EATING

DISORDER

BY
ATHIRA S NAIR
MPHIL CPT 1st YEAR

CHAIRED BY
Mr. SONU S DEV
CLINICAL PSYCHOLOGIST AND
LECTURER
According to American Psychiatric Association, “eating disorders are behavioural conditions
characterized by severe and persistent disturbance in eating behaviors and associated
distressing thoughts and emotions.”

According to NIMH, “Eating disorders (ED) are all those disorders that include irregular or
disturbed eating practices. They are characterized by either excessive intake or inadequate
intake of food.”

In the late 1800s, eating disorders were accepted as psychogenic illnesses. Anorexia nervosa,
which was regarded as a psychophysiological reaction, was the first eating disorder listed in
the Diagnostic and Statistical Manual of Mental Disorders (DSM) in its first edition (DSM-I)
APA. However, despite the fact that weight phobia, a crucial aspect of eating disorders, was
initially explored in the 1930s, the British psychiatrist Gerald Russell first identified Bulimia
nervosa in 1979 Castillo M, et al.

Eating disorders (EDs) are polysymptomatic syndromes, defined by maladaptive attitudes

and behaviors around eating, weight, and body image, but typically accompanied by
disturbances of self-image, mood, impulse regulation, and interpersonal functioning.

The current system of psychiatric diagnosis, DSM-5, includes four official ED syndromes—
anorexia nervosa (AN), bulimia nervosa (BN), the formerly provisional diagnosis, binge
eating disorder (BED), and a new classification—avoidant/restrictive food intake disorder
(ARFID) in which individuals have a minimized or limited food intake due to some
psychological conditions, pica, where the patient eats non-food items, rumination syndrome,
where the individuals regurgitates undigested or barely digested food, and a group of other
specific feeding or eating disorders. There are two additional categories addressing atypical
ED variants that do not full fill criteria for one of the four syndromes noted but that
nonetheless constitute a significant detriment to individuals’ adjustment—other specified
feeding and eating disorder (OSFED) and unspecified feeding and eating disorder (USFED).

Epidemiology of eating disorder

A wide range of gender, age, and cultural disparities, as well as differences in the
methodologies employed for diagnosis and measurement, can be seen in estimates of the
incidence of eating disorders. Anorexia affects 0.4% and bulimia impacts 1.3% of young
females in the developed countries in a given year, respectively. In any given year, 0.8% of
men and 1.6% of women are affected with binge eating disorder. A study by Smink FR, et al.
found that up to 4% of women may experience anorexia at some point in their lives, and up to
2% will experience bulimia and binge eating disorders. It seems that less developed nations
have lower rates of eating problems. Females are about ten times as likely as men to suffer
from anorexia and bulimia. Eating disorders typically first appear in late childhood or early
adulthood.

Even though they are very frequent, eating disorders are not well understood in India. 14.8%
of the sample group had the syndrome of eating distress, according to Srinivasan TN, et al.
research of 210 medical students in Chennai utilising the eating attitudes test (EAT) and
BITE self-report questionnaires. The following study, conducted by Bhugra D, et al., found
that 0.4% of North Indians have bulimia nervosa. According to the findings of Abraham SF,
et al., Indian females tend to externalize their problems and explain their eating disorder-
related feelings and behaviours in medical and physical terms. They also accept the physical
effects of their eating disorders on their health more readily than the psychological ones.
Silawat R did a study in India to compare the incidence of eating anxiety among several zonal
female basketball players in India. According to the findings, India’s east zone had the
highest prevalence, followed closely by the north zone. The incidence of eating distress was
low in the west and south zones, with the south zone scoring the lowest.

Classification
ICD -11 Feeding and eating disorders
DSM 5 (Feeding and Eating Disorders)
Pica- 307.52 Anorexia nervosa- 6B80

Rumination- 307.53 Bulimia nervosa- 6B81

Avoidant/ restrictive food intake disorder- 307.59 Binge-eating disorder- 6B82

Anorexia nervosa- F 307.50 Avoidant-restrictive food intake disorder- 6B83

Bulimia nervosa- 307.51 Pica- 6B84

Binge eating disorder- 307.51 Rumination-regurgitation disorder- 6B85

Other feeding and eating disorder Other specified feeding or eating disorder- 6B8Y

Unspecified feeding and eating disorder Feeding or eating disorder, unspecified- 6B8Z

ANOREXIA NERVOSA
DSM-5

A. Restriction of energy intake relative to requirements, leading to a significantly low body

weight in the context of age, sex, developmental trajectory, and physical health. Significantly
low weight is defined as a weight that is less than minimally normal or, for children and
adolescents, less than that minimally expected.

B. Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes
with weight gain, even though at a significantly low weight.

C. Disturbance in the way in which one's body weight or shape is experienced, undue
influence of body weight or shape on self-evaluation, or persistent lack of recognition of the
seriousness of the current low body weight.

Clinical subtypes

Food-restricting category (Food intake is highly restricted, and the patient may be relentlessly
and compulsively overactive, with overuse athletic injuries)

Purging category (alternate attempts at rigorous dieting with intermittent binge or purge
episodes)

ICD-11

Essential (required) features:

• Significantly low body weight for the individual’s height, age, developmental stage and
weight history that is not due to the unavailability of food and is not better accounted for by
another medical condition. A commonly used guideline is body mass index (BMI) less than
18.5 kg/m2 in adults and BMI-for-age under 5th percentile in children and adolescents. Rapid
weight loss (e.g., more than 20% of total body weight within 6 months) may replace the low
body weight guideline as long as other diagnostic requirements are met. Children and
adolescents may exhibit failure to gain weight as expected based on the individual
developmental trajectory rather than weight loss.

• A persistent pattern of restrictive eating or other behaviors that are aimed at establishing or
maintaining abnormally low body weight, typically associated with extreme fear of weight
gain. Behaviors may be aimed at reducing energy intake, by fasting, choosing low calorie
food, excessively slow eating of small amounts of food, and hiding or spitting out food, as
well as purging behaviors, such as self-induced vomiting and use of laxatives, diuretics,
enemas, or omission of insulin doses in individuals with diabetes. Behaviors may also be
aimed at increasing energy expenditure through excessive exercise, motor hyperactivity,
deliberate exposure to cold, and use of medication that increases energy expenditure (e.g.,
stimulants, weight loss medication, herbal products for reducing weight, thyroid hormones).

• Low body weight is overvalued and central to the person’s self-evaluation, or the person’s
body weight or shape is inaccurately perceived to be normal or even excessive. Preoccupation
with weight and shape, when not explicitly stated, may be manifested by behaviors such as
repeatedly checking body weight using scales, checking one’s body shape using tape
measures or reflection in mirrors, constant monitoring of the calorie content of food and
searching for information on how to lose weight or by extreme avoidant behaviors, such as
refusal to have mirrors at home, avoidance of tight-fitting clothes, or refusal to know one’s
weight or purchase clothing with specified sizing.

Prevalence

1. Based on international data, the lifetime prevalence of anorexia nervosa for females
ranges from 0.3%-1.5% and for males range from 0.1%-0.5%.

2. Anorexia nervosa has a mortality rate that is around 12 times higher than the mortality
rates from all other causes.

3. Females with anorexia nervosa outnumber males with anorexia nervosa on a 10:1
ratio

Prognosis

Remission in AN varies. Three-fourths of patients treated in out-patient settings remit within

5 years and the same percentage experience intermediate-good outcomes (including weight
gain). Relapse is more common in patients who are older with a longer duration of disease or
lower body fat/weight at the end of treatment, have co-morbid psychiatric disorders, or
receive therapy outside of a specialized clinic. Patients who achieve partial remission often
develop another form of eating disorder (ex. bulimia nervosa or unspecified eating disorder).

All-cause mortality is greater in AN compared to the rest of the population. It has one of the
highest mortality rates of all eating disorders due to medical complications, substance abuse,
and suicide. Patients with AN have increased rates of suicide and this accounts for 25% of
deaths associated.
BULIMIA NERVOSA

DSM-5

A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of

the following:

1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that
is definitely larger than what most individuals would eat in a similar period of time under
similar circumstances.

2. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot
stop eating or control what or how much one is eating).

B. Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such as

self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or
excessive exercise.

C. The binge eating and inappropriate compensatory behaviors both occur, on average, at
least once a week for 3 months.

D. Self-evaluation is unduly influenced by body shape and weight.

E. The disturbance does not occur exclusively during episodes of anorexia nervosa.

ICD-11

Essential (required) features:

• Frequent, recurrent episodes of binge eating (e.g., once a week or more over a period of at
least 1 month). Binge eating is defined as a distinct period of time during which the
individual experiences a loss of control over his or her eating behavior. A binge eating
episode is present when an individual eats notably more and/or differently than usual and
feels unable to stop eating or limit the type or amount of food eaten. Other characteristics of
binge eating episodes may include eating alone because of embarrassment, eating foods that
are not part of the individual’s regular diet, eating large amounts of food in spite of not
feeling hungry, and eating faster than usual.

• Repeated inappropriate compensatory behaviors to prevent weight gain (e.g., once a week
or more over a period of at least 1 month). The most common compensatory behavior is self-
induced vomiting, which typically occurs within an hour of binge eating. Other inappropriate
compensatory behaviors include fasting or using diuretics to induce weight loss, using
laxatives or enemas to reduce the absorption of food, omission of insulin doses in individuals
with diabetes, and strenuous exercise to greatly increase energy expenditure.

• Excessive preoccupation with body weight and shape. When not explicitly stated,
preoccupation with weight and shape may be manifested by behaviors such as repeatedly
checking body weight using scales, checking one’s body shape using tape measures or
reflection in mirrors, constant monitoring of the calorie content of food and searching for
information on how to lose weight or by extreme avoidant behaviors, such as refusal to have
mirrors at home, avoidance of tight-fitting clothes, or refusal to know one’s weight or
purchase clothing with specified sizing.

• There is marked distress about the pattern of binge eating and inappropriate compensatory
behavior or significant impairment in personal, family, social, educational, occupational or
other important areas of functioning.

• The symptoms do not meet the definitional requirements for Anorexia Nervosa.

Prevalence

1. The lifetime prevalence of bulimia nervosa for adult women ranges from 1.7%-2.0%
and for men ranges from 0.5-0.7%.

2. The prevalence of bulimia nervosa in ethnic minority youth is 5.1% for girls and 2.3%
for boys.

3. Among youth with bulimia nervosa, 49% meet criteria for major depression and 66%
meet criteria for an anxiety disorder.

BINGE EATING DISORDER

A. Recurrent episodes of binge eating. An episode of binge eating is characterized by

both of the following:
a. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food
that is definitely larger than most people would eat in a similar period of time under
similar circumstances
b. The sense of lack of control over eating during the episode (e.g., a feeling that one
cannot stop eating or control what or how much one is eating)
B. Binge-eating episodes are associated with three (or more) of the following:
 1. Eating much more rapidly than normal
2. Eating until feeling uncomfortably full
3. Eating large amounts of food when not feeling physically hungry
4. Eating alone because of being embarrassed by how much one is eating
5. Feeling disgusted with oneself, depressed, or very guilty after overeating
C. Marked distress regarding binge eating is present.
D. The binge eating occurs, on average,
1. at least 2 days a week for 6 months (DSM-IV frequency and duration criteria)
2. at least 1 day a week for 3 months (DSM-5 frequency and duration criteria)
E. The binge eating is not associated with the regular use of inappropriate compensatory
behavior (e.g., purging, fasting, excessive exercise) and does not occur exclusively
during the course of anorexia nervosa or bulimia nervosa.

ICD-11

Essential (required) features:

• Frequent, recurrent episodes of binge eating (e.g., once a week or more over a period of 3
months). Binge eating is defined as a distinct period of time during which the individual
experiences a loss of control over his or her eating behavior. A binge eating episode is
present when an individual eats notably more or differently than usual and feels unable to
stop eating or limit the type or amount of food eaten. Other characteristics of binge eating
episodes may include eating alone because of embarrassment, or eating foods that are not part
of the individual’s regular diet.

• The binge eating episodes are not regularly accompanied by inappropriate compensatory
behaviors aimed at preventing weight gain.

• The symptoms and behaviors are not better explained by another medical condition (e.g.,
Prader-Willi Syndrome) or another mental disorder (e.g., a depressive disorder) and are not
due to the effect of a substance or medication on the central nervous system, including
withdrawal effects.

• There is marked distress about the pattern of binge eating or significant impairment in
personal, family, social, educational, occupational or other important areas of functioning.

Epidemiology and Prevalence

Binge eating disorder is more common in women compared to men, often starting in late
adolescence or early adulthood. This condition is also more common in students and those
without a college education. The lifetime prevalence of binge eating disorder averages 1.9%
in international surveys and 2.6% in studies conducted in the United States. Approximately
79% of people with a history of binge eating disorder have at least 1 lifetime psychiatric
comorbidity. In an estimated 48.9% of people, ≥3 comorbid conditions are observed,
including:

 Anxiety disorder in 56.1%, with phobia being the most common

 Mood disorder in 46.1%, with major depressive disorder being the most common
 Disruptive behavior disorder in 25.4%, with intermittent explosive disorder and
attention-deficit/hyperactivity disorder being the most common
 Substance use disorder in 23.7%, with alcohol use disorder being the most common

Etiology

It is widely held that EDs have a multidimensional etiology, including genetic liabilities
(affecting mood, behavioral controls, sensitivity to reward, energy metabolism and appetite),
developmental processes (conducive to self-image or adjustment problems, or excessive
concerns with achievement and social approval), environmental stresses (such as perinatal
insults or childhood traumata), state-related effects (owing to the nutritional and mental
status), and ultimately, social inducements toward intensive dieting.

Sociocultural Factor

Researchers have long recognized that sociocultural pressures—from media, family, peers,
and romantic partners—play a major role in the development and continuation of eating
disorders in women.

Studies (e.g., Stice, 1994; Striegel-Moore et al., 1986) have shown that:

 Pressure to be thin is strongly linked to eating disorder symptoms, especially in

adolescents and college-aged women.

 These pressures cause women to internalize the "thin ideal"—the belief that being thin
equals beauty, success, and worth.
  This internalization often leads to body image disturbance, where women feel
dissatisfied and ashamed of their bodies because they don't match unrealistic beauty
standards shown in media.

According to Objectification Theory (Fredrickson & Roberts, 1997):

 Women in such cultures often experience sexual objectification—where their value is
based on how their bodies look.
 Over time, they start to self-objectify—judging themselves from an outsider’s
perspective and constantly monitoring their appearance.
 This results in body shame, low self-esteem, and greater risk for disordered eating.
Additionally, theorists like Pipher (1994) and Maine (2000) argue that:
 Constant pressure to be thin can lead women to feel unsupported by others and
experience negative emotions such as sadness or worthlessness.

The socio-cultural theory of anorexia nervosa, initially advanced by Hsu (1988), highlights
the significant role of societal and cultural factors in the development of the disorder. This
theory emphasizes the high value placed on slimness, the evolving roles of women in society,
and the increased vulnerability of adolescent girls from upper and middle socioeconomic
classes, particularly in Western or Western-influenced cultures. Attie, Gunn, and Peterson
(1990) further supported this perspective by situating anorexia within a historical and
ideological context, where concerns about body weight and shape are culturally constructed
and deeply embedded in social norms. Expanding on this, Iancu et al. (1994) proposed that
while not all women exposed to socio-cultural pressures will develop anorexia, certain
cultural elements—such as careers that emphasize physical appearance, ongoing gender
inequality, and devaluation of motherhood—create a fertile ground for the disorder. The
theory also notes that the disorder commonly begins in adolescence and is more prevalent
among individuals in higher socioeconomic strata. Moreover, cultural practices like labeling
foods as "good" or "bad" reflect deeper symbolic beliefs that contribute to unhealthy eating
behaviors. Fundamentally, the socio-cultural theory posits that female attractiveness is
closely tied to thinness, and in the face of changing societal expectations and limited gender
equality, many women experience role confusion and insecurity, which may intensify their
drive for control and perfection—central features in the manifestation of anorexia nervosa.

Psychological factors
The first studies in the 1970s found that people with anorexia nervosa (AN) often showed
traits like being obsessive, anxious in social situations, introverted, and depressed. These
studies also noticed a difference between those who only restrict food (AN-R) and those who
binge eat or purge (AN-B/P). People with AN-R were usually seen as emotionally reserved
and rule-following, while those with AN-B/P were more impulsive and had trouble
controlling emotions.

Later studies also found that bulimia nervosa (BN) tends to be linked with impulsive and
risk-taking traits. In general, people with AN-R tend to care a lot about social approval and
show compulsive behaviors, while those with BN or AN-B/P may be more emotionally
unstable or rebellious.

However, not everyone with the same diagnosis has the same personality traits. Researchers
have found three general personality patterns in eating disorders:

1. Psychologically intact but perfectionistic

2. Overcontrolled (inhibited and compulsive)

3. Dysregulated (impulsive and reactive)

AN-R is usually linked to the overcontrolled type, while AN-B/P and BN can fall into any of
the three. The dysregulated type is more likely to have other issues like depression, self-harm,
substance use, and a harder time recovering in treatment.

Specific traits

1. Perfectionism

 People with AN (Anorexia Nervosa), BN (Bulimia Nervosa), and BED (Binge Eating
Disorder) often score high on perfectionism.

 They tend to set very high standards for themselves, are highly self-critical, and worry
a lot about what others think.

 These traits often exist before the eating disorder, stay even after recovery, and are
seen in family members too.

 Perfectionism is linked to strict dieting and obsession with body image.

2. Impulsivity
  Seen more in binge/purge types (BN, AN-BP) than in restrictive types (AN-R).

 Includes behaviors like self-harm, substance use, stealing, and suicide attempts.

 Impulsivity can lead to more severe ED symptoms and might even appear before the
ED begins.

3. Body-Image Disturbance

 A central issue in AN and BN: distorted view of one's body and harsh body criticism.

 Some studies confirm this, while others argue it’s more about emotions and attention
than actual misperception.

4. Dietary Restraint

 Refers to mental rules about eating, like believing low-calorie foods are always better
or feeling guilt after eating.

 These restrictive beliefs can actually lead to binge eating, especially after triggers like
sadness, low self-worth, or drinking alcohol.

 People who diet and feel depressed are more likely to start binge-eating later.

5. Emotion Dysregulation

 Negative emotions often trigger binge-eating episodes.

 Binge eating may temporarily relieve emotional pain, making it a self-reinforcing

behavior.

 Studies using real-time tracking support this emotion-based model.

6. Neurocognitive Traits

 EDs are linked to challenges in memory, attention, and problem-solving.

 AN is especially tied to problems with:

o Set-shifting (difficulty switching tasks or thoughts)

o Central coherence (focusing too much on details instead of the big picture)

 These traits may also show up in relatives of people with AN, suggesting a possible
genetic or trait link.
  Decision-making is also impaired in some EDs, but other issues (like substance
abuse) might play a role.

 Cognitive remediation therapy has shown promise in improving thinking patterns in

ED patients.

Early Theories on Family Dynamics in Eating Disorders (EDs)

 In earlier psychological models, Anorexia Nervosa (AN) was often seen as a response
to excessive familial control and overprotectiveness. The theory suggested that when
families are too intrusive or emotionally overinvolved, a child might refuse food as a
form of self-assertion or rebellion against this control.

 For Bulimia Nervosa (BN), early models described patients as coming from families
that were emotionally neglectful, disengaged, or chaotic. In this view, bulimic
behaviors—such as bingeing and purging—were understood as ways to manage mood
swings and emotional distress arising from family dysfunction. Eating behavior
became a coping mechanism for handling feelings of rejection or abandonment.

 However, these models often put blame on families, which caused guilt and stigma
for relatives, and had limited empirical support. Over time, such perspectives were
recognized as too simplistic and potentially harmful.

Shift in Contemporary Understanding

 The Academy for Eating Disorders (AED) now clearly states that families are not the
primary cause of eating disorders. While family factors can influence risk or help
maintain the disorder, they do not cause anorexia or bulimia on their own.

 The AED rejects blame-based models of ED causation and stresses the complexity of
EDs, which involve multiple biological, psychological, and social factors beyond
family functioning.

Empirical Findings on Family Functioning

 Research shows some patterns in family characteristics associated with different ED

types:
 o Anorexia Nervosa (AN) families tend to show higher enmeshment, meaning
family members may be overly involved with one another and lack healthy
boundaries or independence.

o Families of individuals with bulimia nervosa often exhibit disengagement,

conflict, hostility, and low nurturance—suggesting emotional distance and
tension.

o Those with binge eating disorder (BED) tend to come from families described
as incohesive, unexpressive, conflictual, and controlling.

 However, these observations come mainly from cross-sectional and retrospective

studies—meaning they look at families and patients at one point or ask patients to
recall past experiences, which limits understanding of cause and effect.

Neurobiological Alterations in Eating Disorders (EDs)

Several neurobiological systems are implicated in the development and maintenance of eating
disorders.

Serotonin (5-HT):
Serotonin regulates mood, social behavior, impulsivity, and eating. Increased 5-HT activity
suppresses appetite, while reduced activity promotes binge eating. Various abnormalities in
central and peripheral 5-HT function have been reported in anorexia nervosa (AN), bulimia
nervosa (BN), and binge eating disorder (BED). Notably, persistent 5-HT anomalies have
been observed in individuals recovered from AN and BN, suggesting a trait marker. For
example, altered 5-HT2A receptor binding and reduced platelet paroxetine binding have been
documented. These anomalies may have a hereditary component, as unaffected first-degree
relatives of BN patients also show altered 5-HT uptake.

Other Neurotransmitters and Neuropeptides:

 Dopamine (DA): DA influences reward, novelty seeking, executive control, affect,

and food intake. Altered DA function has been noted in active and recovered AN and
BN cases, including increased D2/D3 receptor binding in the striatum in recovered
AN and decreased DA metabolites and transporter availability in BN.
  Brain-Derived Neurotrophic Factor (BDNF): BDNF regulates food intake and energy
balance and is involved in neural plasticity. Reduced serum BDNF levels have been
reported in AN and BN. Genetic variants such as the BDNF Val66Met polymorphism
have been linked to BN.

Hypothalamic–Pituitary–Adrenal (HPA) Axis:

The HPA axis is the primary stress response system. AN and BN show alterations in HPA
function, influenced by malnutrition, comorbid mood/anxiety disorders, trauma, and the
disorder itself. Severity of ED psychopathology often correlates with HPA-axis dysfunction.

Gut Peptides and Hormones:

 Cholecystokinin (CCK) and Peptide YY (PYY): Both promote satiety by acting on

the hypothalamus. Plasma levels are reduced in BN, possibly facilitating binge
episodes.

 Leptin: Regulates appetite and energy expenditure; levels are abnormally low in
active AN and normal-weight BN individuals.

 Ghrelin: Influences short-term appetite and long-term energy balance; elevated in

BED.

Sex Hormones:
Given the higher prevalence of EDs in females, sex hormones like androgens and estrogens
may influence risk. Studies suggest prenatal androgen exposure may protect against ED
development, evidenced by findings in opposite-sex twins and second-to-fourth digit ratio
correlations with ED symptoms. Puberty may activate genetic risk for ED through hormonal
changes.

Genetics and Eating Disorders (EDs)

Family and Twin Studies:
 Eating disorders (EDs) show familial transmission, especially among female relatives
of affected individuals.
 Twin studies strongly support a genetic component, with heritability estimates
ranging widely but significantly:
o Anorexia Nervosa (AN): 33% to 84%
o Bulimia Nervosa (BN): 28% to 83%
 o Binge Eating Disorder (BED): 41% to 57%
 Shared environmental factors (e.g., family environment) appear to have a smaller
influence than genetics.

 Genetic predispositions can interact with environmental stressors (like childhood abuse) to
influence ED risk.

 For example, low-function alleles of serotonin transporter genes combined with childhood
trauma increase impulsivity, affective instability, and novelty seeking.

 Similar interactions have been noted with dopamine receptor gene polymorphisms and
glucocorticoid receptor variants in the context of childhood abuse and ED symptoms.

 AN risk may be amplified by puberty-related hormonal changes, dieting, and malnutrition,

which interact with genetic factors.

MODELS OF EATING DISORDER

Multidimensional Model of Eating Disorders
Eating disorders like anorexia nervosa and bulimia nervosa are complex and arise from
multiple interacting factors, categorized into three main groups: predisposing, precipitating,
and perpetuating factors.
1. Predisposing Factors:
these include individual psychological and biological traits, family dynamics, and
cultural influences that create vulnerability to eating disorders.
o Psychological: Depression, anxiety, personality disorders, distorted thinking,
emotional difficulties, body image issues, and trauma (e.g., sexual abuse).
o Biological: Genetics, prenatal or birth-related risks, tendencies toward obesity,
and hormonal or neurochemical imbalances.
o Familial: Dysfunctional family roles, such as an overly controlling mother or
passive father, and unhealthy family interactions like enmeshment or conflict
avoidance.
o Cultural: Societal pressure to be thin, leading to body dissatisfaction and
dieting.
2. Precipitating Factors
These are triggers that initiate the onset of an eating disorder.
o Dieting and dissatisfaction with body weight or shape.
o Depression, mood disorders, poor coping skills, and stressful life events.
3. Perpetuating Factors
These maintain and worsen the disorder once it has begun.
o The physical and psychological effects of starvation, which can worsen mood
and increase obsession with food and control.
o Binge eating, purging (like vomiting or laxative use), and non-purging
behaviors (such as excessive exercise or diet pills) that reinforce the cycle of
the disorder.
The model highlights how these factors interact over time to contribute to the development
and persistence of eating disorders. For example, cultural pressure leads to dieting
(precipitating), which leads to starvation effects and compensatory behaviors (perpetuating),
all building on pre-existing vulnerabilities.
Dual-Pathway Model of Eating Pathology
This model explains how eating disorders develop through two main routes (pathways), both
triggered by body dissatisfaction, which arises mainly from societal pressures to be thin
(family, peers, media).
1. Background:
o Pressure to conform to the "thin ideal" leads to body dissatisfaction.
o Body dissatisfaction then increases the risk of developing eating problems.
2. Two Pathways from Body Dissatisfaction:
o Dieting Pathway: Unhealthy dieting behaviors (like severe calorie restriction)
can lead to eating disorders.
o Negative Affect Pathway: Experiencing negative emotions (such as sadness,
anxiety) can also lead to eating disorders.
3. Interaction Between the Pathways:
o Dieting can increase negative emotions because of failure to maintain strict
diets and the mood effects of starvation.
o Negative emotions can trigger binge eating as a way to cope or distract from
these feelings.
4. Outcome:
o Either extreme dieting or chronic negative emotions alone—or a combination
of both—can lead to eating pathology (disordered eating behaviors).
In brief, societal pressure leads to body dissatisfaction, which then causes eating disorders
either through unhealthy dieting, negative emotions, or both.

Trans diagnostic Model of Eating Disorders

Fairburn et al. describe a “transdiagnostic” model of eating disorders and provide evidence
that patients with anorexia, bulimia and atypical eating disorders display many common
clinical features (e.g. excessive preoccupation with figure, weight and their control). The line
of argument for transdiagnostic mechanisms is the transformation of the symptoms of one
type of eating disorder into another type during the course of treatment (and afterwards) (e.g.
symptoms of anorexia nervosa converted to symptoms of bulimia nervosa), and the fact that
the symptoms of eating disorders are non transformed into other mental illnesses . It is worth
pointing out that this evidence leads to the use of the transdignostic model of eating dis orders
in enhanced cognitive–behavior therapy (CBT-E) [23]. The basis for the transdiagnostic
model of eating disorders was the cognitive–behavioral mod el of anorexia and bulimia. The
core psycho pathology of eating disorders is a dysfunction al cognitive schema related to low
self-esteem, high perfectionism, mood intolerance and difficulties in relationships with other
people. These psychopathological symptoms of bulimia nervosa play a relevant role in the
emergence of an excessive preoccupation with figure, weight and their control, self-
monitoring, and restrictive eating. The only symptoms of bulimia which are not related to the
core psychopathology are paroxysmal overeating and inappropriate use of compensatory
behaviors (self-induced vomiting and laxatives). In addition, the emergence of these
symptoms is often associated with difficult life issues and negative mood. Some of the
symptoms of bulimia are also characteristic of anorexia. The cognitive–behavioral theory of
anorexia nervosa (restricting subtype) encompasses the following common elements:
excessive preoccupation with figure, weight and their control, and non-compensatory weight
control (restrictive diet). Body image disturbance and maladaptive behaviors lead to
excessive concentration on eating, social withdrawal, severity of obsessive thoughts and
behaviours in relation to the body, and excessive satiety. These symptoms reinforce other
maintaining mechanisms. Anorexia and bulimia also differ in the level of the relationship
between food restriction and binge episodes. The first type of eating disorder is related to
dieting. Instead, patients with bulimia exhibited more severe paroxysmal over eating than
restrictive eating. The clinical features and maintaining mechanisms which are characteristic
of anorexia nervosa and bulimia nervosa play a relevant role in the occurrence and
maintenance of atypical eating disorders. The core psychopathology of all types of eating
disorders is related to very similar symptoms and many elements of the maintaining
mechanism are repeated in all types.

Reward-Centred Model of Anorexia Nervosa

This model highlights how neurobiological and psychological reward mechanisms contribute
to the development and persistence of anorexia nervosa.

 Certain behaviors related to anorexia (like food restriction or weight loss) activate the
brain’s reward system, particularly by increasing dopamine activity.
 This reinforces the disordered behaviors, making them feel rewarding, which leads to
their repetition and maintenance.

Factors Involved:
A. Triggers:

 Emotional suppression (avoiding or not expressing feelings).

B. Socio-emotional Factors:

 Social influences, such as seeking approval, control, or empowerment through weight

loss.

C. Physiological Factors:

 Biological predispositions, including heightened dopamine response to anorexia-

related behaviors.

D. Personality Factors:

 Traits like perfectionism or obsessive tendencies increase vulnerability.

E. Behavioral Changes:

 Initial attempts at dieting or weight control evolve into compensatory behaviors (e.g.,
excessive exercise or restriction) that become habit-forming due to the reward system
activation.

How the Cycle Works:

 These factors interact and reinforce each other.

 The dopamine reward system strengthens the belief that weight loss is “good,” and
this reward system maintains the eating disorder by:
o Enhancing negative cognitive biases (e.g., fear of weight gain, distorted body
image).
o Making anorexic behaviors more psychologically satisfying, even when
physically harmful.
Transtheoretical Model of Eating Disorders

It’s a way of understanding why eating disorders like anorexia and bulimia continue over
time, even when the person wants to get better. This model doesn't just focus on food or
weight—it looks at underlying emotional, cognitive, and relational issues that keep the
disorder going.

According to MANTRA Model: The Four Main Factors That Keep Anorexia Going

1. Thinking Style
o People with anorexia often have a very rigid and perfectionistic way of
thinking.
o They focus too much on small details and fear making mistakes.
o This makes it hard for them to be flexible or accept change, even in recovery.
2. Emotional Struggles
o They may struggle to identify or express emotions (a condition called
alexithymia).
o They experience intense negative emotions (like sadness, fear, or anxiety).
 o They often compare themselves to others and feel they aren’t good enough.
3. Relationship Difficulties
o Some have trouble in social relationships or feel emotionally disconnected.
o They may feel things like shame, guilt, or fear when dealing with others.
4. Pro-Anorexia Beliefs
o They may believe that having anorexia helps them feel in control or safe.
o For example, “If I stay thin, I’m successful” or “Starving helps me deal with
life.”

Role of Starvation

Starvation actually reinforces these four factors.

 It makes thinking more rigid, emotions harder to manage, and social withdrawal
worse.
 It also feeds the false belief that anorexia is helping them cope.

Emotional Abuse and Bulimia

Research shows:

 People with bulimia often have a history of emotional neglect or abuse.

 This trauma makes it harder for them to deal with emotions.
 They might turn to binge eating or purging as a way to cope with emotional pain.
 Emotional dysregulation (not being able to manage feelings) is a key problem.

Emotional Eating

 When emotions get overwhelming, some people eat to soothe themselves.

 This is called emotional eating, and it’s common in bulimia and binge eating.
 After eating, they may feel shame or guilt, which triggers more disordered eating.
MANAGEMENT
Enhanced cognitive behavioural therapy (CBT-E)

CBT-E is the abbreviation for “enhanced cognitive behaviour therapy”, and is one of the
most effective treatments for eating disorders. It is a “transdiagnostic” treatment for all forms
of eating disorder including anorexia nervosa, bulimia nervosa, binge eating disorder and
other similar states.

Four Stages of CBT-E (for Non-Underweight):

Stage 1
Engage the patient in treatment and change
 Many patients are ambivalent. Building trust and motivation early is essential.
 Encourage the patient to take ownership of their recovery.
Create a personalized case formulation
 A collaborative visual diagram that explains how the eating disorder is maintained.
 Helps patients see that their problems are understandable and changeable.
 It's provisional and evolves over time.
Introduce real-time self-monitoring
 Track eating, thoughts, feelings, and events in the moment.
  Helps build self-awareness and opens space for behavior change.
 Reviewed in every session and guides the session agenda.
Begin collaborative “weekly weighing”
 Therapist and patient weigh together weekly.
 Provides accurate, balanced information about weight changes.
 Reduces frequent or avoidant self-weighing behavior.
Provide psychoeducation
 Teach patients about:
o Features of eating disorders
o Body weight regulation
o Why vomiting/laxatives/diuretics don’t work for weight loss
o Dangers of dieting and rigid food rules
Establish “regular eating”
 Eat 3 meals + 2–3 snacks daily, no more than 4 hours apart.
 Eat only during these planned times, with no compensatory behavior.
 Focuses on consistency over calorie count.
 Helps prevent binge eating and introduces nutritional structure.
 Support sticking to the plan
 Use two strategies to resist urges to binge or eat between meals:
o Distraction techniques (e.g., go for a walk, leave the kitchen)
o Urge-surfing (learning to ride out the urge without acting on it)
 Involve significant others (if appropriate)
 If others can support the patient or are hindering progress, involve them—with patient
consent.
 Useful when family or partners make unhelpful comments or can help with
accountability
Stage 2
 Continue Stage 1 strategies
 Regular eating, self-monitoring, weekly weighing, and engagement are still ongoing.
 Conduct a joint review of progress
 Celebrate improvements and reinforce helpful changes.
  Identify areas that are still problematic or where change has been minimal.
 Update the case formulation
 Modify the original diagram based on new insights from the first stage.
 Address emerging maintaining mechanisms.
 Identify and understand obstacles
 If progress is limited, explore why:
o Are there unaddressed maintaining processes?
o Are new issues coming up?
Stage 3
Addressing Overevaluation of Shape and Weight

 Many people with eating disorders base their entire self-worth on shape, weight, and
control over eating. This "overevaluation" is the main target in Stage 3.

 Patients are helped to identify how their self-worth is overly tied to

weight/appearance, and how this leads to harmful behaviors like extreme dieting,
binge eating, and body checking.

 A detailed "extended formulation" is developed with the therapist, showing how

thoughts and behaviors (like body checking and feeling fat) keep the disorder going.

 To reduce this, patients are encouraged to reinvest in other parts of life (e.g., hobbies,
work, relationships) and make these part of how they value themselves.

 Body checking and avoidance are reduced by raising awareness, challenging faulty
comparisons, and gradually increasing body exposure.

 “Feeling fat” is reframed as a misinterpretation of emotions (like sadness, stress, or

fullness). Patients learn to recognize the actual feelings behind it.

 Later in this stage, origins of body image issues are explored to help patients
understand how their beliefs developed and why they no longer serve them.

2. Addressing Dietary Rules and Event-Triggered Eating

 Many patients follow rigid, unrealistic food rules. These are identified, tested, and
broken down during sessions. The aim is to reduce dieting and introduce flexibility.
  For those who binge eat, "food avoidance" (avoiding certain “forbidden” foods) is
tackled by reintroducing feared foods in a safe, controlled way.

 Patients also learn to manage changes in eating behavior triggered by mood or events
(like stress, sadness, or social pressure). This is done through problem-solving skills
and healthy emotion regulation.

3. Addressing Broader Issues (Clinical Perfectionism, Low Self-Esteem, Interpersonal

Problems)

If these issues are maintaining the eating disorder, they are directly treated:

 Perfectionism: Similar to overevaluation of shape/weight, perfectionists base their

worth on constant achievement. Patients learn how this mindset is harmful, reduce
unrealistic goals, and address perfectionist behaviors (like checking performance,
procrastination, etc.).

 Core Low Self-Esteem (CLSE): Some patients believe they are fundamentally flawed
regardless of success. This deep-rooted belief is challenged through cognitive
restructuring and behavioral experiments that help patients form a more balanced
view of themselves.

 Interpersonal Problems: Issues like loneliness, conflict, or poor relationships may

contribute to or worsen the eating disorder. These are addressed using Interpersonal
Psychotherapy (IPT) alongside CBT-E to improve relationships and emotional health.

Stage 4
 Gradual winding down of treatment routines
 Patients stop self-monitoring.
 Begin weekly weighing at home (instead of with the therapist).
 Create a personalized relapse prevention plan
 Covers the months until the post-treatment review (~20 weeks later).
 May include:
o Continued work on body checking, food avoidance, and problem-solving.
 o Encouragement to develop new interests and activities.
 Build realistic expectations about recovery
 Emphasize that minor setbacks are normal and manageable.
 Teach patients to view problems as “lapses,” not relapses.
 Strengthen confidence in using CBT-E tools independently when difficulties arise.

DBT for Eating Disorders

1. DBT is Based on an Emotion Regulation Model
One of the features that makes DBT unique is its focus on understanding and working with
emotions. Targeting emotions in the treatment of EDs was not a central part of standard ED
treatments (e.g., CBT, FBT). However, research has shown that focusing on emotion
regulation is a necessary part of treatment and recovery.

For example:

▪Many individuals with an ED report difficulty describing, tolerating, and expressing

emotions. For many, emotions are experienced as threatening, confusing and completely
overwhelming. Other people report feeling numb, empty, and unable to connect with
emotions.

▪ Clients with EDs often report that they do not have the skills to cope with their emotions in
healthy, adaptive ways during treatment or post intensive treatment.

▪Without adequate emotion regulation skills, ED symptoms can become a way of regulating
overwhelming and uncomfortable feelings and body states (e.g., gastrointestinal distress), at
least temporarily. Many people have reported that their symptoms help them tolerate and
control intense and painful emotions. Binge eating, purging, and fasting have been described
as coping strategies, “physical escapes”, “ways of withdrawing” or as a “temporary relief”
from emotional pain and discomfort.

Negative emotions are one of the most common triggers for ED symptoms. Studies which
have tracked emotional states before and after episodes of binge eating have shown that
depression, anger, guilt, loneliness and self-blame are significantly higher on days in which
people engage in symptoms.

▪If left untreated, emotion dysregulation may increase a person’s vulnerability to relapse
following treatment. Several studies have found that people are more likely to maintain their
recovery from an ED when they feel that they can better identify, accept and tolerate
emotions.

2. DBT Focuses on Motivation as a Central Treatment

Target EDs are known for their ego-syntonic nature (e.g., having qualities that a person
doesn’t want to get rid of) and can be characterized by anosognosia, a neurological condition
in which a person is not aware of the seriousness of their illness). Motivation to change
waxes and wanes and DBT uses a set of strategies to work with this throughout treatment.

3. The Driver in DBT is to Build a Life Worth Living

For many clients, symptom focused treatments have not been sufficient and, for some, have
been experienced as traumatic and coercive. DBT balances the need for safety and medical
stability with truly chasing a life worth recovering into. For many, the goal of stopping
purging because they have an ED is not enough.

4. DBT Helps People Learn and Hone Skills to Build That Life Worth Living!
It is difficult, if not impossible, to change over-learned behaviours that have served to help a
person cope without learning new ways of being in the world (and in one’s body). Our clients
and their families often tell us that they need help tolerating anxiety and anger around meals
and beyond or navigating suicidal and self-injurious thoughts and behaviours while trying to
decrease ED symptoms.

In DBT, clients receive in-depth training across 4 domains:

Mindfulness skills: designed to teach people how to focus attention on the present moment
without judgment. Very often, people with EDs have difficulty staying in the “here and now”.
Connecting with emotions, with the body, and with food is very triggering for someone with
an ED. Mindfulness skills help individuals gain insight into their patterns and behaviours and
allows them to observe thoughts and feelings without judging or acting on them.

Interpersonal Effectiveness: Individuals with EDs often report that they have difficulty
asserting their needs, saying no to others, and putting their goals and desires before those of
others. Often this comes from a place of fear (e.g., fearful of being rejected/disliked by
others) or shame (e.g. the belief that one’s needs are not important).Interpersonal
effectiveness skills teach people how to effectively communicate with others and how to
increase the likelihood of getting their needs met.

Distress Tolerance: These skills are designed to help clients get through a crisis without
making matters worse. In this module, clients learn a range of strategies for coping with
stress and crises in a way that minimizes harm and are in line with the life values of our
clients. These are often the first skills people learn to use to interrupt symptoms and gain
confidence that there is a different way of navigating difficult situations.

Emotion Regulation: Unlike distress tolerance skills, emotion regulation skills are the daily
things we teach clients to do to improve quality of life and reduce vulnerability to “emotion
mind”. People will learn how to observe and describe their emotional world without fear,
judgment, or self-hatred. These skills emphasize the adaptive nature of all emotions, teaches
clients how to problem-solve, change their emotions when needed, and challenge myths
about emotions.

Family-Based Treatment (FBT) for Eating Disorders

FBT is a leading outpatient, evidence-based treatment for adolescents with eating disorders,
particularly Anorexia Nervosa (AN) and Bulimia Nervosa (BN). It aims to restore physical
and psychological health by empowering the family—especially the parents—as the primary
agents of change.

FBT for Anorexia Nervosa (AN)

Three Phases of FBT for AN:
Phase 1: Weight Restoration (Parental Takeover)
 Parents temporarily take full responsibility for the adolescent’s eating and physical
activity, much like an inpatient team would:
o Decide what, how much, and when the adolescent eats.
o Monitor all food intake closely.
o Restrict excessive physical activity.
 Due to the ego-syntonic nature of AN, adolescents are unlikely to make health-
promoting choices.
 Siblings are not involved in mealtime enforcement but encouraged to support the
adolescent emotionally.
 Second session: Involves a “family meal” conducted in the therapist’s office.
o Therapist observes and coaches the family in feeding the child effectively.
o The meal is an opportunity to boost parental confidence and demonstrate that
change is possible.
 This phase ends when:
o The adolescent shows steady weight gain.
o Eating behaviors are less resistant.
o Parental control is effective and consistent.
Phase 2: Returning Control to the Adolescent
 Gradual and age-appropriate return of autonomy over food-related decisions to the
adolescent.
 Example: Instead of parents plating food, the adolescent may begin to serve
themselves—with parental oversight.
 Parental involvement remains in place to supervise and intervene if the adolescent’s
intake is inadequate.
 Helps adolescents practice responsibility while minimizing risk of relapse or
regression.
Phase 3: Rebuilding Normal Life & Identity
  Focuses on psychosocial development, healthy autonomy, and reintegration into
normal adolescent roles.
 Addresses upcoming developmental challenges (e.g., school stress, peer relationships)
and provides tools for navigating them without using the eating disorder as a coping
mechanism.
FBT for Bulimia Nervosa (BN)
FBT has been adapted for BN in adolescents. While the overall structure is similar to FBT-
AN, the goals and tone differ due to the ego-dystonic nature of BN and the emotional
environment typically surrounding it.
 Parents still take the lead, but the approach is more collaborative:
o Adolescents with BN are often distressed by their behaviors, making them
more open to change and less resistant to parental involvement.
 Special attention is paid to:
o Reducing shame, secrecy, and guilt related to binge-purge behavior.
o Modifying parental criticism, which tends to be higher in families of
adolescents with BN.
o Encouraging open communication and emotional support.
 FBT-BN allows for more flexibility than FBT-AN:
o Sessions may also address comorbid conditions (e.g., depression, impulsivity,
substance use) that are more common in BN.
o Behavioral issues or emotional dysregulation can be directly addressed within
treatment.
 Focus on developing healthy coping strategies to replace binge-purge behaviors.
Interpersonal Psychotherapy for Eating Disorders (IPT-ED)

The therapist explains that eating disorders often persist because of interpersonal difficulties,
even if the patient is not fully aware of them due to their preoccupation with food, shape, and
weight. The treatment focuses on current interpersonal relationships, not directly on eating
behaviors. The assumption is: by resolving interpersonal issues, disordered eating behaviors
will improve. The information gathering involves exploring the interpersonal history
surrounding the onset and development of the eating disorder, which helps highlight links
between relational experiences and disordered eating. The therapist also conducts an
interpersonal inventory—a detailed assessment of the patient’s current social network,
relationships, and life circumstances—to understand their present interpersonal functioning.
Additionally, the therapist identifies interpersonal triggers for recent changes in eating
behavior, as these events often signal unresolved interpersonal problems that may be
maintaining the disorder.

Common Interpersonal Problem Areas:

1. Lack of intimacy / interpersonal deficits – Feeling isolated or lacking close
relationships.
2. Role disputes – Ongoing conflicts with significant people due to differing
expectations.
3. Role transitions – Struggles with life changes like moving out, starting college, or
new jobs.
4. Complicated grief – Difficulty coping with the loss of a loved one.
5. Life goals – Uncertainty about the future and personal aspirations.

OTHER APPROCHES
In understanding eating disorders beyond the dominant cognitive-behavioral models,
humanistic approaches focus on the individual's capacity for growth, self-actualization, and
meaning-making. These therapies emphasize empathy, unconditional acceptance, and a deep
understanding of the person's inner world.

They view mental health as deeply connected to the realization of personal needs and
authentic self-expression. For individuals with eating disorders, treatment is centered on
discovering intrinsic meaning, developing self-worth beyond physical appearance, and
rebuilding a connection with one’s true self.

The therapist’s role is to create a safe, non-judgmental space that allows the client to explore
their emotional pain, foster self-awareness, and reclaim personal agency in healing.

Systemic approaches view eating disorders within the context of interpersonal and familial
relationships.

Minuchin’s Structural Family Therapy highlights how anorexia can serve to maintain family
homeostasis, often in families characterized by enmeshment, rigid boundaries,
overprotectiveness, and poor conflict resolution.

The Milan Systemic Model (Palazzoli) adds that sociocultural and familial pressures, such as
expectations to be thin or academically perfect, contribute to the development of anorexia.
Weber and Stierlin’s systemic approach further emphasizes transgenerational patterns where
maladaptive beliefs about control, perfection, or emotional suppression are passed down, and
the process of separation and individuation is disrupted.

Emotional abuse, parental neglect, or trauma (like sexual abuse) are also identified as
significant risk factors, especially in bulimia, often leading to poor emotional regulation and
reliance on compensatory behaviors such as purging or bingeing. Research supports the link
between emotional difficulties and the intensity of bulimic behaviors, which are frequently
moderated by traits like perfectionism.

Lastly, integrative and body-oriented therapies offer a holistic understanding and treatment of
eating disorders by addressing predisposing, triggering, and maintaining factors.

Slade’s integrative model posits that vulnerabilities such as perfectionism or dysfunctional

family dynamics (predisposing), experiences like body-shaming (triggers), and reinforcement
through compliments for weight loss or the false sense of control (maintaining factors) all
interact to sustain the disorder. Since body image disturbance is a key feature in all eating
disorders, body-oriented therapies are crucial. These include dance movement therapy, yoga,
kinesiotherapy, and body-centered psychotherapy, all aiming to enhance interoceptive
awareness—helping individuals recognize bodily signals such as hunger or stress and
differentiate them from emotional needs.

Approaches like the Hakomi Method and other somatic techniques help patients reconnect
with their bodies, process stored trauma, and gain better control over disordered eating
behaviors by grounding them in their bodily experiences.

AVOIDANT-RESTRICTIVE FOOD INTAKE DISORDER

DSM-5

A. An eating or feeding disturbance (e.g., apparent lack of interest in eating or food;

avoidance based on the sensory characteristics of food; concern about aversive consequences
of eating) as manifested by persistent failure to meet appropriate nutritional and/or energy
needs associated with one (or more) of the following:
 1. Significant weight loss (or failure to achieve expected weight gain or faltering growth
in children)
2. Significant nutritional deficiency.
3. Dependence on enteral feeding or oral nutritional supplements.
4. Marked interference with psychosocial functioning.

B. The disturbance is not due to an associated gastrointestinal or other general medical

condition (e.g., esophageal reflux).

C. The eating disturbance does not occur exclusively during the course of anorexia nervosa or
bulimia nervosa, and there is no evidence of a disturbance in the way in which one’s body
weight or shape is experienced.

D. The eating disturbance is not attributable to a concurrent medical condition or not better
explained by another mental disorder. When the eating disturbance occurs in the context of
another mental disorder, the severity of the eating disturbance exceeds that routinely
associated with the condition or disorder and warrants additional clinical attention.

ICD-11

Essential (required) features:

• Avoidance or restriction of food intake that results in either or both of the following:

o The intake of an insufficient quantity or variety of food to meet adequate energy or

nutritional requirements that has resulted in significant weight loss, clinically significant
nutritional deficiencies, dependence on oral nutritional supplements or tube feeding, or has
otherwise negatively affected the physical health of the individual.

o Significant impairment in personal, family, social, educational, occupational or other

important areas of functioning (e.g., due to avoidance or distress related to participating in
social experiences involving eating).

• The pattern of eating behavior is not motivated by preoccupation with body weight or shape
or by significant body image distortion.

• Restricted food intake and consequent weight loss (or failure to gain weight) or other impact
on physical health is not due to unavailability of food, not a manifestation of another medical
condition (e.g., food allergies, hyperthyroidism), and not due to the effect of a substance or
medication (e.g., amphetamine), including withdrawal, and not due to another mental
disorder.

Prevalence

Prevalence in the general child population ranging from 0.35% to 3.2% and globally in adult
populations from 0.3% to 3.1% (Zickgraf et al., 2016).

Some studies have shown males with ARFID have a higher prevalence than females,
especially in pediatric populations (Nicely et al., 2014).

DSM-V indicates a more balanced sex distribution of ARFID compared to other eating
disorders (e.g., anorexia nervosa and bulimia nervosa), which predominantly affect females.

Etiology

Three-dimensional model of the neurobiology of ARFID (Thomas et al., 2017)

 Oversensitivity in taste perception itself

 Differences in activation of the brain’s appetite-regulating centers

 Hyper activation of this defense motive system (i.e., amygdala, anterior cingulate, and
VPFC hyper activation)

PICA

DSM-5
 A. Persistent eating of nonnutritive, nonfood substances over a period of at least 1
month.
B. The eating of nonnutritive, nonfood substances is inappropriate to the developmental
level of the individual.
C. The eating behavior is not part of a culturally supported or socially normative
practice.
D. If the eating behavior occurs in the context of another mental disorder (e.g.,
intellectual disability [intellectual developmental disorder], autism spectrum disorder,
schizophrenia) or medical condition (including pregnancy), it is sufficiently severe to
warrant additional clinical attention.

ICD-11

Essential (required) features:

• Regular consumption of non-nutritive substances, such as non-food objects and materials

(e.g., clay, soil, chalk, plaster, plastic, metal and paper), or raw food ingredients (e.g., large
quantities of salt or corn flour).

• The ingestion of non-nutritive substances is persistent or severe enough to require clinical

attention. That is, the behavior causes damage to health, impairment in functioning, or
significant risk due to the frequency, amount or nature of the substances or objects ingested.

• Based on age and level of intellectual functioning, the individual would be expected to
distinguish between edible and non-edible substances. In typical development, this occurs at
approximately 2 years of age.

• The symptoms or behaviors are not a manifestation of another medical condition (e.g.,
nutritional deficiency).

Epidemiology

Children and adolescents with autism spectrum disorder and intellectual disability

Up to 15 percent of persons with severe intellectual disability have engaged in pica

Affect both sexes equally

Etiology

Nutritional Factors
  Iron and/or zinc deficiency

 Anemia related to sickle-cell dis-ease, kidney/liver disease (e.g., dialysis patients),

celiac disease in childhood

 Malnutrition due to neglect

Environmental Factors

 Stressful events

 Impoverished environments

 Lack of active participation in activities

Mental Health Factors

Obsessive–compulsive disorder (OCD), pathological anxiety, schizophrenia, emotional

disturbance, depression…

Sensory/Physiological Factors

 Take pleasure in the texture, smell, and/or taste of the items they ingest (Rose et al.,
2000)

 Physiologic effects of these substances.

Management of Pica

Pharmacological Interventions
Selective serotonin reuptake inhibitors (SSRIs) may be used to address underlying anxiety,
obsessive-compulsive traits, or mood disturbances that can contribute to pica behaviors,
helping reduce the compulsive ingestion of non-food items.

Nutritional Interventions
Iron and zinc supplements are often administered when nutritional deficiencies are suspected
to be triggers for pica. These supplements can help correct deficiencies that may be causing
cravings for non-nutritive substances.

Behavioral Interventions
  Overcorrection: This technique involves requiring the individual to engage in effortful
corrective behaviors after exhibiting pica, such as cleaning the area or performing a
related task, to reduce the frequency of the behavior.
 Habit Reversal: This includes three key components:
o Awareness Training to help the person recognize the urge or occurrence of
pica behavior.
o Competing Response Training to teach the person to perform an incompatible
behavior instead of pica (e.g., holding a toy or object).
o Social Support involves family or caregivers providing encouragement and
reinforcement for positive behavior change.

Environmental Enrichment
Providing play and other recreational activities can reduce boredom or sensory seeking that
might drive pica behavior. Engaging the individual in stimulating and meaningful activities
helps decrease the occurrence of pica.

Dietary Modifications
Introducing highly spiced or flavored foods may reduce cravings for non-food substances by
making eating more interesting and satisfying.

Reinforcement
Positive reinforcement strategies encourage desirable behaviors and discourage pica by
rewarding the individual for abstaining from non-food ingestion.

Facial Screening/Physical Restraint Procedures

In more severe cases, facial screening devices or physical restraints may be used temporarily
to prevent access to harmful objects or substances, ensuring the safety of the individual while
behavioral interventions take effect.

RUMINATION-REGURGITATION DISORDER

DSM-5
A. Repeated regurgitation of food over a period of at least 1 month. Regurgitated food may
be re-chewed, re-swallowed, or spit out.

B. The repeated regurgitation is not attributable to an associated gastrointestinal or other

medical condition (e.g., gastroesophageal reflux, pyloric stenosis).

C. The eating disturbance does not occur exclusively during the course of anorexia nervosa,
bulimia nervosa, binge-eating disorder, or avoidant/restrictive food intake.

ICD-11

Essential (required) features:

• The intentional and repeated bringing up of previously swallowed food back to the mouth
(i.e., regurgitation), which may be re-chewed and re-swallowed (i.e., rumination), or may be
deliberately spat out (but not as in vomiting).

• The regurgitation behavior is frequent (at least several times per week) and sustained over a
period of at least several weeks.

• The diagnosis should only be assigned to individuals who have reached a developmental
age of at least 2 years.

• The regurgitation behavior is not a manifestation of another medical condition that directly
causes regurgitation (e.g., esophageal strictures or neuromuscular disorders affecting
esophageal functioning) or causes nausea or vomiting (e.g., pyloric stenosis).

Development and Course

Age at onset in infants is usually between ages 3 and 12 months

Frequently remits spontaneously, but its course can be protracted and can result in medical
emergencies Can have an episodic course or occur continuously until treated.

High rate of spontaneous remission.

Etiology

Rumination is associated with high intragastric pressure and the ability to contract the
abdominal wall to cause retrograde movement of the gastric contents into the esophagus.
Several studies have elucidated other gastrointestinal symptoms such as gastroesophageal
reflux that may accompany rumination.
Management

Diaphragmatic Breathing
This technique helps counteract involuntary, unnoticed contractions of the abdomino-thoracic
muscles by promoting controlled, deep breathing. Patients are guided to sit comfortably and
place one hand on their chest and the other on their abdomen. During slow, deep breaths (6 to
8 per minute), only the hand on the abdomen should rise, indicating proper diaphragmatic
movement while keeping the chest still. This encourages diaphragmatic contraction and
abdominal expansion, improving respiratory efficiency and relaxation. The effectiveness of
diaphragmatic breathing can be monitored using biofeedback tools such as electromyography
(EMG) or high-resolution impedance manometry (HRIM), which provide visual feedback to
help patients better understand and perform the technique.

Medical Therapy
Medications like Baclofen and Buspirone may be considered for patients who do not respond
adequately to initial behavioral treatments.

Orthorexia Nervosa

Orthorexia nervosa (ON) refers to a strong preoccupation with a healthy diet with negative
emotional, cognitive, or social consequences when trying to approach this goal and when the
eating behaviour deviates from these self-imposed rules. In the literature, there is an ongoing
debate over whether ON should be considered simply a lifestyle phenomenon or a psychiatric
disorder. In this vein, ON seems to share psychopathological characteristics with both eating
disorders (EDs) and obsessive-compulsive disorder (OCD). However, there are insufficient
data to reconcile the debate.
Vaccari et al. [52] analyzed the prevalence and intensity of ON symptoms (measured using
the ORTO-15) in patients who had been diagnosed with obsessive-compulsive symptoms
(measured using the OCI-R), in comparison to 42 subjects with anxiety or depression
disorders and 236 subjects with no psychiatric morbidity. The main finding was that patients
with OCD presented higher ON symptoms when compared to patients in the other groups
(p = 0.0005).
Novara et al. [51] examined whether ON may be related to and differentiated from OCD,
EDs, perfectionism, anxiety, and depression in 302 individuals from the general population.
The sample was divided into two groups, named “High EHQ” and “Low EHQ,” based on
scores on the Eating Habits Questionnaire (EHQ-21). The results showed a correlation
between ON and EDs and non-adaptive perfectionism constructs, which emerged
independently of obsessive-compulsive symptoms. The same pattern was observed when
comparing the High and Low EHQ groups.
Reference
Linardon, J. (2024, May 16). Bulimia Nervosa Statistics 2024: 25 Shocking Facts. Break
Binge Eating. https://breakbingeeating.com/bulimia-nervosa-statistics/
Linardon, J. (2024, May 18). Anorexia Nervosa Statistics 2024: 14 Shocking Facts. Break
Binge Eating. https://breakbingeeating.com/anorexia-nervosa-statistics/
Shah, M. (2023). Eating Disorders in India: A Systematic Review. Acta Neurophysiologica,
4(3). https://academicstrive.com/ANPL/ANPL180022.pdf
Mars, J. A., Iqbal, A., & Rehman, A. (2024, August 11). Binge Eating Disorder. StatPearls
Publishing. Retrieved from
https://www.ncbi.nlm.nih.gov/books/NBK551700/ncbi.nlm.nih.gov
Moore, C. A., & Bokor, B. R. (2023, August 28). Anorexia Nervosa. StatPearls Publishing.
Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK459148/
Nair, I. V., & Mohan, A. K. (2023). Impact of Anorexia Nervosa – A Social Work
Perspective in the Indian Context. We the People DSNLU Journal of Social Sciences, 1(1),
101.
Tylka, T. L., & Subich, L. M. (2004). Examining a multidimensional model of eating
disorder symptomatology among college women. Journal of Counseling Psychology, 51(3),
314–328. https://doi.org/10.1037/0022-0167.51.3.314
Blaney, P. H., Krueger, R. F., & Millon, T. (Eds.). (2009). Oxford textbook of
psychopathology (3rd ed.). Oxford University Press.
Brytek-Matera, A., & Czepczor, K. (2017). Models of eating disorders: A theoretical
investigation of abnormal eating patterns and body image disturbance. Archives of Psychiatry
and Psychotherapy, 19(1), 16–26. https://doi.org/10.12740/APP/68422
Linardon, J. (2021, January 6). CBT-E: A guide to enhanced cognitive-behavioral therapy
(CBT-E) for eating disorders. Break Binge Eating. Retrieved from
https://breakbingeeating.com/cbt-e/
Federici, A. (2024). Dialectical behaviour therapy for the treatment of eating disorders.
Originally published 2009. Retrieved from https://www.nedic.ca
Champion, L., & Power, M. J. (2012). Interpersonal psychotherapy for eating disorders.
Clinical Psychology & Psychotherapy, 19(2), 150–158. https://doi.org/10.1002/cpp.1780
Rienecke, R. D. (2017). Family-based treatment of eating disorders in adolescents: Current
insights. Adolescent Health, Medicine and Therapeutics, 8, 69–79.
https://doi.org/10.2147/AHMT.S115775
Ammerman, R. T. (Ed.). (Year). Comprehensive handbook of personality and
psychopathology: Volume 3. Child psychopathology (M. Hersen & J. C. Thomas, Eds.-in-
Chief). Publisher.
Abraham, S. F., Brown, T., & Llewellyn-Jones, D. (2003). Eating disorders in India: Some
observations. Indian Journal of Psychiatry, 45(2), 58–60.

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental

disorders (5th ed.). https://doi.org/10.1176/appi.books.9780890425596
Bhugra, D., Bhui, K., Gupta, K. R. (2000). Bulimia nervosa in North India: A population-
based survey. International Journal of Eating Disorders, 28(1), 101–104.
Silawat, N. R. (2018). A comparative study of eating anxiety among zonal female basketball
players in India. International Journal of Yogic, Human Movement and Sports Sciences, 3(2),
235–237.
Smink, F. R., van Hoeken, D., & Hoek, H. W. (2012). Epidemiology of eating disorders:
Incidence, prevalence and mortality rates. Current Psychiatry Reports, 14(4), 406–414.
https://doi.org/10.1007/s11920-012-0282-y
Srinivasan, T. N., Suresh, T. R., & Jayaram, V. (1995). Emergence of eating disorders in
India: Study of eating distress syndrome and development of a screening questionnaire.
International Journal of Social Psychiatry, 41(2), 132–136.
https://doi.org/10.1177/002076409504100208
Bardone-Cone, A.M.; Wonderlich, S.A.; Frost, R.O.; Bulik, C.M.; Mitchell, J.E.; Uppala, S.;
Simonich, H. Perfectionism and eating disorders: Current status and future directions. Clin.
Psychol. Rev. 2007, 27, 384–405. [Google Scholar] [CrossRef]