3. Biology of eating
Disorders
Prof. Hani Hamed Dessoki, M.D.PsychiatryProf. Hani Hamed Dessoki, M.D.Psychiatry
Prof. PsychiatryProf. Psychiatry
Chairman of Psychiatry DepartmentChairman of Psychiatry Department
Beni Suef UniversityBeni Suef University
Supervisor of Psychiatry DepartmentSupervisor of Psychiatry Department
El-Fayoum UniversityEl-Fayoum University
APA memberAPA member

4. HistoryHistory
• In Western Europe of the 12In Western Europe of the 12thth
and 13and 13thth
centuries,centuries, “miracle“miracle
maidens,” or women who starved themselves, were highlymaidens,” or women who starved themselves, were highly
regarded, and their behavior was imbued with religiousregarded, and their behavior was imbued with religious
interpretations.interpretations.
• Catherine of Siena (1347 – 1380), whose complete controlCatherine of Siena (1347 – 1380), whose complete control
over her food intake was seen as a sign of religious devotion,over her food intake was seen as a sign of religious devotion,
was regarded as a saint (Heywood, 1996).was regarded as a saint (Heywood, 1996).
• ““Holy anorexia” was, however, short-livedHoly anorexia” was, however, short-lived
• By the 16By the 16thth
century the Catholic Church began to disapprovecentury the Catholic Church began to disapprove
of asceticism.of asceticism.
• Some anorexics were subsequently viewed as witchesSome anorexics were subsequently viewed as witches
(Brumberg, 2000).(Brumberg, 2000).

5. History cont’d
• First cases reported in 1689 by RichardFirst cases reported in 1689 by Richard
Morton –Morton – “wasting” disease of nervous“wasting” disease of nervous
etiology in one male and one femaleetiology in one male and one female
(Gordon, 2000).(Gordon, 2000).
• The first formal description of AN, however, isThe first formal description of AN, however, is
credited to Sir William Gull, physician tocredited to Sir William Gull, physician to
Queen Victoria, who in 1868 named theQueen Victoria, who in 1868 named the
disorder anorexia hysterica, emphasizingdisorder anorexia hysterica, emphasizing
what he believed to be its psychogenicwhat he believed to be its psychogenic
origins.origins.

6. History: Bulimia NervosaHistory: Bulimia Nervosa
• Bulimia Nervosa (BN), by contrast, was first clinicallyBulimia Nervosa (BN), by contrast, was first clinically
described in 1979described in 1979
• Historical accounts date to 1398, whenHistorical accounts date to 1398, when “true“true
boulimus” was described in an individual having anboulimus” was described in an individual having an
intense preoccupation with food and over eating atintense preoccupation with food and over eating at
very short intervals, terminated by vomiting (Stein &very short intervals, terminated by vomiting (Stein &
Laakso, 1988).Laakso, 1988).
• The word bulimia is derived from Greek and meansThe word bulimia is derived from Greek and means
“ravenous hunger,” quite the opposite of anorexia.“ravenous hunger,” quite the opposite of anorexia.

7. The Celebrity Thin IdealThe Celebrity Thin Ideal

8. The Impact of Media
• 90% of all girls ages 3-11 yrs have a Barbie Doll
• If Barbie were a real woman, her measurements
would be 38-18-33
• The body type portrayed in advertising as the ideal is
possessed naturally by only 5% of females
• The diet industry came on the scene in the 1960’s

9. Barbie and BodiesBarbie and Bodies
• Seven feet tallSeven feet tall
• 38 inch chest38 inch chest
• 21 inch waist21 inch waist
• 36 inch hips36 inch hips
• VirtuallyVirtually
unattainable for anunattainable for an
adult womanadult woman

10. Eating Disorders and Cross-
Cultural Influences
• Eating disorders more prevalent in industrialized
societies which emphasize thinness.
– US, Canada, Japan, Europe
• As countries become more “westernized”, eating
disorders increase.
• When women from countries with low prevalence
rates more 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.

11. Statistics
• Over one-half of teenage girls and one-
third of teenaged boys use unhealthy
weight control behaviors such as skipping
meals, smoking, fasting, vomiting, or
taking laxatives

12. Some statisticsSome statistics
• Eating disorders have
increased threefold in the last
50 years
• 10% of the population is
afflicted with an eating
disorder
• 90% of the cases are young
women and adolescent girls
• Up to 21% of college women show sub-threshold symptoms
• 61% of college women show some sort of eating pathology

13. Statistics
• Americans spend over $40 billion on
dieting and diet related products each year

14. Messages about FoodMessages about Food
What messages have you received (from
parents, peers, media, etc.) about food?
How are messages about food different for
women and men?

15. Eating Disorders
• Anorexia Nervosa
–Restricting Type
–Binge Eating/Purging (Bulimic) Type
• Bulimia Nervosa
–Purging Type
–Nonpurging Type
• Eating Disorder NOS

16. AnorexiaAnorexia
Risk of Death:
The Deadliest of all
Psychological Disorders

17. 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

20. Body Mass Index
• Weight in kg divided by height in m2
• NORMAL BMI : 18 to 24 years of age
BMI < 18 : suspect malnutrition
BMI 24 to 30 : overweight
BMI 30 to 40 : obesity
BMI above 40 = morbid obesity

21. Obesity
• Defined as 20% over ideal body weight
or BMI > 30
• Not an eating disorder per se and unlike
an eating disorder is not an mental illness.
However, many people who binge eat
become obese and can have mental health
problems
• 1/3 of NYC public high school students
are overweight or obese

22. What does our weight cost?
• Direct CostsDirect Costs
• Indirect CostsIndirect Costs
• 1995 = $99 billion1995 = $99 billion
• 2000 = $117 billion2000 = $117 billion
• Most of the cost associated with obesity is dueMost of the cost associated with obesity is due
to type 2 diabetes, coronary heart disease, andto type 2 diabetes, coronary heart disease, and
hypertension.hypertension.

23. Why are we so overweightWhy are we so overweight??
• GenesGenes
• DietDiet
• ExerciseExercise
• Nutrition EducationNutrition Education
• Social (single parent, no time to prepare meals,Social (single parent, no time to prepare meals,
etc.)etc.)

24. Vicious Cycle of Bulimia

25. 22Chapters:
1. Neurodevelopmental Disorders
2. Schizophrenia Spectrum & Other
Psychotic Disorders
3. Bipolar & Related Disorders
4. Depressive Disorders
5. Anxiety Disorders
6. Obs-Compulsive & Related
7. Trauma- & Stressor-Related
8. Dissociative Disorders
9. Somatic Symptom Disorders
10.Feeding & Eating Disorders
11.Elimination Disorders
12.Sleep/Wake Disorders
13. Sexual Dysfunctions
14. Gender Dysphoria
15. Disruptive, Impulse-Control &
Conduct Disorders
16. Substance Related & Addictive
Disorders
17. Neurocognitive Disorders
18. Personality Disorders
19. Paraphilic Disorders
20. Other Mental Disorders
21. Medication-induced Movement…
Med Effects
22. Other Conditions (v codes)

26. Feeding and Eating Disorders:
Cont…
Pica and Rumination Disorder:
• Criteria has been revised to allow diagnosis for individuals of all ages.
Avoidant/Restrictive Food Intake Disorder:
• 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.

27. Feeding and Eating Disorders:
Cont…
Anorexia Nervosa:
• The requirement for amenorrhea has been eliminated.
• Clarity and guidance: how to judge if an individual is at “significantly
low weight” has been added.
• Criterion B has been expanded to include not only “overtly expressed
fear of weight gain” but also “persistent behavior that interferes w/
weight gain”.

28. Feeding and Eating Disorders:
Cont…
Bulimia Nervosa :
• The only change is the reduction in the required
minimum average frequency of binge eating &
inappropriate compensatory behavior frequency
from twice to once weekly for 3 months.

29. Feeding and Eating Disorders:
Cont…
Binge Eating Disorder:
• Elevated to main body of manual from appendix B
in DSM-IV.
• The only change is the minimum average
frequency of binge eating required for diagnosis is
once weekly over the last 3 months (identical to
frequency criterion for bulimia nervosa).

30. Causes of Eating Disorders
• Personality Traits
• Genetics
• Environmental Influences
• Biochemistry

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

32. Personality traits contribute to the
development of eating disorders because:
• 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

33. Genetic Factors May Predispose
People to Eating Disorders
*Studies Suggest:
• Increased risk of anorexia nervosa among first-degree
biological relatives of individuals with the disorder
• increased risk of mood disorders among first-degree
biological relatives of people with anorexia, particularly the
binge-eating/purging type.
• Twin studies
– concordant rates for monozygotic twins is significantly higher
than those for dizygotic twins.
• Mothers who are overly concerned about their
daughter’s weight and physical attractiveness might
cause increase risk for development of eating
disorders.
• Girls with eating disorders often have brothers and a
father who are overly critical of their weight.

34. Environmental Factors
- Interpersonal and Social
• Interpersonal Factors
– troubled family and personal relationships
– difficulty expressing emotions and feelings
– history of being teased or ridiculed based on
size or weight
– history of trauma, sexual, physical and/or
mental abuse
• 60-75% of all bulimia nervosa patients have a
history of physical and/or sexual abuse

35. Etiology: Biological Theory
• Biological theories focus on the role of the hypothalamus
(the region concerned with the regulation of body
functions, such as temperature, weight, appetite, & general
homeostasis); 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)

36. Hypothalamus
• Neurotransmitter links to these eating disorders stem
from studies done primarily on the hypothalamus.
• Specifically, the ventromedial and lateral hypothalamus
have been shown to govern eating behavior in humans,
as well as in many laboratory animals.
• 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.

37. • 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.

38. • Decreasing the level of epinephrine in the
ventromedial hypothalamus of rats was
correlated with their exhibiting anorexic
type behaviors.
• That is, they would adopt a low rate of
eating, increase their rate of activity,
reduce their carbohydrate intake, and
rebound with overeating.

39. Biochemical Factors
• Chemical imbalances in the neuroendocrine system
– 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
– representing a link between depression and eating
disorders
• Excessive levels of cortisol in both anorexia and
depression
– caused by a problem that occurs in or near the
hypothalamus

40. Etiology: Biological Theory (2(
• There is also evidence of a central
neurotransmitter system dysregulation affecting
5HT, DA, and NOREPI; the strongest evidence
supports reduced NOREPI activity and turnover
• Vomiting leads to an increase in DA levels which
reinforces/rewards the vomiting behavior
• Theories of serotonergic hyperfunctioning in
anorexia and serotonergic hypofunctioning in
bulimia are attractive but don’t explain why
SSRIs are sometimes helpful for both

41. • This indicates that 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 successful treatment of bulimia with
SSRIs suggests the importance of
serotonin in eating disorders.

42. • Anorexic patients, on the other hand, may
have overactive serotonerigic response
centers, leading to a need to reduce the
levels of serotonin in their brains by
restricting their food intake.
• Actually, 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.

43. • Low serotonin levels have been linked to depression
which is a commonly concurrent disorder in people with
eating disorders.
• Both eating disorders and depression can be seen as
disorders that occur when the I-function, a sense of self,
is not in agreement with external reality.
• For example, the depressed person often has a feeling
of helplessness, hopelessness, and exceedingly low self
esteem regardless of their actual situation in life.

44. • A person suffering from anorexia or bulimia feels they are overweight when in fact they are
underweight (anorexia( or of normal weight (bulimia(. The I-function has somehow adopted an
unhealthy self image.
• The body presented by the I-function to the self is not the same body
which others see.
• Researchers looking for biological treatments for these disorders are
in effect looking for ways to bring the I-function's body image into
agreement with the body as seen by the outside world.
• Ultimately, the I-function must be a conglomeration of neurons whose arrangement was
determined through genetic programming.
• As neurons communicate by neurotransmitters an aberrant neurotransmitter system could affect
the I-function, and therefore self perception.
• Possible reasons for the faulty neurotransmitter system range from genetic to environmental
influences.

45. • Success of drug therapies suggest that the I-function can be
positively affected by artificial augmentation of the neuro-chemical
environment.
• Treatment with anti-depressant medication correlates with an
increase in self esteem among depressed individuals.
• That is, an I-function which was previously supplying a poor self
image can be changed, allowing for a healthier, more accurate view
of the self.
• A bulimic's or anorexic's I-function may also be positively affected by
drugs which can change its neuro-chemical environment.
• In this chemical fashion relief may be found for affected individuals.

46. • Two newly discovered hormones, orexin A and orexin B, are
connected with feeding behavior in rats.
• By modulating feelings of hunger and satiety the scientists can
influence how much a rat eats.
• Following injection of these hormones into the lateral hypothalamus
the rats were found to immediately begin eating eight to ten times
more food than normal.
• Following up on this finding they measured elevated hormone levels
when the rat was starved.
• These researchers have not yet been able to see if a decrease of
orexin A and B result in decreased appetites.

47. • 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.

48. Why do we eat?
The hypothalamus is the controller stimulated
by:
• OREXIGENIC PEPTIDES (appetite inducers)
e.g. agouti-protein and neuropeptide Y
• ANOREXIGENIC PEPTIDES (appetite
suppressants)
e.g. melano-cortin which, with effects on
specific receptors (MC1R(, decreases food
intake and increases energy expenditure

49. Central Controls are Influenced
by Circulating HORMONES:
• INSULIN: provides signals related to blood
glucose levels
• LEPTIN: signaling consistency of body fat
stores
and, in addition
• The GUT HORMONES

50. The GUT HORMONES
• GRELIN: secreted by the stomach fundus (when empty( increases
appetite and hence food intake (orexigenic(
• NO: nitric oxide (not a hormone but dilates the empty stomach hence
very orexigenic(
• CHOLECYSTOKININE and PEPTIDE YY3-36: secreted by endocrine
lining cells of the distal gut and colon when food present hence appetite
suppressants (anorexigenic(
Can these hormones be manipulated therapeutically?
Not easily!
ANY LOSS OF BODY FAT stimulates a defensive system which acts in
order to RESIST THE LOSS OF FAT
IN CONCLUSION: the GUT TALKS to the BRAIN
‫بتصوصو‬ ‫بطنه‬ ‫عصافير‬ ‫بيقولك‬

52. Thorough Medical Assessment
• Physical Exam
– Check weight
– Blood pressure, pulse, and temperature
– Heart and lungs
– Tooth enamel and gums
• Nutritional assessment/evaluation
– Eating patterns
– Biochemistry assessment—how chemistry
with eating disorders contributes to additional
appetite decline and decreased nutritional
intake

53. Thorough Medical Assessment
• Lab & other diagnostic tests
– Blood tests
– X-rays
– Other tests for heart and kidneys
• Interviews
– History of body weight
– History of dieting
– Eating behaviors
– All weight-loss related behaviors
– Past and present stressors
– Body image perception and dissatisfaction

54. Treatment Strategies
For Eating Disorders

55. Treatment Strategies:
• Ideally, treatment addresses physical and
psychological aspects of an eating disorder.
• People with eating disorders often do not
recognize or admit that they are ill
– May strongly resist treatment
– Treatment may be long term
• E.D. are very complex and because of this
several health practitioners may be involved:
– General practitioners, Physicians, Dieticians,
Psychologists, Psychiatrists, Counselors, etc.
• Depending on the severity, an eating disorder is
usually treated in an:
– Outpatient setting: individual, family, and group
therapy
– Inpatient/Hospital setting: for more extreme cases

56. Anorexia Treatment
• Three main phases:
– Restoring weight lost
– Treating psychological issues, such as:
• Distortion of body image, low self-esteem, and
interpersonal conflicts.
– Achieving long-term remission and
rehabilitation.
• Early diagnosis and treatment increases
the treatment success rate.

57. Eating Disorder Treatment
• Medical Treatment
– Medications can be used for:
• Treatment of depression/anxiety that co-exists with
the eating disorder
• Restoration of hormonal balance and bone density
• Encourages weight gain by inducing hunger
• Normalization of the thinking process
– Drugs may be used with other forms of
therapy
• Antidepressants (SSRI’s)
– May suppress the binge-purge cycle
– May stabilize weight recovery

58. Eating Disorder Treatment
• Individual Therapy
– Allows a trusting relationship to be formed
– Difficult issues are addressed, such as:
• Anxiety, depression, low self-esteem, low self-confidence,
difficulties with interpersonal relationships, and body image
problems
– Several different approaches can be used, such as:
• Cognitive Behavioral Therapy (CBT)
– Focuses on personal thought processes
• Interpersonal Therapy
– Addresses relationship difficulties with others
• Rational Emotive Therapy
– Focuses on unhealthy or untrue beliefs
• Psychoanalysis Therapy
– Focuses on past experiences

59. Current Opinion in Psychiatry
A Review of Eating Disorders in Males
Anu Raevuori, Anna Keski-Rahkonen, Hans W. Hoek
DisclosuresCurr Opin Psychiatry. 2014;27(6):426-430.
• Abstract
• Purpose of review Research in eating disorders in males has been active lately compared to the
past. This review aims to provide an overview of the recently published studies of eating
disorders in males.
• Recent findings Publication of the Diagnostic and Statistical Manual of Mental Disorders, 5th
edition has outlined more sex-neutral diagnostic criteria for eating disorders. Data of
socioeconomic factors, prenatal influences, clinical characteristics, assessment, and mortality for
eating disorders have been reported independently for males. Unlike in females, higher parental
education showed no association with eating disorders in males, but twin or triplet status and
lower gestational age at birth had an independent association with anorexia nervosa in males.
Contrary to earlier suggestions, no differences in eating disorder symptoms such as binging,
vomiting, or laxative abuse were observed between the sexes.
• Yet, males tended to score lower on eating disorder symptom measures than females. High rates
of premorbid overweight and higher BMIs at various stages of eating disorders have been
confirmed repeatedly.
• Higher age and lower BMI at admission, and restrictive anorexia nervosa subtype predicted fatal
outcome for anorexia nervosa in males.
• Summary Contemporary research provides grounds for improved recognition, diagnosis, and
treatment for males suffering from eating disorders.

60. ‫واسمه‬ ‫نفسى‬ ‫مرض‬ ‫بقى‬ ‫السيلفى‬ ‫كده‬ ‫خل ص‬
‫سيلفيتيس‬
HEALTH & MEDICINE, HUMAN INTEREST,
INTERNATIONAL
AMERICAN PSYCHIATRIC ASSOCIATION
MAKES IT OFFICIAL: ‘SELFIE’ A MENTAL
DISORDER
MARCH 31, 2014
Chicago, Illinois – The
American Psychiatric
Association (APA) has
officially confirmed what
many people thought all
along: taking ‘selfies’ is a
mental disorder.

61. APA said there are three levels of the disorder:
Borderline selfitis : taking photos of one’s self at least three
times a day but not posting them on social media
Acute selfitis: taking photos of one’s self at least three
times a day and posting each of the photos on social
media
Chronic selfitis: Uncontrollable urge to take photos of one’s
self round the clock and posting the photos on social
media more than six times a day
Types of Selfitis

62. According to the APA, while there is currently no cure for
the disorder, temporary treatment is available through
Cognitive Behavioral Therapy (CBT). The other good
news is that CBT is covered under Obamacare.
This is unwelcome news for Makati City in the Philippines,
especially for its mayor, Junjun Binay, son of the
incumbent vice president. Makati was recently named
selfie capital of the world by Time Magazine. The mayor
even organized a ticker tape parade after his city was
bestowed the rare honor.

64. Medscape Medical News > Psychiatry
More Than 50% of Antipsychotics Prescribed Off Label
Liam Davenport, December 30, 2014
More than half of the prescriptions for
antipsychotics in the United Kingdom are
prescribed to individuals with no diagnosis of a
serious mental illness (SMI), a major study of
primary care records has revealed.
Investigators at University College London also
found that off-label antipsychotic prescribing is
more likely to occur in women, older people, and
socially and economically disadvantaged
individuals.

65. More Than 50% of Antipsychotics Prescribed
Off Label
Serious Side Effects
International and national guidelines urge caution concerning the use
of antipsychotics; for patients who do not have a diagnosis of
psychosis, their use is recommended only in a limited number of
cases.
The drugs are associated with serious adverse effects, including
extrapyramidal symptoms with first-generation antipsychotics and
weight gain and lipid/glucose dysregulation with second- generation
agents. Moreover, antipsychotics may be linked to increased rates
of stroke and all-cause mortality in patients with dementia.
However, the researchers note that the drugs may be prescribed off
label, potentially to "augment antidepressants in complex or
treatment-resistant cases of obsessive compulsive disorder, anxiety
and personality disorders."