8.7% met the ED criteria, and 23.1% exhibited sub-threshold ED psychopathology. The female-to-male ratio of ED diagnosis was 2.5:1. These rates vary substantially from population norms (3–5% prevalence, female-to-male ratio of 10:1) and may suggest an underlying vulnerability in the neurodivergent population that predisposes them to ED pathology [ 4 , 13 ]. As an illustration, a diagnosis of autism is associated with an increased risk for both AN and BED [ 13 ]. Furthermore, a recent review identified that 20% of children diagnosed with ADHD will go on to develop an ED [ 14 ]; although the risk is highest for BN and BED, the risk is also significantly elevated for AN [ 15 ].

Not only are those with NDs at increased risk of developing an ED, they have an increased risk for poor treatment outcomes [ 16 , 17 , 18 , 19 ]. Individuals with autism or ADHD have been identified as having greater ED symptom severity [ 17 , 18 ], reduced treatment efficacy [ 16 , 17 , 20 ], prolonged course of illness, and increased risk of chronicity [ 16 , 17 , 18 ]. These poor outcomes may come, in part, due to delays in identifying EDs within ND cohorts, on account of variations in their presentation [ 4 , 21 ]; however the factors that contribute to underlying vulnerability among ND cohorts may also contribute to these poor outcomes.

This increased prevalence of EDs and poorer outcomes among ND cohorts has prompted research exploring the relationships between specific EDs and traits of autism or ADHD that may contribute to these factors [ 13 , 15 , 19 , 22 , 23 , 24 , 25 , 26 ]. One pathway of interest is the role of executive functions (EF), as several neurocognitive difficulties, including task-switching and inhibitory control, have been identified in both NDs and EDs [ 27 , 28 , 29 , 30 , 31 ].

Executive functions

Executive functions are cognitive processes that facilitate goal-directed behaviours [ 32 ]. Though the understanding of the scope of EFs varies, most researchers include the ability to resist impulses (inhibitory control), plan and initiate tasks, direct attention, retain information (working memory), adapt approach (cognitive flexibility) and regulate emotions [ 32 , 33 ]. While the EFs have distinct functions, there is a commonality between them in the task of managing goals [ 34 ].

Relatedly, EF impairments appear to be a transdiagnostic phenomenon in psychopathology, though the breadth and extent of these impairments vary between disorders [ 35 ]. These impairments may reflect underlying vulnerabilities for psychopathology, and may be reinforced as the various symptoms utilise critical EF resources [ 36 , 37 , 38 ]. Attentional control theory suggests that impairments in one EF reduce the cognitive resources available for other EFs. This reduction of available resource impacts processing efficiency, and, where the cognitive demand is high, impairs performance [ 34 , 36 , 37 , 39 ]. In turn, impaired performance appears to maintain or exacerbate the impairment underpinning psychopathology [ 40 ]. Thus, is possible that within an ND cohort, underlying variations in inhibitory control redirect essential EF resources, increasing susceptibility for the development of EDs.

Importantly, there are strong similarities between the range of EF impairments that underpin both ADHD and autism and EDs [ 30 , 41 , 42 , 43 ]. Research exploring these shared EF impairments has focused on aspects of EF in the relationship between particular NDs and EDs, such as cognitive flexibility within AN and autism [ 44 , 45 , 46 ]. Due to its perceived association with impulsivity, inhibitory control has been identified as a common vulnerability between ADHD and BED, BN, and AN-BP [ 47 , 48 , 49 ]. Although inhibitory control is a common vulnerability between ADHD and these EDs, and an identified impairment within both autism [ 50 , 51 ] and EDs [ 43 , 52 , 53 ], it has not been explored as an overlapping factor between them. These shared inhibitory control difficulties in NDs and EDs will, therefore, be the focus of the present thesis.

Impulsivity and inhibitory control

Although impulsivity is not an EF, it is a trait thought to reflect diminished abilities in inhibitory control [ 54 , 55 ], and measures of impulsivity are frequently used as a part of diagnostic assessments for various psychiatric, psychological, and neurodevelopmental disorders, including ADHD [ 55 , 56 , 57 , 58 , 59 ]. Impulsivity is a construct that includes rapid, unplanned, and inappropriate behaviours [ 55 , 60 , 61 ]. It comprises three subdomains: motor impulsivity, or spontaneous action; non-planning impulsivity, or a focus on the present over the future; and attentional impulsivity, or the inability to sustain attention on a specific stimulus [ 60 , 62 ].

These domains of impulsivity, particularly motor and attentional, are thought to recruit domains of inhibitory control in behavioural action and directing attention [ 54 , 55 ], as shown in Fig. 1 . This has led to neurocognitive measures of inhibitory control frequently being used as a behavioural measure of impulsivity in research [ 48 , 49 , 63 , 64 , 65 ]; however, there is a lack of clear correlation between self-report measures of trait impulsivity and performance on these neurocognitive tasks. Where associations exist, they are strongest in the presence of complex cognitive or emotional stimuli [ 58 , 66 , 67 , 68 ]. Due to the inconsistency of findings in the relationship between impulsivity and inhibitory control, trait impulsivity needs to be distinguished from inhibitory control to clearly understand the relationship between EDs, EFs and NDs.

Domains of impulsivity and inhibitory control

This figure illustrates the multidimensional models of both trait impulsivity and the executive function of inhibitory control. The overlap between the trait impulsivity domains and inhibitory control domains illustrates where trait impulsivity is thought to draw on and reflect abilities within the domains of inhibitory control

Inhibitory control

Inhibitory control is also a multidimensional construct that is implicated in ADHD, autism, and EDs [ 13 , 19 , 23 , 25 , 26 ]. It is comprised of the subdomains of response inhibition and attentional control, as illustrated in Fig. 1 [ 32 , 69 ]; these functions work across cognitive, motor and emotion domains [ 70 ]. Though these subdomains are separate, they are often closely correlated [ 69 ] and work together to facilitate goal-directed behaviour [ 34 , 56 ].

Response inhibition

Response inhibition is the cognitive capacity to withhold an action or suppress a response to an impulse or behavioural response urge [ 56 , 68 ]. When a stimulus triggers an urge to act, response inhibition enables the ability to withhold this action [ 56 ]. Failure of response inhibition is theorised to result in both impulsive and compulsive behaviours [ 56 ]; impulsive behaviours involve acting without a plan, whereas compulsive behaviours arise from an inability to cease the action despite intent [ 56 ].

Attentional control

Attentional control is the cognitive ability to suppress interfering information from distracting stimuli by monitoring for salient cues and suppressing cognitive responses to irrelevant cues [ 56 ]. This process keeps attention focused on task-related information and supports response inhibition by suppressing cognitive responses to irrelevant stimuli that would otherwise trigger a behavioural response urge [ 69 , 71 , 72 ]. Where attentional control is impaired, there is a greater responsiveness to irrelevant stimuli and a subsequent redirection of cognitive resources [ 36 ].

Inhibitory control in NDs and EDs

Inhibitory control impairments have been identified separately in both NDs and EDs [ 28 , 50 , 51 , 73 ]. These impairments include difficulties in attentional control, most notably seen in an attentional bias to emotionally salient stimuli that underpin the restricted interests in autism and AN [ 50 , 74 , 75 ]. Impaired attentional control likely results in a failure to suppress a cognitive response to the salient stimuli; in autism this triggers engagement in restricted special interests and rigid routines. In anorexia, with the overvaluation of shape and weight [ 76 ] this pattern leads to compulsive thoughts and behaviours, similar to the impairment pattern found in those with obsessive-compulsive disorder [ 77 , 78 , 79 ].

Impairments in response inhibition are associated with impulsive behaviours in NDs [ 30 ], and in the EDs, including AN [ 38 , 64 , 66 , 80 , 81 ]. When cognitive responses to salient stimuli are not suppressed, a behavioural urge is triggered. In ND’s this may look like repetitive and/or impulsive motor behaviours, while in EDs this may present as binge-eating and purging behaviours [ 64 , 66 , 81 ]. Aims and Rationale.

There appear to be parallels between the expression of inhibitory control impairments in the EDs and NDs. It is possible that these underlying impairments within NDs may represent a unique vulnerability for EDs, and this same mechanism may contribute to the poorer treatment outcomes within the neurodivergent cohort. Consequently, it is important to explore the dimensions of inhibitory control as a potential vulnerability factor for EDs in a neurodivergent population.

Although several studies have identified inhibitory control impairments in each of these disorders separately, there is very little research exploring inhibitory control as a shared vulnerability between the disorders, leaving a substantive gap in the existing knowledge base. This review seeks to determine the state of the literature concerning the construct of inhibitory control and whether it is implicated in the overlap of EDs and neurodivergence as a shared vulnerability. A systematic scoping review was therefore determined to be the appropriate approach. To explore the breadth of knowledge about inhibitory control in this overlap, this review will include both clinical and non-clinical populations and seeks to answer the questions: What is known about the role of inhibitory control in the relationship between EDs and NDs ? and, a re there differences in inhibitory control performance where EDs and ND overlap, compared to either ND or ED alone?

A scoping review of the literature was conducted following the method outlined by the Preferred Reporting Items for Systematic Reviews and Meta-analysis extension for Scoping Reviews (PRISMA-ScR) [ 82 ]. The PRISMA-ScR checklist is provided in the supplementary material. Scoping reviews are undertaken to determine the state of the literature and identify key knowledge gaps, as well as identifying key themes and areas that may be under-researched [ 82 , 83 , 84 ].

To be included in the review, studies needed to measure symptoms of EDs, and traits of autism and/or ADHD in participants. Studies had to measure inhibitory control utilising a task-based neurocognitive measure, and report errors of omission and/or commission, which reflect difficulties with attentional control and response inhibition, respectively. To ensure a comprehensive review, no restrictions were placed on the age of participants, and both clinical and non-clinical populations were included. Where studies included cohorts with both ND and EDs, results had to distinguish those with both diagnoses from those with a singular diagnosis. Studies had to be published within the last ten years due to the potential impact of technological changes from paper-based instruments to computerised tests. Though both forms have high reliability, the scores between formats do not correlate, possibly due to additional confounds [ 85 ], and thus cannot be easily compared. To ensure a full exploration of the literature, a secondary search was run without date restrictions; however, no additional studies met the inclusion criteria.

The following databases were searched systematically, following PRISMA guidelines: EMBASE, Medline, Scopus, PsycInfo and ProQuest. Because NDs are associated with longer illness duration for EDs, and ED diagnoses can change over time, all ED diagnoses were included in the search. The search query was developed in conjunction with a librarian from Deakin University and included the following keywords: autism, eating disorder, anorexia, bulimia, binge eating, ADHD, impulsivity , and inhibitory control . Full search terms are provided in the Supplementary Material. The search was completed on the 18th of February 2023, and updated on the 23rd of August 2023; references were managed using Covidence ( https://www.covidence.org ).

A systematic process was used to identify the final articles for review. Database search results were loaded into Covidence. After removing duplicates, the author and a second reviewer (LB or MK) completed title and abstract screening and a blind full-text review of the remaining articles. Results were unblinded, and where a consensus could not be made, a meeting was held with JS and MK to decide. Upon completion of full-text screening, reference lists were searched, and a key author search was conducted in Google Scholar, Web of Science and Scopus.

Although scoping reviews do not require a quality assessment of the evidence to appropriately aggregate findings [ 83 ], the quality was assessed utilising the Mixed Methods Appraisal Tool (MMAT) [ 86 ] to strengthen the overall appraisal of the existing subject knowledge. The MMAT is designed to critically appraise methodological quality across mixed study reviews, providing appraisal criteria for each study category: qualitative studies, randomised control trials, non-randomised studies, mixed-method studies and quantitative descriptive studies The MMAT asks whether the study meets the appraisal criteria, with responses including “yes”, “no” and “can’t tell”, to contrast methodological quality between studies [ 86 ]. Studies in this review utilised appraisal criteria from quantitative descriptive studies and non-randomised studies and were assessed on the relevancy of their methods to the research question, the appropriateness of measurements used, and representativeness of the sample to the target population.

Search results

The combined searches yielded 1491 results. After removing duplicates, 979 studies remained to be screened. A title and abstract screen left 96 studies for full-text review. In total, 4 studies met the inclusion criteria for this review, with an inter-rater agreement of 93%, (33.4% specific positive agreement and 98.8% specific negative agreement). The full screening and selection process is outlined in Fig. 2 , and an overview of the included studies and their findings is provided in Table 1 .

Study selection & screening

The PRISMA diagram illustrates the study selection and screening process. It identifies the number of results returned by the search, the process of screening for eligibility, the number of studies excluded, including how many were excluded for each reason. This PRISMA diagram was created with PRISMA2020 [ 128 ]

Study characteristics

All four studies utilised a cross-sectional design [ 42 , 56 , 58 , 73 ]; two of the four included at least one comparison group [ 42 , 56 ], whereas the remaining studies explored the prevalence of traits or strength of association within a single population [ 58 , 73 ].

The quality of the studies was evaluated using the quantitative non-randomised and quantitative descriptive criterion in the MMAT [ 86 ], which assesses a range of methodological factors that can lead to risk of bias. Factors are assessed on a yes (1), no/can’t tell (0) basis. Most studies were of high methodological quality; however, all studies failed to clearly define a target population or outline participant inclusion and exclusion criteria. One study was assessed to have only moderate quality due to a significant amount of missing data and the potential for this to reflect response bias. The full quality analysis is presented in Table 2 .

Participant characteristics

In total, 379 participants were included in these studies, with a reported age of 15 to 35 years, and mean ages between 19 and 23.7 years. The populations were predominantly female, with a BMI in the normal range, reflecting a majority BN population. Three studies utilised clinical samples [ 49 , 63 , 87 ], with two utilising clinical interviews to confirm the diagnoses [ 49 , 63 ].

Neurodevelopmental disorders

No studies measured autistic traits or reported diagnoses of autism; however, all studies measured symptoms of ADHD. Participants were recruited from the general population and university undergraduate programs, while two studies also sought out participants with a diagnosis of ADHD [ 87 ] or an ED [ 49 ] by recruiting via support groups and treatment programs. Where participants had a diagnosis of ADHD or ED, this was confirmed via clinical assessment in three studies [ 49 , 63 , 87 ], with one study also requiring participants with ADHD to report the age they were diagnosed by a professional [ 87 ]. The remaining study explored the presence of ADHD symptoms but did not report formal diagnoses [ 65 ].

Where diagnoses were confirmed, one study included participants that used stimulant medication, the effects of which were controlled for in analyses [ 87 ], whereas participants in the other two studies were not medicated at the time of the study [ 49 , 63 ]. The study by Seitz et al. [ 49 ] reported the prevalence of lifetime stimulant use in all participants; no significant differences existed between those with and without ADHD.

All studies utilised self-report measures to assess the presence and severity of current ADHD symptoms, using total scores in their analysis. Utilising the Connors’ Adult ADHD Rating Scale Self-Report Screening Version (CAARS-S: SV) subscales for hyperactivity/impulsivity and inattentive symptoms, one study also explored whether there were specific relationships between each of these core ADHD symptoms and patterns of restrictive or binge-eating [ 87 ].

Eating disorders

The presence of eating disorder psychopathology was established using self-report measures in all four studies, with the range of measures outlined in Table 1 . Two studies also conducted clinical interviews to further assess ED symptoms and severity [ 49 , 63 ]. All four studies measured binge-eating symptoms, predominantly utilising the Binge Eating Scale (BES), while two also measured restrictive eating behaviours [ 49 , 87 ]. Only one of studies reported findings related to restrictive eating behaviours [ 87 ].

Role of inhibitory control

All studies used neurocognitive measures of inhibitory control as a behavioural measure of impulsivity. Studies sought to explore the relationship between ADHD symptoms of impulsivity and disordered eating behaviours, with two focusing on mediation effects [ 65 , 87 ] and two exploring whether there are cumulative effects of impulsivity in a comorbid ADHD and ED presentation [ 49 , 63 ].

Studies utilised a variety of neurocognitive measures, including the go/no-go task [ 49 , 65 , 87 ], the TAP incompatibility task [ 49 ], and the Connors continuous performance task (CCPT-2) [ 63 ]. Psychometric properties of these tests in the current studies were not reported, however other studies utilising the CCPT-2 have reported a Cronbach’s alpha ranging from 0.85 to 0.96 across omission errors, commission errors and response times [ 88 ]. An analysis of go/no-go tests have shown Cronbach’s alpha of greater than 0.45 [ 89 ].

Three studies reported data for commission errors on the go/no-go task [ 63 , 65 , 87 ]. Two studies utilising clinical samples found no significant associations between ADHD and performance on the go/no-go task [ 63 , 87 ]. Where those with ADHD were not taking stimulant medication, no significant differences were found between those with ADHD, ADHD and an ED, and healthy controls in response inhibition measures [ 63 ]. However, in the non-clinical sample, symptoms of ADHD predicted errors of commission on the go/no-go task. ADHD symptoms predicted errors of commission, however when they were controlled for, errors of commission did not predict binge-eating symptoms [ 65 ].

Two studies explored the relationships between diagnosed ADHD, EDs and attentional control. They found the presence of an ED was associated with more omission errors on the tasks [ 49 , 63 ]. There were no significant differences between those with ADHD and healthy controls, and there were no significant differences for those with ADHD and BN compared to those with BN alone [ 49 ].

Trait impulsivity

All studies utilised self-report measures of trait impulsivity, the Barratt Impulsivity Scale (BIS) [ 49 , 63 , 65 , 87 ], with a Cronbach’s alpha of 0.85 Symptoms of ADHD and symptoms of EDs were associated with higher scores on these measures. The presence of ADHD was associated with higher scores on the Barratt Impulsivity Scale (BIS); there was no significant difference in scores between those with ADHD and those with comorbid ADHD and ED [ 63 ]. Scores were significantly higher for those with ADHD and ED than those with ED alone [ 49 ]. When looking at the mediation effect of impulsivity on the relationship between ADHD and ED, impulsivity mediated the relationship in a clinical sample [ 87 ] but not in a non-clinical sample [ 65 ].

Impairments in EFs may represent a unique vulnerability for developing an ED among the ND population, with a range of inhibitory control difficulties present in EDs and NDs. This study sought to clarify what is known about inhibitory control in the overlap of EDs and NDs, with findings suggesting a multifaceted relationship. Key differences emerged between the domains of inhibitory control, with the most consistent impairments found in the attentional control domain. Although the existing research is quite limited, the mixed findings may attentional control theory; although impairments may exist, performance impairments may only emerge in the presence of high cognitive demand [ 34 , 36 , 37 , 39 ].

Response inhibition has been frequently utilised in the literature, and in this review, as a behavioural measure of impulsivity [ 49 , 54 , 63 , 64 , 65 , 87 ], which is a key diagnostic criterion of ADHD [ 90 ]. Errors of commission reflect an inability to withhold a primed response, reflecting response inhibition impairments [ 91 ], yet the association between trait impulsivity and errors of commission were not significant in either the clinical or non-clinical samples [ 63 , 65 , 87 ]. It is possible that, the effect of medication for ADHD could reduce impairments in response inhibition among clinical samples [ 92 ]. Medication status was not reported in all studies [ 49 , 87 ]; however, in a study with participants who were not medicated, there was still no association between impulsivity and response inhibition [ 63 ]. This may suggest that trait impulsivity and inhibitory control are related, yet distinct constructs [ 35 , 58 , 93 ], with other aspects of neurocognitive function implicated in the impulsive symptoms of ADHD, such as impairments in reward signalling [ 56 ].

No significant relationships were found between response inhibition and binge-eating symptoms [ 65 , 87 ] despite binge-eating having a strong association with trait impulsivity in a clinical sample [ 49 , 87 ]. These findings contrast with the literature showing an association between response inhibition and binge-eating behaviours in those with a clinical ED [ 64 , 81 ]. Although Kaisari et al. [ 87 ] utilised a clinical sample, this was for an ADHD population. The association trended positive but did not reach significance, which could be due to lower ED symptom severity levels, which were not reported. The association between ADHD symptoms and response inhibition also trended positive, however, did not reach significance. This may reflect the low cognitive demand of the task, as individuals with ADHD often perform similarly to typically developing individuals when demand is low [ 94 ].

Other studies have found that the ability to detect these impairments emerges in the presence of salient stimuli [ 52 , 53 ]. In the current review, only one study used a salient stimulus, the food paradigm on the go/no-go task, to see whether this mediated the relationship between ADHD and disordered eating. Because no association was found with ADHD symptoms, no further analysis was conducted; therefore, the impact of salience on inhibitory control performance is unknown [ 87 ]. Future research should explore the relevance of salient stimuli on inhibitory control performance in the relationship between ADHD and disordered eating.

It is also possible that the impairments in response inhibition in ADHD and EDs are similar, but there is no cumulative effect when these disorders co-exist. In a review by Steadman and Knouse [ 65 ], which used a non-clinical sample, although ADHD symptoms and response inhibition were correlated, there was no further predictive utility for binge-eating symptoms. Equally, in a clinical sample, performance on measures of response inhibition was not able to be differentiated between those with BN and those with comorbid ADHD and BN [ 49 ], which may also suggest that the impairments in response inhibition are not cumulative. In both these examples, it is possible that the impairments that occur within ADHD leave individuals more vulnerable to developing an ED, but are not further exacerbated by the ED.

Impairments in attentional control were significant in both individuals with ADHD and individuals with EDs [ 49 , 63 ]. Poor attentional control has been linked to the inattentive symptoms of ADHD [ 95 ] as well as compulsive behaviours, due to the inability to direct attention away from these urges [ 77 , 78 , 79 ]. These findings are also consistent for those with EDs, with recent research suggesting that the compulsive symptoms of binge-eating may reflect the inattentive symptoms of ADHD more than the impulsive symptoms [ 80 , 96 , 97 , 98 , 99 ]. Similarly, Seitz et al. [ 49 ] found that inattentive symptoms of ADHD explained more variance in ED symptoms than hyperactivity or impulsivity within an ADHD and BN sample. These findings could suggest that impaired attentional control is an underlying vulnerability factor for developing an ED among those with ADHD [ 100 ]. This is consistent with findings in a longitudinal study, which identified that the combination of higher inattentive and hyperactive/impulsivity symptoms of ADHD in childhood increased the susceptibility to disordered eating in adolescence [ 101 ].

Individuals with ADHD and ED also performed worse on measures of attentional control than those with ADHD alone [ 63 ], which may suggest the impairments have a cumulative effect. This potential cumulative effect was not found when comparing those with ADHD and ED to those with an ED alone; however, participants with ADHD and ED had more severe ED symptoms [ 49 ]. It is possible that, for those with ADHD, impaired attentional control may enhance the attentional bias towards weight and shape that is commonly found in EDs [ 76 ], contributing to their severity [ 25 , 97 ].

Secondary findings

Two additional studies that emerged in the literature did not report results in a way that distinguished those with an ED from those with comorbid ED and ND. Consequently, they could not be included in the formal review findings, yet they highlight key relationships between these conditions, which are noted here.

The first study explored the impact of disordered eating (orthorexia nervosa; ON) on EFs and included participants diagnosed with autism or ADHD. This group made up 12% of the total participants, and 33% of those with ON [ 102 ], reflecting a greater prevalence of NDs among those with disordered eating. This study utilised a validated self-report measure of EFs and found a moderate association between ON symptoms and impairments in inhibition after accounting for demographic variables, including a diagnosis of autism or ADHD. As an association was found after controlling for this variable, the impairments might be associated with ON symptoms in addition to NDs; however, the results were not reported in a way to determine the nature of this relationship.

The second study examined the relationship between ADHD, higher-weight status (HWS), and binge-eating, exploring whether those with HWS and ADHD shared common neuropsychological vulnerabilities and whether those were heightened in those with binge-eating [ 103 ]. This study found that among individuals with HWS, those with binge-eating performed worse on a measure of response inhibition than those without binge-eating [ 103 ]. When controlling for inattentive symptoms of ADHD, these differences became non-significant [ 103 ]. Because both groups included a typically developing population and those with ADHD, and prevalence rates were not reported, the relationship between ADHD, response inhibition, and binge-eating is unclear.

Methodological limitations in the present literature

The research exploring inhibitory control in the overlap of EDs and NDs has a few significant methodological limitations. Firstly, this research base is limited; studies exploring inhibitory control in EDs often exclude participants with a co-existing ND [ 104 , 105 ] rather than controlling for these traits. Where studies include participants with both diagnoses, results were not reported comparing those with an ED to those with both an ND and ED, as described above [ 102 , 103 ].

A second limitation is the use of inhibitory control tasks as a behavioural measure of impulsivity. Much of the existing research on inhibitory control in EDs and NDs has focused on trait impulsivity rather than the neurocognitive domain. Inhibitory control impairments are also often linked to trait impulsivity in the EDs [ 30 ], despite a lack of clear association between these constructs [ 35 ].

The relationship between self-report measures of trait impulsivity and performance on neurocognitive tasks measuring inhibitory control has been explored substantially in the literature, with several studies indicating that, although related, these are separate constructs and self-report measures do not correlate to behavioural tasks [ 106 , 107 , 108 ]. In this review, no association was found between self-report measures of impulsivity and the behavioural measures of inhibitory control [ 49 , 63 , 65 , 87 ]. It is likely that while self-report measures of impulsivity may reflect difficulties with inhibitory control, they are not exclusively measuring this EF, but rather a broader construct that includes reward mechanisms and affect [ 54 , 68 , 108 ]. This reflects findings from a previous systematic review which identified that the cognitive factor of impulsivity includes reward-driven behaviour in addition to inhibitory control. This study encouraged the exploration of both of these mechanisms to increase understanding of the underlying processes in the relationship between ADHD and disordered eating [ 48 ]. As impairments in inhibitory control may represent unique vulnerabilities within an ND population, it is important to utilise neurocognitive measures of inhibitory control to better understand the relationship between NDs, EF and EDs.

A final limitation of these studies was that the majority focused on a singular domain of inhibitory control, whereas there are a few related but distinct domains [ 34 , 108 , 109 ]. The go/no-go task is designed primarily to measure response inhibition [ 110 ]. Errors of omission can provide some information about attentional control; however, a task of congruent and incongruent information, such as the Stroop Colour Word Test (SCWT) [ 111 ], is designed to measure both domains, giving greater insight into variable abilities in attentional control. Future research ought to utilise a range of performance-based measures, with both neutral and salient cues, including the antisaccade task, stop-signal task, Flanker task and cued recall [ 112 ], to develop a more robust understanding of the relationship between the various domains of inhibitory control and symptoms of EDs and NDs.

Although this review attempted to capture the breadth of the existing knowledge on this topic, its approach inevitably has limitations. Whereas restricting the studies to those that utilised a behavioural task measure of inhibitory control would have strengthened the distinction between this construct and trait impulsivity, excluding self-report measures may have excluded some relevant contributions to the topic as they reflect a subjective view of one’s behaviour [ 54 ]. Limiting the initial search to studies published within the last ten years may also have excluded some relevant papers; however, changes in the administration of neurocognitive tasks, and to diagnostic criteria for ADHD, autism and EDs in the DSM-5 would have limited the comparability of earlier studies. Additionally, the reference list and key author search results attempted to account for this by including studies published at any time, and no earlier studies were identified.

Directions for future research

A significant knowledge gap exists in understanding the broader relationship between EDs and NDs. Notably, there is a substantial clinical overlap between autism and ADHD, with both contributing to an increased risk of developing an ED. Though some individual studies have identified inhibitory control impairments in specific EDs and NDs, as documented in this review, there has been limited exploration of the relationship between these two families of disorders. Inhibitory control impairments may contribute to the relationship between the two families of disorders [ 113 ], but no study has explored this to date.

Autism is associated with impairments in inhibitory control [ 50 , 51 , 114 ] and increased risk of EDs [ 13 ], yet no study in this review included an autistic cohort, leaving a substantial gap in knowledge of factors that could contribute to development and severity of ED symptoms. Studies focusing on autism have identified that greater symptom severity is associated with poorer inhibitory control [ 115 ], and females appear to show poorer response inhibition than their male counterparts [ 116 ]. Although a strong association exists between autism and AN [ 23 ] and EDs are diagnosed more frequently in females, the potential common vulnerability of inhibitory control has not been explored in this population. Future research should explore the role of inhibitory control in the relationship between autism and EDs, differentiating between impulsivity and inhibitory control by using self-report measures and a range of neurocognitive tasks to capture the full breadth of inhibitory control abilities.

The reviews in this study also focused predominantly on the relationship between ADHD and binge-eating symptoms, yet a diagnosis of ADHD is associated with an increased risk of all EDs, including those with AN [ 14 , 15 ]. Research indicates that inhibitory control impairments may be present in AN as well [ 80 , 96 , 117 ], yet very few studies explore the relationship between inhibitory control, ADHD, and anorexia, as evidenced in this review. Here future research ought to explore inhibitory control within the relationship between ADHD and each of the EDs, ensuring the use of neurocognitive tasks that will capture both domains of inhibitory control. As symptoms of impulsivity and inattention are key diagnostic criteria for ADHD [ 90 ], the use of self-report measures of trait impulsivity alongside the neurocognitive tasks may help distinguish between trait impulsivity and EF impairments in the relationship between ADHD and EDs.

To further the understanding of the role of inhibitory control in the relationship between NDs and EDs, future research should recruit participants with NDs, EDs, and those with both an ND and ED. Data collection should include the use of stimulant and psychotropic medications as well as other substance use, to control for these effects. It is also important that studies use a wide range of inhibitory control neurocognitive tasks to capture all the domains of inhibitory control. The use of validated self-report measures may add ecological utility and enhance findings by providing insight into ‘real world’ impact [ 35 ].

Clinical implications

Amongst ED cohorts, those with a co-morbid ND have been identified as having an increased risk for poorer treatment outcomes [ 16 , 17 , 18 , 19 ]. For those with an ED, a co-existing diagnosis of ADHD or autism is associated with greater symptom severity, reduced treatment efficacy, and prolonged illness [ 16 , 17 , 18 ]. Considering the heightened mortality risk and poor prognosis for those with EDs, it is important to identify and understand the unique vulnerabilities within the neurodivergent cohort to improve their treatment outcomes.

Impaired inhibitory control is a component of NDs, and this mechanism may pose a unique vulnerability for the development of an ED and contribute to its treatment resistance. Because an overvaluation of weight and shape characterises EDs, cognitive responses to stimuli associated with these factors may prove more challenging to inhibit due to their congruent, goal-oriented nature. Failure to inhibit these cognitive responses may result in attention being directed towards the stimuli and triggering the impulse for behavioural response. This, in turn, may contribute to the ongoing maintenance of the disorder by reinforcing maladaptive cognitions and impairing behaviour-change processes [ 81 , 118 , 119 ].

Improved understanding of these neurocognitive processes may lead to more targeted interventions [ 120 , 121 , 122 , 123 , 124 ]. Mindfulness based interventions have been associated with small improvements in inhibitory control accuracy, resulting in less mind wandering [ 124 ]. Global EF improvements have also been found in AN and autism after undergoing cognitive remediation therapy, which may improve treatment responsiveness [ 120 , 121 , 122 , 123 ]. Other brief EF training interventions have also shown promise in improving EFs and self-regulation in those with severe mental illness [ 121 , 125 , 126 ].

Greater understanding of the association between neurocognitive processes and symptoms may also result in interventions tailored to more salient stimuli, which may increase the ecological efficacy of treatment. A recent proof-of-concept trial utilised virtual reality training based on the go/no-go paradigm to target response inhibition in disorders with binge-eating. Though this pilot trial was small, there was a significant reduction in loss-of-control of eating and a small reduction in impulsivity among the participants during the treatment and follow-up period [ 108 ]. An improved understanding of the underlying neurocognitive processes may lead to other, similar targeted interventions and improve treatment outcomes [ 120 ].

The role of inhibitory control in the overlap of EDs and NDs is an area that is currently under-researched. Existing research suggests that this may be implicated in the overlap of ADHD and disordered eating, particularly through the subdomain of attentional control. Future research should expand the knowledge base by including individuals with autism, exploring both domains of inhibitory control, and continuing to differentiate between the constructs of impulsivity and inhibitory control.

Data availability

All data generated or analysed during this study are included in this published article.

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BN conceptualised and designed the project, completed data collection and analysis, interpreted the results, and prepared the manuscript. JS and MK contributed to the conceptualisation and study design, data collection and analysis, and interpretation of results. LB contributed to data collection and analysis. PGE and MFT contributed to the study design and interpretation of results. All authors contributed to and approved the final manuscript.

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Norton, B., Sheen, J., Burns, L. et al. Overlap of eating disorders and neurodivergence: the role of inhibitory control. BMC Psychiatry 24 , 454 (2024). https://doi.org/10.1186/s12888-024-05837-6

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Eating Disorders

Ethical Considerations for Patients With Eating Disorders

What are the benefits and drawbacks of in-person or virtual relationships.

Posted May 31, 2024 | Reviewed by Tyler Woods

What Are Eating Disorders?
Find counselling to heal from an eating disorder

From the mid-1990s until 2014, I founded and was the Executive Director of Cedar Associates, an outpatient treatment center for eating disorders with two locations in Westchester County, New York. We were a group of qualified eating disorder specialists joined together for a common cause—to provide coordinated and expert care to our patients.

One ethical issue we pondered was whether or not we had created a cottage industry for those most vulnerable. We wondered if we were somehow taking advantage of those in need as we were part of the new 'niche' industry created by the rapid increase in the prevalence of eating disorders. There was now a steady influx of patients in desperate need of help. Having an eating disorder is terrifying, debilitating, and costly for patients and their families. Eating disorders remain the leading cause of death among all mental health conditions.

Our dilemma was about money. We simultaneously believed that we were entitled to a solid living wage and that patients were entitled to solid and expert care; both could be true and acceptable. Most healthcare practitioners struggle with healthcare services' delivery, costs, and payment. These ethical issues remain unresolved due to the politicization of healthcare, the complexity of insurance, and other factors. However, clinicians have always been able to assert their training, competency, and expertise in providing treatment unequivocally; these bona files remain ethically foundational.

We now have a choice of mental health care delivery, which has created new ethical considerations. COVID-19 set precedence for conducting sensitive meetings virtually, especially in health care. Whether to see a patient in-person or virtually is now part of the clinical decision-making mix. Deciding whether or when to treat in person versus virtually takes a mindful and clinically astute clinician.

Some factors to consider when deciding between in-person and virtual meetings:

Establishing a prudent care plan involves routinely choosing the type of treatment based on the patient's clinical needs. Eating disorders, like others with complex symptoms, occur among the most psychologically vulnerable people. Assessing the level of severity can be very difficult. Keep in mind all the factors that help in assessment: type, frequency, and use of the symptom are all important, as well as assessing the level of depression , how isolated the person is, the family dynamics, and the level of support the person has in the recovery process.

Since eating disorders manifest in many and with various constellations of symptoms, it isn't always easy to tell by looking at someone what state they are in. Patients can conceal their bodies through layered clothing and hide the truth about their behavior due to shame , anger , and fear .

Eating disorders are also disorders of relationships—the ones we have with our self-concept and our relationships with others. (Zerbe, 2008, Scheel, 2011). Is the clinician confident that a relationship that fosters support, safety, and appropriate boundaries is possible virtually? Is the clinician comfortable not experiencing the most nuanced communication during online sessions? Since eating disorders are the vehicle for communication about relationships, internal conflicts, and lability in mood, does seeing a person virtually contribute to further relational disconnect? Is a real relationship possible virtually?
Eating disorder clinicians often must face working with families in despair, who would never have consented to the treatment had it not been for their child, adolescent, or adult child in physical distress. The family member with the eating disorder is often the family symptom-bearer. Family members can blame and attack those who are most trying to help; they can sometimes bully school officials and therapists and can resist recommendations or, worse, manipulate or lie about therapeutic interventions to save their reputations. Is the clinician prepared to coordinate care among various professionals while being able to reduce or eliminate divisiveness among family members and other involved professionals? It can be enormously complex for family members to accept the psychological underpinnings of the eating disorder and the metaphoric use of the symptom to talk about family dynamics and issues. Will virtual sessions impede this process of discovery?

In the past, clinicians relied solely on their transparency to patients about their training in treating eating disorders. Although this remains true today, there is a certification process and credentials for clinicians to treat eating disorders, further qualifying competency and commitment to ethical treatment standards (IAEDP). Certified eating disorder specialists (CEDSs) now provide the care, and most clinicians incur additional costs in ongoing training, supervision, and personal therapy.

We need competent and expert therapists. More therapists are receiving advanced training; however, training in evidence-based treatment alone cannot allow someone to understand the complexities of a severe condition. Trauma , major depression, debilitating anxiety , borderline personality disorder, and a high degree of family dysfunction surround and underlie the development of an eating disorder. Do virtual appointments add another layer to an oversimplification of the needs of this population?

Skills in here-and-now approaches like cognitive behavioral therapy, acceptance and commitment therapy, short-term interpersonal therapies, mindfulness , and motivational approaches are insufficient in treating eating disorders. Therapists require additional training in understanding human motivation , even the use of the eating disorder as a symbol and metaphor. Are virtual appointments ethically consistent with providing a holistic treatment protocol for a patient with an eating disorder? (Freeman, 2007)

Telehealth contributions and considerations:

Telehealth has allowed vast populations to have access to mental health treatment, sometimes for the first time. Medically and psychologically home-bound people, rural communities with difficult access to larger towns, adult family members who cannot easily drive their child to treatment, and many others praise telehealth's ability to service specific populations and meet the demands of more and more people considering psychotherapy for the very first time.

Is some form of therapy, like telehealth, better than no therapy? Absolutely, but with the caveat that these treatments are best suited for those who are not suffering from major depressive conditions, significant anxiety, personality disorders masquerading as 'merely' relationship issues, or those with severe symptoms like an eating disorder. Often, patients with minor anxiety do very well in teletherapy because of the protective veil of physical distance and how the camera orients eye contact.
Mental health issues confront one in every five Americans (CDC). Adding a layer of disconnect via telehealth requires prudent decision-making to proceed, especially when the therapist is new to the field of eating disorders, or new to the field of treating mental health conditions.
Serious assessment and consideration are required to determine which patients may be most suited to benefit from telehealth and those for whom it poses risks.

We are in an age of disconnect from human contact, with artificial intelligence , virtual meetings, and connections based and maintained on social media . If only we could extract our humanity from being human, we might be in better mental health living in a virtual world.

CDC.gov. Center for Disease Control: mental health statistics (2024).

Freeman, C. & Power, M. Handbook of Evidence-Based Psychotherapies: A guide for research and practice. 1st edition. Wiley. (2007).

Greenson, R. The technique and practice of psychoanalysis: Volume 1. England: Routledge Press. (1967).

iaedp.com. International association of eating disorders. certified eating disorder specialist overview. (2024)

Scheel, J. When Food is Family: A loving approach to heal eating disorders. Washington: Idyll Arbor Inc. (2011).

Zerbe, K. Integrated Treatment of Eating Disorders: Beyond the Body Betrayed. New York: W.W. Norton & Co. (2008)

Judy Scheel, Ph.D., L.C.S.W. , is the author of When Food Is Family , and is the founder and Executive Director of the Cedar Associates Foundation.

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J Eat Disord

Risk factors for eating disorders: findings from a rapid review

Sarah barakat.

1 InsideOut Institute for Eating Disorders, University of Sydney, Sydney Local Health District, Sydney, Australia

4 Faculty of Medicine and Health, Charles Perkins Centre (D17), InsideOut Institute, University of Sydney, Level 2, Sydney, NSW 2006 Australia

Siân A. McLean

2 School of Psychology and Public Health, La Trobe University, Melbourne, Australia

Emma Bryant

3 Healthcare Management Advisors, Melbourne, Australia

Stephen Touyz

Sarah maguire, associated data.

Not applicable—all citations provided.

Risk factors represent a range of complex variables associated with the onset, development, and course of eating disorders. Understanding these risk factors is vital for the refinement of aetiological models, which may inform the development of targeted, evidence-based prevention, early intervention, and treatment programs. This Rapid Review aimed to identify and summarise research studies conducted within the last 12 years, focusing on risk factors associated with eating disorders.

The current review forms part of a series of Rapid Reviews to be published in a special issue in the Journal of Eating Disorders, funded by the Australian Government to inform the development of the National Eating Disorder Research and Translation Strategy 2021–2031. Three databases were searched for studies published between 2009 and 2021, published in English, and comprising high-level evidence studies (meta-analyses, systematic reviews, moderately sized randomised controlled studies, moderately sized controlled-cohort studies, or population studies). Data pertaining to risk factors for eating disorders were synthesised and outlined in the current paper.

A total of 284 studies were included. The findings were divided into nine main categories: (1) genetics, (2) gastrointestinal microbiota and autoimmune reactions, (3) childhood and early adolescent exposures, (4) personality traits and comorbid mental health conditions, (5) gender, (6) socio-economic status, (7) ethnic minority, (8) body image and social influence, and (9) elite sports. A substantial amount of research exists supporting the role of inherited genetic risk in the development of eating disorders, with biological risk factors, such as the role of gut microbiota in dysregulation of appetite, an area of emerging evidence. Abuse, trauma and childhood obesity are strongly linked to eating disorders, however less conclusive evidence exists regarding developmental factors such as role of in-utero exposure to hormones. Comorbidities between eating disorders and mental health disorders, including personality and mood disorders, have been found to increase the severity of eating disorder symptomatology. Higher education attainment, body image-related factors, and use of appearance-focused social media are also associated with increased risk of eating disorder symptoms.

Eating disorders are associated with multiple risk factors. An extensive amount of research has been conducted in the field; however, further studies are required to assess the causal nature of the risk factors identified in the current review. This will assist in understanding the sequelae of eating disorder development and in turn allow for enhancement of existing interventions and ultimately improved outcomes for individuals.

Supplementary Information

The online version contains supplementary material available at 10.1186/s40337-022-00717-4.

Plain English summary

Research into the risk factors associated with eating disorders (EDs) is necessary in order to better understand the reasons why people develop EDs and to inform programs which aim to reduce these risk factors. In the current study we reviewed studies published between 2009 and 2021 which had researched risk factors associated with EDs. This study is one review of a wider Rapid Review series conducted as part the development of Australia’s National Eating Disorders Research and Translation Strategy 2021–2031. The findings from this review are grouped into nine main risk factor categories. These include (1) genetics, (2) gastrointestinal microbiota and autoimmune reactions, (3) childhood and early adolescent exposures, (4) personality traits and comorbid mental health conditions, (5) gender, (6) socio-economic status, (7) ethnic minority, (8) body image and social influence, and (9) elite sports. Further research is needed to better understand the relationship between the risk factors, in particular the ways in which they may interact with each other and whether they cause the ED or are just associated with the ED.

Introduction

Eating disorders (ED) are complex psychiatric conditions associated with significant psychological and physical impairment. Individuals with EDs are at greater risk of suicide attempts, mortality, and poorer quality of life relative to both the general population and individuals with other psychiatric conditions [ 1 – 3 ]. Central to addressing the pervasive nature of EDs is understanding the circumstances which make individuals more vulnerable to developing these psychiatric conditions. The development of an ED is dependent on a myriad of variables ranging from sociocultural, to biological and genetic, and psychological factors. Despite the variation and complexity present in the aetiology of EDs, efforts have been made by researchers to identify risk factors which commonly predict onset [ 4 – 6 ]. Understanding the range of risk factors and their potential contribution to onset of an ED is crucial to identifying at risk groups and providing effective screening and prevention programs, as well as targeted interventions [ 7 , 8 ].

EDs can be severe and are often chronic in nature, particularly if not addressed in a timely manner. A recent study of ED patients identified an average delay of 5.28 years between ED symptom onset and treatment-seeking [ 9 ]. A factor considered to contribute to this delay is health professionals’ lack of awareness of indicators of disordered eating behaviours, meaning EDs often go unrecognised by treating clinicians [ 10 ]. Identification of risk factors for EDs offers an opportunity for targeted education of health professionals to assist in distinguishing patterns of psychosocial, biological, and genetic vulnerabilities for disordered eating even in the absence of any overt weight or dietary concerns [ 11 ].

Knowledge of the risk factors for EDs offers the opportunity for early identification of high-risk groups and in turn a timely and tailored response via avenues such as public policy development or initiation of targeted prevention programs [ 12 ]. Prevention and early intervention programs based upon aetiological models may help to prevent movement along the spectrum from at-risk to full threshold disorder [ 13 ]. Additionally, EDs are complex psychiatric conditions with a somewhat limited range of efficacious evidence-based interventions [ 14 , 15 ]. In addition, a significant number of patients with EDs do not respond to current evidence-based treatments [ 16 – 20 ]. As such, attempts to better understand the role of risk factors in aetiological and causal pathways of EDs are necessary in order to form more nuanced conceptualisations of these illnesses. This may inform the development of more effective treatments, especially for those with persistent and chronic course [ 21 ].

The current Rapid Review paper forms part of a series of reviews commissioned by the Australian Federal Government to inform the Australian National Eating Disorders Research and Translation Strategy 2021–2031[ 22 ]. This paper aims to identify and explore the risk factors associated with EDs by summarising the existing evidence related to aetiological underpinnings. Importantly, the review is inclusive of research which considers risk factors to be either causal in nature or associated with the onset of ED.

The Australian Government Commonwealth Department of Health funded the InsideOut Institute for Eating Disorders (IOI) to develop the Australian Eating Disorders Research and Translation Strategy 2021–2031 [ 1 ] under the Psych Services for Hard to Reach Groups initiative (ID 4-8MSSLE). The strategy was developed in partnership with state and national stakeholders including clinicians, service providers, researchers, and experts by lived experience (including consumers and families/carers). Developed through a two-year national consultation and collaboration process, the strategy provides the roadmap to establishing EDs as a national research priority and is the first disorder-specific strategy to be developed in consultation with the National Mental Health Commission. To inform the strategy, IOI commissioned Healthcare Management Advisors (HMA) to conduct a series of RRs to broadly assess all available peer-reviewed literature on the six DSM-5 listed EDs.

A RR Protocol [ 23 ] was utilised to swiftly synthesise evidence in order to guide public policy and decision-making [ 24 ]. This approach has been adopted by several leading health organisations including the World Health Organisation [ 25 ] and the Canadian Agency for Drugs and Technologies in Health Rapid Response Service [ 26 ], to build a strong evidence base in a timely and accelerated manner, without compromising quality. A RR is not designed to be as comprehensive as a systematic review – it is purposive rather than exhaustive and provides actionable evidence to guide health policy [ 27 ].

The RR is a narrative synthesis and sought to adhere to the PRISMA guidelines [ 28 ]. It is divided by topic area and presented as a series of papers. Three research databases were searched: ScienceDirect, PubMed and Ovid/Medline. To establish a broad understanding of the progress made in the field of EDs, and to capture the largest evidence base from the past 12 years (originally 2009–2019, but expanded to include the preceding two years), the eligibility criteria for included studies into the rapid review were kept broad. Therefore, included studies were published between 2009 and 2021, in English, and conducted within Western healthcare systems or health systems comparable to Australia in terms of structure and resourcing. The initial search and review process was conducted by three reviewers between 5 December 2019 and 16 January 2020. The re-run for the years 2020–2021 was conducted by two reviewers at the end of May 2021.

The RR had a translational research focus with the objective of identifying evidence relevant to developing optimal care pathways. Searches therefore used a Population, Exposure, Outcome (PEO) approach [ 29 ] whereby search terms are specified to identify literature relating to the population or group of interest (i.e., individuals of any age or background with the propensity to develop and eating disorder), exposure to the risk factors that are associated with the development of an eating disorder, and the outcome of interest (i.e., the development of an eating disorder). By using the three PEO components to guide the search strategy, the PEO approach aims to facilitate a thorough and systematic examination of existing literature. Purposive sampling focused on high-level evidence studies such as: meta-analyses; systematic reviews; moderately sized randomised controlled studies (RCTs) ( n > 50); moderately sized controlled-cohort studies ( n > 50), or population studies ( n > 500). However, the diagnoses ARFID and UFED necessitated a less stringent eligibility criterion due to a paucity of published articles. As these diagnoses are newly captured in the DSM-5 (released in 2013, within the allocated search timeframe), the evidence base is emerging and fewer studies have been conducted. Thus, smaller studies (n = < 20) and narrative reviews were also considered and included. Grey literature, such as clinical or practice guidelines, protocol papers (without results) and Masters’ theses or dissertations, was excluded. Other sources (which may not be replicable when applying the current methodology) included the personal libraries of authors, yielding four additional studies (see Additional File 1 ). This extra step was conducted in line with the PRISMA-S: an extension to the PRISMA Statement for Reporting Literature Searches in Systematic Reviews [ 30 ].

Full methodological details including eligibility criteria, search strategy and terms and data analysis are published in a separate protocol paper [ 31 ]. The full RR included a total of 1320 studies (see Additional File 1 for PRISMA flow diagram). Data from included studies relating to risk factors for EDs were synthesised and are presented in the current review.

The Rapid Review identified 284 studies for inclusion in the ‘Risk Factors’ category. When referring to ‘risk factors’ in this review, we are not always referring to causal risk factors. Accordingly, some of the risk factors included in this review are correlated or associated with increased risk of an ED, without evidence of causation. As the aim of a Rapid Review is to broadly synthesise findings, we did not narrow to studies only providing evidence regarding the causal relationship of risk factors. Rather, the current review focused on a range of research including prospective, experimental and correlational studies to identify a large number of potential correlates which have risk capacity for EDs. According to the Kraemer et al. (2001) criteria, this review covers research related to the following technical terms: “correlate” (a measure associated with the outcome), “risk factor” (a measure which precedes the outcome), and “causal risk factor” (a risk factor, which when manipulated, causes a change in the outcome) [ 32 ]. Therefore, the factors identified in this review are associated or predictive factors, unless in cases where a causative link has been demonstrated. A summary of the key risk factors associated with EDs is provided in Table Table1 1 and are discussed in this section. Results are subdivided into nine categories: (1) genetics, (2) gastrointestinal microbiota and autoimmune reactions, (3) childhood and early adolescent exposures, (4) personality traits and comorbid mental health conditions, (5) gender, (6) socio-economic status, (7) ethnic minority, (8) body image and social influence, and (9) elite sports. A full list of included studies for this topic, including population, aims, design, and outcome measures is available in Additional File 1 .

Risk factors associated with EDs

Risk factor category	Features of risk factor	Associated ED
Genetic	See Sect. and Table 2 for details	AN, BN, BED
Gut microbial dysbiosys	CIpB)	AN
Autoimmune disease	Diabetes, inflammatory gastrointestinal disease	AN, BN, EDNOS
Childhood weight status	Low BMI	AN
	High BMI	BN, BED
Relationship with parents	Parent perception that the child is overweight	AN-BP, BN, BED, PD
	Parental teasing about weight	AN-BP, BN, BED
	Perceived pressure from parents to eat	ARFID
Neglect/abuse/trauma		AN, BN, BED, PD
	Post-traumatic stress disorder	BED
Personality traits	Perfectionism	AN-R, A-AN
	Obsession	AN-R, A-AN
	Impulsiveness	AN-BP, BN, BED, PD
Comorbid conditions	Obsessive compulsive disorder	AN
	Social anxiety disorder	BN, AN
	Borderline personality disorder	BN, BED, PD
	Bipolar disorder	BN, BED
	Depression	All EDs
Social/environmental	Exposure to ‘thin ideal’	All ED
	Body dissatisfaction	BN, BED, PD
	Early puberty development	BN, AN
	Food insecurity	Binge eating behaviours
	High educational attainment	Restricting type ED behaviours
	Involvement in elite sports	All ED

ED eating disorder; AN anorexia nervosa; BN bulimia nervosa; BED binge eating disorder; EDNOS eating disorder not otherwise specified; BMI body mass index; AN-BP anorexia nervosa (binge-purge subtype); PD personality disorder; ARFID avoidant restrictive food intake disorder; AN-R anorexia nervosa (restrictive subtype); A-AN atypical AN

1. Genetics: endocrines and neurotransmitters

Genetic risk factors and polymorphisms (variations in gene expression), relating to core EDs have been widely studied. Research conducted within twins and family groups as well as large-scale genomic studies have indicated a genetic component to risk of Anorexia Nervosa (AN), Bulimia Nervosa (BN) and Binge Eating Disorder (BED) [ 33 ]. Incidence rates in individuals with a parent with a history of ED have been found to be over twice as high compared to individuals with parents with no history of an ED [ 34 ]. Familial studies have demonstrated a strong genetic association for AN in particular. An individual is 11 times more likely to develop AN if they have a relative with the disorder as compared to someone with no family history. Similarly, an individual is 9.6 times more likely to develop BN, and 2.2 times more likely to develop BED if they have a relative with the disorder [ 33 ]. Evidence of genetic risk factors for other EDs is growing [ 33 ], although there have been no genetic studies to date conducted with Avoidant Restrictive Food Intake Disorder (ARFID) [ 35 ].

Anorexia nervosa and bulimia nervosa

Genetic factors have been shown to strongly contribute to both AN and BN [ 36 ]. There is evidence to suggest approximately half of the genetic factors implicated in AN and BN are shared between the disorders, with the remaining 50% being unique to one or the other [ 36 ]. An older study of Norwegian twins found some support for different features of AN being more heritable than others; having found weight/shape concern to have greater genetic association than low BMI and amenorrhea [ 37 ]. In contrast the landmark 2019 study by two international genome-wide association consortiums found that both metabolic and anthropometric related genetic loci associated with BMI lowering alleles have strong correlations with AN [ 38 ].

Hereditary patterns of EDs have been shown to disproportionately affect females [ 34 ]. In a sample of adolescent twins aged 15 to 17, Baker et al. (2009) found females were at greater genetic risk for disordered eating than males [ 39 ]. This is consistent with earlier evidence suggesting drive for thinness and body dissatisfaction showed lower heritability in males [ 40 ]. Baker et al. [ 39 ] found that only half of the genetic risk factors predicting drive for thinness and body dissatisfaction in females predicted the same traits in males. A possible explanation for this difference was offered in a study of French and German cohorts whereby inherited variations in an estrogen receptor gene (ESR1) significantly increased risk of restrictive eating and subsequently development of AN restrictive subtype (AN-R) [ 41 ].

Comorbidities

Genetic risk has been implicated in co-occurrence of EDs and other psychiatric diagnoses. Genetic associations have been found between Attention-Deficit/Hyperactivity Disorder (ADHD) and all EDs, with the strongest correlation to binge/purge-type ED behaviours [ 42 , 43 ]. Strong positive genetic associations have also been identified between AN and other psychiatric comorbidities, including Obsessive Compulsive Disorder (OCD), major depressive disorder, suicidality, schizophrenia, neuroticism, autism, and neurodevelopmental delay [ 44 – 48 ]. Genetic risk for comorbid AN and Generalised Anxiety Disorder (GAD) has also been identified [ 46 , 47 ].

The contribution of comorbid mental health disorders to ED risk and outcomes are further discussed in Sect. Results and in another topic paper of the Rapid Review, ‘Psychiatric Comorbidities and Medical Complications.’

Genes and polymorphisms

Several genomic studies have attempted to locate specific gene loci implicated in the development of EDs. See Table Table2 2 for a summary of genes and polymorphisms identified in ED genomic studies. A recent genome-wide association study published in 2021 has suggested that there is a distinct difference in the underlying biology between binge-type EDs (BN and BED) and AN. The study reported that both BN and BED shared genomic variant with overweight and obesity, whereas the directions of these associations were reversed for AN [ 49 ].

Genes and polymorphisms identified in the development of EDs

ED	Polymorphism (allele)	Function
AN		Cell adhesion molecule 1
		O-6-methylguanine-DNA methyltransferase
		Cell and tissue-specific gene transcription
		Polypyrimidine tract binding protein primarily expressed in the brain
	G861	5-hydroxytryptamine receptor 1B
	rs13338499	Agouti-related protein (appetite stimulator)
	5-HTTLPR (S)	Serotonin transporter
	rs2254298	Oxytocin receptor
	rs3798577	Estrogen receptor
	rs2291635	Cholesterol metabolism/BMI
	rs550942	Ciliary neurotrophic factor receptor
BN	rs928554	Estrogen receptor
	Rs1049353	Cannabinoid receptor
	5-HHTLPR	Serotonin receptor
	Rs1800497(Taq1A)	Dopamine receptor D2

	Rs4680 (Va1158Met)	Catechol-O-methyltransferase
	Rs9939609	BMI and fat mass
	Bc11	Glucocorticoid receptor
	rs1078947	Tyrosine receptor kinase (obesity and mood disorder related)
	rs6198	Glucocorticoid receptor
BED	Rs696217	Ghrelin
		Melanocortin 4 receptor
	rs6277	Dopamine receptor D2
	rs1800497
	Rs1800497 (Taq1A)	Ankyrin repeat and kinase domain containing 1
	Rs2270912	Dopamine transporter 1
	Rs2863130
	5-HHTLPR	Serotonin transporter
	Rs1799971 (118A/G)	Dopamine receptor D2
	Rs6265 (Val66Met)	Brain derived neurotropic factor
	rs1558902	BMI and fat mass

ED eating disorder; AN anorexia nervosa; BN bulimia nervosa, BED binge eating disorder

Genetic susceptibility to AN was explored in a landmark meta-analysis of 33 datasets from international genome-wide association studies. Watson et al. [ 38 ] compared the DNA of almost 17,000 individuals with AN to the DNA of 55,000 people without AN around the world. Eight loci associated with significant risk of developing AN were identified [ 38 , 50 ], including genetic correlations with certain psychiatric, anthropometric, and metabolic traits, as well as physical activity. Positive associations were found for physical activity, anxiety and schizophrenia disorders, and HDL cholesterol. Negative associations were found for metabolic (including glycemic), lipid, and anthropometric traits including fat mass, fat-free mass, BMI, obesity, type 2 diabetes, fasting insulin, insulin resistance, and leptin [ 48 ]. Analysis of causality revealed a bi-directional relationship between potential AN genes and risk for low body mass index (BMI). However, there is stronger evidence that low-BMI-causing alleles increase risk of AN than there is for AN-risk genes leading to low BMI [ 38 ].

A study of Norwegian adolescents found an association between poor appetite and undereating, and the COMT gene, which is responsible for regulating dopamine levels through the production of the COMT enzyme [ 51 ]. Brain studies of patients with AN have indicated that, due to disturbances in regular serotonin and dopamine reward pathways, individuals with AN may use restricted eating as a mechanism to reduce anxiety [ 52 ]. In one study of patients with AN and BN, mutations in genes with heightened expression in brain tissue (CNTF, NTRK) were associated with a higher minimum lifetime BMI and earlier ED onset [ 53 ].

Six genetic polymorphisms have been associated with the development of BN in people with obesity [ 54 ]. Of the six genetic polymorphisms, three are thought to be related to the neuroendocrine receptors of dopamine, serotonin, and cannabinoid. This association is supported by evidence that genetic variations which lead to low dopamine production and neurotransmission are associated with an increased risk of binge/purge type EDs [ 55 ]. The remaining three polymorphisms identified in BN aetiology were associated with an estrogen receptor, the production of an enzyme expressed in brain tissue, and the FTO gene (which has a role in BMI regulation) [ 54 ]. While dopamine and serotonin receptor genes (DRD2 and SLC6A4, respectively) are implicated in the development of both BN and BED, differing polymorphisms in these genes appear to be associated with increased risk of developing one disorder over the other [ 54 ]. Further, triallelic 1 variations in a serotonin receptor allele (5-HTTLPR) have also been observed to contribute to compulsive personality traits and the development of AN, BN, and eating disorder not otherwise specified (EDNOS) [ 56 , 57 ]. A polymorphism of the oxytocin receptor gene (OXT-R) was also found to distinguish between risk of onset for restricting type EDs or binge/purge type EDs, indicating the potential role of oxytocin in the development and maintenance of EDs [ 58 ]. Additional research has identified an association between a polymorphism in a neurotransmitter inhibition gene (HTR1B) and an increased risk of developing BN as well as greater severity of AN symptoms, including low BMI [ 59 ].

Expression of genes associated with the production of appetite and weight control endocrines (leptin, melanocortin, and neurotrophin) are thought to have a role in ED development and severity [ 45 ]. A case–control study by Zeeland et al. [ 60 ] found a significant number of AN participants with a polymorphism in a cholesterol metabolism gene (EPHX2), which was also associated with lower BMI (see Table Table2). 2 ). Yilmaz et al. (2014) examined 20 single-nucleotide polymorphisms 2 (SNPs) in the endocrine system genes in a sample of individuals with BN (n = 745) and AN (n = 245). Although no significant differences were observed between either ED diagnosis or control participants, two SNPs associated with regulation of BMI were found to have an impact on disease severity (See Table Table2) 2 ) [ 61 ].

Consequences of variations in endocrine signalling in individuals with ED also include reduced capacity for interoception 3 particularly relating to gastric interoception. A systematic review of interoception in individuals with ED found the strongest correlations were observed in individuals with AN who consistently had lower gastric interoception relating to satiety and self-reported fullness, while individuals with BN were found to have lower pain interoception resulting in higher pain thresholds. However, researchers were unable to ascertain whether lack of gastric interoception in individuals with AN was a result of conscious processing of satiety cues or disruptions in endocrine signalling [ 62 ].

Non-shared vs. shared environments

A Swedish study of female monozygotic (identical) and dizygotic (fraternal) twins aged between 20 and 47 found that nonshared environmental factors between twins had a greater impact on ED risk than shared environmental factors [ 36 ]. This finding was further supported by a study of an Australian twin sample, which concluded that nonshared environmental factors contributed to the genetic factors associated with weight loss behaviours and overeating behaviours in AN and BN, respectively [ 63 ]. Shared environmental factors were not observed to have an impact on disordered eating behaviours [ 63 ].

Exposure to childhood trauma has been linked to polymorphisms in genes expressed in the glucocorticoid receptor pathway which are associated with increased risk of developing BN, binge eating, and loss of control over eating [ 51 , 64 – 66 ]. This finding is supported by research conducted by Monteleone et al. [ 67 ], who found significantly lower levels of cortisol in individuals with AN and BN with a history of childhood maltreatment than healthy controls and those ED patients with no history of childhood trauma. Exposure to childhood trauma was also found to interact with gene expression through creating higher levels of DNA methylation 4 in women with BN [ 68 ]. Analysis of evidence from seven studies found a strong additive effect for serotonin transporter 5-HTTLPR polymorphism combined with childhood experiences of physical and sexual abuse in the development of BN [ 69 ]. Childhood trauma and abuse as a risk factor for EDs, particularly related to environmental influence, will be further discussed in Sect. Results .

Binge eating disorder

Variation in genes linked to appetite and satiety modulating hormones such as ghrelin are often implicated in the development of BED, as well as several genes related to regulation of BMI and fat storage. A study of 4,360 adolescents aged 14 or 16 found that frequency of binge eating was associated with expression of a polymorphism in the FTO gene, thought to play a role in BMI and obesity [ 70 ]. Further, mutations of the MC4R gene, involved in metabolism and feeding, is also associated with BED and obesity [ 71 , 72 ].

As previously discussed, polymorphisms in genes responsible for the production of neuroendocrine receptors such as dopamine and serotonin are also commonly associated with BN and BED [ 54 ]. Reward responses to food have long been implicated in the development and perpetuation of BED. The expression of two alleles in the dopamine D2 receptor has been found to be positively associated with BED in a sample of 230 individuals with obesity [ 73 ]. The authors concluded that expressions of these alleles was associated with hypersensitivity to reward, likely having a causal relationship with BED [ 73 ]. In a study of female twins in the US, increased binge eating frequency was also found to be associated with genetic factors related to the personality traits neuroticism and conscientiousness [ 74 ].

Night eating syndrome

Genetic research relating to Night Eating Syndrome (NES) is less developed than the primary EDs. Work in animal models has implicated variants of the VGF, a gene responsible for production of a neuropeptide precursor in NES aetiology [ 75 , 76 ]. One familial study was identified assessing the heritability of NES involving families where at least one parent had obesity. Night eating symptoms in mothers were strongly associated with similar behaviours in their sons and daughters, while no such correlation was observed for fathers [ 77 ]. Interestingly, the association was slightly stronger in sons (r = 0.19) than in daughters (r = 0.15), whereas heritability relationships are typically stronger in female offspring in other ED diagnoses [ 34 , 77 ]. This finding was further supported by evidence from a Swedish twin registry study where males were more likely to endorse night eating traits associated with genetic factors, while females were more likely to endorse binge eating [ 76 ]. Further research is required to understand any potential genetic risk factors associated with NES.

There is considerable evidence pointing to genetic risk in the development of EDs, with the highest heritability conferred for AN [ 33 , 34 ]. Females are also at greater genetic risk for disordered eating in comparison to males [ 39 ]. When considering the specific genetic variations thought to contribute to increased ED risk, genetic associations have been found between EDs and other psychiatric comorbidities, however the type of comorbidity differs according to the ED diagnosis. For binge-type EDs (BN and BED) strongest genetic correlations are observed with ADHD [ 42 , 43 ] whilst AN has strong correlations with OCD, MDD, suicidality, schizophrenia, neuroticism, autism, and neurodevelopmental delay [ 44 – 48 ]. In a similar manner, genetic correlations with metabolic traits appear to differ between ED diagnoses, such that BN and BED have been found to share genomic variants with overweight and obesity [ 49 ] whereas potential AN genes uphold a bi-directional relationship with low BMI [ 38 ]. Genes associated with other metabolic functions, including appetite and weight control endocrines (leptin, melanocortin, neurotrophin) have also been implicated in ED development and severity, however fewer differences between ED diagnoses are apparent. Polymorphisms in the genetic loci responsible for neurotransmitters associated with reward processing and appetite regulation hormones, including dopamine, serotonin, and cannabinoid have been identified as a risk factor across several ED diagnoses including AN, BN, and EDNOS [ 45 , 50 – 62 ]. Additionally, genetic polymorphisms in the glucocorticoid receptor pathway responsible for the stress response have been linked to individuals who have experienced trauma and are associated with increased risk for BN [ 51 , 65 , 66 ].

2. Gastrointestinal microbiota and autoimmune reactions

Gastrointestinal microbiota.

The role of gut microbiota and immune system reactions in the development and perpetuation of EDs is an emerging field, however is receiving growing attention. Endocrines produced in the gastrointestinal (GI) tract communicate with the brain to regulate functions of appetite and satiety. Given the role of these functions in EDs, it is thought that dysregulation of the gut microbiome may be partially responsible for ED psychopathology [ 78 – 80 ]. A review of evidence on the gut microbiome suggests that the growth cycle of gut bacteria and their metabolites 5 may contribute to patterns of accelerated and/or prolonged satiety in AN and periodic lack of satiation in BN [ 78 ]. In a study of 33 AN patients undergoing refeeding, Hanachi et al. [ 81 ] found the AN patients to have significant gut microbial dysbiosis compared with 22 healthy controls.

Several studies of AN have investigated the role of a protein (CIpB) produced by the Escherichia Coli ( E. Coli ) bacteria. The CIpB protein has a similar structure to the human hormone responsible for simulating secretion of satiation peptide YY. The peptide YY has been detected in high levels in the blood plasma of individuals with AN compared to healthy controls [ 78 , 82 , 83 ]. Peptide YY levels have also been found to be elevated among individuals with AN-R as compared to those with AN-BP and healthy controls [ 84 ]. Intestinal infections and chronic inflammation can lead to large increases in the number of E. coli bacteria in the GI tract, therefore increasing the levels of peptide YY and potentially increasing risk of ED [ 83 ]. The CIpB protein produced by E. Coli also prompts an immune reaction whereby autoantibodies are created. The position on the receptor for this autoantibody has been shown to differentiate between risk for BN and BED or AN [ 78 ]. Despite such emerging evidence indicating a role for gut microbiome dysregulation in EDs, researchers consider much of the evidence to be in an observational phase or using murine models 6 and lacking the capacity to explain aspects of ED pathology [ 79 , 85 ].

Autoimmune and autoinflammatory diseases

Gut microbiota are also known to interact with autoimmune responses, which have been investigated as a potential risk factor for EDs. In a large population-based cohort study, autoimmune and autoinflammatory diseases were identified as a significant predictor in the development of EDs and were associated with a 36% increased chance of developing AN. Interestingly, risk of BN and EDNOS was much higher at 73% and 72%, respectively [ 86 ]. Among a sample of patients hospitalised for EDs in Finland, higher prevalence of type 1 diabetes and Crohn’s disease was observed compared with healthy controls [ 87 ]. A recent meta-analysis has also identified a bidirectional association between coeliac disease and EDs. In particular, patients with AN are at a significantly greater risk of coeliac disease than healthy adults without AN [ 88 ]. Further, researchers argue that symptoms of ED commonly mimic those of chronic inflammatory GI and endocrine disease, including inflammatory bowel disease and diabetes type 1 and 2, emphasising the importance of screening for possible co-occurrence [ 89 ]. Unlike the vast majority of other risk factors associated with EDs, autoimmune and autoinflammatory diseases represented a greater risk for male participants as compared to females [ 86 ].

As a type of autoimmune disease, diabetes is commonly associated with EDs. There is a substantial evidence base indicating an increased prevalence of disordered eating behaviours among individuals with both type 1 and type 2 diabetes [ 90 , 91 ]. However, much of the evidence is observational and there are limitations in distinguishing between avoidance of certain food groups due to presence of an ED versus a feature of diabetes management [ 92 , 93 ]. Nevertheless, high rates of ED behaviours not related to food restriction (e.g., excessive exercise, vomiting, and laxative abuse) have been observed in adolescents and adults with diabetes [ 94 , 95 ]. Insulin manipulation or restriction has also been observed in adolescents with diabetes resulting in poor glycaemic control and poorer outcomes [ 89 , 90 , 94 – 96 ]. Interestingly, a study of adults has revealed that weight/shape overvaluation was lower in participants with diabetes (31.5%) compared to those who did not have diabetes (41.2%). The authors suggest that this may indicate that BED, as an ED for which weight/shape overvaluation is not a diagnostic criteria, may be of particular concern among adults with diabetes [ 97 ].

In terms of biological risk factors, evidence has largely focused upon proteins produced by gut bacteria, which have been implicated in dysregulation of appetite and satiety in individuals with EDs. The metabolites of gut bacteria are thought to play a role in disordered eating patterns, including prolonged satiety in AN and periodic absence of satiety in BN [ 78 – 80 ]. For example, a protein produced by E. Coli bacteria has been found to mimic the structure of the satiation peptide YY, a protein that is higher in individuals with AN as compared to healthy controls [ 83 , 84 ]. Findings such as these have led researchers to consider intestinal infections and chronic inflammation as a potential risk factor for EDs. However, research in this field is emerging, with further studies needed to better understand the association between gut microbiome dysregulation and EDs. Large studies have indicated that having an autoimmune or autoinflammatory disease, such as Crohn’s disease, inflammatory bowel disease, diabetes type 1 and 2, and coeliac disease, is also significantly associated with increased risk of BN and EDNOS, and to a lesser extent, AN [ 90 – 95 ].

3. Childhood and early adolescent experiences

A range of childhood experiences have been linked to the development of EDs later in life, including in-utero exposures, family dynamics and parental characteristics, childhood weight, and experiences of abuse and trauma.

In utero exposures

There is evidence to suggest that exposure to certain levels of hormones during foetal development could increase risk of ED development later in life. In a large cohort study of women in the UK, daughters whose mothers had a lifetime diagnosis of BN were found to have been exposed to high levels of prenatal testosterone in the womb, which was implicated in an increased risk of BN and binge eating [ 98 ]. However, a large multinational twin study was unable to find any link to in utero exposure to sex hormones and ED onset later in life [ 99 ].

Research has indicated that in-utero exposure to high levels of cortisol through maternal stress is associated with later development of ED [ 100 , 101 ]. A further study in the UK found that individuals who were born preterm had an increased risk of ED associated with structural brain alterations linked to underdevelopment [ 102 ]. Additional risk factors include the use of substances during pregnancy (e.g., nicotine) and maternal illness leading to malnutrition (e.g., anaemia), which have also been linked to an increased risk of AN and BN in the child later in life [ 103 ].

Risk factors conferred during foetal development are further supported by findings that risk of BED is associated with high weight at birth or being large for gestational age, while AN was associated with low weight at birth. No significant foetal developmental risk factors have been identified for BN [ 104 ]. Moreover, stressful events experienced by mothers in the year prior or during pregnancy, in particular the death of a close relative in the six months preceding pregnancy, have been shown to have an impact on the development of feeding or EDs in infants and toddlers [ 105 ]. Feeding issues in babies of mothers who had an ED diagnosis during pregnancy were also noted in this cohort [ 106 ].

A recent systematic review identified an association between AN and older maternal age, preterm birth (< 32 weeks), lower birth size, and maternal health complications (e.g., preeclampsia, eclampsia). The review also reported an association between BN and maternal stress during pregnancy [ 107 ].

There appears to be an impact of pregnancy upon the eating behaviours of women with an ED diagnosis. One study has found that ED behaviours across diagnoses tended to improve significantly during the pregnancy period, although this may not be maintained after [ 108 ]. It has also been reported that pregnancy is associated with remission of BN but an increased risk of BED onset [ 109 , 110 ]. Women with a history of psychosocial adversities have been found to possess a significantly greater risk for BN during pregnancy [ 111 ].

Family dynamics and parental characteristics

Research has shown that children are more likely to develop an ED if their parents display characteristics commonly associated with ED psychopathology, such as drive for thinness and perfectionism [ 112 ]. Specifically, maternal history of an ED has been shown to be associated with higher rates of emotional eating in children as young as four years old [ 113 ]. The children of women with lifetime AN have also been found to exhibit deficits in cognitive functioning, including social understanding, visual-motor function, planning, and abstract reasoning [ 114 ].

Additionally, Larsen et al. [ 115 ] reported that general parental psychiatric illness is associated with increased risk of BN and EDNOS. The authors also identified the experience of childhood adversity and significant family disruption as significant risk factors for development of BN and EDNOS. Interestingly, no associations between childhood adversities and risk of AN could be identified by authors, although a separate study identified maternal depressive symptoms as a predictor of AN [ 116 ].

Adopted individuals have also been identified as having a greater risk of binge eating and extreme weight loss behaviours, as well as increased risk of a lifetime diagnosis of an ED [ 117 ]. Other parental characteristics which have been associated with ED behaviours include high maternal BMI at 16 weeks’ gestation and when their child is eight years old, high maternal education attainment, and low parental self-esteem [ 118 – 120 ].

Individuals’ perceptions of the quality and nature of their parental relationship has been investigated as a potential risk factor for development of an ED. Research has found that female individuals diagnosed with AN or BN report significantly lower perceived emotional connectedness prior to disorder onset than their healthy sisters. In a family-based study of 332 female individuals, low emotional connectedness conferred a greater risk of developing BN over AN-R [ 121 ]. Further, females who report low maternal warmth have a higher risk of developing binge/purge type EDs [ 122 ]. Low parental warmth appears to be a risk factor for ED development in females but not males [ 123 ]. A study of AN patients and their healthy siblings found that both siblings in these families perceived low maternal care and high maternal overprotection. Siblings affected by AN developed insecure attachment compared with their siblings and had higher preoccupation with relationships, while healthy siblings were able to develop secure attachment and low need for approval and high self-transcendence [ 124 ]. Other risk factors include an oppressive parental relationship and childhood unhappiness [ 122 ].

Parents’ communication about food, as well as parental eating behaviours, have been shown to be a significant risk factor for EDs in their children. Several studies have found that exposure to disordered eating behaviours such as dietary restriction in parents is likely to have an impact on the early development on EDs in children, beyond the influence of genetics [ 125 , 126 ]. One study identified maternal distress as a mediating factor in the relationship between maternal ED and infant feeding difficulties [ 127 ]. Maternal dieting and poor communication among family members have also been associated with long-term risk for restrictive disordered eating [ 128 ]. Conversely, parental conversations regarding healthy eating, rather than dieting or weight, and regular family meals were found to be protective against development of EDs among child and adolescent samples in Europe and the US [ 129 , 130 ]. Parental pressure to eat, early negative experiences with food, and high disgust sensitivity were found to predict picky eating behaviours associated with ARFID. Parental encouragement around food in childhood was observed as a protective factor. Being male was also found to be a significant risk factor for adult picky eating behaviour and potential ARFID [ 131 ].

The experience of stressful life events, including bereavement, separation from family members, or involvement in an accident have been found to have an impact on ED development, in particular BN and BED. The occurrence of three or more events in combination with external criticism of weight or shape has been shown to be significant predictors in the year prior to BN onset [ 132 ]. No significant differences were observed between BN and BED in terms of the number or types of events experienced prior to onset [ 133 ].

Childhood weight

Research on the association between childhood weight and risk of eating pathology in later years is ambiguous. Several studies have reported that higher weight during childhood poses an increased risk of developing an ED in later years, including among culturally and linguistically diverse (CALD) individuals, as well as males [ 134 – 138 ]. Analysis of specific ED behaviours among adolescents in the US between 1999 and 2010 found that ED symptomatology and weight/shape concern persisted beyond adolescence for individuals who were overweight. Contrastingly, for non-overweight individuals, unhealthy weight control behaviours and body dissatisfaction decreased over time [ 139 ]. Other studies have found that adolescents with a weight history in the overweight range experience a significantly greater drop in BMI, higher levels of ED psychopathology and comorbid mental health difficulties, and take much longer to be identified than adolescents without a history of overweight [ 140 ], 141 .

Contrastingly, explorations of the association between weight history and AN specifically have found that low baseline BMI is a significant risk factor for development of both atypical AN and AN [ 38 , 142 , 143 ].

It has been suggested that parental perception of their child as being overweight may be a more powerful predictor of ED development than the child’s weight itself [ 118 , 144 , 145 ]. The significant impact of parental behaviours on ED risk has been supported by a study comparing individuals with BN to healthy controls and individuals with other psychiatric conditions. While being overweight or obese in childhood was identified as a risk factor, high maternal expectations and negative parental attitudes about weight and obesity in childhood were more strongly associated with the onset of BN among participants [ 146 , 147 ]. These risk factors are also associated with onset of BED [ 148 ]. Negative parental attitude towards childhood weight, including parental teasing about weight, has been shown to have a strong positive association with ED behaviours in both males and females, in particular binge eating behaviours [ 146 , 149 , 150 ]. Parental comments about their child’s weight and eating behaviours are also significantly associated with increased drive for thinness and body dissatisfaction [ 151 , 152 ].

Abuse and trauma

Experience of childhood trauma and abuse has been consistently identified as a non-specific risk factor for the development of EDs, although these experiences are more strongly associated with binge-purge type disorders such as BN, BED, and AN-BP [ 153 – 157 ]. Evidence from several studies suggests that emotional abuse is a significant predictor of binge/purge symptomology in women, while sexual abuse and physical neglect were associated with symptoms in men [ 158 – 160 ]. Sexual harassment has also been identified as a risk factor for EDs however little is known about the causal relationship or the role of mediating factors [ 161 ]. Attempts to investigate the association between types of childhood trauma and specific ED diagnoses have found that emotional abuse is a risk factor for all core ED symptoms [ 162 ]. A large-scale study of young adults in the US found that participants who reported multiple types of maltreatment in childhood were almost twice as likely to report binge eating and skipping meals as compared to those who reported no or low maltreatment [ 163 ]. Verbally abusive fathers have been shown to be strongly associated with AN-BP and BN, and verbally abusive mothers influence the development of BN [ 164 ].

Studies conducted in groups of women with obesity have found relationships between binge eating and childhood abuse and neglect. The severity of the abuse, rather than the type of abuse, appears to have a role in the development of BED and severity of food addiction [ 165 , 166 ]. A recent study has found that childhood food neglect is associated with increased risk for BN and BED even after adjusting for other adverse experiences and financial difficulties experienced during childhood [ 167 ]. A study on the impact of childhood emotional abuse and ED risk found that low self-perception and self-esteem caused by the abuse contributed to an increased risk of BED and NES [ 168 ]. Further, individuals with both an ED diagnosis and a history of childhood trauma and abuse have been found to have increased risk of lifetime suicide attempts [ 169 , 170 ].

The experience of childhood bullying has been found to increase risk of AN, and to a lesser extent BN, in children and adolescents [ 171 – 173 ]. However, increased risk of EDs was not found to carry on into early adulthood [ 171 ]. Weight-based teasing has also been associated with emotional eating, eating in the absence of hunger, and disordered eating attitudes and behaviours [ 174 ]. Consistent with existing evidence, an observational study of 182 adolescents receiving treatment for EDs found bullying was the most common form of trauma experienced by patients [ 175 ]. Assessment of the impact of cyberbullying also found the experience predicted onset of AN, BN, and EDNOS in a group of individuals with an ED diagnosis and increased ED symptomology and depression among a group of high-risk individuals [ 176 ]. Exposure to online content and risk of ED development is discussed further in Sect. Gender .

An overview of the evidence regarding the impact of early experiences in terms of ED risk has identified a range of factors starting from the in-utero environment through to adolescence. In-utero exposure to high levels of testosterone, cortisol, or substances have been associated with increased risk of EDs [ 98 – 100 , 102 , 103 ]. There is also evidence to linking high birth weight to BED and low birth weight to AN [ 104 ]. Weight persists as a risk factor throughout childhood and adolescence, with research findings that high maternal expectations and negative parental attitudes about weight are also associated with ED risk. The quality and nature of one’s parental relationship is considered another risk factor for EDs, such that lower ratings of parental warmth or emotional connectedness have been reported by individuals with AN and BN as compared to their healthy siblings [ 121 – 124 ]. Experiences of childhood adversity, significant family disruption, childhood trauma (including neglect and emotional or sexual abuse) are well-documented risk factors, with evidence suggesting that they are most likely to contribute to the development of binge/purge type disorders (AN-BP, BN, BED, PD) [ 115 , 153 – 156 ]. Researchers have also suggested that the link between EDs and trauma is likely to be underestimated due to non-disclosure [ 207 ].

4. Personality traits and comorbid mental health conditions

Traits such as anxiety, perfectionism and obsessive-compulsivity are frequently associated with increased risk of EDs and may play a substantial role in the severity of symptoms, response to treatment, and risk of relapse [ 178 ].

Perfectionism, impulsivity, compulsiveness, and avoidance motivation

Rather than being linked to diagnostic type, a meta-analysis of personality traits (Farstad et al., 2016) found a more robust association with specific behaviours and symptomatology. Studies have shown that relative to controls, individuals with ED have elevated levels of perfectionism (setting of excessively high standards for performance, accompanied by overly critical self-evaluation); neuroticism (tendency to experience negative effects such as anger, anxiety, self-consciousness, irritability, emotional instability, and depression); impulsivity, particularly negative urgency (tendency to engage in impulsive behaviour when experiencing strong negative emotion); compulsivity (tendency toward overcontrolled behaviour); avoidance motivation (tendency to move away from or avoid situations associated with punishment); sensitivity to social rewards; introversion; and self-directedness (goal-oriented behaviour) [ 178 – 186 ].

Perfectionistic traits are common in both AN and BN. A systematic review and meta-analysis concluded that individuals with AN tended to place greater emphasis on high personal standards, while individuals with BN were more likely to perceive high levels of parental criticism [ 178 ]. The contribution of perfectionism to ED symptomatology (including dietary restriction and shape and weight overvaluation) was further supported by Joyce et al. [ 180 ] in a community-based sample of women. The study was inconclusive as to whether perfectionism was the cause of the ED symptoms. However, a significant positive association between perfectionism and weight and shape overvaluation was observed [ 180 ].

Among a sample of adolescent females recruited from an ED service in Australia, researchers found both a direct relationship between perfectionism and AN symptoms as well as an indirect relationship when mediated by depression [ 187 ]. The two different relationships were found to be equally viable, further supporting the notion of a reciprocity of symptoms between anxiety, depression, and AN, which are preceded by perfectionism.

In a 10-year follow-up study of university-aged adults in the US perfectionism was associated with the onset of AN, BN, and EDNOS and found to contribute significantly to disorder maintenance [ 188 ]. The tendency toward perfectionism in AN has been linked to a trait of vulnerable narcissism, ‘hiding the self,’ described as an unwillingness to show one’s faults or needs to others. The ability to exhibit control over emotional needs and relationships was correlated with AN-R in a comparison study involving individuals with AN and BN. However, the cross-sectional design was unable to determine whether this trait preceded AN-R and the sample size was relatively small [ 189 ].

Obsessiveness has also been found to be strongly associated with AN. Among a clinical sample of patients with AN and atypical AN, obsessiveness was positively correlated with a drive for thinness, a key aspect of AN symptomatology. The study did not find any significant differences between AN and atypical AN in terms of obsessive behaviours [ 190 ].

Studies seeking to assess personality traits contributing to differences in clinical presentation between restricting and binge/purge ED subtypes conclude that alexithymia – the inability to identify or verbally describe feelings or emotions – plays a role in the emotional dysregulation displayed by both AN-R and BN patients [ 191 , 192 ]. Higher levels of alexithymia have been associated with greater risk of re-hospitalisation in a three-year follow-up study of women with both AN and BN [ 193 ]. Prefit et al.’s [ 194 ] meta-analysis of studies into EDs and associated personality traits found lack of emotional awareness and inability to regulate emotions leading to maladaptive ED symptomology was not diagnosis specific [ 194 ]. Findings from the meta-analysis support Brown et al. (2018), suggesting a need for emotion-focused treatment approaches such as dialectical behaviour therapy (DBT) [ 192 , 195 ].

While binge/purge presentations are consistently associated with impulsivity and greater emotional dysregulation [ 196 , 197 ], one study demonstrated no significant differences in ability to regulate emotions between AN-R and BN patients with high levels of alexithymia [ 192 ]. However, in another study involving clinical samples of AN-R, AN-BP and BN patients, individuals with AN-R were found to have fewer fluctuations in mood than individuals with AN-BP and BN. Only in groups exhibiting binge/purge symptomology were these behaviours observed as a method for alleviating negative affect [ 198 ]. Similarly, among a group of 139 female college students, lower impulsivity in addition to lower self-esteem was found to be associated with AN risk [ 199 ]. A recent systemic review has warned that due to methodological limitations in the studies conducted to date, there is insufficient evidence to support the characterisation of AN and BN as being low and high in impulsivity, respectively [ 200 ].

Individuals with binge/purge subtypes EDs, including AN-BP, BN, BED and various OSFEDs, have been found to have higher levels of avoidance motivation, impulsivity, emotional dysregulation, anxiety, depression, and paranoia than healthy controls [ 178 ]. Within a clinical sample of AN patients, individuals displaying binge/purge symptoms were more likely to engage in non-suicidal self-injurious behaviour and have lower self-directedness and co-operation than individuals with AN only [ 201 ]. However, the literature is inconclusive as to whether these traits contribute to ED onset or are symptoms of it.

Several studies have observed high levels of impulsivity in individuals with BN, with these individuals commonly displaying negative urgency, lack of planning and sensation seeking. Farstadt et al. (2016) in their meta-analysis also argue a role for compulsiveness (i.e., the tendency towards overcontrolled behaviour), suggesting that the interaction of personality traits such as impulsiveness and compulsiveness can have implications for ED symptomology and disorder severity [ 161 , 180 , 183 , 184 ]. In this manner, impulsivity was found to have a significant impact on the types of ED symptomatology displayed by the individual and clinical presentation [ 178 , 195 ]. In contrast, Waxman [ 195 ] found no significant differences in impulsivity between ED diagnoses. Waxman [ 195 ] suggested that while there is a lack of evidence from longitudinal studies to determine conclusively that impulsivity is a risk factor in the development of ED, evidence from studies using proxy measures such as delinquency found these behaviours preceded BN onset. One further study has reported an association between NES and impulse control disorder [ 202 ]. It has also been suggested that impulsivity and addiction-like mechanisms may explain the association between ED psychopathology and both high-risk sexual behaviours and substance misuse [ 203 , 204 ].

A study of 83 sister pairs found participants with a lifetime ED diagnosis displayed higher levels of internalising behavioural issues (social withdrawal, anxiety, depression) and/or externalising behavioural problems (aggression and delinquency) than their healthy sisters [ 205 ]. Internalising behaviours were found to be a strong predictor for AN-R, while externalising behaviours were strongly associated with later onset of bulimic symptoms and BN [ 205 ].

Two models illustrating risk of bulimic behaviours among young females have attempted to account for both the role of personality traits and traditional ED concepts of the ‘thin ideal’ [ 206 ]. Pearson’s integrated model of risk combines the ‘state-based’ pathway, which shows binge eating as an impulsive lack of control behaviour and purging as a compulsive correction, and the ‘trait-based’ pathway, which emphasises negative urgency as a consistent tendency toward impulsivity and stress alleviation through binge eating. The ‘trait-based’ pathway also considers the role of inherited ED risk and predisposing childhood exposures [ 206 ]. Pearson et al. argue that integration of the ‘trait-based’ model considers the important role of heritability and negative urgency that is absent from the Stice model [ 207 ]. Further investigation of disease models of bulimic behaviour by Dakanalis et al. [ 208 ] indicate that risk factors are more complex than can be mapped by the dual pathway model, citing bi-directional relationship between dietary restriction and negative affect.

Negative urgency has also been found to be an independent predictor of food addiction among individuals displaying binge-eating symptomology [ 209 ]. A further study by Utschig et al. [ 210 ] indicated that fear of negative evaluation from others is a predictor for body dissatisfaction and pressure to be thin, contributing to an internalised ‘thin ideal’ in individuals with BN and feeding into the state-based model. Fear of negative evaluation is considered an aspect of social anxiety and relates to heightened sensitivity to social rewards, a trait found to be elevated across ED diagnoses [ 178 , 210 ].

Personality disorders

The central role of certain personality traits in the perpetuation and potential development of ED symptomology reflects established relationships between some personality disorders and EDs [ 211 – 213 ]. Comorbidity studies have found borderline personality disorder (BPD) to most commonly occur with BN and other binge/purge ED subtypes [ 212 ]. This finding is supported by research on personality traits in EDs where avoidant behaviours and low emotion regulation flexibility are elevated in bulimic-type disorders and also a core feature of BPD [ 178 , 212 , 214 ]. However, some researchers argue that the co-occurrence of EDs and personality disorders may have been inflated in previous studies [ 215 ]. In a sample of 132 females with ED, prevalence of any personality disorder was 21%, lower than in other studies where reported figures were between 27 and 95% [ 215 ]. However, findings from von Lojewski et al. [ 215 ] were consistent with existing evidence that BPD traits were significantly associated with binge/purge EDs compared with AN-R. Individuals with comorbid BPD and ED were also more likely to report self-induced vomiting as compared to any other personality disorder. Co-occurrence of EDs and BPD has also been associated with increased risk of engaging in non-suicidal, self-injurious behaviours within a clinical sample [ 212 ]. Meta-analysis of 20 studies published between 1987 and 2010 found comorbidity of BPD with EDNOS (now OSFED) to be 38%, and 29% with BED. Researchers indicated that ED and personality disorder comorbidity are more common among individuals with AN and BN than BED and EDNOS [ 216 ]. However, among patients with BED or EDNOS, avoidant personality disorders were found to be the most common, followed by BPD [ 216 ]. It should however be noted that two of three studies identified by the Rapid Review concerning ED and personality disorders were restricted to relatively small clinical samples without control groups. They were also limited by their cross-sectional design in their capacity to investigate the temporal relationships between disorders.

Anxiety, mood disorders and psychiatric comorbidities

Co-occurring and preceding mental health conditions, particularly those with shared genetic and experiential influences such as anxiety and mood disorders, are also risk factors for EDs. While it is difficult to assess which condition precedes the other without use of prospective study designs [ 217 ] these relationships have been widely studied in AN and BN, and there is some evidence for anxiety and mood disorders including depression and bipolar disorder preceding ED symptomatology. Evidence from a three-year prospective study of 615 pairs of twins in the US suggests elevated risk for AN is associated with higher levels of depression and anxiety in combination with a high drive for thinness, rather than either risk factor alone [ 218 ]. There is less conclusive evidence on the relationship between BN, anxiety, and depression although some preliminary research was identified indicating several key symptoms were shared between the three disorders [ 219 ].

Mood disorders

In clinical ED populations, prevalence of mood disorders is frequently high [ 220 ]. In one study, major depressive disorder (MDD) was found to affect 64% of individuals with AN-R and over 75% of binge/purge ED subtypes (AN-BP, BN). Sequencing of disorder onset found that mood disorders preceded ED onset in a third of the AN-R cases and 40% of the AN-BP/BN cases. The remaining comorbid cases were either co-occurring or onset following ED diagnosis. These findings from Godart et al. [ 220 ] indicate that depressive disorders can be both a predictor and consequence of ED, as well as a comorbidity caused by malnutrition further complicating management and treatment of EDs.

Assessment of the temporal relationship between depression and disordered eating in an eight-year longitudinal study found depressive symptoms predicted increases in BN behaviours, which in turn predicted increases in depressive symptoms [ 221 ]. These findings indicate there may be a reciprocal relationship between the two conditions. A reciprocal relationship was also identified in a larger cohort of adolescent females where individuals who reported depressive symptoms were twice as likely to engage in overeating and binge eating at four-year follow-up, and individuals reporting overeating and binge eating were also more likely to report depressive symptoms at follow-up [ 222 ].

Anxiety disorders

There is evidence to suggest that anxiety is the most commonly occurring comorbidity with ED [ 223 ]. Childhood anxiety disorders have repeatedly been found to precede the onset of an ED, particularly AN [ 224 – 228 ]. Studies have identified a greater incidence of childhood obsessive–compulsive traits in individuals diagnosed with AN in comparison to control groups without an ED [ 177 ]. Micali et al. [ 211 ] conducted a longitudinal study of 231 young people diagnosed with OCD over a nine year period. Of the 126 participants who completed the follow up assessment, 12.7% had a diagnosis of an ED. Such findings highlight predictive value of childhood anxiety disorders in the later development of EDs, especially AN.

A reciprocal relationship between GAD and AN was indicated in a large twin study by Thornton et al. [ 229 ] whereby having GAD significantly increased likelihood of AN and having AN significantly increased likelihood of GAD. The group with AN and GAD had the lower mean adult BMI than both AN only and GAD only groups and healthy controls. These findings indicate the presence of comorbid mental health conditions may exacrerbate EDs and increases severity of symptoms. Sihvola et al. (2009) found co-occurrence of MDD and GAD at age 14 was strongly associated with onset of ED at follow-up (age 17). Weaker associations were observed for both MDD and GAD alone [ 230 ].

Ciarma and Mathew [ 231 ] investigated the relationship between social anxiety disorder (SAD) and disordered eating among adults aged between 18 and 35 living in the community. This study found self-esteem and stress reactivity resulting from interpersonal conflict to be partial mediators, indicating that ED symptoms can be elicited by heightened responses to stress from social conflict and negative self-view. However, the partial mediation effect observed indicated that other unidentified factors may also have a role in the relationship. A further study of adolescents found evidence of a bidirectional relationship whereby depression and anxiety were risk factors for disordered eating behaviours, which in turn led to increased depression and anxiety [ 232 ].

Prevalence of social anxiety was also found to be high among a separate clinical sample of Australian adults with an ED, where 42% were found to have social phobia. It was also the most commonly diagnosed anxiety disorder within each of the ED subtypes, including 33% of those diagnosed with BN, 26% for AN and 25% for EDNOS. Investigations into the temporal relationship between ED diagnosis and anxiety disorder have found many individuals have anxiety prior to their ED diagnosis [ 225 – 227 ]. However, in one systematic review, this was supported only by the included retrospective case–control and cohort studies, and was not supported by evidence from prospective studies included in the review [ 227 ]. This discrepancy highlights the potential role of recall bias that may be present across studies relating to anxiety and EDs [ 227 ]. OCD and SAD also tend to precede onset of ED, and BN in adolescence may increase risk of SAD and panic disorders in adulthood [ 233 ].

In some individuals, shame has been found to predict later onset of BN and social anxiety, indicating a shared risk factor for both conditions [ 234 ]. Impaired psychosocial functioning and capacity to maintain interpersonal relationships associated with shame or shyness was also found to predict ED onset among adolescents in the US [ 235 ].

Psychiatric comorbidities of ED diagnoses other than AN/BN

Evidence relating to mental health comorbidities for EDs other than AN and BN is less developed. Studies conducted investigating BED and NES are confined to clinical samples with cross-sectional designs, highlighting a need for further work in this area, especially considering the high prevalence of psychiatric comorbidities detected in individuals with these diagnoses. Among patients receiving treatment for BED, 74% had a lifetime psychiatric disorder diagnosis, and 43% had a current diagnosis [ 236 ]. In a population of overweight and obese patients with severe mental illness, 25% were diagnosed with NES and 6% with BED [ 237 ]. Other studies measuring NES in patient samples with depression and bipolar disorder (BD) found the prevalence to be 32.5% and 8.8% respectively [ 238 , 239 ]. Higher prevalence of NES was detected in both depression and BD groups compared with healthy controls, indicating increased risk among these individuals.

ED and BD comorbidities are also commonly reported in research, with association between BD and BN/BED considered particularly significant, although the casual and temporal relationships between the disorders are not well understood [ 240 – 242 ]. While it is likely that some risk factors are shared, lack of data regarding disorder onset limits commentary on the relative risk BD confers to the development of ED [ 241 ]. One review found incidence of BD to be 4.7 times higher in individuals with BN, 3.6 times higher in individuals with BED and 3.5 times higher for binge/purge ED subtypes overall. Due to the low prevalence of AN and BD in the general population, an accurate estimation of this comorbidity is difficult to obtain [ 241 , 243 ]. BD in individuals with ED is associated with increased severity of core symptoms including body dissatisfaction, weight/shape concern, eating concern, impulse regulation, interoceptive awareness and perfectionism [ 244 ]. Mood instability is also significantly higher in individuals with a BD/ED comorbidity compared to those with BD alone. Systematic review of BD and its clinical correlates by McDonald et al. [ 245 ] suggests this finding indicates shared aetiology between ED and BD through emotional dysregulation.

ADHD and autism spectrum disorders

There is an emerging body of literature exploring associations between EDs and attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorders (ASDs), however few have examined the conditions as risk factors in the development of ED. A 2016 meta-analysis of twelve studies found a three-fold increased risk of ED among individuals with ADHD [ 246 ]. Similarly, a 2020 matched cohort screening study found the same three-fold increase—almost one third of children and adolescents with ADHD were at risk of ED, compared to 12% of healthy controls. Here, BMI was a statistically significant predictor of risk [ 247 ]. Impulsivity and inattention symptoms of childhood ADHD have been positively associated with the development of overeating and bulimic-type behaviours in adolescence [ 248 ]. A longitudinal study of a large sample of adolescents reported that the onset of emotional and behavioural issues, including those associated with ADHD and conduct disorder, was observed to occur prior to the onset of disordered eating behaviours [ 249 ].

A 2013 systematic review found elevated rates of ASDs in ED populations compared with healthy controls, however, six of the eight studies in this review were based on longitudinal research using the same community sample [ 250 ]. The authors suggested a need to integrate appropriate, well-structured ASD assessment tools into routine care of ED service users, with the prevalence of ASD traits potentially contributing to ‘high treatment resistance to conventional therapies’ [ 250 ]. Dell’ Osso et al. [ 251 ] tested such an instrument in a sample of 138 individuals meeting DSM-5 criteria for an ED and 160 controls. They found significantly higher autism spectrum traits in participants with EDs, particularly verbal and non-verbal communication, inflexibility and adherence to routine, and restricted interest and rumination. Individuals with restrictive EDs were more likely to display ASD traits. Similarly, as part of a large, population-based prospective study of women and their children, Schaumberg et al. (2021) found autistic-like social communication difficulties during middle childhood were associated with BN symptoms during adolescence in both males and females [ 252 ]. They also discovered that misattribution of faces as sad or angry at 8.5 years of age was associated with a diagnosis of AN and purging behaviours at age 14. Contrarily, Dinkler et al. [ 253 ] in their prospective twin cohort study found no association between traits of autism in nine-year-old children and a later AN diagnosis, as well as noting a marked elevation in restricted/repetitive behaviour and interests only in the subgroup of individuals with acute AN. They questioned previous reports of elevated prevalence of ASD in AN and instead wondered if autistic traits may be best conceptualised as an epiphenomenon of the acute phase of AN.

Post-traumatic stress disorder

Although there is a large body of evidence relating to childhood trauma and abuse as a risk factor for the development of ED, few studies were identified investigating the role of post-traumatic stress disorder (PTSD) specifically as a risk factor. No distinction was made in the search methodology for this review between complex trauma and early childhood adverse events, with all studies captured under the search term ‘risk factors.’ Studies presented in this section, focused on the link between diagnosed PTSD and development of ED.

Results from two cohort studies observed an association between PTSD and severity of ED symptoms as well as relatively high prevalence rates within sample populations [ 254 , 255 ]. Among a patient sample in Sweden who had experienced trauma either prior to ED onset, after onset or within a year of onset, lifetime prevalence of PTSD was observed to be 24.1% [ 255 ]. An almost identical PTSD prevalence was found within a smaller ethnically diverse sample of obese women with BED in the US, at 24% [ 254 ]. Analysis of the impact of timing of trauma exposure on ED symptom severity in the Swedish sample found the association was only significant in the group who had experienced trauma in the same year of their ED diagnosis [ 255 ]. This analysis was not undertaken in the US study. Brewerton et al. [ 256 ] assessed adults entering ED treatment at seven US sites and found 49.3% had PTSD. It was found that individuals who were significantly more symptomatic had a higher propensity towards binge-type disorders and reported worse quality of life than those without PTSD. Co-occurrence of PTSD and AN was reported by Reyes-Rodriguez et al. (2011) as part of their cross-sectional study of 753 women with AN. They found 13.7% of the sample of AN patients also met criteria for PTSD with childhood sexual traumas being the most common traumatic event associated with the diagnosis [ 257 ].

Evidence from three studies relating to EDs in veteran populations—a meta-analysis (Barlett and Mitchell [ 259 ]); a retrospective chart review (Forman-Hoffman et al. [ 258 ]); and a retrospective cohort study of female veterans (Mitchell et al. [ 260 ])—found an association between increased ED prevalence and PTSD and trauma. Through a telephone interview with 1004 veterans, Formann-Hoffman et al. [ 258 ] determined that 16% of their sample had a lifetime ED with many of the cases also experiencing comorbid PTSD or lifetime sexual trauma. However, increased risk for ED among the veteran population could not be solely attributed to trauma, as unhealthy weight control behaviours are also common in this population due to strict weight and fitness requirements within the military [ 259 – 261 ].

The prevalence of personality traits appear to differ according to the ED diagnostic category. Elevated levels of perfectionism are common amongst AN and BN, obsessiveness strongly associated with AN, and binge/purge presentations consistently associated with impulsivity and greater emotional dysregulation, whereas lack of emotional awareness is not ED specific and common amongst most ED diagnoses [ 178 – 183 , 196 ]. Although co-occurrence of ED and personality disorders has been consistently identified in studies of comorbidity (e.g., BPD and binge/purge EDs), mood and anxiety disorders represent the most common psychiatric comorbidities in individuals with EDs (e.g., MDD affects over 75% of binge/purge EDs, SAD affects 42% of adults with an ED) [ 212 , 220 , 223 , 225 – 227 ]. There is also good evidence to suggest that the presence of a diagnosable childhood anxiety disorder (e.g., OCD) precedes the onset of an ED later in life [ 177 , 211 ]. Other psychological factors which appear to contribute to the risk of EDs include diagnoses of PTSD, ADHD, or ASD [ 246 , 250 , 254 ].

5. Gender differences

EDs impact a higher number of females with greater symptom severity. While common risk factors are shared across genders, such as low self-esteem and high shape/weight concern, males have been identified as less likely to engage in severe dieting behaviours compared with their female counterparts [ 262 , 263 ].

Puberty is a period of significant risk for ED development in both males and females. Research has implicated increased production of sex hormones during puberty, in particular estrogen, in the onset of EDs [ 264 ]. Evidence has consistently demonstrated that early onset of puberty is strongly associated with increased risk for ED development in both young males and females. Favaro et al. [ 265 ] linked earlier age of menarche with a younger mean age of onset of AN and BN. It has been suggested that if an individual experiences changes to their body shape, associated with menarche, at an earlier time than their peers, this may lead to heightened body dissatisfaction and which in turn may contribute to early the onset of EDs.

Despite the commonality between males and females in terms of the risk of ED development posed by puberty, it had been suggested that bodily changes experienced during this time possess a stronger impact for females as compared to males. It is thought that changes to one’s body shape move females further away from the thin ideal, whereas the changes for males move them closer to ideals around muscularity [ 266 ]. These findings have been supported by a cohort study, which found that bulimic symptoms and body dissatisfaction were associated with early puberty in females and late puberty in males [ 267 ]. Similarly, having a higher BMI comparative to peers has been associated with ED risk among teenage girls but not boys in a US school cohort [ 265 ].

Comorbidity

Research into gender differences has found that an equal proportion of male and female adolescents with an ED experience comorbid anxiety or depression [ 268 ]. A further four-year retrospective study in male adolescents with a diagnosed ED supported the assertion that comorbid anxiety and depression posed considerable ED risk to males [ 269 ]. Research has also identified increased prevalence of compulsive disorders, including gambling and substance use, among males as compared to females in a cohort of individuals at risk of ED [ 270 ]. While male ED risk has been associated with compulsive and depressive symptoms in these studies, evidence presented in a longitudinal study of adolescents found depression to be associated with higher ED symptomology in 12-year-old girls but not in boys [ 271 ]. Further research into EDs and depression in males is required to clarify the impact of this association.

Gender roles

Gender roles have been investigated as a potential contributor to ED risk. Exposure to media ideals has been found to be associated with increased body dissatisfaction and ED symptomology in university-aged males [ 272 ]. Research has also indicated that increased femininity in heterosexual males is negatively associated with muscle dissatisfaction [ 273 ]. Weak associations have also been found between femininity in women and eating pathology and body satisfaction. Among both sexes, masculinity was found to have a significant negative relationship with eating pathology, also conferring modest protection to body dissatisfaction [ 273 ].

Interactions between societal gender roles and sexual orientation is also known to play a role in ED risk with researchers suggesting that greater social body image pressures are present among gay males. A systematic review of disordered eating among sexual minority individuals has reported that elevated ED symptomology exists across all LGBTQI + groups as compared to heterosexual males and females [ 274 ]. A further study of men aged 18 to 35 found that disordered eating and body dissatisfaction was higher in gay and bisexual men compared to heterosexual men, as was susceptibility to social messaging around body image [ 275 ]. The occurrence of body image disorders has also been found to be higher among sexual minorities as compared to heterosexual samples [ 276 ]. A recent study involving a sample of transgender and gender non-binary individuals reported that increased internalised transphobia was associated with increased likelihood of disordered eating symptoms [ 277 ]. There is insufficient evidence currently available to separate risk of engagement in specific types of ED behaviours according on sexual identity [ 274 ].

The literature indicates that whilst both males and females are susceptible to risk factors for EDs such as early puberty onset and elevated weight/shape concerns, it appears that these factors have a stronger impact upon females as compared to males in terms of risk of developing disordered eating behaviours and psychopathology (e.g., severe dieting, bulimic symptoms and body dissatisfaction) [ 292 , 294 , 297 – 300 ]. Recent findings also indicate that LGBTQI + groups are at a higher risk of ED symptomology and body image disorders as compared to heterosexual individuals [ 305 – 307 ].

6. Socio-economic status

Despite the pervasive view that EDs disproportionately affect more affluent groups, evidence suggests that disordered eating behaviours occur at similar rates across all income levels and regardless of employment status [ 278 ]. Differences between socio-economic status (SES) seem to emerge in the types of disordered eating. Specifically, a positive correlation has been reported between non-fulltime workers and binge eating and purging behaviours. Also, a trade or certificate qualification has been shown to be positively associated with strict dieting as compared to groups with no higher education [ 278 ]. In contrast, a large study conducted in Sweden failed to find a relationship between social class and household income and incidence of EDs in females. However, in males, lower household income was associated with increased risk of BN and EDNOS, although the study observed a very low rate of BN in males [ 279 ].

Recent studies in the US have found low food security to be a predictor for disordered eating behaviours [ 280 ]. Among higher SES adolescents, binge eating behaviours were associated with weight-related teasing by family members [ 281 ]. In an adult sample, experience of low food security was more common among individuals with BN and BED as compared to healthy weight controls [ 282 ]. Lower food security in these individuals was associated with more frequent binge eating episodes and, in individuals with BN, unhealthy compensatory behaviours [ 282 ].

High levels of parental education have also been identified as a predictor of EDs [ 119 , 283 ]. Higher educational attainment by both parents as well as maternal grandparents has been associated with higher incidence of AN, BN, and EDNOS equally across diagnoses in females [ 279 , 284 ]. In males a positive association was found between parental education and AN, but not for BN or EDNOS [ 279 ].

Research into sociocultural risk factors for EDs suggests that income has little impact on overall ED risk although available evidence points to specific indicators that have an influence [ 278 ]. Higher education attainment is associated with restrictive ED behaviours, while experience of food insecurity is associated with binge-type behaviours and EDs [ 279 , 282 , 284 ].

7. Ethnic minority

Although there is no evidenced association between ethnic background and the risk of ED onset, specific aspects of ED psychopathology do appear to differ between ethnic groups [ 285 , 286 ]. A cohort study of females aged between nine and 22 years old found those with an ED were more likely to be non-Hispanic White, come from well-educated households, and be well-educated themselves [ 287 ]. A recent study of a treatment-seeking community sample in US found that Black individuals displayed higher rates of BED as compared to other ethnic groups, however overall Asian and Black individuals were less likely to report ED symptoms than White individuals [ 288 ]. Significantly higher thin ideal internalisation has been observed among Asian-American participants as compared with other groups [ 285 ]. Additionally, the association between fear of losing control of eating and depressive symptoms has been found to be stronger in Asian and Pacific Islander minorities than other ethnic groups [ 289 ]. In a study comparing thin-ideal internalisation among young Australian and Malaysian women, a stronger association between body dissatisfaction and restrained eating practices was observed in the Australian sample [ 286 ].

Further investigation of ethnic minority status has implicated perceived ethnic discrimination as a risk factor in ED development. In a cohort of college students, perceived discrimination based upon one’s ethnicity was associated with increased prevalence of key ED symptoms including restraint, weight/shape concern, body dissatisfaction and bulimia [ 290 ]. Perceived discrimination was also found to increase drive for muscularity among males in the sample but not drive for thinness among females. These findings indicate a potentially growing risk for ED in CALD individuals [ 290 ].

A small body of evidence was identified in the current RR regarding the association between ethnic minority status and ED risk. Of the studies reviewed, unique associations have been found between particular ethnic groups and specific aspects of ED psychopathology. For example, in comparison to other ethnic groups, higher rates of BED have been observed in Black-Americans and greater thin ideal internalisation in Asian-Americans [ 286 , 289 ]. Given that a significant proportion of ED research has been conducted using White/Caucasian participants, greater research efforts are needed to better understand the features of EDs in ethnically diverse groups.

8. Body image and social influence

Weight/shape concern, overvaluation of weight/shape and drive for thinness, referred to here using the term body image concerns, are key concepts in ED [ 291 , 292 ]. Along with the social and cultural factors that contribute to body image concerns, these concerns have been extensively investigated as risk factors for the development of EDs. Research in this area has been concentrated among women and girls whose body image concerns are characterised by a focus on low body weight and the thin-ideal [ 293 ], but greater recent focus on men and boys with regard to the muscular/lean ideal has been seen due to increasing recognition of muscle orientated EDs in males. Engagement with particular environments that shape social norms for appearance and promote pursuit of the ideal body shape or weight, or involvement in certain activities with a culture of strict dieting and excessive exercise is encouraged, such as college level or professional sports, are also well studied risk factors in ED literature.

Body image and appearance ideals

Studies using prospective designs have found evidence for body image concerns predicting development of EDs and ED behaviours. In an eight-year longitudinal study of adolescent girls, higher levels of perceived pressure to be thin, thin-ideal internalisation, and body dissatisfaction were significant predictors of later onset ED (BN, BED, and purging disorder) [ 294 ]. Among an adolescent sample, dissatisfaction with weight and shape, but not overvaluation or preoccupation, was a predictor of onset of an ED after 12 months [ 295 ]. The authors suggest that while body dissatisfaction may impart risk for ED development, the other body image-related constructs of overvaluation and preoccupation, may indicate presence of ED psychopathology. A systematic review of the impact of anti-obesity public health messages has found that endorsement of thin ideals and drive for thinness are exacerbated in response to exposure to messages which are stigmatising towards individuals who are overweight or obese [ 296 ]. In a large longitudinal sample of adolescent boys and girls, body image concerns predicted binge eating over 5 years to young adulthood [ 297 ] and persistent disordered eating 10 years later among both males and females [ 298 ], and body dissatisfaction, preoccupation with body weight and shape, and overvaluation predicted increases in disordered eating 15 years later, particularly in females [ 299 ]. Similarly, in a cohort of this sample characterised as having BMI in the overweight category, higher body image concerns predicted prevalence and onset of disordered eating (binge eating and extreme weight control behaviours) over five years [ 300 ]. Findings for body image concern as a risk factor for development of AN are mixed. In this regard, a systematic review of 46 longitudinal studies by Glashouwer et al. [ 301 ] with a pooled sample of 4,928 patients with AN was unable to definitively determine whether body dissatisfaction was a causal factor in disorder onset.

Media, social media, and the internet

The impact of media depictions of appearance ideals on ED symptoms have been examined with studies of varying methodologies. A meta-analysis of laboratory-based experimental studies found that viewing idealised images resulted in a small but non-significant increase in body dissatisfaction. However, exposure to these images was found to have a greater impact on groups considered at high-risk for developing EDs [ 302 ]. Of note, there were no differences observed in the impact of these images based on gender, indicating that men and women are equally affected by media portrayals of idealised bodies [ 302 ].

Among 574 women aged between 14 and 36, social expectations to be thin were found to mediate the relationship between protective self-presentation and disordered eating [ 303 ]. This finding aligns with research on exposure to negative parental attitudes regarding weight to be a risk factor in the later development of ED, discussed previously [ 118 , 303 ].

As with traditional media, the effects of portrayal of idealised bodies on the internet and on social media has been explored. Among young women, use of social media was found to impact weight and shape concerns [ 304 ] and among a predominantly female sample of participants with AN, use of appearance-focused social media was found to be associated with higher levels of ED symptoms [ 305 ]. A systematic review found that general internet use was associated with body image and eating concerns [ 306 ]. Further exploration of problematic internet use suggested excessive use of social media was associated with increased risk of AN and BN, while video gaming was associated with risk of BED [ 307 ]. However, recent proliferation of pro-AN or pro-ED websites and social media networks may create online environments that are more detrimental to the health of individuals at risk of ED than other forms of media. Even among females with normal BMI and no history of ED, one week of exposure to pro-ED website content resulted in a significant reduction (20%) in calorie intake among participants compared to groups who were exposed to other website content including health and fitness websites [ 308 ]. Dangers associated with pro-ED websites is not restricted to females, with a content analysis study finding that up to 25% of participants on pro-AN forums are male, suggesting that these sites may have a substantive negative impact with males engaged with these sites expressing negative experiences including body dissatisfaction [ 309 ].

Body image concerns are a well-known risk factor for EDs. High levels of body dissatisfaction and internalisation of the thin ideal have been found to be predictors of ED onset, whereas related constructs of overvaluation and preoccupation with weight and shape are considered to reflect current ED psychopathology [ 270 – 277 ]. Exposure to the thin ideal via either traditional media or social media is associated with greater risk of an ED, with evidence suggesting that both males and females are equally impacted by this content [ 278 – 283 ].

9. Elite sports, female athlete triad, and excessive exercise

Engagement in activities that accept or promote strict dieting practices and endorsement of low body fat has the potential to contribute to development and maintenance of ED symptoms [ 310 ]. Consistent with this, EDs among elite and college/university level athletes were observed at higher rates than in non-athlete comparison groups [ 311 ], although no difference in prevalence of EDs was found between athletes engaged in sports with an emphasis on aesthetics and/or weight and athletes engaged in sports without this focus. The female athlete triad (FAT), characterised by low energy availability (through increased physical activity or dietary restriction), amenorrhea and low mineral bone density, is considered a consequence of training for elite level sports and pursuit of lean physiques [ 312 ]. Features of FAT have also been observed in elite para-athletes (n = 260) with no difference in risk between genders or sport type [ 313 ].

In relation to ED behaviours, among elite athletes (n = 224), high prevalence of clinically significant ED symptomology (22.8%) has also been found [ 314 ].Similarly, in a sample of college level female gymnasts and swimmers (n = 325), 4.6% (n = 15) engaged in intentional vomiting, 1.5% (n = 5) used laxatives and 2.5% (n = 8) used diuretics for weight control. Additionally, 10.5% (n = 3.4) engaged in binge eating two or more times a week, while almost all participants engaged in binge eating once a week, 96.6% (n = 314) [ 315 ]. However, in a smaller UK sample of male and female gymnasts (n = 51) no purging behaviours were observed, although 31% of male gymnasts in this group scored highly on ED self-report questionnaires [ 316 ].

However, other studies have not found these differences between athlete and non-athlete groups. For example, a cohort study comparing elite and non-elite athletes to controls (n = 725) was also unable to find any differences between the three groups in terms of ED behaviours. However, it did highlight distinct differences associated with social pressures and influences on body image and weight in athletes versus non-athletes. There is some evidence to suggest that unlike female athletes, male athletes are not at greater risk of developing EDs than non-athletes [ 317 ]. Evidence from a meta-analysis of 31 studies of ED athletes indicated that, with the exception of wrestling, male athletes were not at greater risk of disordered eating than non-athletes. Although, researchers noted that studies were heterogenous and measurements were impacted by the potential inappropriateness of ED assessment tools for male populations [ 318 ].

Among non-elite populations, recognising excessive physical activity or exercise levels among women in the community is particularly important in risk assessment of ED, as these individuals were found to be 2.5 times as likely to have an ED diagnosis than non-excessively exercising individuals [ 319 ]. Furthermore, participation in activities promoting lean body types such as yoga and pilates has also been highlighted as a potential risk factor for ED development. However, in a large cohort study (n = 2,287) of young adults no association was found between participating in yoga and pilates and ED symptomology among female subjects but increased risk of unhealthy and extreme weight control behaviours as well as binge eating was observed in males [ 320 ]. Further research is required to understand the unique associations identified in this study.

Similar to athletic settings, other physical activity pursuits take place in environments that may promote ED symptoms. A systematic review and meta-analysis observed higher rates of ED among dancers, where dancers were found to have three times greater risk of having AN or EDNOS but not BN, than the general population and risk was particularly heightened among ballet dancers [ 321 ].

Involvement in elite sports is a potential risk factor for disordered eating behaviours among both male and female athletes [ 311 – 317 ]. Increased attention should be paid towards excessive exercise by non-elite populations in the community as risk factor for EDs and to support screening and early intervention activities [ 318 – 320 ].

This review to aimed to summarise recent peer-reviewed evidence relating to risk factors associated with EDs. An extensive number of research studies were identified, exploring a multitude of risk factors. For the purposes of this review, the research findings were broadly characterised into nine primary categories: (1) genetics, (2) gastrointestinal microbiota and autoimmune reactions, (3) childhood and early adolescent experiences, (4) personality traits and comorbid mental health conditions, (5) gender, (6) socio-economic status, (7) ethnic minority, (8) body image and social influence, (9) and elite sports.

Identification of the recent evidence relating to key risk factors offers valuable knowledge to researchers, clinicians, and policy makers, such that it may inform the development of evidence-based approaches for the care and treatment of individuals with EDs. An understanding of risk factors is essential for the development and refinement of aetiological models [ 8 ]. In a recent review of existing models of disordered eating, Pennesi and Wade [ 21 ] reported that very few of the existing theoretical models (18.5%) have informed the development of effective interventions. The authors call upon researchers to use empirically supported risk-factors to modify existing theories, which then can inform prevention and treatment interventions [ 21 ].

The findings of the current review can be used to determine which risk factors are differentially appropriate targets for prevention, early intervention, and/or treatment efforts [ 322 ]. For example, modifiable risk factors such as negative parental comments towards weight and eating behaviours may be best approached using targeted prevention parenting programs to assist with modelling of healthy eating patterns and family dialogue. There is evidence to suggest targeted prevention programs addressing early signs of disordered eating in adolescents (e.g., the Body Project, StudentBodies2-BED ) are effective in significantly reducing future onset of EDs [ 323 , 324 ]. They represent a targeted, efficient way of addressing modifiable risk factors rather than approaching the population as a whole in a largely non-specific manner.

Identifying risk factors which are less amenable to modification, such as genetic risk factors and autoimmune conditions, may represent an opportunity for enhanced screening measures to recognise early signs of disordered eating prior to onset of full ED diagnosis. Research has identified low levels of screening and poor detection rates of EDs by health practitioners, in particular non-stereotypical presentations of EDs in primary care settings [ 325 – 327 ]. A noteworthy outcome of the current review pertains to the growing field of evidence supporting increased risk of EDs within the sexual minority groups as compared to heterosexual samples. Given the high levels stigma surrounding both LGBTQI and EDs, particularly for young males, it is of particular importance that clinicians thoroughly assess for disordered eating behaviours within sexual minority groups [ 328 , 329 ]. Accordingly, the findings of this review may offer an opportunity for advances in the development of resources (e.g., screening instruments) to assist practitioners in recognising evidenced risk factors for EDs.

Finally, awareness of comorbid psychiatric illnesses or personality traits may inform targets for treatment interventions, including as specific programs for individuals with comorbid personality disorders and ED. Enhanced Cognitive Behaviour Therapy (CBT-e) offers an example of the way in which comorbid psychological traits, considered to be “external” to the ED itself, can be addressed to create a more efficacious, tailored treatment for patients [ 330 ]. The inclusion of additional treatment targets to address comorbid psychological mechanisms (clinical perfectionism, core low self-esteem, and interpersonal problems) allows for cognitive behaviour therapy treatment to meet the needs of non-responders for whom comorbid psychopathology may have interfered with their treatment response [ 331 ].

Additionally, given the search strategy of the review adopted a timeline which overlaps between two versions of the Diagnostic and Statistical Manual of Mental Disorders [ 332 ], namely Version 4 and 5 (i.e., DSM-IV and DSM-5), our findings were able to highlight inconsistences in the degree of research conducted across various ED diagnoses. In particular, the findings demonstrate that considerably less is known about the risk factors associated with EDs which were recently included as formal diagnoses in the DSM-5, including ARFID, BED, rumination disorder, and pica, highlighting the need for more focused research efforts to be put towards these diagnoses.

In this review, gaps in the existing literature were identified. Many of the research studies included in the review adopted a cross-sectional study design and therefore focused upon associations and correlations between EDs and potential risk factors. Consequently, some studies were limited in their capacity to delineate temporal or causal relationships, or how in fact the associations connect the factor with the illnesses. For example, although an understanding of psychiatric comorbidities of EDs (e.g., perfectionism, impulsivity etc.) provides value, without longitudinal research it is difficult to disentangle whether these traits contribute to ED onset or are symptoms of it. Similarly, identification of trauma and abuse as a risk factor for eating disorders needs further clarification as this association has been described for many other mental health conditions such as anxiety and depression [ 333 ], and is not likely a specific association to eating disorders. Additionally, several of the studies included in the current review were not able to distinguish between factors related to onset and factors related to maintenance in EDs, which represents an important differentiation of different classes of risk factors and their influence [ 207 ]. It is possible that some of the constructs reviewed in the present paper have a role as maintenance factors, even if they may not have a role as a causal risk factor. An understanding of whether one psychiatric condition precedes another can assist clinicians in treatment planning and inform sequencing of treatment targets. Taken together, these considerations represent a limitation in our ability to understand the implications of these identified risk factors. For risk factors which have relied heavily upon cross-sectional studies, future research is encouraged to adopt experimental or prospective study designs to better capture the nature of the variable being examined.

Several of the studies included in the review examined risk factors in isolation from one another and thus assessment of their association with EDs occurred as though they were independent contributors of risk. This is markedly distinct from real world environments in which EDs develop in response to a multitude of risk factors and consequently, weakens the ecological validity of the reported findings. An understanding of the ways in which various risk factors interact with each other (e.g., whether they are cumulative in nature), is necessary to form a detailed conceptualisation of illness profiles for both clinicians and researchers, which can in turn inform the development of targeted interventions. Conversely, in the absence of this information, the mechanisms of change are less clear. Future research would benefit from adopting an approach towards risk factors as co-occurring, interactional variables as opposed to a siloed view.

Given the attempt to summarise peer-reviewed ED literature in a broad-reaching and prompt manner, there are some limitations of the review. First broad search terms, required to fulfil the purpose of the large series of rapid reviews, of which this paper forms part, were used to collate evidence, which may have compromised the specificity of the included studies for individual ED diagnoses and/or phenotypes and individual risk factors. Additionally, research studies were excluded if they reported on unpublished data, implementation research, or if they were observational studies; and included studies were mostly limited to those conducted in Western cultures with high-resource health systems. Finally, having a specified time period for the review meant that seminal studies conducted prior to the start date were not included.

Conclusions

This review has identified risk factors for which a substantial evidence-base exists as well as emerging areas requiring further investigation (e.g., ADHD) and ED diagnoses where there is less available evidence (e.g., BED, ARFID). A broad review of the literature has been provided, however future studies are required which critique the strength of evidence of the causal nature of these risk factors.

Acknowledgements

The authors would like to thank and acknowledge the hard work of Healthcare Management Advisors (HMA) who were commissioned to undertake the Rapid Review. Additionally, the authors would like to thank all members of the consortium and consultation committees for their advice, input, and considerations during the development process. Further, a special thank you to the carers, consumers and lived experience consultants that provided input to the development of the Rapid Review and wider national Eating Disorders Research & Translation Strategy. Finally, thank you to the Australian Government—Department of Health for their support of the current project.

Abbreviations

ED	Eating disorder
BN	Bulimia nervosa
AN	Anorexia nervosa
BED	Binge eating disorder
AN-R	Anorexia nervosa (restrictive subtype)
ARFID	Avoidant restrictive food intake disorder
AN-BP	Anorexia nervosa (binge-purge subtype)
EDNOS	Eating disorder not otherwise specified
A-AN	Atypical anorexia nervosa
BMI	Body mass index
NES	Night eating syndrome
ADHD	Attention-deficit/hyperactivity disorder
ASD	Autism spectrum disorder
DBT	Dialectical behaviour therapy
BPD	Borderline personality disorder
MDD	Major depressive disorder
SAD	Social anxiety disorder
BD	Bipolar disorder
PTSD	Post-traumatic stress disorder
SES	Socioeconomic status
CALD	Culturally and linguistically diverse
FAT	Female athlete triad

Author contributions

PM, ST and SM oversaw the Rapid Review process; AL carried out and wrote the initial review; SB, SMC and EB wrote the first manuscript; all authors edited and approved the final manuscript.

The RAPID REVIEW was in-part funded by the Australian Government Department of Health in partnership with other national and jurisdictional stakeholders. As the organisation responsible for overseeing the National Eating Disorder Research & Translation Strategy, InsideOut Institute commissioned Healthcare Management Advisors to undertake the RAPID REVIEW as part of a larger, ongoing, project. Role of Funder: The funder was not directly involved in informing the development of the current review.

Availability of data and materials

Declarations.

Not applicable.

ST receives royalties from Hogrefe and Huber, McGraw Hill and Taylor and Francis for published books/book chapters. He has received honoraria from the Takeda Group of Companies for consultative work, public speaking engagements and commissioned reports. He has chaired their Clinical Advisory Committee for Binge Eating Disorder. He is the Editor in Chief of the Journal of Eating Disorders. ST is a committee member of the National Eating Disorders Collaboration as well as the Technical Advisory Group for Eating Disorders. AL undertook work on this RAPID REVIEW while employed by HMA. A/Prof Sarah Maguire is a guest editor of the special issue “Improving the future by understanding the present: evidence reviews for the field of eating disorders.”

1 having three different alleles at the same locus.

2 Polymorphism is a DNA sequence variation.

3 perception or awareness of sensations inside the body.

4 DNA methylation is a process that controls the expression/suppression of a gene without changing the genetic sequence.

5 Small molecules formed in or necessary for metabolism.

6 Models using rates and mice.

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Patient Care & Health Information
Diseases & Conditions
Celiac disease

Your small intestine is lined with tiny hairlike projections called villi, which absorb sugars, fats, proteins, vitamins, minerals and other nutrients from the food you eat. Gluten exposure in people with celiac disease damages the villi, making it hard for the body to absorb nutrients necessary for health and growth.

Celiac disease is an illness caused by an immune reaction to eating gluten. Gluten is a protein found in foods containing wheat, barley or rye.

If you have celiac disease, eating gluten triggers an immune response to the gluten protein in your small intestine. Over time, this reaction damages your small intestine's lining and prevents it from absorbing nutrients, a condition called malabsorption.

The intestinal damage often causes symptoms such as diarrhea, fatigue, weight loss, bloating or anemia. It also can lead to serious complications if it is not managed or treated. In children, malabsorption can affect growth and development in addition to gastrointestinal symptoms.

There's no definite cure for celiac disease. But for most people, following a strict gluten-free diet can help manage symptoms and help the intestines heal.

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The symptoms of celiac disease can vary greatly. They also may be different in children and adults. Digestive symptoms for adults include:

Weight loss.
Bloating and gas.
Abdominal pain.
Nausea and vomiting.
Constipation.

However, more than half the adults with celiac disease have symptoms that are not related to the digestive system, including:

Anemia, usually from iron deficiency due to decreased iron absorption.
Loss of bone density, called osteoporosis, or softening of bones, called osteomalacia.
Itchy, blistery skin rash, called dermatitis herpetiformis.
Mouth ulcers.
Headaches and fatigue.
Nervous system injury, including numbness and tingling in the feet and hands, possible problems with balance, and cognitive impairment.
Joint pain.
Reduced functioning of the spleen, known as hyposplenism.
Elevated liver enzymes.

Children with celiac disease are more likely than adults to have digestive problems, including:

Chronic diarrhea.
Swollen belly.
Pale, foul-smelling stools.

The inability to absorb nutrients might result in:

Failure to thrive for infants.
Damage to tooth enamel.
Irritability.
Short stature.
Delayed puberty.
Neurological symptoms, including attention-deficit/hyperactivity disorder (ADHD), learning disabilities, headaches, lack of muscle coordination and seizures.

Dermatitis herpetiformis

Gluten intolerance can cause this blistery skin disease. The rash usually occurs on the elbows, knees, torso, scalp or buttocks. This condition is often associated with changes to the lining of the small intestine identical to those of celiac disease, but the skin condition might not cause digestive symptoms.

Health care professionals treat dermatitis herpetiformis with a gluten-free diet or medicine, or both, to control the rash.

When to see a doctor

Consult your health care team if you have diarrhea or digestive discomfort that lasts for more than two weeks. Consult your child's health care team if your child:

Is irritable.
Is failing to grow.
Has a potbelly.
Has foul-smelling, bulky stools.

Be sure to consult your health care team before trying a gluten-free diet. If you stop or even reduce the amount of gluten you eat before you're tested for celiac disease, you can change the test results.

Celiac disease tends to run in families. If someone in your family has the condition, ask a member of your health care team if you should be tested. Also ask about testing if you or someone in your family has a risk factor for celiac disease, such as type 1 diabetes.

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Your genes, combined with eating foods with gluten and other factors, can contribute to celiac disease. However, the precise cause isn't known. Infant-feeding practices, gastrointestinal infections and gut bacteria may contribute, but these causes have not been proved. Sometimes celiac disease becomes active after surgery, pregnancy, childbirth, viral infection or severe emotional stress.

When the body's immune system overreacts to gluten in food, the reaction damages the tiny, hairlike projections, called villi, that line the small intestine. Villi absorb vitamins, minerals and other nutrients from the food you eat. If your villi are damaged, you can't get enough nutrients, no matter how much you eat.

Risk factors

Celiac disease tends to be more common in people who have:

A family member with celiac disease or dermatitis herpetiformis.
Type 1 diabetes.
Down syndrome, William syndrome or Turner syndrome.
Autoimmune thyroid disease.
Microscopic colitis.
Addison's disease.

Complications

Celiac disease that is not treated can lead to:

Malnutrition. This occurs if your small intestine can't absorb enough nutrients. Malnutrition can lead to anemia and weight loss. In children, malnutrition can cause slow growth and short stature.
Bone weakening. In children, malabsorption of calcium and vitamin D can lead to a softening of the bone, called osteomalacia or rickets. In adults, it can lead to a loss of bone density, called osteopenia or osteoporosis.
Infertility and miscarriage. Malabsorption of calcium and vitamin D can contribute to reproductive issues.
Lactose intolerance. Damage to your small intestine might cause you abdominal pain and diarrhea after eating or drinking dairy products that contain lactose. Once your intestine has healed, you might be able to tolerate dairy products again.
Cancer. People with celiac disease who don't maintain a gluten-free diet have a greater risk of developing several forms of cancer, including intestinal lymphoma and small bowel cancer.
Nervous system conditions. Some people with celiac disease can develop conditions such as seizures or a disease of the nerves to the hands and feet, called peripheral neuropathy.

Nonresponsive celiac disease

Some people with celiac disease don't respond to what they consider to be a gluten-free diet. Nonresponsive celiac disease is often due to contamination of the diet with gluten. Working with a dietitian can help you learn how to avoid all gluten.

People with nonresponsive celiac disease might have:

Bacterial overgrowth in the small intestine.
Poor pancreas function, known as pancreatic insufficiency.
Irritable bowel syndrome.
Difficulty digesting sugar found in dairy products (lactose), table sugar (sucrose), or a type of sugar found in honey and fruits (fructose).
Truly refractory celiac disease that is not responding to a gluten-free diet.

Refractory celiac disease

In rare instances, the intestinal injury of celiac disease doesn't respond to a strict gluten-free diet. This is known as refractory celiac disease. If you still have symptoms after following a gluten-free diet for 6 months to 1 year, you should talk to your health care team to see if you need further testing to look for explanations for your symptoms.

Celiac disease care at Mayo Clinic

Rubio-Tapia A, et al. American College of Gastroenterology guidelines update: Diagnosis and management of celiac disease. American Journal of Gastroenterology. 2023; doi:10.14309/ajg.0000000000002075.
Catassi C, et al. Coeliac disease. The Lancet. 2022; doi:10.1016/S0140-6736(22)00794-2.
Singh P, et al. Who to screen and how to screen for celiac disease. World Journal of Gastroenterology. 2022; doi:10.3748/wjg.v28.i32.4493.
What is celiac disease? Celiac Disease Foundation. https://celiac.org/about-celiac-disease/what-is-celiac-disease/. Accessed April 26, 2023.
Feldman M, et al., eds. Celiac disease. In: Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management. 11th ed. Elsevier; 2021. https://www.clinicalkey.com. Accessed April 26, 2023.
Celiac disease. National Institute of Diabetes, Digestive and Kidney Diseases. https://www.niddk.nih.gov/health-information/digestive-diseases/celiac-disease. Accessed April 26, 2023.
Ami TR. AllScripts EPSi. Mayo Clinic. March 24, 2023.
Khanna S (expert opinion). Mayo Clinic. May 12, 2023.

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Open access
Published: 07 June 2024

Avoidant restrictive food intake disorder: recent advances in neurobiology and treatment

Natasha K. O. Fonseca ORCID: orcid.org/0000-0003-4661-5740 1 ,
Vitória D. Curtarelli 2 ,
Juliana Bertoletti 3 ,
Karla Azevedo 2 , 6 ,
Tiago M. Cardinal 4 ,
Júlia D. Moreira ORCID: orcid.org/0000-0002-2256-7222 5 , 6 &
Luciana C. Antunes ORCID: orcid.org/0000-0002-0106-0721 4 , 5 , 6

Journal of Eating Disorders volume 12 , Article number: 74 ( 2024 ) Cite this article

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Avoidant restrictive food intake disorder (ARFID) is an eating disorder characterized by persistent insufficient nutritional and/or energy intake. ARFID, before referred to as “selective eating disorder”, was introduced recently in the DSM-5 as a replacement for and expansion of the previous diagnosis. Individuals with ARFID may limit food variety and intake due to avoidance based on the sensory characteristics of the food or related to any adverse consequences of eating without the intention of losing weight and concerns of body image. The limited understanding of avoidant and restrictive eating poses challenges to effective treatment and management, impacting directly on the growth and development of children and adolescents. The ARFID neurobiological concept has not yet been clearly defined to clinical practice for nutritionists, thereby hindering screening and impeding the development of treatment recommendations. This narrative review provide useful practical information to consult the pathophysiology, the neurobiology, the clinical features, the assessment and the treatment for healthcare professionals seeking to enhance their clinical knowledge and management of this disorder.

Plain English summary

Avoidant restrictive food intake disorder (ARFID) is an eating disorder characterized by persistent insufficient nutritional and/or energy intake. Individuals with ARFID exhibit limited food intake and variety, often due to a lack in eating, without the primary goal of weight loss. The limited understanding of avoidant and restrictive eating poses challenges in terms of effective treatment and management, which directly impacts the growth and development of children and adolescents, as well as their nutrition and psychosocial well-being. ARFID is a relatively recent diagnostic classification, representing a burgeoning field of study. The identification of diagnostic criteria and the pursuit of new knowledge in this area have only recently begun. Consequently, assessment tools and treatment strategies are still in the process of development and validation. This narrative review explored the neurobiological perspective of ARFID using the three-dimensional model, examined its etiology and risk factors, evaluated clinical screening and evaluation tools, discussed common clinical complications, and presented different types of nutritional, behavioural, and pharmacological interventions used in ARFID treatment.

Introduction

Eating behaviour relies on the successful integration of various neurobiological functions, as well as family and interpersonal relationships, during early human development. Disruptions in one or more of these multisystemic areas can lead to dysfunctional eating behaviours or eating disorders [ 1 ]. When a specific aspect of eating behaviour deviates from the norm or cultural norms and causes suffering, disability, and impairment in daily activities, it is highly likely to be classified as an eating disorder [ 2 ]. Eating disorders have a multifactorial etiology determined by genetic, sociocultural predispositions, biological and psychological vulnerabilities and patterns of interpersonal relationships [ 3 ].

Individuals with Avoidant Restrictive Food Intake Disorder (ARFID) may restrict their food intake and variety due to an apparent lack of interest in eating (low interest), exhibit avoidant eating behaviour based on sensory characteristics of foods (sensory limitations) and/or express concern about the aversive consequences of eating (fear) [ 4 ].

Studies on the neurobiological basis of ARFID support a three-dimensional model that explains the three primary clinical presentations: neurobiological alterations in sensory perception, appetite homeostasis, and negative valence systems. These alterations can create a negative and stressful environment surrounding food intake [ 5 , 6 ].

To synthesize recent advancements in understanding ARFID and identify current gaps in the literature, we conducted a comprehensive literature review using the MedLINE/PubMed and Scopus databases until April 2023. We selected all articles published in English and Portuguese since 2013. The keywords and terms employed in the review encompassed the following: Avoidant Restrictive Food Intake Disorder/ARFID; ARFID and Selective eating; ARFID and sensory sensitivity; ARFID and sensory hypersensitivity; ARFID Neurobiology; ARFID complication; ARFID treatment. Additionally, we actively searched for recently published meta-analyses and systematic reviews, as well as examined the reference lists of research articles for further relevant sources.

Avoidant restrictive food intake disorder

Prior to the DSM-5, it became evident that a subset of children, adolescents, and young adults experienced eating difficulties that did not fit into existing diagnostic categories. These patients often received various diagnoses, including the residual diagnosis of Eating Disorder Unspecified [ 7 , 8 ], which was inadequate as these individuals did not exhibit weight and/or shape concerns [ 1 ]. ARFID is a comprehensive term encompassing a range of eating-related issues, including apparent lack of interest in eating, selective and demanding eating, food phobia, avoidance based on sensory characteristics of food, emetophobia, functional dysphagia, and globus hystericus, which refers to anxiety about the aversive consequences of eating [ 8 , 9 , 10 ].

Initially, the diagnostic category was limited to children under the age of 6 and focused on the dysfunctional relationship between the eating disorder and caregiver-child interactions [ 1 ]. It is common for children to exhibit food-related complaints such as selectivity or avoidance during their developmental stages. They may have idiosyncratic preferences for specific flavours and consistencies, but these are typically self-limiting inclinations that are part of natural and transient development, seldom necessitating intervention [ 11 , 12 ]. However, when a persistent condition arises, causing clinically significant problems and interfering with physical, social, and emotional development, the diagnosis of ARFID should be considered.

Definition and diagnostic criteria

ARFID is characterised as a persistent eating disorder that exhibits clinical heterogeneity. According to the DSM-5, ARFID is defined by the following criteria: Criterion A—an eating disorder characterized by the persistent failure to meet appropriate nutritional and/or energy needs, resulting in (i) clinically significant weight loss, or, in the case of children, failure to achieve expected and adequate growth or delayed growth; (ii) significant nutritional deficiencies; (iii) reliance on enteral or oral nutritional supplementation; and/or (iv) substantial impairment in psychosocial functioning [ 13 ]. Criterion B states that the eating disorder cannot be better explained by the unavailability of food or a culturally accepted practice. Criterion C specifies that the eating disorder should not occur exclusively during Anorexia Nervosa (AN) or Bulimia Nervosa (BN), and there should be no evidence of disturbance in the perception of weight or body shape. Criterion D emphasizes that food restriction/avoidance should not be better explained by or co-occur with another medical condition or eating disorder. The eating disorder is not attributable to a co-occurring medical condition or better explained by another mental disorder, such as AN. When an eating disorder occurs in the context of another condition or disorder, its severity exceeds that usually associated with the condition or disorder and warrants additional clinical attention [ 13 ].

Restriction by the sensory characteristics of foods tends to appear in the first decade of child development and can last throughout adult life [ 13 ]. ARFID can have a chronic course that significantly impacts the psychosocial functioning of both the patient and their family. The diagnosis of ARFID is made when the individual fails to meet appropriate nutritional requirements (such as anemia and vitamin deficiency), resulting in significant weight loss that they are not influenced or motivated by body shape, lack of weight gain or growth in children, or when the behaviour markedly interferes with psychosocial functioning [ 10 , 14 ].

Clinical characteristics

Three subtypes were identified based on motivations for food avoidance and corresponding to the descriptive presentations of ARFID, according to the DSM-5: (1) ARFID-low appetite, individuals with limited food intake who had low appetite, lack of interest in food; had difficulties with the act of eating, such as small bites, prolonged time to finish meals; (2) ARFID-sensory limitations, those with limited variety associated with sensory problems and aversions related to certain foods or profound rigidity involving the act of eating such as food selectivity, food neophobia; and (3) ARFID-aversive, individuals with avoidance histories/nutritional restriction that occurred and/or evolved as a result of an event (choking, vomiting) or specific fear (fear of choking, pain or nausea).

However, although the DSM-5 criteria include these commonly observed clinical presentations of ARFID, there is a lack of evidence supporting the etiology behind these presentations. Thus, these clinical subtypes serve as illustrative examples to aid in accurate diagnosis, recognizing that other causal processes may contribute to food restriction in children with ARFID [ 15 ].

A strategy used in previous studies to understand the clinical presentation of patients with ARFID has been to compare them with cases of AN and BN [ 7 , 16 , 17 ]. When compared with individuals with AN or BN, individuals diagnosed with ARFID tended to be significantly younger (mean age in ARFID ranged from 11.1 to 14.6 years versus 14–15.6 years in AN and 14.9– 16.7 years in BN), have a longer duration of illness (12–33 months in ARFID vs. 8–23 months in other EDs) and have more male patients (men ranging from 21 to 50%); although female patients continue to be the majority among all diagnostic groups and, in general, the pediatric sample with ARFID is equally common in boys and girls [ 18 ]. Patients with ARFID were more likely to have a medical condition or an anxiety disorder compared to patients with AN or BN, however, they were less likely to have mood disorders [ 7 , 16 ]. In terms of weight, patients with ARFID consistently are at a lower weight than patients with BN, but at a similar weight or a slightly higher weight compared to patients with AN [ 7 , 15 , 17 , 19 ]. Patients with ARFID, during admission interviews for daily programs targeting eating disorders, report no body image distortion or desire for weight loss. They also exhibit fewer compensatory behaviors commonly associated with eating disorders, such as purging or excessive exercise [ 16 ].

Etiology and risk factors

It is important to highlight that the majority of the available knowledge on ARFID is based on studies involving relatively small clinical samples, primarily comprising individuals from eating disorder programs or those seeking specialized medical help [ 15 ]. Furthermore, due to the relatively recent establishment of diagnostic criteria, investigations into the prevalence and etiology of ARFID have mainly relied on retrospective studies [ 7 , 16 , 17 , 19 , 20 ]. Another knowledge gap lies in understanding the characteristics associated with ARFID in adults, as most studies have focused on pediatric samples covering childhood and adolescence [ 21 ]. Even without exact data, a prevalence range of 0.5–5% is estimated in the general population, both in adults and children [ 22 ]. The incidence of ARFID in children 5 to 18 years of age was 2.02 (95% CI 1.76–2.31) per 100.000 patients in a study with 207 children and adolescents based on the Canadian Paediatric Surveillance Program survey [ 23 ]. In this same study, Kaztman et al. (2021) show that age- and sex-specific differences were noted for diagnostic criteria, medical characteristics, psychiatric comorbidities, eating behaviors, and hospitalization [ 23 ].

ARFID has a heterogeneous group of presentations with likely multiple etiologies, such as neurobiological, neurodevelopment, genetic, sociobehavioral among others. Most individuals diagnosed with ARFID have primary medical diagnoses comorbid food difficulty and restriction, most commonly neurological or gastroenterological disorders. Nonetheless, even when associated, these disorders are not considered the reason for the development of ARFID, as Criterion D states that the eating behavior is not better explained by something else.

Neurodevelopmental disorders are comorbid some presentations and are more common especially Autism Spectrum Disorder (ASD) and Attention Deficit Hyperactivity Disorder (ADHD). [ 14 ]. Patients with comorbid autism spectrum disorder (ASD; 28%) showed more food-related sensory sensitivities (RR = 1.26) and greater lack of interest in eating (RR = 1.18) than those of patients without ASD (49%) [ 24 ]. While other patients may or may not have another associated medical condition. Patients' anxiety traits showed the greatest positive correlations with symptoms of concern about aversive consequences of eating [ 24 ]. Certain presentations of ARFID bear similarities to anxiety disorders (e.g., choking phobia) and are likely to have a similar etiology (psychiatric and general medical factors are involved and may be a response to environmental stressors) [ 14 ].

Zickgraf et al. (2019) suggests that etiological and maintenance factors that influence eating behavior in ARFID may be associated with distinct patterns of restrictive eating [ 25 ]. While Thomas et al. (2017) hypothesize that the clinical presentation of an individual with ARFID can be understood as a single point along a three-dimensional space, that is, the three presentations described above vary in severity but are not mutually exclusive (sensory perception, homeostatic appetite and negative valence systems). The available data supporting the dimensional model suggest that the majority of diagnosed individuals undergoing psychological treatment present eating difficulties in several domains of the ARFID [ 6 ].

According to Brigham et al. (2018), the etiology of ARFID may involve biological factors, sensory sensitivity, anxiety traits, and the interplay between homeostatic and hedonic aspects of eating behaviour, which can contribute to increased vulnerability and act as predisposing factors [ 26 ]. Coglan and Otasowie (2019) propose a framework for understanding the contributing factors to ARFID, categorizing them into three groups, similar to models proposed for other eating disorders: predisposing, precipitating, and perpetuating factors [ 10 ] (Fig. 1 ).

Predisposing, precipitating, and perpetuating factors of the ARFID framework

Predisposing factors encompass neurodevelopmental disorders, such as ASD and ADHD, which serve as the foundation for certain clinical presentations of ARFID. Sensory hypersensitivity, often observed in individuals with ASD, can interfere with the consumption of specific foods, resulting in dietary restrictions. The distractibility and agitation associated with ADHD can impact eating behaviour, leading to decreased interest in food and heightened arousal levels during mealtimes. Additionally, a primary medical condition can act as a predisposing factor, as a significant proportion of children with feeding difficulties have gastrointestinal or neurological disorders, as well as food allergies [ 10 ].

Among the precipitating factors are traumatic episodes or some specific event in which individual has been experienced or witnessed such as vomiting, choking, and abdominal discomfort. Stressful events that may contributed on the pathogenesis of eating disorders depends on how each individual reacts to situations and the resources that each one has to respond to them [ 4 ].

A previous study retrospectively determined the incidence of ARFID in children and adolescents using the DSM-5 diagnostic criteria in a pediatric eating disorder program [ 27 ]. The authors observed that 71.4% of patients reported a triggering factor for their eating disorder, including abdominal pain, bullying, death of a family member or friend, initiation of a medication, vomiting or witnessing vomiting, food allergy concern, and animal rights concern [ 27 ].

Among the factors that perpetuate or maintain the ARFID are the frustration of the parents at feeding moment; the restrictive offer of the child's favorite foods; and not being introduced to new foods or new ways of eating preparation. All these examples are recognized for contributing to children's feeding problems and may be one of the explanations for the maintenance of dysfunctional behaviors associated with the disorder [ 10 , 16 ].

Neurobiology of ARFID

Various studies have examined the neurobiological basis of ARFID (Fig. 2 ). Patients with ARFID often exhibit restrictive eating behaviours that can be categorized into different functional domains described below [ 5 ].

The neurobiological basis of ARFID

ARFID and sensory sensitivity

Individuals with ARFID who exhibit food avoidance behaviour based on discomfort associated with the sensory properties of food (such as texture, temperature, colour, smell, and presentation) often report intensely negative taste experiences with non-preferred foods [ 6 , 13 , 28 , 29 ]. This domain of ARFID involves the selective refusal of specific food items while accepting preferred foods without difficulty [ 30 ].

Sensory sensitivity, considered an intrinsic characteristic, involves differences in the perception, reactivity, and integration of sensory information, including taste (bitterness, sweetness), touch sensations (viscosity, food texture), and odours, which vary among individuals. Sensory sensitivity and sensory integration disorders have been associated with food selectivity [ 7 , 31 ].

Hyperresponsiveness or hypersensitivity refers to an exaggerated response to sensory stimuli. In individuals with ASD, food selectivity may be related to sensory sensitivity, sensory processing dysfunction, and altered responses to sensory inputs, particularly in terms of sensory modulation, resulting in hyper or hyporesponsiveness [ 32 , 33 ]. Both food avoidance and food selectivity are commonly observed in individuals diagnosed with ASD and ADHD. Parents and clinicians frequently report that children with ASD exhibit highly selective eating patterns and have a limited variety of foods in their diet [ 32 , 34 ]. In these cases, sensory hyperresponsiveness appears to be associated with food selectivity [ 33 ].

On average, 13–50% of patients with ARFID present comorbidities with ASD [ 35 ]. Bourne and collaborators (2022) state that although the literature on children and young people with autism reliably highlights the three main reasons for food avoidance and restriction in ARFID, according to the original diagnostic guidelines, sensory sensitivities are currently the most cited. Given the atypical sensory processing associated with ASD, texture aversion is the most commonly reported concern, although sensitivity to taste, temperature, type, color, and appearance have also been described [ 35 ].

One consistent feature of ASD is that it is more commonly diagnosed in boys than in girls [ 36 ]. On the other side, Katzman et al. (2021) show that boys had a higher rate of refusal based on sensory characteristics (51.2%; 95% CI 40.2–62.2%) compared with girls (31.5%; 95% CI 23.9–40.2%; P = 0.007) in a sample of 207 children and adolescents with ARFID [ 23 ]. The DSM-V shares that ARFID is more common in men than women in those with comorbid ASD. What still remains a gap in the literature is whether the sensory profile would be greater in men than in women and whether sex could predict this characteristic of sensory sensitivity.

Thomas et al. (2017) hypothesized that sensory hypersensitivity influences taste perception [ 6 ]. A study by Kauer et al. (2015) found that adults self-identified as "picky eaters" were more likely to reject foods with bitter or sour tastes but not those that were sweet or salty [ 37 ]. Moreover, they rated sweet and bitter flavours as more intense compared to the control group. Individuals who were more sensitive to bitterness were referred to as "supertasters" and exhibited aversive reactions and subsequent refusal of foods [ 30 ]. Research on food selectivity in children suggests that food avoidance may be based on hypersensitivity to food texture, indicating that texture can influence flavour perception. Children with sensory defensiveness, particularly in the tactile domain, exhibit aversion and high sensitivity to specific textures and consistencies of food [ 37 , 38 ]. The rate of refusal based on sensory characteristics (5–9 years of age: 66.7%; 95% CI 47.9–81.3%; 10–14 years of age: 38.6%; 95% CI 30.7–47.3%; 15–18 years of age: 22.2%; 95% CI 12.3–36.9%; P < 0.001) was higher among younger children whit ARFID [ 23 ].

Individuals with sensory hyperresponsiveness exhibit faster, more intense, and longer-lasting responses to sensory stimuli compared to those with typical sensory responsiveness. This non-gradual, maladaptive response is postulated to stem from difficulties in regulating and organizing the degree and intensity of sensory input response in individuals with sensory modulation dysfunction [ 32 , 33 , 39 ]. Christol et al. (2018) explored the hypothesis that patients with oral sensory hypersensitivity exhibit structural differences in brain areas associated with taste perception [ 32 ]. Children with sensory food aversions (SFAs), commonly referred to as "picky eaters" or "selective eaters," also display hypersensitivity to sensory experiences beyond meal contexts [ 30 ].

Genetic studies have revealed an inherited pattern of food sensitivity, particularly concerning sensitivity to the bitter taste of 6-n-propylthiouracil (PROP), which influences food choices. Certain polymorphisms in the taste receptor gene family, specifically the Tas2r gene, have been found to differentiate "supertasters" from "non-tasters" [ 30 , 40 , 41 ]. Selective eating associated with hypersensitivity in taste perception may co-occur with the ARFID domain of sensory avoidance and fear of aversive consequences, where an extreme aversive reaction to a particular food can result in nausea or vomiting [ 30 ].

ARFID and inappetence

Food restriction or avoidance is characterized by a general lack of interest in food and eating, low appetite, early satiety, difficulties with the physical act of eating (such as taking small bites or pieces), prolonged mealtime, reporting a lack of hunger at mealtimes, forgetting to eat, or feeling full faster than others [ 13 , 28 ]. According to the hypothesis proposed by Thomas et al. (2017), this clinical presentation of ARFID may be associated with differences in the activation of regulatory centers involved in hunger and satiety perception [ 6 ].

The initiation of a meal is influenced by various factors, including external or non-homeostatic factors such as social situations or time constraints, as well as internal or homeostatic factors related to energy substrates, hunger, and satiety [ 42 ]. Homeostatic regulation involves the integration of hormonal and metabolic signals with information from the gastrointestinal tract and autonomic nervous system activity in the brainstem and hypothalamus, resulting in a coordinated regulatory response for energy homeostasis [ 43 , 44 ]. The hypothalamus and insular cortex play crucial roles in integrating hunger and satiety signals. Hunger appears to increase hypothalamic activity, while satiety exerts an inhibitory effect [ 42 , 45 ]. Distinct centers responsible for appetite and satiety have been identified: the lateral hypothalamus (LH) regulates the termination of feeding, whereas the paraventricular nucleus of the hypothalamus (PVN) is associated with the initiation of feeding [ 46 , 47 ].

Thomas et al. (2017) discussed the neurobiology of individuals exhibiting inappetence or low interest in food, proposing that there may be a distinct pattern of activation in the centers responsible for regulating hunger and satiety perception [ 6 ]. The findings of a study by Kerem et al. (2022) support the existence of divergent neurobiological foundations for restrictive/avoidant eating behaviour in individuals with ARFID and body mass index (BMI) associations [ 48 ]. The authors identified significant hyperactivation in the brain regions of the orbitofrontal cortex and anterior insula (regions associated with food anticipation and reward processing in response to visual cues of palatable food) in fasted individuals with ARFID and overweight/obesity, compared to individuals with ARFID and normal weight. However, it is important to question the directional relationship of these findings, namely whether such changes result from the neurobiology of a specific clinical subtype of ARFID or if they are consequences of the nutritional status impairment in these patients.

Nevertheless, there is no consensus regarding the plausibility of homeostatic dysregulation being associated with the acute onset of restrictive behaviour explained by inappetence, while deficits in reward sensitivity have been found in other eating disorders, particularly AN [ 25 ].

According to neuroendocrine findings, the literature shows that this patients with ARFID may to have distinct patterns of secretion of gut-derived appetite-regulating hormones, especially those have a low-weight, compare to AN and healthy controls. Higher levels of fasting ghrelin, high anorexigenic peptide YY (PYY) levels post-meal, higher levels of plasma fasting cholecystokinin (CCK) and higher basal or post-prandial levels of glucagon-like peptide 1 (GLP-1) are hypotheses explored in these patients, such as in AN [ 49 ]. Becker et al. (2021) show low-weight ARFID showed lower levels of total ghrelin around a meal than AN, low-weight ARFID did not differ from AN or healthy controls in PYY levels and did not show sustained high PYY levels post-meal [ 50 ]. Murray et al. (2022) found fasting CCK was higher in those with full/subthreshold ARFID versus healthy controls with a large effect, controlling for age, sex, and BMI percentile [ 51 ]. Aulinas et al. (2020) also observed distinct medical and endocrine alterations in ARFID compared to AN, such as a lower number of menses missed, higher total T3 levels, and lower total T4: total T3 ratio [ 52 ]. Neuroendocrine changes must be highly interconnected with homeostatic dysregulation and must be further studied in the future, especially in research with weight recovery, to assess whether there is normalization in neuroendocrine levels, and thus identify whether this change is part of the pathophysiology of the disorder or directly associated with malnutrition. Better understanding this mechanism can assist in differential diagnosis, in addition to providing new treatment targets.

ARFID and fear of aversive consequences of eating

Restrictive avoidant eating behaviour may arise as a conditioned negative response linked to the fear of experiencing aversive consequences while eating, following a traumatic event or specific fear. The ARFID subdomain known as the "fear of aversive consequences" typically manifests suddenly after a traumatic incident that resulted in unpleasant outcomes such as pain, nausea, choking, vomiting, or invasive clinical procedures involving the gastrointestinal tract (e.g., upper digestive endoscopy, esophagoscopy) [ 13 ].

Individuals who have undergone food-related trauma and subsequently develop avoidance behaviours to protect themselves from negative experiences may exhibit restrictive avoidant eating behaviour [ 26 , 28 , 30 ]. Any aversive encounter associated with food can trigger a conditioned fear of eating in susceptible individuals. Several patterns can be observed that contribute to this restriction, including the fear of eating after a single traumatic event, such as a choking incident; fear of eating in children who have undergone painful or unpleasant oral procedures; and fear in children who were tube-fed, lacked significant feeding milestones, or had limited experiences with food, leading to a sense of threat when food is presented orally [ 53 ].

According to Brigham et al. (2018), individuals within this domain of ARFID often possess an inherent predisposition to anxiety, resulting in the generalization of food avoidance beyond the initial target food. This may extend to similar foods, entire food groups, or environments that evoke memories of the traumatic event [ 26 ]. Thomas et al. (2017) propose hypotheses regarding the neurobiological mechanisms associated with the ARFID subdomain of fear of aversive consequences, suggesting a possible hyperactivation of brain circuits involving the amygdala and anterior cingulate cortex, which are key structures in the limbic system involved in fear processing, or hyperactivation of the defence system [ 6 , 21 ].

Anxiety plays a prominent role in theoretical models of avoidant eating behaviour, with previous studies indicating elevated anxiety symptoms in children with ARFID [ 54 ]. Conceptually, fear and anxiety can be understood as brain states triggered by external or internal stimuli, giving rise to specific measurable behavioural, physiological, hormonal, and autonomic reactions ( 55 ). Fear and anxiety elicit defensive behavioural responses that evolved to enable organisms to avoid or mitigate harm and ensure survival—a vital adaptation mechanism in potentially hostile environments. However, in humans, excessive fear and chronic anxiety transition from adaptive responses to maladaptive ones, causing damage and dysfunction [ 55 ].

Previous studies have emphasized the involvement of specific brain regions in generating fear and anxiety, as well as the contribution of synaptic and neuromodulatory processes within these regions. Indeed, studies using the Pavlovian model of conditioned fear have revealed the existence of a network distributed across brain regions involved in fear learning and expression. These structures include but are not limited to, the amygdala, medial prefrontal cortex (mPFC), and hippocampus [ 55 ]. One fundamental principle of fear learning is the requirement for activity-dependent plasticity within the amygdala. Sensory inputs from various modalities converge in the lateral amygdala (LA), receiving auditory, visual, and somatosensory information related to conditioned and unconditioned stimuli. Plasticity in the LA, induced by conditioning, precedes that in the cortex and thalamus, develops more rapidly than the conditioned behavioural response, and is believed to drive the expression of conditioned fear behaviour [ 55 ].

Specific phobias entail intense and persistent fears of certain objects or specific situations, which often result in avoidant behaviour. On the other hand, Post-Traumatic Stress Disorder (PTSD) arises from a traumatic event. However, it is important to note that specific phobias can either stem from a traumatic event (experimental phobia) or have no experiential basis (non-experiential phobia) [ 56 , 57 , 58 ]. The individual's response to trauma depends not only on the characteristics of the event or stressor but also on specific factors unique to the individual, such as genetic or experiential predispositions [ 59 ]. In light of this, Thomas et al. (2017) suggests that a subgroup of individuals who develop ARFID after a traumatic eating experience may have had a pre-existing vulnerability, which contributes to an increased phobic response [ 6 ].

Chatoor, Conley, and Dickson (1988) conducted a review of cases involving children who exhibited food refusal and acute onset of food-related anxiety after episodes of choking. These children also experienced intense anticipatory eating anxiety. The study termed this phenomenon "Post Traumatic Eating Disorder" since the children's reactions to the aversive episode resembled those of individuals who had experienced a traumatic event and developed PTSD [ 30 ].

Behaviours associated with specific experiential phobias can be sustained and perpetuated by dysfunctions in the fear mechanism that is dependent on learning. This can include impairments in fear extinction and a lack of habituation to fear, which refers to the failure to acquire a reduced fear response through repeated exposure to the fear-inducing stimulus. The maintenance of specific experiential phobias can be attributed to operant conditioning of fear, which reinforces avoidance behaviours [ 56 ]. In the case of ARFID, children may avoid the target food or mealtime to escape the discomfort or anxiety it generates, thus negatively reinforcing the avoidance behaviours and perpetuating the eating psychopathology [ 60 ]. However, unlike the effectiveness observed in exposure-based treatments for patients with anxiety disorders [ 61 ], daily exposure to the visual, olfactory, and harmless consequences of consuming food alone does not appear to reduce avoidant behaviour in individuals with ARFID [ 62 , 63 ]. Potential hypotheses as to why exposures do not improve food selectivity in ARFID may include cognitive factors that impede experiential learning [ 64 ].

Another crucial factor to consider is the role of repulsion in the manifestation of anxious symptoms in individuals with ARFID. The relationship between repulsion and anxiety offers new insights, as disgust is functionally associated with preventing contamination by pathogens (as may occur with the ingestion of contaminated food) and is resistant to extinction mechanisms. An exploratory study involving 1,644 adults analysed the contributions of sensory sensitivity, anxiety, and the experience of disgust to elucidate the potential role of disgust in food avoidance within ARFID. The findings revealed that disgust fully mediated the association between anxiety and ARFID. Thus, repulsion may play a significant role in food avoidance and could provide an explanation for novel approaches towards more effective treatments.

Clinical screening and evaluation tools of ARFID

The identification of ARFID as a diagnostic entity is relatively new, and currently, there is a lack of a standard assessment tool for its specific psychopathology. This gap hampers the identification of ARFID in clinical settings, understanding its etiology and associated risk factors, assessing the effectiveness of treatment, and verifying the epidemiology and natural course of the disorder [ 12 ]. It has been observed that many psychometric measures commonly used in eating disorder contexts are not specific enough to facilitate a diagnosis of ARFID, thereby resulting in low sensitivity if used as assessment tools [ 27 ]. However, screening tools for ARFID are in the early stages of development and validation.

Several screening and diagnostic instruments have been developed, which can be divided into assessments structured clinical interviews (EDA-5, Eating Disorder Assessment for DSM-5; SCID-5, Structured Clinical Interview for DSM-5; PARDI, Pica, ARFID, and Rumination Disorder Interview; EDE, Eating Disorder Examination) and self-reported questionnaires (EDY-Q, Eating Disorders in Youth-Questionnaire; NIAS, Nine-Item ARFID Screen; FNS, Food Neophobia Scale; PARDI-AR-Q, Pica, ARFID, and Rumination Disorder – ARFID Questionnaire) to evaluate specific type of use for clinicians and researchers [ 15 , 65 ].

Pica , ARFID and rumination disorder interview (PARDI)

Bryant-Waugh et al. (2019) evaluated the feasibility, acceptability, reliability, and validity of the PARDI's psychometric properties [ 66 ]. PARDI is a structured interview developed to assess the presence and severity of diagnoses for evaluation and treatment planning in clinical and research settings, specifically focusing on ARFID. It encompasses the clinical presentations of the three phenotypes of ARFID, namely sensory sensitivity, lack of interest in eating, and fear of aversive consequences. These distinct explanations for dietary restriction may require different treatment approaches. PARDI shows promise as a tool, with initial data indicating good feasibility, adequate acceptability, and good internal consistency for the three-dimensional phenotypes of ARFID. Internal consistency of the three ARFID profiles was in the adequate to good range, with Cronbach’s alphas as follows: sensory sensitivity (0.77), lack of interest food or eating (0.89), fear of aversive consequences (0.79), and overall severity (0.89). Cohen’s κ for the ARFID diagnosis (coded as yes or no) was 0.75. However, clinical measures for validation and convergence between self-report and parent/caregiver reporting have not been examined [ 66 ].

Eating disorder examination (EDE-ARFID)

In a similar study, Schmidt et al. (2019) presented a pilot study proposing the inclusion of ARFID criteria in the children's and parents' version of the Eating Disorder Examination (EDE), referred to as EDE-ARFID [ 67 ]. Based on 22 items rated on a 7-point Likert scale (0 = never/not at all to 6 = every day/extremely), the EDE subscales restraint, eating concern, weight concern, and shape concern are built, with higher subscale and global mean scores indicating more eating disorder psychopathology over the past 28 days. For this study, the subscales weight and shape concern and the global score were used, with Cronbach's α in this study of 0.81, 0.94, and 0.94 for the EDE [ 68 ]. In a non-clinical sample of children aged 8 to 13 years with low weight and/or restrictive eating behaviors, the EDE-ARFID module demonstrated high reliability, convergent and divergent validity, and the ability to distinguish between children with and without ARFID based on anthropometric and clinical characteristics [ 67 ]. The EDE-ARFID tool serves as both a diagnostic instrument and a means to collect clinical information related to the psychopathology of ARFID [ 15 , 67 , 69 ].

Eating disorders in youth-questionnaire (EDY-Q)

The EDY-Q [ 70 ] is a self-report tool consisting of 14 items designed to detect early-onset eating disorders in children aged 8 to 13 years. The total mean score had an internal consistency of Cronbach's α = 0.62, reflecting heterogeneity of EDY-Q items [ 70 ]. Twelve of these items specifically address the symptoms of ARFID, including the three variants proposed by the DSM-5 [ 13 ]. The EDY-Q focuses on assessing restrictive eating behaviors while excluding concerns about weight or shape. It can be utilized as a quick screening tool for ARFID-related symptoms [ 15 , 70 ]. Other tools such as the Behavioral Pediatrics Feeding Assessment Scale (BPFAS) and the Child Food Neophobia Scale (CFNS) can also aid in distinguishing ARFID from demanding eating during normal development in younger children [ 71 ].

Nine item ARFID screen (NIAS)

Zickgraf and Ellis (2019) conducted a validation study of the NIAS, a brief, multidimensional, self-report screening tool developed to assess selective and restrictive eating behaviors in adults. The NIAS addresses food restriction behaviors associated with the three eating patterns related to ARFID, namely appetite, fear, and sensory sensitivity. The results from a non-clinical sample of adult college students and a sample of adults potentially at risk for ARFID support the use of the NIAS to assess restrictive eating behavior, characterized by picky eating, lack of appetite or limited interest in eating, and fear of negative consequences from eating [ 25 ]. Acceptable Cronbach's alpha and omega coefficients for the total scaleand subscales were obtained, in the entire sample. For the total scale α = 0.84, ω = 0.90; the selective/neophobic eating subscale was α = 0.77, ω = 0.77, while the appetite subscale was α = 0.74,ω = 0.70, and lastly, for fear subscale were α = 0.80, ω = 0.80 [ 72 ].

Food neophobia scale (FNS)

The FNS is a 10-item measure that measures reluctance to try new foods [ 73 ]. This scale was originally validated for se in adults and has been adapted in children [ 74 ]. Higher scores on the FNS are indicative of behavioral responses to novel foods (e.g., eating fewer unfamiliar foods presented). Cronbach's alpha for the Food Neophobia Scale was 0.82, indicating a high degree of internal validity. Food neophobia scores were normally distributed with a mean ± SE of 29.6 ± 0.70 [ 75 ].

Clinical complications in ARFID

The diagnosis of ARFID encompasses patients with diverse presentations, resulting in different clinical outcomes [ 13 , 26 , 76 ]. ARFID poses a significant impact on the variety, quality, and quantity of the diet, as it is associated with an inadequate composition of macronutrients and micronutrients. Consequently, there is an increased risk of nutritional deficiencies, improper linear growth, dependence on enteral nutrition and nutritional supplements, and the need for hospitalization to restore nutritional status [ 69 , 77 ].

Regarding studies on individuals with food selectivity, the results do not consistently indicate a correlation between selectivity and low body weight [ 62 , 78 , 79 ]. However, some studies have reported weight loss [ 27 , 80 , 81 ]. There is no demonstrated association between food selectivity and overweight/obesity [ 79 ]. Individuals with ARFID commonly have a diet characterized by processed and refined carbohydrates, and foods with added sugars, with lower consumption of proteins, vegetables, and fruits. Compared to children without eating disorders, children diagnosed with ARFID exhibit lower levels of vitamin K (due to reduced vegetable consumption) and vitamin B12 (resulting from decreased consumption of animal proteins) [ 77 , 82 ].

Similar to other eating disorders, ARFID can have profound clinical, nutritional, and psychosocial implications, particularly during childhood and adolescence. These implications may include severe limitations in food acceptance and reduced daily energy intake. Prepubertal infants, children, and adolescents diagnosed with ARFID may experience delays in typical development or growth, which can negatively impact their learning abilities [ 13 , 60 ].

Patients with ARFID and growth deficits may require enteral nutrition or oral nutritional supplements to ensure adequate caloric and nutritional intake [ 69 , 81 ], depending on the severity of the condition. ARFID shares some clinical complications, such as malnutrition, weight loss, or failure to gain weight due to restriction/avoidance, with AN [ 25 , 71 , 77 ]. However, compared to the clinical course of AN, patients diagnosed with ARFID tend to develop the eating disorder at an earlier age and require longer hospital stays for medical and nutritional stabilization [ 76 , 83 , 84 ]. Although patients with ARFID may have a similar BMI to those with AN, they typically experience less significant weight loss before treatment [ 76 ]. Furthermore, during hospitalization, patients with ARFID more frequently require enteral nutrition to meet their energy needs and exhibit less resistance and distress during the therapeutic process compared to those with AN [ 80 , 81 , 84 ].

In severe cases of ARFID, patients may display signs and symptoms of malnutrition, such as fatigue, lethargy, difficulty concentrating, memory deficits, presyncope, constipation, hypersensitivity to cold, hypothermia, electrolyte abnormalities (e.g., hypokalemia), dry skin, lanugo, alopecia, bradycardia, orthostatic postural tachycardia, hypotension, and a sunken abdomen. These symptoms are attributed to deficiencies in macronutrients and micronutrients [ 26 , 69 , 71 , 85 ].

Moreover, female patients with ARFID may experience pubertal delay before the onset of menstruation. Primary amenorrhea may occur, and in postmenarcheal patients, secondary amenorrhea may result from low body weight. These findings are associated with lower bone mineral density [ 26 , 69 , 71 , 85 ]. In cases of extreme food restriction, individuals may become malnourished and require medical stabilization in specialized inpatient units [ 40 , 85 ].

Children with ARFID may exhibit impairments in recognizing satiety signals and have difficulty following appropriate eating habits. Those who reject foods that require extensive chewing, such as meats and tough vegetables, and only accept softer textures or pureed consistencies, may experience delays in oral motor development due to lack of experience with chewing. Additionally, they may also experience speech delays [ 1 , 30 ].

In addition to significant clinical and nutritional complications, ARFID's selective and restricted eating patterns have a negative impact on social and emotional development, leading to higher levels of stress and family conflict in food-related contexts [ 13 ], as well as greater likelihood of comorbid neurodevelopmental disorders, disruptive behavior disorders and conduct disorders [ 86 ]. The severity of ARFID, particularly in terms of fear of aversive consequences related to eating, is associated with higher levels of anxiety, obsessive–compulsive disorder, and trauma-related disorders [ 86 , 87 , 88 ].

Undoubtedly, the presence of comorbidities has a more reserved course and prognosis. Children's initial knowledge about food is incomplete, and it is through experiences with caregivers, family members, and social interactions involving food that their knowledge is enhanced [ 7 , 31 ]. Selectivity and extreme food avoidance can hinder a child's experiences in social settings, including interactions related to eating at school or with peers. The implications of this significant gap in child development may persist throughout the individual's lifespan.

Treatment of ARFID

The management of ARFID (see Fig. 3 ) aims to determine the appropriate level of care, whether it be outpatient or in a hospital setting. The goals of treatment include clinical stabilization of the patient, restoration of nutritional status, addressing fear and/or pain associated with food, gradually expanding food variety, and facilitating the recovery of hedonistic aspects of food and psychosocial relationships related to eating [ 85 ]. Patients diagnosed with ARFID may not present just one of the domains. As such, it is important not to isolate patients into sub-profiles and treat them solely as “sensory” patients, for example, but rather to target personalized treatment to each individual.

The treatment of ARFID

There is limited evidence available to guide healthcare professionals in the treatment of ARFID, and no specific guidelines or consensus have been established. This lack of guidance can potentially lead to prolonged hospitalizations and the need for intensive care for complex cases [ 8 , 26 ]. Like other eating disorders, the treatment of ARFID requires a multidisciplinary approach involving a team of healthcare professionals, ideally including paediatricians, psychiatrists, psychologists, nurses, nutritionists, and occupational therapists. This multidisciplinary team addresses all aspects of the individual's functioning [ 9 , 89 ]. In many cases, patients with ARFID follow eating disorder programs that employ a range of strategies and approaches, similar to those used for other eating disorders, particularly AN. Treatment modalities can vary from outpatient care with a multidisciplinary team to hospitalization for close monitoring and rehabilitation of clinical and nutritional status [ 26 , 89 ].

Therefore, given the heterogeneous clinical presentation of ARFID, the treatment plan for each patient should incorporate strategies tailored to their specific needs. It is essential to recognize that the requirements of patients with ARFID may differ based on the clinical presentation of the disorder and the presence of associated neuropsychiatric comorbidities. This approach allows for the identification of the precipitating and maintaining factors of restrictive eating behaviours and food avoidance. Moreover, understanding the dietary characteristics and associated clinical and psychiatric comorbidities is crucial, considering the complexity that can accompany the diagnosis [ 8 , 90 , 91 , 92 ].

Nutritional intervention in ARFID

The clinical manifestations of ARFID may result in impaired nutritional status, as indicated by insufficient weight gain, low body weight, growth deficits, and malnutrition. Addressing these complications is of utmost therapeutic importance and should be initiated promptly.

The primary objective is to restore body weight initially. Nutritional strategies employed for weight recovery and prevention of further weight loss should ensure adequate nutrient intake, particularly concerning calories. This can be achieved through the consumption of foods that are more readily accepted by the individual, as well as the prescription of nutritional supplements via oral or enteral nutrition. These approaches facilitate the necessary initial increase in food volume to promote weight gain, without immediately incorporating new or avoided foods into the diet [ 26 , 71 , 92 , 93 ].

AN and ARFID share common challenges such as malnutrition, nutrient deficiencies, and psychosocial impairment resulting from restrictive eating behaviours. While these disorders differ in their precipitating and sustaining factors, the treatment of both conditions involves similar components, including the normalization of weight and eating behaviour as therapeutic targets [ 26 , 91 ]. However, patients with ARFID and AN may have distinct therapeutic needs regarding dietary and nutritional treatment, and the dietary prescription may vary in terms of quality, quantity, and food choices. For instance, it is known that patients with ARFID tend to reject foods that are considered "safe" by individuals with AN while preferring those deemed "dangerous" by AN patients. This can present a challenge when implementing the same treatment strategies and environmental structures for both disorders [ 9 ].

One of the main objectives is to adapt the eating routine or supplementary to provide all macro and micronutrient needs. When avoiding and restricting specific consumption of cereals and grains, it will be necessary to pay attention to the recovery of Carbohydrates and Fiber; when restricting animal products, legumes and dairy products, pay attention to the intake of Protein (relevant in the process of malnutrition) and Riboflavin/Vitamin B2, Cobalamin/vitamin B12, Iron, Selenium and Zinc; when restricting fish and seafood, pay attention to the recovery of Vitamin D and Omega-3 acids; in fruits and vegetables, pay attention to Vitamin C, folates and other minerals; and finally, when restricting animal and fruit/vegetable fats, pay attention to recovering the intake of Fats and Vitamin E, Vitamin A, Vitamin K [ 94 ].

In a hospital or outpatient setting, the nutritionist or dietitian, as an integral part of the multidisciplinary team, typically calculates the dietary therapy prescription, estimates energy and fluid requirements for oral intake, assesses the adequacy of macro and micronutrients, and plans meal schedules. Furthermore, the nutritionist is responsible for establishing goals for nutritional therapy, defining a plan for monitoring the dietary therapy prescription, which includes assessing nutritional and hydration status, tracking progress in oral intake, adjusting oral and enteral feeding when necessary, and providing appropriate guidance on nutritional needs while developing an individualized meal plan [ 93 , 95 , 96 , 97 , 98 ].

Another objective is to reintroduce of new foods or those previously avoided and this is gradually integrated into the individual's routine through exposure experiences led by professionals from the multidisciplinary team. Notably, the severity of food refusal observed in individuals diagnosed with ARFID increases the likelihood of requiring enteral nutritional support, in comparison to those with AN [ 6 , 84 , 92 ]. Within specialized treatment centres, the use of enteral nutrition is a common practice for cases of restrictive eating disorders. However, during the initiation of the refeeding protocol, close monitoring for electrolyte abnormalities, which may arise from refeeding syndrome—a serious and potentially fatal complication—is essential [ 26 , 95 ]. Protocols and guidelines have been proposed and are widely utilized in clinical practice to safely commence refeeding in severely malnourished individuals with eating disorders or those who have experienced prolonged periods of starvation [ 93 , 96 , 99 , 100 , 101 , 102 , 103 , 104 ].

Considering that long-term dependence on enteral nutritional support may be a component of the diagnostic criteria for ARFID, enteral administration is regarded as a temporary measure as part of the treatment. However, caution is required when opting for its use, as it can lead to iatrogenic effects such as reduced expectations regarding the consumption of solid foods, hindering the development of sensory skills related to eating, gastrointestinal symptoms, and other discomforts associated with food intake [ 6 , 90 , 105 ]. Once the patient's nutritional and fluid needs are met, leading to clinical stabilization, other therapeutic strategies can be initiated. These may include nutritional counselling, specific psychological interventions, restoration of healthy dietary patterns that facilitate social interactions and well-being, desensitization to avoided foods, and the introduction of new foods into the diet [ 30 , 97 , 105 , 106 ].

And finally, nutritional counselling plays a vital role in addressing dysfunctional eating behaviours in eating disorders. Its primary objective is to guide individuals towards adopting a normal diet across all dimensions, thereby restoring physical and psychological health. In children and adolescents, this process also aims to facilitate age-appropriate development. To achieve this, nutritionists provide guidance, support, and strategies to prepare individuals for the challenges they may encounter during treatment, such as behavioural and emotional difficulties, gastrointestinal discomfort, changes in body composition, and potential medical issues [ 93 ]. Signs and symptoms of specific vitamin-mineral deficiencies could be invetigated due to group of dietary restrictions and supplemented or reinserted in different preparations [ 94 ]. Another fundamental tool in the treatment of eating disorders is the development of a food plan by a nutritionist. This plan offers practical, organized, and tailored guidance on energy and nutrient requirements, with gradual modifications. Initially, the focus is on meeting energy needs, followed by an emphasis on macronutrients and micronutrients [ 93 ].

Pharmacological intervention in ARFID

Currently, there is limited empirical evidence regarding pharmacological treatments for the management of ARFID. However, case reports and small case series studies have explored the use of certain psychotropic drugs as adjunctive therapeutic interventions for ARFID and its associated psychiatric comorbidities [ 26 , 95 ].

Olanzapine, a second-generation atypical antipsychotic, has been associated with reduced cognitive rigidity in beliefs about food and increased appetite and subsequent weight gain [ 26 , 89 ]. Its mechanism of action involves blocking histaminergic and serotonergic receptors in the lateral hypothalamus, thereby stimulating food intake [ 107 , 108 , 109 ]. Clinical research examining the effects of olanzapine on weight recovery in patients with AN has yielded modest results, demonstrating an association between olanzapine use and gradual weight gain in AN patients over time [ 110 , 111 , 112 , 113 ]. A case study analyzed the use of low-dose olanzapine as an adjunct to conventional treatment, including individual, group and family therapy, nutritional counselling, and pharmacotherapy, in an eating disorder program for children and adolescents. The study compared individuals who received olanzapine with those who did not and found a statistically significant difference in weight gain. Adjuvant olanzapine also helped reduce associated anxiety, depressive symptoms, and cognitive impairments [ 26 , 95 ].

Another psychotropic drug of interest is Mirtazapine, an antidepressant known for its safety and efficacy in treating depressive and anxious symptoms in adults. The rationale for its use in ARFID is its antagonistic activity on H1 histaminergic receptors, which can promote an orexigenic effect, induce weight gain, and increase gastric emptying [ 114 , 115 , 116 , 117 ]. Gray et al. (2018) reported the use of mirtazapine to enhance appetite and facilitate weight gain while reducing nausea and vomiting [ 118 ]. The study observed an average weekly change in BMI of 0.10 before starting mirtazapine and an average weekly change in BMI of 0.23 after mirtazapine treatment, suggesting that mirtazapine may promote weight gain in patients with ARFID. Mirtazapine was found to be well tolerated and associated with a higher rate of weight gain compared to standard weight restoration programs [ 15 , 118 ]. Tanidir and Herguner (2015) described the use of mirtazapine in the treatment of a pediatric patient with food avoidance due to an aversive eating experience and diagnosed with ARFID. The patient exhibited a reduction in anxiety and fear symptoms, increased appetite, and weight gain following the initiation of mirtazapine treatment [ 119 ].

Buspirone, which has shown efficacy in treating Generalized Anxiety Disorder, has also been explored as a potential treatment for anxiety symptoms in adolescents with ARFID. A case report described the successful use of buspirone in reducing anxiety symptoms, improving eating behaviours by reducing fear of vomiting, and promoting weight gain in a female adolescent with ARFID resulting from an aversive eating experience [ 15 , 120 ]. This case study suggests further investigation into the potential usefulness of buspirone in ARFID treatment [ 120 , 121 ]. Additionally, a case series detailed six patients diagnosed with ARFID who received treatment in a hospital-based eating disorder program. The treatment approach included family therapy, cognitive-behavioural therapy, medical monitoring, and pharmacological treatment with olanzapine, fluoxetine, and cyproheptadine (used as an appetite stimulant in two cases). After treatment, all six patients achieved the desired BMI [ 122 ].

There is currently no psychotropic medication for treatment of ARFID approved by the U.S. Food and Drug Administration. Future placebo-controlled randomized clinical trials are necessary to establish the efficacy of these pharmacological interventions as potential strategies for the treatment of ARFID [ 26 ].

Behavioral intervention in ARFID

Psychotherapeutic approaches to managing ARFID, along with the aforementioned therapeutic modalities, necessitate an individualized assessment of restrictive behaviours. This assessment serves as the basis for developing a tailored plan to address specific avoidant and restrictive behaviours and expand the consumption of diverse food groups [ 5 ].

While treatment protocols similar to those used for other eating disorders, such as AN, have been employed for ARFID, it is important to recognize that ARFID represents a distinct clinical entity. Therefore, adopting identical therapeutic protocols is not considered sufficient or recommended, as ARFID patients exhibit unique psychopathology and present distinct predisposing, precipitating, and maintaining factors (in addition to not always being underweight) [ 66 ].

Solid evidence on effective treatments for ARFID is limited. Nonetheless, findings from single case studies, case series, and non-randomized clinical trials employing psychological interventions show promising results in reducing ARFID symptoms. Cognitive-Behavioural Therapy (CBT) adapted for ARFID has been increasingly studied as a potential intervention [ 123 , 124 , 125 , 126 , 127 , 128 ], as well as the utilization of Family-Based Therapy (FBT) as a treatment strategy [ 122 , 125 , 129 ].

A case report by King, Urbach, and Stewart (2015) highlighted the successful treatment of a patient with limited food intake due to fear of aversive consequences using a cognitive-behavioural therapy approach. Positive outcomes included weight gain, increased daily caloric consumption, improvements in cognition and energy levels, and a general reduction in anxiety [ 124 ].

Dumont et al. (2019) presented a clinical case series involving eleven patients aged between 10 and 18 years who received four weeks of daily cognitive-behavioural therapy specifically designed to target the causal factors of food restriction and avoidance in adolescents with ARFID. This protocol incorporated inhibitory learning principles and repeated exposures to food stimuli, demonstrating preliminary success in treating various clinical presentations of ARFID by reducing symptoms, such as increased food acceptance, reduced anxiety, and decreased psychosocial interference. Tube feeding was discontinued in six out of the eleven patients observed [ 123 ].

Thomas et al. (2020) evaluated the feasibility, acceptability, and preliminary efficacy of Cognitive-Behavioral Treatment for ARFID (CBT-AR) in individuals aged 10 years and older, encompassing all clinical presentations of ARFID. Preliminary results indicated a significant reduction in symptoms and ARFID severity scores on the PARDI. Patients also exhibited increased variety in their food consumption, incorporating new foods into their routines following treatment, and weight gain was observed in underweight patients [ 127 ].

In an adult clinical sample, Thomas et al. (2021) conducted a proof-of-concept study on the use of CBT-AR, which yielded promising results and justified further investigation into the safety and efficacy of this approach [ 128 ]. Significant decreases in ARFID severity scores on the PARDI and sensory sensitivity were observed, along with notable weight gain. However, anxiety and depression levels did not show significant changes.

Family-Based Therapy (FBT), commonly utilized in the treatment of eating disorders in adolescents, particularly for AN and BN, focuses on educating and training caregivers to support patient recovery in an outpatient setting [ 125 , 130 ]. FBT places emphasis on modifying eating behaviours through caregiver management, recognizing them as key agents in driving change in dysfunctional eating behaviours [ 122 , 125 ].

Lock et al. (2018) presented three case reports illustrating the application of family-centred treatment adapted for ARFID (FBT-ARFID) in preadolescents diagnosed with the disorder. These reports demonstrated significant clinical progress in reducing symptoms, including weight gain, increased food variety in the diet, and decreased anxiety symptoms. The authors suggested that such an intervention could be employed for ARFID, considering the unique clinical presentations of patients. While the available data is limited and should be interpreted with caution due to methodological limitations such as study design, small sample sizes, and short follow-up periods, the findings suggest that FBT-ARFID may be a viable, potentially promising, and effective approach for this population [ 122 , 125 , 130 ].

Future directions for research

Further epidemiological studies are required to investigate the trajectory of ARFID over time, contributing to a more comprehensive understanding of the mechanisms underlying food restriction and avoidance, as well as the etiology, risk factors, and therapeutic interventions. Patients with ARFID exhibit distinct biological foundations, thus a thorough characterization of the various clinical presentations is crucial for developing a better conceptual understanding. This understanding will aid in determining the implications of these phenotypes in terms of diagnosis, treatment, course, and prognosis, which may vary for each patient. Additionally, it can provide guidance for the necessary and appropriate care of such individuals.

Prospective and long-term follow-up studies are necessary to comprehend the course of the disorder and the potential impairments in the development of physical and social skills. Limited knowledge of avoidant and restrictive eating hampers effective treatment and management, with long-term consequences for the growth, development, nutrition, and psychosocial functioning of children and adolescents.

Moving forward, several areas of research are particularly intriguing. One such area is the validation of screening instruments that are sensitive to the heterogeneity of clinical characteristics. While initial evidence supports the sensitivity and validity of existing screening and diagnostic tools, larger-scale studies are required to test their psychometric properties in more extensive samples and cohorts from diverse clinical settings over extended observation periods. Future investigations could also delve into the neurobiology associated with ARFID, thereby contributing to a greater understanding of the processes and mechanisms underlying food avoidance and its perpetuation in children, adolescents, and adults. Although significant progress has been made in understanding the pathogenesis of ARFID, further studies are needed to examine the long-term outcomes and consequences of delayed diagnosis.

Furthermore, in-depth research into existing neurobiological models for ARFID is crucial. This disorder involves alterations in sensory perception, sensory hypersensitivity, dysregulation of appetite homeostasis, and differences in the activation of regulatory centres for hunger and satiety perception. Additionally, excessive activity in negative valence systems that correlate with phobic characteristics has been observed. Exploring the neurobiological bases and hypotheses that have already been proposed may yield promising avenues for comprehending the etiology, pathophysiology, and personalized treatment of ARFID.

Moreover, it is important to evaluate the outcomes and efficacy of the various therapeutic interventions that have been proposed for the specific characteristics of ARFID. Rigorous randomized clinical trials, incorporating reliable control conditions and standardized measures, are needed to determine which treatments or combinations of treatments are effective for different presentations and phenotypes of ARFID, as well as their responsiveness to various therapeutic option. Lastly, educational and awareness programs targeting health professionals are of utmost importance to promote best practices in the care and treatment of this relatively unknown and highly challenging eating disorder.

Conclusions

ARFID is a relatively recent diagnostic classification, representing a burgeoning field of study. The identification of diagnostic criteria and the pursuit of new knowledge in this area have only recently begun. Consequently, assessment tools and treatment strategies are still in the process of development and validation. This narrative review explored the neurobiological perspective of ARFID using the three-dimensional model, examined its etiology and risk factors, evaluated clinical screening and evaluation tools, discussed common clinical complications, and presented different types of nutritional, behavioural, and pharmacological interventions used in ARFID treatment.

Availability of data and materials

Not applicable.

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Fonseca, N.K.O., Curtarelli, V.D., Bertoletti, J. et al. Avoidant restrictive food intake disorder: recent advances in neurobiology and treatment. J Eat Disord 12 , 74 (2024). https://doi.org/10.1186/s40337-024-01021-z

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Sustainability

Microplastics Are Everywhere. Here’s How to Avoid Eating Them.

By Katie Okamoto

Katie Okamoto is an editor on the discovery team. She’s covered the intersections of products, sustainability, and health for more than a decade.

Microplastics and nanoplastics are everywhere.

The teeny tiny pieces of plastic have been found in everything from drinking water to chicken nuggets, apples, and broccoli.

Recent studies have linked these pollutants to heart disease , lung disorders , and more worrying health issues.

But unfortunately, microplastics are now so pervasive that they’re nearly impossible to avoid.

If you’re concerned about the health effects linked to microplastics, the experts I spoke with said that you can lower your risk by taking care of your general health: getting plenty of sleep and exercise, eating a balanced diet, lowering stress, and seeking preventative care.

Still, it’s probably a good idea to lower your exposure to microplastics even if you can’t avoid them completely. Although you can cut back your exposure in as many ways as there are sources of plastic, the experts I spoke with recommended focusing on exposures from water, food, and air.

I talked to three doctors and a research scientist for tips on how to reduce the amount of tiny plastics and their chemicals that you (or your kids ) might ingest. Here’s what they recommend.

1. Cut back on bottled water

Some research indicates plastic bottled water may be a significant source of microplastics. While scientists are still studying just how significant, one study from 2019 of water and other commonly consumed food and drink found it to be the most concentrated source .

There is emerging evidence that on average, bottled water contains more microplastics than tap. (One study published in 2024 suggests that we have underestimated measured concentrations.)

Drinking bottled water in a pinch isn't the end of the world, but if you have concerns about it, you could always consider carrying a reusable steel or glass bottle or tumbler when out and about.

2. Get an NSF-certified water filter

Switching to tap water from plastic bottled water will likely significantly reduce your routine exposure to plastics. But while the average plastic water bottle contains more microplastics and nanoplastics than tap, research shows that tap water may also be a source of microplastics.

Several of our water filter picks are specifically NSF/American National Standards Institute–certified to reduce microplastics, which means they’ve been rigorously tested in an accredited lab. They’re certified only to reduce since the filters cannot guarantee total elimination. Our picks include under-sink filters , such as the Aquasana AQ-5200 , and the Brita Elite , a pitcher filter .

Aquasana AQ-5200

Exceptional, affordable under-sink filtration.

Certified for the most contaminants, widely available, affordable, and compact.

Buying Options

$100 + FS w/code AQWC50

Brita Elite Filter

Ace filtration, long lifespan.

This 10-cup, user-friendly model is rated to last six months between replacements.

Yes, it’s ironic that most NSF/ANSI-certified water filters contain plastic. But any microplastic shedding from using the plastic filter is likely to be minimal, as long as you avoid running hot water through the filter and store your water in the fridge, since heat accelerates plastic degradation.

Research suggests that boiling tap water, cooling it, and then filtering it may be especially effective at reducing microplastics, although it’s less practical for most people than simply using a filter.

3. Don’t use plastic to store food

Plastic food storage and packaging is so common that it’s difficult to avoid entirely. But your safest bet is to avoid storing food or liquid in plastic when possible and to minimize exposing any plastic (even those that say they’re BPA-free or microwave-safe) to high heat. Sunlight, acids, and physical erosion can also degrade plastic.

4. Don’t reuse single-use plastics for food and drinks

It’s great to reuse single-use plastic —just not for food. Unless you’re using the plastic in the freezer, save it for something that isn’t food storage or reheating, said Dr. Gillian Goddard, an endocrinologist and author at ParentData , a science-based online resource for parents. That means don’t reuse plastic takeout containers, breastmilk bags, or drink bottles.

5. Don’t microwave in plastic

Avoid microwaving or heating food or water in plastic—even if it says it’s microwave-safe, said Tracey Woodruff, director of the Program on Reproductive Health and the Environment at University of California San Francisco. Instead, consider glass or ceramic. The Pyrex Simply Store 18-Piece Set is our pick for the best food storage containers , and they survived our drop tests, stack neatly, and come with user-friendly lids (although you may not want to microwave the plastic lids). Our runner-up, the leakproof Glasslock 18-Piece Container Set , is another great option.

Pyrex Simply Store 18-Piece Set

The best glass container set.

The Pyrex Simply Store containers stack neatly and are made from durable tempered glass. The colorful lids make it easier to match their shape to the corresponding container, though you may need to replace them over time.

Glasslock 18-Piece Container Set

The best leakproof glass container set.

The Glasslock containers have locking lids that will prevent leaks. But these lids also put stress on the lips of the containers, so the glass may be prone to chipping over time.

6. Wash plastic by hand

Dishwasher temperatures run very hot and can degrade plastic—even dishwasher-safe plastic—and lead to microplastic shedding. Try to wash your plastic food containers by hand.

7. Use wood or bamboo cutting boards

Some research suggests that plastic cutting boards can be a significant source of microplastics in your diet, since repeated cutting on their surface can dislodge particles that adhere to food. Wood cutting boards also have some other advantages: They’re better for your knife blades and last longer than plastic when properly maintained.

Teakhaus Medium Professional Carving Board with Juice Canal 109

The best wood cutting board.

This beautiful teak board requires more careful cleaning than a plastic board, but it feels better under a knife and is easier to maintain than the other wood boards we tested.

Our cutting board pick, the Teakhaus Medium Professional Carving Board with Juice Canal 109 , is made from sustainably harvested teak. If you still prefer plastic for certain uses, use it sparingly and replace it after heavy scarring.

8. Clean your air

The air we breathe is also a potential source of microplastics, in the form of dust. Reducing airborne dust in your home, then, may reduce your exposure to inhaled microplastics.

SEBO Airbelt K3 Premium

The best canister vacuum.

This bagged canister vacuum excels on both bare floors and carpets, and has many adjustment options and useful attachments. It should last for the long haul.

7-Year Standard Warranty

10-Year Extended Warranty

That means doing boring stuff, like vacuuming regularly with a bagged, sealed-system vacuum that has a HEPA or S-class filter and mopping and wiping down surfaces with a damp sponge or cloth (since dusting kicks those tiny particles back up into the air).

Coway Airmega AP-1512HH Mighty

Exceptional, efficient, affordable.

Perfect for bedrooms, playrooms, and living rooms, this air purifier is one of the highest-performing, most-durable, and most-economical models we’ve tested.

You should also take care of seasonal chores like cleaning fans and AC unit filters and changing HVAC filters, and consider getting an air purifier if you live near a busy road.

Take special steps for infants and young children

Infants may be exposed to microplastics and nanoplastics in much higher concentrations than adults. Research shows that this exposure may be cause for concern, particularly at critical stages of early development. But much like health risks to adults, it’s important to think of microplastics exposure as just one piece of a child’s overall health.

“I emphasize that before putting much energy and resources into minimizing unknown risks, it is worth attending to reducing the risks we know about,” said Dr. Carlos Lerner, a pediatrician and professor of clinical pediatrics at UCLA Health. He cited following safe sleep recommendations for infants, avoiding secondhand smoke, and practicing good nutrition as examples.

If you want to take a more precautionary approach, avoid using plastic to warm formula or breastmilk. This is the main point of advice from the experts I spoke with, as well as the Cleveland Clinic .

1. Avoid microwaving or heating formula in plastic

Recent evidence shows that polypropylene-bottle-fed babies may swallow very high levels of tiny plastics due to the high temperatures used to sterilize bottles and prepare formula, as well as shaking the bottles to mix. If you want to feed your baby warmed formula and use plastic bottles, consider premixing the formula in a glass container, then cooling it down before transferring it to the feeding bottle.

2. Rinse heat-sterilized plastic bottles before adding formula or breastmilk

If you use heat to sterilize plastic bottles, leave them to cool then rinse them several times before filling them with formula or breastmilk, Lerner suggested.

3. Consider glass or silicone over plastic bottles

If your baby prefers warmed milk or formula, consider heating it in a glass or silicone bottle. (If you don't use a bottle warmer, we have advice about how to safely do this without one.) The Philips Avent Glass Natural Response Baby Bottle is our recommendation for the best glass baby bottle.

Philips Avent Glass Natural Response Baby Bottle

Our favorite glass bottles.

With only three pieces and a large, easy-to-screw-on collar, this glass bottle is simple to use and didn’t leak in our test. But the very wide nipple may not work well for all babies.

4. Wash hands before eating

For young kids who eat with their hands, try to establish a habit of handwashing before eating, said Woodruff. While handwashing is not always possible, it can help reduce exposure from touching microplastics in dust and soil (and maybe, just maybe, stem the tide of germs).

How worried should you be about microplastics?

Scientists are still studying the exact connections between these teeny tiny pieces of plastic and human health. But it’s clear that exposure to plastic—whether it’s those tiny particles, the chemicals they leach, or a combination—is being linked to a variety of worrying health issues.

Some of those connections still require more research, such as ties to colon cancer , respiratory disease , metabolic function , and disruption to endocrine systems , while others—like a recent study that found those with levels of plastics in their arteries were at a higher risk for heart attacks, strokes, and death—seem a little more clear.

It’s important to remember that these links point to concerns about the impact of microplastics on public health, but they are not specific, predictable outcomes. “What I’m thinking about is population risk, not a risk to a specific individual,” said Goddard.

The tricky thing is that microplastics and nanoplastics are impossible to avoid, no matter how diligent you are: They’re in the air we breathe , our drinking water , and our food. But scientists aren’t sure what levels of microplastics and nanoplastics we’re each taking in from those sources.

The oft-cited estimate that the average person eats a credit card’s worth of plastic every week has been called into question . But our bodies are certainly taking in plastic, and that’s more than nature intended.

Given the growing body of evidence, it’s possible that we’ll start to see more public health measures that address microplastic pollution. Until then, taking care of your overall health is the first line of defense, followed by taking reasonable steps to reduce microplastic exposure.

This article was edited by Christine Cyr Clisset and Ben Frumin.

Tracey Woodruff, director of the Program on Reproductive Health and the Environment at UCSF , phone interview , April 25, 2024

Gillian Goddard, MD, endocrinologist and adjunct assistant professor at NYU Langone Hospital and author of “Hot Flash” newsletter from ParentData , phone interview , April 26, 2024

Carlos Lerner, MD, pediatrician at the Children’s Health Center at UCLA and professor and Jack H. Skirball endowed chair in Pediatrics at UCLA , email interview , April 26, 2024

Hayley Goldbach, MD, board-certified physician and dermatologic surgeon at Brown University , email interview , April 29, 2024

Meet your guide

Katie Okamoto

Katie Okamoto is an editor on the discovery team and leads Wirecutter’s sustainability coverage. She has been covering products—from food to furniture—and their intersections with environmental impact and environmental health for more than a decade. Previously, Katie was an editor at Metropolis Magazine.

Mentioned above

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After more than 30 hours researching hundreds of models, we’ve found the best under-sink water filtration systems for most people. Here’s what we recommend. The Best Under-Sink Water Filter
Water filters and pitchers are the simplest, most affordable way to get reliable filtered water at home. The Best Water Filter Pitcher and Dispenser
Most plastic isn’t actually recycled. These 12 tips can help you reduce your overall plastic use—and make a difference in the global plastic pollution problem. 12 Ways to Break Up With Single-Use Plastics
After years of using and abusing food-storage containers, we recommend the glass Pyrex Simply Store 18-Piece Set and the Snapware Total Solution 20-Piece Set. The Best Food Storage Containers

Silicone Kitchen Gear Isn’t As Sustainable As Many People Think. Try These Solutions Instead.

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Our favorite alternatives to plastic or disposable food storage include silicone food-storage bags, beeswax wraps, and cloth produce bags.

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IMAGES

Eating Disorder Infographic
Australia’s first national strategy for eating disorders released
Eating Disorders: Prevalence, Risk Factors and Treatment Options
Eating Disorders (infographic)
Exciting News in the Eating Disorder Field
Eating Disorders Research paper

COMMENTS

Current approach to eating disorders: a clinical update
Advances and the current status of evidence‐based treatment and outcomes for the main eating disorders, anorexia nervosa, bulimia nervosa and BED are discussed with focus on first‐line psychological therapies. Deficits in knowledge and directions for further research are highlighted, particularly with regard to treatments for BED and ARFID ...
The association between eating disorders and mental health: an umbrella
Positive association between ADHD and disordered eating. Impulsivity symptoms of ADHD were positively associated with overeating in anorexia nervosa and bulimia nervosa. Further research is needed to determine the direction of relationship and underlying mechanisms. 90%.
Home page
Aims and scope. Journal of Eating Disorders is the first open access, peer-reviewed journal publishing leading research in the science and clinical practice of eating disorders. It disseminates research that provides answers to the important issues and key challenges in the field of eating disorders and to facilitate translation of evidence ...
Eating disorder outcomes: findings from a rapid review of over a decade
Research in eating disorder genetics is a rapidly emerging area with potential clinical implications for assessment and treatment. Bulimia nervosa (BN) Overall, studies pertaining to a diagnostic profile of BN report remission recovery rates of around 40-60%, depending on criteria and FU period, as detailed below.
Articles
Eating disorders (ED) are associated with symptoms across body image, disordered eating, and exercise-related domains, and while predominantly affecting females, ED in males is also a significant concern. Howe... Andreas Birgegård, Rasmus Isomaa, Elin Monell and Johan Bjureberg. Journal of Eating Disorders 2024 12 :68.
Eating disorders
Eating disorders are disabling, deadly, and costly mental disorders that considerably impair physical health and disrupt psychosocial functioning. Disturbed attitudes towards weight, body shape, and eating play a key role in the origin and maintenance of eating disorders. Eating disorders have been increasing over the past 50 years and changes in the food environment have been implicated.
Statistics & Research on Eating Disorders
Research Review: What we have learned about the causes of eating disorders - a synthesis of sociocultural, psychological, and biological research. J Child Psychol Psychiatry, 56(11), 1141-1164. By age 6, girls especially start to express concerns about their own weight or shape. 40-60% of elementary school girls (ages 6-12) are concerned ...
Eating Disorder Statistics
While we know that eating disorders impact people of all genders, ages, races, religions, ethnicities, sexual orientations, body shapes and weights, to date, the majority of eating disorder research studies lack this representation. As you read through the findings below please note that the information may be limited due to this lack of inclusion.
Eating disorders
Eating disorders are disabling, deadly, and costly mental disorders that considerably impair physical health and disrupt psychosocial functioning. Disturbed attitudes towards weight, body shape, and eating play a key role in the origin and maintenance of eating disorders. Eating disorders have been increasing over the past 50 years and changes ...
Trends in US Patients Receiving Care for Eating Disorders and Other
This study included 3 281 366 individuals (2 053 432 females [62.6%]) with a mean (SD) age of 37.7 (16.2) years. Patient characteristics were similar across years, except that the age of patients with eating disorders decreased over time ().The number of patients with inpatient care for eating disorders remained approximately 0.3 per 100 000 members per month until May 2020 when it more than ...
Prevalence of eating disorders over the 2000-2018 period: a systematic
Eating disorders (EDs) lead to multiple psychiatric and somatic complications and thus constitute a major public health concern. ... The characteristics of the research were a priori precisely defined to allow the sorting of articles. Thus, only articles regarding the general population (excluding populations with specific pathologies, e.g ...
Treatment of eating disorders: A systematic meta-review of meta
14 Eating Disorders Center for Treatment and Research, Department of Neuroscience, University of Turin, Turin, Italy. 15 Department of General Psychology, University of Padova, Padova, Italy. 16 Department of Medicine, Surgery and Dentistry 'Scuola Medica Salernitana', Section of Neurosciences, University of Salerno, Salerno, Italy.
New insights on eating disorders
Still other eating disorders fall into a catchall category known as "eating disorders not otherwise specified." What all of these disorders share is a dangerously maladaptive approach to food. Unsurprisingly, binge-eating disorder is often associated with obesity. People with anorexia and bulimia, on the other hand, fear gaining weight.
Binge eating appears more widespread, persistent than thought
What's the prevalence of binge eating in society? That's a tricky question because the research doesn't entirely agree. The National Comorbidity Survey Replication, which was done in 2007 by my mentor, Jim Hudson, and Ron Kessler, suggested that the prevalence of DSM-4 binge-eating disorder was around 2.6 percent [chance over a] lifetime in the U.S.
Current Discoveries and Future Implications of Eating Disorders
Recent research on eating disorders has highlighted the complexity of these conditions including the significance of early period intervention measures in treatment, the role of genetics and social factors, and the impact of the COVID-19 pandemic. Eating disorders are associated with a range of negative health outcomes, including malnutrition ...
Recent Advances in Developmental and Risk Factor Research on Eating
The Diagnostic and Statistical Manual of Mental Disorders (i.e., DSM-5) currently recognizes three primary eating disorders: anorexia nervosa, bulimia nervosa, and binge eating disorder. The origins of eating disorders are complex and remain poorly understood. However, emerging research highlights a dimensional approach to understanding the ...
Special Report: Youth With Eating Disorders—Time Is of the Essence in
Despite these shocking statistics, eating disorder research has historically been significantly underfunded. For example, recent estimates of U.S. federal funding amounted to just $.73 per person impacted with an eating disorder, compared with almost $87 per person for schizophrenia and $59 per person for autism spectrum disorder. In Canada ...
Binge eating disorder may last longer than previously thought
The research team said its results contradict previous studies that documented faster remission times. "The big takeaway is that binge-eating disorder does improve with time, but for many people ...
(PDF) Overview on eating disorders
Abstract and Figures. There is a commonly held view that eating disorders are lifestyle choice. Eating disorders are actually serious and often fatal illnesses, obsessions with food, body weight ...
Eating disorder outcomes: findings from a rapid review of over a decade
Eating disorders (ED), especially Anorexia Nervosa (AN), have amongst the highest mortality and suicide rates in mental health. While there has been significant research into causal and maintaining factors, early identification efforts and evidence-based treatment approaches, global incidence rates have increased from 3.4% calculated between 2000 and 2006 to 7.8% between 2013 and 2018 [].
Overlap of eating disorders and neurodivergence: the role of inhibitory
Neurodivergence and eating disorders: the role of inhibitory control. Eating disorders (EDs) are complex mental illnesses that typically emerge in childhood and adolescence, although they can impact individuals across the lifespan [].EDs are estimated to impact 2.2% of the population in a given year, with a lifetime prevalence of 11.1% [2, 3].When subthreshold diagnoses are considered, however ...
An update on the prevalence of eating disorders in the general
Introduction. Eating disorders (EDs) are a group of syndromes characterized by eating behaviors and psychological disorders accompanied by weight changes and/or social disorders that have a significant influence on quality of life and social function [1, 2].Moreover, individuals with eating disorders may develop severe somatic complications that can cause a higher risk of suicide [] and ...
The association between eating disorders and mental health: an umbrella
Eating disorders (ED) such as anorexia nervosa, bulimia nervosa and binge eating disorders lead to higher physical and psychological morbidity, disabilities, and mortality rates [].The prevalence of eating disorder is increasing, with the lifetime prevalence between 3.3 and 18.6% among women and between 0.8 and 6.5% among men [].Risk factors such as dieting and body dissatisfaction have been ...
Ethical Considerations for Patients With Eating Disorders
Eating disorders are also disorders of relationships—the ones we have with our self-concept ... M. Handbook of Evidence-Based Psychotherapies: A guide for research and practice. 1st edition. ...
Can TikTok exacerbate eating disorders?
Recent research published in the International Journal of Eating Disorders suggests a connection between the use of TikTok, a popular video-based social media platform, and eating disorder symptoms.
Risk factors for eating disorders: findings from a rapid review
This study is one review of a wider Rapid Review series conducted as part the development of Australia's National Eating Disorders Research and Translation Strategy 2021-2031. The findings from this review are grouped into nine main risk factor categories. These include (1) genetics, (2) gastrointestinal microbiota and autoimmune reactions ...
Risk factors for eating disorders: findings from a rapid review
Risk factors represent a range of complex variables associated with the onset, development, and course of eating disorders. Understanding these risk factors is vital for the refinement of aetiological models, which may inform the development of targeted, evidence-based prevention, early intervention, and treatment programs. This Rapid Review aimed to identify and summarise research studies ...
Celiac disease
Diarrhea. Fatigue. Weight loss. Bloating and gas. Abdominal pain. Nausea and vomiting. Constipation. However, more than half the adults with celiac disease have symptoms that are not related to the digestive system, including: Anemia, usually from iron deficiency due to decreased iron absorption.
Avoidant restrictive food intake disorder: recent advances in
Avoidant restrictive food intake disorder (ARFID) is an eating disorder characterized by persistent insufficient nutritional and/or energy intake. ARFID, before referred to as "selective eating disorder", was introduced recently in the DSM-5 as a replacement for and expansion of the previous diagnosis. Individuals with ARFID may limit food variety and intake due to avoidance based on the ...
Microplastics Are Everywhere. Here's How to Avoid Eating Them
June 2024. Microplastics and nanoplastics are everywhere. The teeny tiny pieces of plastic have been found in everything from drinking water to chicken nuggets, apples, and broccoli. Recent ...

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Special Report: Youth With Eating Disorders—Time Is of the Essence in Achieving Remission

Eating Disorders Can Be Life Threatening Yet Underresearched

Fighting Myths and Misconceptions

Anorexia Nervosa (AN)

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BMC Psychiatry

Ethical Considerations for Patients With Eating Disorders

Some factors to consider when deciding between in-person and virtual meetings:

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Risk factors for eating disorders: findings from a rapid review

Siân A. McLean

Emma Bryant

Stephen Touyz

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