important psychiatric disorders- need specialized attention

1. Seminar
Eating Disorders
Presenter: Dr Diptadhi Mukherjee
Moderator: Dr D.J. Chetia
Dr Hemanta Dutta
LGBRIMH, Tezpur
23/09/15

2. Outline
• Introduction
• History
• Cross-cultural influence
• Epidemiology
• Etiology
• Nosology
• Differential diagnosis
• Comorbidity
• Complication
• Indian scenario
• Management
• Feeding and eating disorders of childhood
• Conclusion

3. Introduction
• Eating disorders are disorders of eating behaviors, associated thoughts,
attitudes and emotions, and their resulting physiological impairments.
• Anorexia nervosa & Bulimia nervosa based on 2 factors:
• (1) Overvaluation of the presumed benefits of weight loss or shape
change
• (2) Fear of fat or somato-visceral discomforts associated with ingesting
food that result in functional medical, psychological, and social
impairment.
• Binge eating disorder- impulsive or compulsive rapid consumption of large
quantities of food and attendant psychological and weight-related
consequences
• They rarely present as sole diagnostic entities- almost always
accompanied by significant comorbid

4. History cont…
• First cases reported in 1689 by Richard Morton – “wasting”
disease of nervous etiology in one male and one female (Gordon,
2000).
• The first formal description of AN, however, is credited to Sir
William Gull, physician to Queen Victoria, who in 1868 named the
disorder “anorexia hysterica”- emphasizing its psychogenic origins.

5. History: Bulimia Nervosa
• The word bulimia is derived from Greek and means “ravenous
hunger,” quite the opposite of anorexia.
• Bulimia Nervosa (BN), by contrast, was first clinically described in
1979 by Russel
• Some authors have hypothesized that bulimia nervosa was
nonexistent before recent times
• Historical accounts date to 1398, when “true boulimus” was
described in an individual having an intense preoccupation with
food and over eating at very short intervals, terminated by
vomiting (Stein & Laakso, 1988).

6. Eating Disorders and Cross-Cultural
Influences
• Eating disorders more prevalent in industrialized societies
which emphasize thinness.
– US, Canada, Japan, Europe
• When women from countries with low prevalence rates move
to countries with higher prevalence rates, prevalence
increases.
• Variations in assessment methods and diagnostic criteria make
it difficult to be certain about differences in prevalence rates
from country to country.

8. Epidemiology
• Prevalence: Anorexia nervosa, approximately 0.4% of young women;
Bulimia nervosa, 1 to 1.5% of young women
• Gender: Women > men (2:1 to 3:1 in community; 10:1 to 20:1 in clinical
series)
• Age: Peaks occur at early and late teen years, but onset can be pre-
pubertal through 8th decade.
• Rural vs. urban: Higher with move from rural to urban setting
• Socioeconomic class: Anorexia nervosa- higher with social class; bulimia
nervosa- independent of social class
• Premature mortality: 0 to 19% on 10- to 20-year follow-up after
hospitalization (medical causes, closely followed by suicide); >50 times
increased suicide rate when an eating disorder co-occurs with alcohol
dependence; anorexia nervosa plus insulin-dependent diabetes mellitus
have 10 times higher mortality than either anorexia or diabetes alone
• Vocational, avocational risks: Ballet, modeling, amateur wrestling, visual
media roles, appearance sports (female gymnastics, figure skating)

10. Etiology of Eating disorders
• A “hijacking” of normal neurobiologically regulated eating
behaviors- abnormal eating pattern becomes autonomous
• Similarities between eating disorders and drug abuse- a
vicious circle
• Multifactorial etiological approach may better account for
current data

11. “The most compelling perspective is a
recognition that eating disorders probably
derive from a cluster of predisposing
vulnerability factors reacting to precipitating
events, especially those occurring during
vulnerable “windows” in development, and
are maintained by sustaining social,
psychological, and biomedical
reinforcements.” - CTP

12. Biological Factors
 Genetic vulnerability-
• Twin studies three times higher concordance in monozygotic
twins than in dizygotic twins
• Monozygotic twins have a 50 to 80 percent concordance rate
for eating disorders.
 Personality, a highly heritable variable, plays a major role
• Restricting-type anorexia nervosa specific genetic endowment
of perseverance, sensitivity, perfectionism, and low
impulsivity
• Binge eating–purging type-Impulsive and extroverted
personality styles

13. Biological factors cont….
 Molecular genetic research-
o loci and polymorphisms associated with genes for the 5-hydroxytryptamine types
1B (5-HT1B), 1D (5-HT1D), 2A (5-HT2A), and 2C (5-HT2C) receptors,
o norepinephrine transporter, dopamine receptor, monoamine oxidase A,
o delta opioid receptor, cannabinoid receptor (CNR1), brain derived
o neurotropic factor (BDNF), preproghrelin,
o CLOCK (endogenous oscillator) system, uncoupling proteins 2
o (UCP2) and 3 (UCP3), beta-type estrogen receptor, hSKCa3 potassium channel, and
human agouti protein (AgRP)
 functional magnetic resonance imaging (fMRI) study of body image
distortion in patients with anorexia nervosa- amygdala activation,
confirming that the amygdala, a major center for the “fear network,” is
involved in distorted and distressed body image

14. Etiology: Biological Theory cont..
• Biological theories focus on the role of the hypothalamus;
• The ventromedial hypothalamus has been called the satiety center. When this
part of the brain is stimulated eating behavior stops, correlating to a feeling of
being satiated. Conversely the lateral hypothalamus, when stimulated,
correlates to eating behavior.
• When operating properly these two areas operate to keep the body at a
specific body weight, termed the set point.
• Damage to either of these regions causes the set point to be altered. Eating
will then reflect the new set point, thus, if it is lower then normal the animal
can literally starve themselves to death.
• Support for this theory comes from neurotransmitter studies showing an
increase in Corticotropin Releasing Factor (CRF) in the CSF of anorexic patients
• When administered to rats, CRF leads to a reduction in food intake, feeding
time, & feeding episodes; it also leads to an increase in grooming time &
grooming episodes
• The occurrence of amenorrhea before weight loss also suggests a
hypothalamic disturbance (occurs in 20% of patients)

15. Biological Theory: Biochemical Factors
• Chemical imbalances in the neuroendocrine system
o These imbalances control hunger, appetite, digestion, sexual function,
sleep, heart and kidney function, memory, emotions, and thinking
• Serotonin and norepinephrine are decreased in acutely ill anorexia
and bulimia patients
o Representing a link between depression and eating disorders
• Excessive levels of cortisol in both anorexia and depression
o Caused by a problem that occurs in or near the hypothalamus
• Vomiting leads to an increase in DA levels which reinforces/rewards
the vomiting behavior

16. Biochemical Factors cont…
• Theories of serotonergic hyperfunctioning in anorexia and serotonergic
hypofunctioning in bulimia are attractive
• This indicates that Anorexic patients, may have overactive serotonerigic
response centers, leading to a need to reduce the levels of serotonin in
their brains by restricting their food intake.
• Excessive levels of serotonin are correlated with a nervous, jittery feeling.
Self-starvation may be an attempt to rid the body of this uncomfortable
feeling.
• On the other hand, Bulimics may have a faulty satiation response center.
• A desire to feel satiated may cause the bulimic to try to flood their brain
with tryptophan, by overeating on sugars which will lead to this precursor.
• The theories don’t explain why SSRIs are sometimes helpful for both
• The successful treatment of bulimia with SSRIs suggests the importance of
serotonin in eating disorders.

17. Biochemical Factors cont…
• A few sources suggested that anorexics are addicted to fasting, apparently
because of the chemical changes brought on by starvation.
• The opioids, enkephalins and endorphins are found to be at elevated
levels in the spinal fluid of patients with anorexia.
• It is unclear however, whether or not the starving was caused by, or was
the cause of, these elevated opioid levels.
• Some studies have found that drugs which inhibit the functioning of these
opioids cause anorexic patients to gain weight.

18. Social Factors
• Practices in society's emphasis on thinness and exercise
• Close yet troubled relationships with their parents.
• Low levels of nurturance and empathy, strained marital relationships in
parents
• Mothers who are overly concerned about their daughter’s weight and
physical attractiveness
• H/O being teased or ridiculed based on size or weight
• H/O trauma, sexual, physical and/or mental abuse- 60-75% of all bulimia
nervosa patients have a history of physical and/or sexual abuse
• Vocational and avocational interests- participation in strict ballet schools
increases the probability of developing anorexia nervosa at least 7-fold
• In high school boys, wrestling is associated with a prevalence of full or
partial eating disordered syndromes during wrestling season of
approximately 17 %
• Gay orientation in men- norms for slimness, albeit muscular slimness, are
very strong in the gay community

19. Psychological factors
• Low self-esteem
• Feelings of inadequacy or lack of control in life
• Fear of becoming fat
• Depressed, anxious, angry, and lonely feelings
• Keep feelings to themselves
• Perfectionists
• Achievement oriented
– Good students
– Excellent athletes
– Competitive careers

20. Psychological factors
• Food and the control of food is used as an attempt to cope with feelings and
emotions that seem overwhelming
• Having followed the wishes of others...
– Not learned how to cope with problems typical of adolescence, growing
up, and becoming independent
• People binge and purge to reduce stress and relieve anxiety
• Anorexic people thrive on taking control of their bodies and gaining
approval from others
• Highly value external reinforcement and acceptance

21. Nosology
• ICD-10
F50 Eating disorders
F50.0 Anorexia nervosa
F50.1 Atypical anorexia nervosa
F50.2 Bulimia nervosa
F5O.3 Atypical bulimia nervosa
F50.4 Overeating associated with other psychological
disturbances
F5O.5 Vomiting associated with other psychological
disturbances
F50.8 Other eating disorders
F50.9 Eating disorder, unspecified

22. Anorexia nervosa

23. Anorexia Nervosa- DSM-5 Diagnostic Criteria
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.
B. Intense fear of gaining weight or becoming fat, even though
underweight.
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 denial of the seriousness of the current
low body weight.
• Subtypes:
Restricting type
Binge-eating/purging type

24. • Period criteria- 3 months
• Severity-
• Mild: BMI ≥ 17 kg/m2
• Moderate: BMI 16-16.99 kg/m2
• Severe: BMI 15-15.99 kg/m2
• Extreme: BMI< 15 kg/m2

25. Bulimia nervosa

26. Bulimia Nervosa- DSM-5 Diagnostic Criteria
A. Recurrent episodes of binge eating characterized by BOTH
of the following:
1. Eating in a discrete amount of time (within a 2 hour
period)large amounts of food.
2. Sense of lack of control over eating during an episode.
B. Recurrent inappropriate compensatory behavior in order
to prevent weight gain (purging).
C. The binge eating and compensatory behaviors both occur,
on average, at least once a week for three months.
D. Self-evaluation is unduly influenced by body shape and
weight.
E. The disturbance does not occur exclusively during
episodes of anorexia nervosa.

27. Period criteria- 3 months
Current severity-
• Mild: 1-3 episodes
• Moderate: 4-7 episodes
• Severe: 8-13 episodes
• Extreme: more that 14 episodes

28. Anorexia vs. Bulimia
• Denies abnormal
eating behavior
• Introverted
• Turns away food in
order to cope
• Preoccupation with
losing more and more
weight
• Recognizes abnormal
eating behavior
• Extroverted
• Turns to food in order
to cope
• Preoccupation with
attaining an “ideal”
but often unrealistic
weight

29. Differential Diagnosis of Anorexia nervosa
• Medical illness- Malignancy/ Brain tumor
• Other Severe Mental Illness-
• Depressive disorders- Differentiating points- Anorexia
nervosa- normal appetite, planned and ritualistic aggression,
preoccupation with recipes, the caloric content, intense fear
of obesity or disturbance of body image
• Somatization disorder- severity of weight loss, morbid fear of
weight loss.
• Schizophrenia- concerned with caloric content vs food to be
poisoned, fear of weight loss, Hyperactivity.
• Bulimia nervosa

30. Differential Diagnosis of Bulimia nervosa
• Anorexia nervosa, binge eating-purging type
• Neurological disease- epileptic-equivalent seizures, central
nervous system tumors, Kluver- Bucy syndrome
• Kleine-Levin syndrome
• Seasonal affective disorder and atypical depression

31. Comorbidity

32. Comorbodity

33. Medical Complications of Eating
Disorders
 Related to weight loss
• Cachexia: Loss of fat, muscle mass, reduced thyroid metabolism (low T3
syndrome), cold intolerance, and difficulty in maintaining core body
temperature
• Cardiac: Loss of cardiac muscle; small heart; cardiac arrhythmias, including
atrial and ventricular premature contractions, prolonged His bundle
transmission (prolonged QT interval), bradycardia, ventricular tachycardia;
sudden death
• Digestive-gastrointestinal: Delayed gastric emptying, bloating, Constipation,
abdominal pain
• Reproductive: Amenorrhea, low levels of luteinizing hormone (LH) and follicle-
stimulating hormone (FSH)
• Dermatological: Lanugo (fine baby-like hair over body), edema
• Hematological: Leukopenia
• Neuropsychiatric: Abnormal taste sensation (?zinc deficiency), apathetic
depression, mild cognitive disorder
• Skeletal: Osteoporosis

34. Medical Complications cont..
 Related to purging (vomiting and laxative abuse)
• Metabolic: Electrolyte abnormalities, particularly hypokalemic,
hypochloremic alkalosis; hypomagnesemia
• Digestive-gastrointestinal: Salivary gland and pancreatic inflammation and
enlargement with increase in serum amylase, esophageal and gastric
erosion, dysfunctional bowel with haustral dilation
• Dental: Erosion of dental enamel, particularly of front teeth, with
corresponding decay
• Neuropsychiatric: Seizures (related to large fluid shifts and electrolyte
disturbances), mild neuropathies, fatigue and weakness, mild cognitive
disorder

35. Scenario in India
• Jha and Awadhia were probably the first to report a
case of eating disorder in India in 1967.
• 6 published case report/case series
• With rapid cultural transformation, the classical
forms of these conditions are being described

37. 2 patients scored above the cutoff for bulimia nervosa, giving a
prevalence of around 0.4%

41. General principles in the management of
eating disorders
• Multidisciplinary approach involving psychiatrists, psychologists,
endocrinologists, dentists, gastroenterologists
• Establish and maintain a therapeutic alliance- addressing patient’s
resistance to treatment and enhancing their motivation for change
• Assessment of eating disorder symptoms-
o Identifying target symptoms and behaviors
o Detailed report of food intake during a single day in the patient’s life may
be quite informative.
o Family history regarding eating disorders and other psychiatric disorders,
alcohol and other substance use disorders, obesity
o KAP of family members in relation to the patient’s disorder, and toward
eating, exercise, and appearance

42. General principles in the management of
eating disorders
• Assessment of eating disorder symptoms cont…
• Instruments to interview patients in a structured format - “gold
standards” to determine clinical diagnoses
• Clinician administered measures like Eating Disorder Examination
(EDE) and Yale-Brown-Cornell Eating Disorder Scale (YBC-EDS)- can
be completed within 10-40 minutes.
• Self reported instruments e.g. Diagnostic Survey for Eating Disorders
(DSED), Bulimia Test-Revised (BULIT-R), Eating Attitudes Test (EAT),
Eating Disorder Examination-Questionnaire (EDE-Q), Eating
Disorders Inventory-2 (EDI-2), Eating Disorders Questionnaire (EDQ)

43. General principles in the management of
eating disorders
• Assessment of patient’s physical status-
o Detailed physical examination- particular attention to -
o Vital signs; physical status (including height and weight); heart rate
and rhythm; jugular venous pressure; heart sounds (especially
midsystolic clicks or murmurs from mitral valve prolapse);
o Acrocyanosis; delayed capillary refill; lanugo;
o Salivary gland enlargement; scarring on the dorsum of the hands
(Russell’s sign);
o Evidence of self-injurious behavior such as ecchymoses, linear scars,
and cigarette burns;
o Muscular weakness; indications of muscular irritability due to
hypocalcaemia, such as in Chvostek’s and Trousseau’s signs;
o Gait and eye abnormalities
o Regular monitoring of BMI

44. Laboratory and other investigation
 For all patients:
• Complete blood count (anemia is frequent)
• Electrolytes- Na/K/Ca/Mg
• Blood urea nitrogen, creatinine
• Thyroid-stimulating hormone, free thyroxine
• Electrocardiogram- Look for Arrhythmia, prolonged QT interval, T wave
changes
• Total protein and prealbumin
• Fasting glucose
• Amylase if purging occurs
• Serum phosphate
 Bulimic syndromes
• In addition to above, amylase (fractionated if abnormal to determine
parotid/salivary gland origin vs. pancreatic origin)
 If amenorrhea >3 months
• Bone mineral density (dual energy X-ray absorptiometry)
 In men with weight loss- Testosterone

45. General principles in the management of
eating disorders
• Choice of treatment setting-
 Intensive inpatient settings (in which subspecialty general medical
consultation is readily available)
 Residential and partial hospitalization programs
 Outpatient care
 Factors determine hospitalization-
o Considerable difficulty gaining healthy weight
o Rapid or persistent decline in oral intake
o Decline in weight despite maximally intensive outpatient care
o Presence of additional stressors, such as dental procedures- may
interfere the patient’s ability to eat
o Weight at which the patient was medically unstable in the past;
o Co-occurring psychiatric problems that merit hospitalization
o Patient’s denial and resistance to participate in his or her own care
in less supervised settings

46. Treatment of Anorexia Nervosa
• Nutritional rehabilitation-
• Goals-
o Restore weight
o Normalize eating patterns
o Achieve normal perceptions of hunger and satiety
o Correct biological and psychological sequelae of malnutrition
• A healthy goal weight for female patients is the weight at
which normal menstruation and ovulation are restored and,
for male patients, the weight at which normal testicular
function is resumed (APA, 2006).

47. • Refeeding programs - Nursing supervised oral refeeding of normal
food in appropriate amounts and composition
• Realistic targets- 1-1.5 Kg/week for hospitalized patients and 0.25-
0.75 Kg/ week for individuals in outpatient programs
• Intake levels start at 30-40 kcal/kg per day (approximately 1,000-
1,600 kcal/day)
• During the weight gain phase, intake advances progressively to as
high as 70-100 kcal/kg per day
• In case of gain > 2-3 Kg/week- carefully monitored for refeeding
syndrome and fluid retention
• 10-15 % require hospital based involuntary treatment
• Forced nasogastric or parenteral feeding- used with caution
• Patients physically resist and constantly remove their nasogastric
tubes- surgically inserted gastrostomy or jejunostomy tubes

48. • Pharmacotherapy-
• Antidepressants-
 SSRI-
o Fluoxetine- 2 RCTs- No significant differences between fluoxetine
and placebo on weight gain, psychological features of eating
disorders, or depression or anxiety measures
o Citalopram- 1 trial- no differences in weight gain after three months
of treatment but modest advantages regarding symptoms of
depression, obsessive-compulsive symptoms, impulsiveness, and
trait anger.
 TCA-
• Amitriptyline and Cyproheptadine- Daily caloric intake significantly
higher for cyproheptadine than for placebo; significantly fewer days
were needed to achieve target weight (in those who did) with both
amitriptyline and cyproheptadine groups than with placebo

49. • Antipsychotics
 Small open-label studies-
• olanzapine, quetiapine may improve weight gain and psychological
indicators- One RCT showed that 87.5% of patients given olanzapine
achieved weight restoration (55.6% placebo).
o low-dose (1-2 mg) haloperidol in addition to standard treatment and were
reported to benefit
• Hormones
o Transdermal testosterone (150 mg or 330 mg) for 3 weeks- greater
decreases in depression in patients who were depressed at baseline, but no
differences in weight gain
o Growth hormone (15 mg/kg/day)- rapid improvement in normal orthostatic
heart rate response to standing challenge
o Estrogen/progesterone versus non-medication control- no differences
between groups on bone density at six months

50. • Antiepileptic drugs-
o Carbamazepine and Valproate may be effective in treating patients
of Anorexia nervosa when they are used to treat an associated
psychiatric (e.g. mood) or neurological (e.g. seizure) disorder;
otherwise, both agents, particularly valproate, are associated with
weight gain (McElroy et al.)
• Nutritional supplement-
o Zinc (14 mg per day)- associated with accelerated increase of BMI
compared to placebo (Birmingham et al.)

51. • Psychosocial interventions-
• Considered to be the mainstay of effective treatment for anorexia nervosa
 Cognitive behavioral therapy (CBT)-
• Monitoring- monitor their food intake, their feelings and emotions, their
binging and purging behaviors, and their problems in interpersonal
relationships
• Cognitive restructuring to identify automatic thoughts, to challenge their
core beliefs
• Problem solving to think through and devise strategies to cope with their
food-related and interpersonal problems.
• Significantly reduced relapse risk- increased the likelihood of good
outcome compared to nutritional counseling based on nutritional
education and food exchanges after inpatient weight restoration
 Nonspecific supportive clinical management (NSCM)> CBT> IPT>
Medication
 Family therapy- patients under the age of 18 benefited from family
therapy, whereas patients over the age of 18 did worse in family therapy
than with the control therapy

52. Treatment of Bulimia Nervosa
• Pharmacotherapy-
• Antidepressants-
 SSRI-
o Fluoxetine (60 mg/day) - Six trials- Fluoxetine was associated with
significant improvements in measures of restraint, weight concern, and
food preoccupation
o Fluvoxamine (150-200 mg /day)/ Sertaline(100 mg/day)- statistically
significant reduction in the number of binge eating crises and purging
compared with the group who received placebo
o Trazodone (400 mg/day)- also may be helpful
 TCA- dropped out more frequently
o Desipramine (200-300 mg/day)- decreasing binge eating, vomiting, and
scores on EAT

53.  5-HT3 antagonist
o Ondansetron
 Other medications-
o Topiramate- efficacious in treating Bulimia nervosa symptoms in 2
randomized trials
o Fenfluramine- banned
o Lithium carbonate
o Opiate antagonist- naltrexone (50-120 mg/day)- not superior to placebo

54. • Psychosocial interventions-
Cognitive behavioral therapy (CBT)
• Considered the benchmark, first-line treatment
• Strict adherence to rigorously implemented, highly detailed, manual-
guided treatments
• 18 to 20 sessions over 5 to 6 months
• Both cognitive and behavioral procedures to-
(1) interrupt the self-maintaining behavioral cycle of bingeing and dieting
(2) alter the individual's dysfunctional cognitions; beliefs about food,
weight, body image; and overall self-concept.
• CBT superior to nutritional counseling alone as well as to supportive-
expressive therapy (a nondirective psycho dynamically oriented
treatment) & Interpersonal therapy

55. Dynamic Psychotherapy
• Concretize introjective and projective defense mechanisms.
• In a manner analogous to splitting
• Patients divide food into two categories: Nutritious items and those that
are unhealthy
• Food that is designated nutritious may be ingested and retained because it
unconsciously symbolizes good introjects.
• Junk food is unconsciously associated with bad introjects and, therefore, is
expelled by vomiting, with the unconscious fantasy that all
destructiveness, hate, and badness are being evacuated.
• Patients can temporarily feel good after vomiting because of the
fantasized evacuation, but the associated feeling of “being all good” is
short-lived because it is based on an unstable combination of splitting and
projection.

56. Self help groups
• Manual including visits with non-specialists in eating disorders
to check on progress
• Self help versus CBT group
Support groups/12-step programs
• ‘Overeaters Anonymous’
• ‘Weight Watchers’

57. Binge Eating Disorder- DSM-5 Diagnostic Criteria
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 (for example, 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. a sense of lack of control over eating during the episode
B. The binge-eating episodes are associated with three (or more) of the following:
A. eating much more rapidly than normal
B. eating until feeling uncomfortably full
C. eating large amounts of food when not feeling physically hungry
D. eating alone because of feeling embarrassed by how much one is eating
E. feeling disgusted with oneself, depressed, or very guilty afterwards
C. Marked distress regarding binge eating is present.
D. The binge eating occurs, on average, at least once a week for three months.
E. The binge eating is not associated with the recurrent use of inappropriate
compensatory behavior (for example, purging) and does not occur exclusively
during the course Anorexia Nervosa, Bulimia Nervosa, or Avoidant/Restrictive
Food Intake Disorder.

58. Binge Eating Disorder
• Most common eating disorder
• 25 % of patients with obesity who seek medical care
• 50-75% of those with severe obesity (BMI>40)
• Twice common in females (4% Vs 2%)
• Impulsive and extroverted personality style are predisposed
• Period of stress- binge may reduce anxiety/ depressive
symptoms
• Obesity- 3% in long term follow up
• 5-years follow up- < 20% had clinically significant symptoms

59. Treatment-
Psychotherapy
Self-help group
Medication- SSRI/ TCA
CBT + Medication > CBT > Medication > Placebo

61. Other Specified Feeding or Eating Disorder (OSFED)
• According to the DSM-5 criteria, to be diagnosed as having OSFED a
person must present with a feeding or eating behaviours that cause
clinically significant distress and impairment in areas of functioning, but
do not meet the full criteria for any of the other feeding and eating
disorders.
• Atypical Anorexia Nervosa
• Atypical Binge Eating Disorder
• Atypical Bulimia Nervosa
• Purging Disorder
• Night Eating Syndrome: Recurrent episodes of night eating. Eating after
awakening from sleep, or by excessive food consumption after the evening
meal. The behavior is not better explained by environmental influences or
social norms. The behavior causes significant distress/impairment. The
behavior is not better explained by another mental health disorder (e.g.
Binge eating disorder).

62. Feeding and Eating Disorders of
Infancy or Early Childhood
• Pica
• Rumination disorder
• Avoidant/Restrictive Food Intake Disorder

63. Pica
 According to the DSM-5 criteria, to be diagnosed with Pica a
child/person must display:
A. Persistent eating of non-nutritive substances for a period of at
least one month.
B. The eating of non-nutritive substances is inappropriate to the
developmental level of the individual.
C. The eating behaviour is not part of a culturally supported or
socially normative practice.
D. If occurring in the presence of another mental disorder (e.g.
autistic spectrum disorder), or during a medical condition (e.g.
pregnancy), it is severe enough to warrant independent clinical
attention.
• Note: Pica often occurs with other mental health disorders
associated with impaired functioning.
• Change: Criteria has been revised to allow diagnosis for individuals
of all ages.

65. • Retrograde diagnosis common- after intestinal obstruction/
infections, lead poisoning.
• 75 percent of 12-month-old infants and 15 percent of 2- to 3-
year-old toddlers placed nonnutritive substances in their
mouth but seldom results in ingestion.
• Commonly comorbid with other developmental disorders
(>15% of IDD)
• Affect both sexes.

66. Etiology
• Several theories-
o Hereditary- higher than expected incidence in the relatives of
persons with the symptoms.
o Nutritional deficiencies- cravings for dirt and ice sometimes
associated with iron and zinc deficiencies- corrected by their
administration.
o Children's psychological deprivation- high incidence of
parental neglect and deprivation associated- suggested that
pica is a compensatory mechanism to satisfy oral needs.
• Most often a transient disorder
• Comorbid depressive symptoms and use of substances
common

67. Laboratory test
• No single test confirms or rules out
• Serum levels of iron and zinc
• Hemoglobin level
• Lead level
Course and Prognosis
• Usually good- children of normal intelligence remits
spontaneously within several months
• In pregnant women- usually limited to the term of the
pregnancy
• In some adults- mentally retarded- can continue for years.

68. Treatment
• No definitive treatment
• The first step- determining the cause
• Neglect or maltreatment- need to be altered immediately.
• Exposure to toxic substances, such as lead, must be eliminated/ rendered
inaccessible
• Emphasize psychosocial, environmental, behavioral, and family guidance
approaches- Ameliorate any significant psychosocial stressors.
• Several behavioral techniques- Positive reinforcement, modeling,
behavioral shaping, and overcorrection treatment
• Increasing parental attention, stimulation, and emotional nurturance
• In some patients, correcting an iron or zinc deficiency has eliminated pica.
• Medical complications (e.g., lead poisoning)- must also be treated.

69. Rumination disorder
• According to the DSM-5 criteria, to be diagnosed as having
Rumination Disorder a person must display:
A. Repeated regurgitation of food for a period of at least one month
Regurgitated food may be re-chewed, re-swallowed, or spit out.
B. The repeated regurgitation is not due to a medical condition (e.g.
gastrointestinal condition).
C. The behaviour does not occur exclusively in the course of Anorexia
Nervosa, Bulimia Nervosa, BED, or Avoidant/Restrictive Food
Intake disorder.
D. If occurring in the presence of another mental disorder (e.g.
intellectual developmental disorder), it is severe enough to
warrant independent clinical attention.
Change: Criteria has been revised to allow diagnosis for individuals of
all ages

70. Epidemiology
• Rumination is a rare disorder.
• more common among male infants- between 3 months and 1 year of age.
• Persists more frequently among children and adults who are mentally
retarded.
• Adults with rumination usually maintain a normal weight.
Etiology
• Rumination and gastroesophageal reflux often coexist- high intra-gastric
pressure
• Self-soothing or produces a sense of relief, leading to a continuation of
behaviors.
• In mentally retarded, the disorder may be to self-stimulatory behavior.
• Psychodynamic theories hypothesize various disturbances in the mother-
child relationship as a contributing factor in the development - increased
levels of marital conflict, leading to understimulation and inadequate
emotional attention to the baby- result in insufficient emotional
gratification and stimulation for the infant who seeks to self-stimulate.
• Overstimulation and tension have also been suggested as causes
• A dysfunctional autonomic nervous system may be implicated.

71. Pathology and Laboratory Examination
• No specific laboratory examination
• Must rule out physical causes of vomiting, such as pyloric stenosis and hiatal
hernia, before making the diagnosis of rumination disorder.
• Can be associated with failure to thrive and varying degrees of starvation-
endocrinological function (thyroid function tests, dexamethasone
suppression test), serum electrolytes, and a hematological workup help
determine the severity of the effects of rumination disorder.
Differential Diagnosis
• Gastrointestinal congenital anomalies/infections/other medical illnesses.
• Pyloric stenosis is usually associated with projectile vomiting and is generally
evident before 3 months of age, when rumination has its onset.
• Associated with various mental retardation syndromes in which other
stereotypic behaviors and eating disturbances, such as pica, are present.
• Can co-occur with other eating disorders, such as bulimia nervosa.
Course and Prognosis
• High rate of spontaneous remission- may develop and remit without ever
being diagnosed.

72. Treatment
• Combination of education and behavioral techniques
• Evaluation of the mother-child relationship-offering guidance to the
mother
• Behavioral technique- Habit-reversal technique- reinforcing an alternate
behavior that becomes more compelling than behaviors leading to
regurgitation
• Aversive behavior intervention- squirting lemon juice into the infant's
mouth whenever rumination occurs
• Anatomical abnormalities (e.g. hiatal hernia)- surgical repair may be
necessary.
• If an infant is malnourished and continues to lose most nutrition through
rumination, a jejunal tube may need to be inserted before other
treatments can be utilized.
• Medications are not a standard part of the treatment- metoclopramide,
cimetidine, haloperidol

73. Avoidant/Restrictive Food Intake Disorder (ARFID)
• According to the DSM-5 criteria, to be diagnosed as having ARFID a
person must display:
A. An Eating or Feeding disturbance as manifested by persistent failure to
meet appropriate nutritional and/or energy needs associated with one
(or more) of the following:
1. Significant loss of weight (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 behavior is not better explained by lack of available food or by an
associated culturally sanctioned practice.
C. The behavior does not occur exclusively during the course of anorexia
nervosa or bulimia nervosa, and there is no evidence of a disturbance in
the way one’s body weight or shape is experienced.
D. The eating disturbance is not attributed to a medical condition, or better
explained by another mental health disorder. When is does occur in the
presence of another condition/disorder, the behavior exceeds what is
usually associated, and warrants additional clinical attention.

74. Changes:
• Previously feeding disorders of infancy or early childhood.
• Criteria is significantly expanded making it a broader category
to capture a wider range of clinical presentations.

75. ICD-10

76. Epidemiology
• Between 15 and 35 % of infants and young children have transient feeding
difficulties
• Prevalence of 4.8 % with equal gender distribution
Differential Diagnosis
• Structural problems with the infants' gastrointestinal tract- feeding
disorders and organic causes of swallowing difficulties often coexist
• Video-fluoroscopic evaluation- 92% sensitive to exclude organic disorders
Course and Prognosis
• Most infants present within the first year of life- appropriate recognition
and intervention- no sign of develop failure to thrive.
• In children 2 to 3 years of age- growth and development can be affected
• 70 % of infants who persistently refuse food in the first year of life
continue to have some feeding problems during childhood.

77. Treatment-
• Individualized and targeting the interactions between the infant and
mother
• Identifying factors that can be changed to promote greater ingestion
• Transactional model of intervention- training process for parents- done in
an intense manner within a short period of time.
o Education for the parents
o Feed on a regular basis at 3- to 4-hour intervals- offer only water between
meals
o Praise for any self-feeding efforts
o Limit any distracting stimulation during meals
• In severe cases hospitalization and nutritional supplementation
• Treatment of comorbid for anxiety and mood symptoms
• Risperidone observed to be associated with an increase in oral intake and
accelerated weight gain

78. Conclusion
• Eating disorders- culture bound syndromes-restricted to countries
with Western culture- formative as well as the pathoplastic effect
on eating disorders.
• The study of eating disorders in developing countries like India
could be illuminating- unique opportunity for testing the role of
culture in the etiology of eating disorders.
• The studies conducted in the management have a limitation of
small sample size and short follow up period- failed to address the
optimal approach to re-nutrition
• Newer medications affecting hunger, satiety, and energy
expenditure as well as novel approach in behavior intervention
need to be developed and tested.

79. References
• Sadock, Benjamin J.; Sadock, Virginia A.; Ruiz, Pedro. Kaplan & Sadock's
Comprehensive Textbook of Psychiatry, 9th Edition.2009 Lippincott
Williams & Wilkins
• Sadock, Benjamin James; Sadock, Virginia Alcott. Kaplan & Sadock's
Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry, 11th
Edition. 2014 Lippincott Williams & Wilkins
• The Maudsley prescribing guidelines in psychiatry / David Taylor, Carol
Paton, Shitij Kapur. – 12th edition.
• The ICD-10 classification of mental and behavioural disorders : clinical
descriptions and diagnostic guidelines.
• DSM-5. APA
• Chakraborty and Basu: Management of eating disorders. Indian J
Psychiatry 52(2), Apr-Jun 2010
• Sharan and Sundar: Eating disorders in women. Indian J Psychiatry 57
(Supplement 2), July 2015

80. THANK YOU