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Physiology of
Appetite and Eating disorders
Presented By: Surg Lt Cdr Jithin Raj M
Moderator: Lt Col Amitabh Saha
Introduction
 Human eating behaviour is complex
 Incompletely understood
Topics covered…
 “Meal” as the unit of analysis
 Controls of meal initiation
 Controls of meal size
 Across meal controls of meal size
 Physiological modulators of eating
 Behavioural neuroscience of psychiatric eating
disorders
Meal-as a unit of analysis
Organisation of ingestive behaviour
Food selection
and initiation
“Hunger”
Maintenance of
eating during the
meal
Termination of
eating(satiation)
Inhibition of eating
after meal
termination(PP
satiety)
Meal size
Timing and frequency of meals
Meal as a unit and eating disorders
Controls of meal initiation
 Numerous stimuli
 Most are conditioned
 Potency depends on indl experience
Controls of meal initiation-Metabolism
 Transient decline in plasma glucose prior to
spontaneous meal
 Temporal dynamics of plasma levels is crucial ie rapid
and large decline are ineffective.
Controls of meal initiation-Ghrelin
 Ghrelin infusion stimulates appetite in rats
 Increased meal frequency without affecting meal size
 Plasma Ghrelin levels increases before meals, increases
during food deprivation and reduces after meals
Relationship of Ghrelin levels and hunger scores
Controls of meal initiation-Ghrelin
 Ghrelin receptors are present in Hypothalamus
(same group of neurons expressing NPY/AgRP in tha
arcuate nucleus)
Controls of meal initiation-Neural mechanisms
 Largely unknown
 Neural afferents in liver
 Specific neurons in the brain, Ghrelin receptors in
hypothalamus
Control of meal size
 Positive and negative feedback of ingested food
 Affect maintenance and termination
Control of meal size-Flavor and reward
(Oropharyngeal food stimuli)
 Flavor is the sensory impression of food or other substance, and is
determined primarily by the chemical senses of taste and smell
 Flavor stimuli arise from olfactory, gustatory, tactile, and thermal
receptors in the oronasopharynx
Control of meal size-Flavor and reward
(Oropharyngeal food stimuli)
 Flavor stimuli contribute to
 (1) detection and discrimination processes; i.e., evaluation of the
presence, type, and intensity of food stimuli
 (2) stimulation or inhibition of eating
 (3) hedonic experience
 (4) associative learning processes
Effects of flavour on feeding-sham
feeding tests
 Technique of sham feeding
 Amount of sham feed depends upon
 Nature of ingestant and the animals
experience with sham feeding
 Example
Sham feeding tests-effects of flavor
 Human sham feeding tests
 Sensory specific satiety—decline in preference for a
consumed food
Flavor and obesity
 Relationship between food flavor and obesity
 Flavor and learning
 Post absorptive consequences
 Specific hungers
Neural mechanism of orosensory
reward-Hindbrain
 The initial processing of flavor stimuli--hindbrain
 Hindbrain alone is sufficient to produce many of the integrated
aspects of the control of eating, including the unconditioned effects
of gustatory stimuli on eating
Neural mechanism of orosensory
reward-Hindbrain
 Harvey Grill experiment-When de-cerebrate rats are
offered various concentrations of sucrose to
eat(normally/ sham feed), their intakes vary exactly
as do those of neurologically intact rats
Neural processes medicating flavors effect on ingestion are
partially independent of those mediating flavor hedonics
Neural mechanism of orosensory
reward-Forebrain
 Poorly understood
 Represented in multiple areas—
nucleus accumbens (NAc)
the amygdala, especially the central (CeA) and basolateral (BLA)
nuclei
parts of the limbic, orbitofrontal, cingulate, and insular cortical
areas,and other brain areas
 Various neurotransmitters
Neural mechanism of orosensory
reward-Forebrain
 Andras Hanjal experiment-Dopamine is released in the NAc in a
dose dependent fashion as rats sham feed of sucrose or oil
 Neural control of eating must be considered as a network
function and not a product of limited no of “centeres”
Satiation-Gastric food stimuli
 Mechano-sensitive mechanism
 Alone not sufficient
Satiation-Instestinal food stimuli
 Mechano and chemoreceptors
 Primacy of intestinal over post absorptive signals
Satiation-Vagal signalling
 Neural negative feedback by gastric
and intestinal food are carried by
vagus to NTS
 Vagal resection-increase in food
intake
 Stimulated by presence of food and
CCK/5HT
Satiation-CCK and other gut peptide signals
 CCK-synthesis
 Reducion in meal size
Satiation-CCK and other gut peptide signals
 CCK InjectionsBehavioural signs of satiation such as grooming and sleep
CCK and obesity
 CCK receptor mutations
Other peripheral peptides
hypothesised to control eating
Across meal controls of meal size
Gut peptides released after meal termination
Metabolic signals in PP period
Adiposity signals
Across meals gut peptide signals
 Effect on food intake that carry over multiple meals
 GLP-1, Peptide YY3-36
Hypothalamic nutrient sensing
 Hypothalamic neurons responds directly to local nutrient concentrations
Adiposity signals
 Lipid stores in adipocytes-Only
substantial stores of energy
 Adiposity signals are factors that
circulate in relation to the mass of
adipose tissue
 Delayed, indirect feedback from past
eating influencing energy homeostasis
by controlling current eating
Adiposity signals
Leptin Insulin
Amylin Ghrelin
Leptin
 Leptin levels are closely correlated with body fat mass
 chronic leptin administration reduces food intake,
increases energy expenditure, and reduces body weight.
 Leptin inhibits eating by selectively reducing meal size.
Insulin and Amylin
 Adiposity signals-tonic plasma levels
 Satiating signals-phasic, meal-related levels
 Both selectively decreases meal size
Hypothalamic mechanism of eating
 2 distinct neuronal populations in ARC
 Nerons expressing propetide POMC
 Neurons expressing NPY and AgRP-orexigenic peptide
Hypothalamic mechanism of eating
 Leptin
 POMCα-MSH (anorexigenic)
 Leptin hyperpolarize these neurons
 Effect on human obesity
Hypothalamic mechanism of eating
 Leptin
NPY and AgRP neurons (orexigenic)
 Leptin hyperpolarize these neurons
 Effect on human obesity
Hyperpolarizes
Hypothalamic mechanism of eating
Hyperpolarizes
Interesting to note that…..
 Research shows that the roles and relative importance of various
molecules will depend both on physiological context and on the
particular brain site considered
 dopamine in the NAc in stimulating eating vs dopamine in the
perifornical hypothalamus inhibits eating
Physiological modulators of eating
Learning
Exercise
Sex differences
Illness anorexia
Learning
 Meal initiation, Food selection and meal size are all
readily conditionable in animals and humans
 For example, when a sound/light CS was presented
to rats before each of six scheduled meals for
several days and then tested during “extinction,”
i.e., when the rats had free access to the same diet,
the CS elicited initiation of a very large meal on
each daily presentation for 3 weeks.
Learning
 Thus, cues that predict food availability during food deprivation
can provoke the initiation of a large meal
in the absence of deprivation.
 Higher order conditioning in humans
 All food selection in humans are appear to be learned
 Importance in behaviour control programs
Exercise
 Inhibitory effects of exercise on food intake
 OTELF rats exercise
Sex differences
 Ovarian cycling and eating
 Increase in plasma estradiol levels
Illness anorexia
 Transient anorexia
 More chronic illness anorexia
 IL1, TNF Alpha and PG E2
Behavioural
neuroscience of
psychiatric eating
disordersnm
Analysis of eating in Bulimia nervosa
patients
 Larger meals compared to controls
 Cognitive stimuli induced binging
 Postingestive negative-feedback satiation signals
are less potent in patients with bulimia
Analysis of eating in Bulimia nervosa
patients
 Postingestive negative-feedback satiation signals are less
potent in patients with bulimia
 Equivalent amounts of food decrease intake less in bulimic
patients than in controls
 Patients with bulimia must eat larger amounts of food to
produce equivalent self-reports of fullness
Analysis of eating in Bulimia nervosa patients
 Volume distention of the stomach produces a decreased
perceptual and mechanical response in patients with
bulimia
 Food-stimulated CCK release is less in bulimic patients
Part II
Overview of
Psychological and
Sociocultural Factors
Associated with
Eating Disorders
Eating disorders
 Disorders of eating behaviour, associated thoughts,
attitudes and emotions physiological impairments
Where to draw the line…?
Most important epidemiological factor
The Beauty Myth: How Images of Beauty Are Used Against Women Naomi Wolf, 1990
Predisposing
factors
Precipitating
factors
Maintaining
factors
Eating disorder
Vulnerability “windows”
In development period
Predisposing
factors
Temperament, Psychological and
Social vulnerability
Biological factors
• Genes related to serotonin
transcription
• Under nutrition
Temperament, Psychological and
Social vulnerability
 Family h/o eating disorders, affective spectrum
disorders, anxiety disorders, OCDs, obesity
 Mood disorders 4x more common in families
Temperament, Psychological and
Social vulnerability
The influence of family functioning –controversial
No single specific family functioning style appears to be necessary or
sufficient, for developing an eating disorder.
Temperament, Psychological and
Social vulnerability
 Childhood or adolescent physical, emotional, or sexual abuse clearly
contributes to psychiatric disorder, but not specifically an eating disorder
Temperament, Psychological and
Social vulnerability
 Tendencies to pay more attention to detail
 Difficulty in global processing of gestalts
 Difficulties in shifting mental sets
 Impaired hedonic mechanisms
Temperament, Psychological and
Social vulnerability
Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
 Mood and anxiety disorders and OCD in childhood
 Early appearance of obsessive compulsive personality
Temperament, Psychological and
Social vulnerability
Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
 Shaky self-esteem, teasing by family or friends, or
comments and directives from authority figure
(doctors, nurses, teachers, coaches)
Temperament, Psychological and
Social vulnerability
Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
 Vocational interests
 Micro cultures
Temperament, Psychological and
Social vulnerability
Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
Vulnerability factors
 The extent to which contributing to societal overvaluation of thinness and
dieting remains controversial.
Becker, A. E., Fay, K. E., Agnew-Blais, J., Khan, A. N., Striegel-Moore, R. H., & Gilman, S. E. (2011).
Social network media exposure and adolescent eating pathology in Fiji. The British Journal of Psychiatry
Vulnerability factors
 Although no single predisposing factor is necessary or
sufficient
 May be related to the number and severity of factors
Precipitating
factorsVulnerability “windows”
In development period
Sympathetic and trained history
Precipitating factors
 In approximately 95 percent of cases, the eating disorder is precipitated by dieting
 In approximately 8 percent of cases, initial weight loss may be inadvertent
(automobile accident requiring jaw wiring, flu, ulcer, etc..)
Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
Other precipitating factors
 Early puberty and accompanied by higher-than-average body weight
 Repugnance toward menses and sexuality
Sustaining
factors
 Social praise commonly provides external
reinforcement for further weight loss
 first sense of internally effective self-control
when the process of puberty is overwhelming
“Anorexia nervosa is an implicitly sanctioned pseudosolution to the existential challenges of adolescence’.
 After significant weight has been lost, attempts at healthy eating may
cause uncomfortable medical symptoms such as gastric bloating or fluid
retention
“Normal
eating is
painful and
impossible”
 Negative expressed emotion
 Anorexic behaviours can act as a regulator of
family dynamics
 Unconscious reinforcement
Calam, R., Waller, G., Slade, P. and Newton, T. (1990),
Eating disorders and perceived relationships with parents. Int. J. Eat. Disorders
Psychopathological
correlates
Psychopathology of eating disorders
 Anorexia nervosa –serve as a long-term
strategy for coping maladaptively with
maturational fears
 Pseudo solutions to core challenges of
adolescence-the challenge of
developing a coherent personal
identity rather than experiencing role
diffusion.
Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
Psychoanalytic explanations
for anorexia—historical interest
 Unconscious confusion between eating and the sexual instinct
 Fantasies and fears of oral impregnation, and confuse fatness with
pregnancy
 Anorexia reflects a regression to an earlier stage of development,
unconscious rejection of adulthood
Psychodynamic viewpoints
 Maturational and existential fears are very commonly
involved with eating disorders.
 Anorexia nervosa seemingly provides escape from
onrushing negative visions of the emerging sexuality and
other biological and social challenges of adolescence
Psychodynamic viewpoints
 sensitive personalities deal with childhood narcissistic
injuries, through self-starvation and disappearing into
“nothingness,”
 Research suggests that some women with anorexia
nervosa, are less “attached to life” than other women
Psychology of later onset ED
 Later-onset disorders differ thematically
 Older adult men may initially slim to increase their sexual
desirability to extramarital partners, enhance their upward
mobility at work etc.
 Some men slim to become more acceptable to gay partners
 Later onset in women may represent attempts at emotional self
regulation when previously unresolved issues present themselves
in late life
Cultural beliefs,
attitudes and
eating disorders
Cultural effects on eating disorders
 Cultural beliefs and attitudes-Significant contributing factors
in the development of eating disorders
 Rates vary among different racial/ethnic and national groups
 Also change across time as cultures evolve
Cultural effects on eating disorders
 Cultural beliefs and attitudes-Significant contributing factors
in the development of eating disorders
 Rates vary among different racial/ethnic and national groups
 Also change across time as cultures evolve
Cultural effects on eating disorders
 The prevalence of eating disorders in non-
Western countries is lower than that of the Western countries
but appears to be increasing
Makino, M., Tsuboi, K., & Dennerstein, L. (2004). Prevalence of Eating Disorders:
A Comparison of Western and Non-Western Countries. Medscape General Medicine, 6(3), 49.
Cultural effects on eating disorders
 Cultural change and vulnerability of eating disorder
 Role of western ideals
 The idealization of the thin body type within Western societies
has been identified as a possible factor leading to the
anorexia nervosa (Bruch 1962)
 Image of beauty that is promoted has changed
 Women’s magazine- More articles on methods for
Weight loss
Garner, Garfinkel, Schwartz, & Thompson, 1980; Owen & Laurel-Seller, 2000; Rubinstein & Caballero, 2000;
Wiseman, Gray, Mosimann, & Ahrens, 1992).
Eating disorders-As culture-bound syndromes ?
 It is important to understand how eating and body image problems present
differently in different cultures
 Many of these non-Western cases lack weight concerns
 Where food is plentiful-the idea of slenderness in constantly
imposed be media and peer pressure
 In countries where food availability fluctuates, plumpness is the
women ideal
Psychol Med. 1983 Nov;13(4):829-37. Cross-cultural differences in the perception of female body shapes.
Furnham A, Alibhai N.
Eating disorders & Indian culture
 information regarding these disorders is very limited
 Study:
 The authors describe five cases of young women who chiefly
presented with refusal to eat, persistent vomiting, marked weight loss,
amenorrhea and other somatic symptoms
 They did not show disturbances in body image seen characteristically
in anorexia nervosa
 Though finally diagnosed and treated as cases of eating disorder, they
presented considerable difficulty in diagnosis
Int J Soc Psychiatry. 1995 Summer;41(2):132-46. Eating disorders: an Indian perspective.
Khandelwal SK1, Sharan P, Saxena S.
Eating Disorders: New Features and
New Treatments
 Cognitive Functioning in Anorexia Nervosa
 Serotonergic abnormalities
Eating Disorders: New Features and
New Treatments
 Negative results with SSRIs in anorexia nervosa
Eating Disorders: New Features and
New Treatments
 Olanzapine in eating disorders
Lisdexamphetamins dimesylate
 In February 2015, Vyvanse (lisdexamfetamine dimesylate)
became the first and only medication approved to treat
moderate to severe Binge Eating Disorder in adults
Summary and take home message
 Need to focus on individuals meals rather than total calorie intake
 Eating behaviour is complex and results from interplay of various
neuronal/hormonal/metabolic sugnals
 Ghrelin- Important in initiation of feeding
 CCK- Satiety signal
 Leptins-Adiposity signal-Complex interaction with feeding behaviour
 There are various vulnerability, precipitating and sustaining factors
leading to the the development of eating disorders
Refrences
 Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
 Murphy, K.G. and Bloom, S.R. (2004), Gut hormones in the control of appetite.
Experimental Physiology, 89: 507–516.doi:10.1113/expphysiol.2004.027789
 Perry, B., & Wang, Y. (2012). Appetite regulation and weight control: the role of gut
hormones. Nutrition & Diabetes, 2(1), e26–. http://doi.org/10.1038/nutd.2011.21
 Eating Disorders: New Features and New Treatments;Medscape reference
 Banks, C. G. (1992). “Culture” in culture-bound syndromes: The case of
 anorexia nervosa. Social Science & Medicine, 34, 867–884.

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Eating behaviour and eating disorder introduction Psychiatry Seminar

  • 1.
  • 2. Physiology of Appetite and Eating disorders Presented By: Surg Lt Cdr Jithin Raj M Moderator: Lt Col Amitabh Saha
  • 3. Introduction  Human eating behaviour is complex  Incompletely understood
  • 4. Topics covered…  “Meal” as the unit of analysis  Controls of meal initiation  Controls of meal size  Across meal controls of meal size  Physiological modulators of eating  Behavioural neuroscience of psychiatric eating disorders
  • 5. Meal-as a unit of analysis
  • 6. Organisation of ingestive behaviour Food selection and initiation “Hunger” Maintenance of eating during the meal Termination of eating(satiation) Inhibition of eating after meal termination(PP satiety) Meal size Timing and frequency of meals
  • 7. Meal as a unit and eating disorders
  • 8. Controls of meal initiation  Numerous stimuli  Most are conditioned  Potency depends on indl experience
  • 9. Controls of meal initiation-Metabolism  Transient decline in plasma glucose prior to spontaneous meal  Temporal dynamics of plasma levels is crucial ie rapid and large decline are ineffective.
  • 10. Controls of meal initiation-Ghrelin  Ghrelin infusion stimulates appetite in rats  Increased meal frequency without affecting meal size  Plasma Ghrelin levels increases before meals, increases during food deprivation and reduces after meals Relationship of Ghrelin levels and hunger scores
  • 11. Controls of meal initiation-Ghrelin  Ghrelin receptors are present in Hypothalamus (same group of neurons expressing NPY/AgRP in tha arcuate nucleus)
  • 12. Controls of meal initiation-Neural mechanisms  Largely unknown  Neural afferents in liver  Specific neurons in the brain, Ghrelin receptors in hypothalamus
  • 13. Control of meal size  Positive and negative feedback of ingested food  Affect maintenance and termination
  • 14. Control of meal size-Flavor and reward (Oropharyngeal food stimuli)  Flavor is the sensory impression of food or other substance, and is determined primarily by the chemical senses of taste and smell  Flavor stimuli arise from olfactory, gustatory, tactile, and thermal receptors in the oronasopharynx
  • 15. Control of meal size-Flavor and reward (Oropharyngeal food stimuli)  Flavor stimuli contribute to  (1) detection and discrimination processes; i.e., evaluation of the presence, type, and intensity of food stimuli  (2) stimulation or inhibition of eating  (3) hedonic experience  (4) associative learning processes
  • 16. Effects of flavour on feeding-sham feeding tests  Technique of sham feeding  Amount of sham feed depends upon  Nature of ingestant and the animals experience with sham feeding  Example
  • 17. Sham feeding tests-effects of flavor  Human sham feeding tests  Sensory specific satiety—decline in preference for a consumed food
  • 18. Flavor and obesity  Relationship between food flavor and obesity  Flavor and learning  Post absorptive consequences  Specific hungers
  • 19. Neural mechanism of orosensory reward-Hindbrain  The initial processing of flavor stimuli--hindbrain  Hindbrain alone is sufficient to produce many of the integrated aspects of the control of eating, including the unconditioned effects of gustatory stimuli on eating
  • 20. Neural mechanism of orosensory reward-Hindbrain  Harvey Grill experiment-When de-cerebrate rats are offered various concentrations of sucrose to eat(normally/ sham feed), their intakes vary exactly as do those of neurologically intact rats Neural processes medicating flavors effect on ingestion are partially independent of those mediating flavor hedonics
  • 21. Neural mechanism of orosensory reward-Forebrain  Poorly understood  Represented in multiple areas— nucleus accumbens (NAc) the amygdala, especially the central (CeA) and basolateral (BLA) nuclei parts of the limbic, orbitofrontal, cingulate, and insular cortical areas,and other brain areas  Various neurotransmitters
  • 22. Neural mechanism of orosensory reward-Forebrain  Andras Hanjal experiment-Dopamine is released in the NAc in a dose dependent fashion as rats sham feed of sucrose or oil  Neural control of eating must be considered as a network function and not a product of limited no of “centeres”
  • 23. Satiation-Gastric food stimuli  Mechano-sensitive mechanism  Alone not sufficient
  • 24. Satiation-Instestinal food stimuli  Mechano and chemoreceptors  Primacy of intestinal over post absorptive signals
  • 25. Satiation-Vagal signalling  Neural negative feedback by gastric and intestinal food are carried by vagus to NTS  Vagal resection-increase in food intake  Stimulated by presence of food and CCK/5HT
  • 26. Satiation-CCK and other gut peptide signals  CCK-synthesis  Reducion in meal size
  • 27. Satiation-CCK and other gut peptide signals  CCK InjectionsBehavioural signs of satiation such as grooming and sleep
  • 28. CCK and obesity  CCK receptor mutations
  • 30. Across meal controls of meal size Gut peptides released after meal termination Metabolic signals in PP period Adiposity signals
  • 31. Across meals gut peptide signals  Effect on food intake that carry over multiple meals  GLP-1, Peptide YY3-36
  • 32. Hypothalamic nutrient sensing  Hypothalamic neurons responds directly to local nutrient concentrations
  • 33. Adiposity signals  Lipid stores in adipocytes-Only substantial stores of energy  Adiposity signals are factors that circulate in relation to the mass of adipose tissue  Delayed, indirect feedback from past eating influencing energy homeostasis by controlling current eating
  • 35. Leptin  Leptin levels are closely correlated with body fat mass  chronic leptin administration reduces food intake, increases energy expenditure, and reduces body weight.  Leptin inhibits eating by selectively reducing meal size.
  • 36. Insulin and Amylin  Adiposity signals-tonic plasma levels  Satiating signals-phasic, meal-related levels  Both selectively decreases meal size
  • 37. Hypothalamic mechanism of eating  2 distinct neuronal populations in ARC  Nerons expressing propetide POMC  Neurons expressing NPY and AgRP-orexigenic peptide
  • 38. Hypothalamic mechanism of eating  Leptin  POMCα-MSH (anorexigenic)  Leptin hyperpolarize these neurons  Effect on human obesity
  • 39. Hypothalamic mechanism of eating  Leptin NPY and AgRP neurons (orexigenic)  Leptin hyperpolarize these neurons  Effect on human obesity Hyperpolarizes
  • 40. Hypothalamic mechanism of eating Hyperpolarizes
  • 41. Interesting to note that…..  Research shows that the roles and relative importance of various molecules will depend both on physiological context and on the particular brain site considered  dopamine in the NAc in stimulating eating vs dopamine in the perifornical hypothalamus inhibits eating
  • 42. Physiological modulators of eating Learning Exercise Sex differences Illness anorexia
  • 43. Learning  Meal initiation, Food selection and meal size are all readily conditionable in animals and humans  For example, when a sound/light CS was presented to rats before each of six scheduled meals for several days and then tested during “extinction,” i.e., when the rats had free access to the same diet, the CS elicited initiation of a very large meal on each daily presentation for 3 weeks.
  • 44. Learning  Thus, cues that predict food availability during food deprivation can provoke the initiation of a large meal in the absence of deprivation.  Higher order conditioning in humans  All food selection in humans are appear to be learned  Importance in behaviour control programs
  • 45. Exercise  Inhibitory effects of exercise on food intake  OTELF rats exercise
  • 46. Sex differences  Ovarian cycling and eating  Increase in plasma estradiol levels
  • 47. Illness anorexia  Transient anorexia  More chronic illness anorexia  IL1, TNF Alpha and PG E2
  • 49. Analysis of eating in Bulimia nervosa patients  Larger meals compared to controls  Cognitive stimuli induced binging  Postingestive negative-feedback satiation signals are less potent in patients with bulimia
  • 50. Analysis of eating in Bulimia nervosa patients  Postingestive negative-feedback satiation signals are less potent in patients with bulimia  Equivalent amounts of food decrease intake less in bulimic patients than in controls  Patients with bulimia must eat larger amounts of food to produce equivalent self-reports of fullness
  • 51. Analysis of eating in Bulimia nervosa patients  Volume distention of the stomach produces a decreased perceptual and mechanical response in patients with bulimia  Food-stimulated CCK release is less in bulimic patients
  • 52. Part II Overview of Psychological and Sociocultural Factors Associated with Eating Disorders
  • 53. Eating disorders  Disorders of eating behaviour, associated thoughts, attitudes and emotions physiological impairments
  • 54. Where to draw the line…?
  • 56. The Beauty Myth: How Images of Beauty Are Used Against Women Naomi Wolf, 1990
  • 58. Predisposing factors Temperament, Psychological and Social vulnerability Biological factors • Genes related to serotonin transcription • Under nutrition Temperament, Psychological and Social vulnerability
  • 59.  Family h/o eating disorders, affective spectrum disorders, anxiety disorders, OCDs, obesity  Mood disorders 4x more common in families Temperament, Psychological and Social vulnerability
  • 60. The influence of family functioning –controversial No single specific family functioning style appears to be necessary or sufficient, for developing an eating disorder. Temperament, Psychological and Social vulnerability
  • 61.  Childhood or adolescent physical, emotional, or sexual abuse clearly contributes to psychiatric disorder, but not specifically an eating disorder Temperament, Psychological and Social vulnerability
  • 62.  Tendencies to pay more attention to detail  Difficulty in global processing of gestalts  Difficulties in shifting mental sets  Impaired hedonic mechanisms Temperament, Psychological and Social vulnerability Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
  • 63.  Mood and anxiety disorders and OCD in childhood  Early appearance of obsessive compulsive personality Temperament, Psychological and Social vulnerability Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
  • 64.  Shaky self-esteem, teasing by family or friends, or comments and directives from authority figure (doctors, nurses, teachers, coaches) Temperament, Psychological and Social vulnerability Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
  • 65.  Vocational interests  Micro cultures Temperament, Psychological and Social vulnerability Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
  • 66. Vulnerability factors  The extent to which contributing to societal overvaluation of thinness and dieting remains controversial. Becker, A. E., Fay, K. E., Agnew-Blais, J., Khan, A. N., Striegel-Moore, R. H., & Gilman, S. E. (2011). Social network media exposure and adolescent eating pathology in Fiji. The British Journal of Psychiatry
  • 67. Vulnerability factors  Although no single predisposing factor is necessary or sufficient  May be related to the number and severity of factors
  • 70. Precipitating factors  In approximately 95 percent of cases, the eating disorder is precipitated by dieting  In approximately 8 percent of cases, initial weight loss may be inadvertent (automobile accident requiring jaw wiring, flu, ulcer, etc..) Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
  • 71. Other precipitating factors  Early puberty and accompanied by higher-than-average body weight  Repugnance toward menses and sexuality
  • 73.  Social praise commonly provides external reinforcement for further weight loss  first sense of internally effective self-control when the process of puberty is overwhelming “Anorexia nervosa is an implicitly sanctioned pseudosolution to the existential challenges of adolescence’.
  • 74.  After significant weight has been lost, attempts at healthy eating may cause uncomfortable medical symptoms such as gastric bloating or fluid retention “Normal eating is painful and impossible”
  • 75.  Negative expressed emotion  Anorexic behaviours can act as a regulator of family dynamics  Unconscious reinforcement Calam, R., Waller, G., Slade, P. and Newton, T. (1990), Eating disorders and perceived relationships with parents. Int. J. Eat. Disorders
  • 77. Psychopathology of eating disorders  Anorexia nervosa –serve as a long-term strategy for coping maladaptively with maturational fears  Pseudo solutions to core challenges of adolescence-the challenge of developing a coherent personal identity rather than experiencing role diffusion. Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition
  • 78. Psychoanalytic explanations for anorexia—historical interest  Unconscious confusion between eating and the sexual instinct  Fantasies and fears of oral impregnation, and confuse fatness with pregnancy  Anorexia reflects a regression to an earlier stage of development, unconscious rejection of adulthood
  • 79. Psychodynamic viewpoints  Maturational and existential fears are very commonly involved with eating disorders.  Anorexia nervosa seemingly provides escape from onrushing negative visions of the emerging sexuality and other biological and social challenges of adolescence
  • 80. Psychodynamic viewpoints  sensitive personalities deal with childhood narcissistic injuries, through self-starvation and disappearing into “nothingness,”  Research suggests that some women with anorexia nervosa, are less “attached to life” than other women
  • 81. Psychology of later onset ED  Later-onset disorders differ thematically  Older adult men may initially slim to increase their sexual desirability to extramarital partners, enhance their upward mobility at work etc.  Some men slim to become more acceptable to gay partners  Later onset in women may represent attempts at emotional self regulation when previously unresolved issues present themselves in late life
  • 83. Cultural effects on eating disorders  Cultural beliefs and attitudes-Significant contributing factors in the development of eating disorders  Rates vary among different racial/ethnic and national groups  Also change across time as cultures evolve
  • 84. Cultural effects on eating disorders  Cultural beliefs and attitudes-Significant contributing factors in the development of eating disorders  Rates vary among different racial/ethnic and national groups  Also change across time as cultures evolve
  • 85. Cultural effects on eating disorders  The prevalence of eating disorders in non- Western countries is lower than that of the Western countries but appears to be increasing Makino, M., Tsuboi, K., & Dennerstein, L. (2004). Prevalence of Eating Disorders: A Comparison of Western and Non-Western Countries. Medscape General Medicine, 6(3), 49.
  • 86. Cultural effects on eating disorders  Cultural change and vulnerability of eating disorder  Role of western ideals  The idealization of the thin body type within Western societies has been identified as a possible factor leading to the anorexia nervosa (Bruch 1962)
  • 87.  Image of beauty that is promoted has changed  Women’s magazine- More articles on methods for Weight loss Garner, Garfinkel, Schwartz, & Thompson, 1980; Owen & Laurel-Seller, 2000; Rubinstein & Caballero, 2000; Wiseman, Gray, Mosimann, & Ahrens, 1992).
  • 88. Eating disorders-As culture-bound syndromes ?  It is important to understand how eating and body image problems present differently in different cultures  Many of these non-Western cases lack weight concerns
  • 89.  Where food is plentiful-the idea of slenderness in constantly imposed be media and peer pressure  In countries where food availability fluctuates, plumpness is the women ideal Psychol Med. 1983 Nov;13(4):829-37. Cross-cultural differences in the perception of female body shapes. Furnham A, Alibhai N.
  • 90. Eating disorders & Indian culture  information regarding these disorders is very limited  Study:  The authors describe five cases of young women who chiefly presented with refusal to eat, persistent vomiting, marked weight loss, amenorrhea and other somatic symptoms  They did not show disturbances in body image seen characteristically in anorexia nervosa  Though finally diagnosed and treated as cases of eating disorder, they presented considerable difficulty in diagnosis Int J Soc Psychiatry. 1995 Summer;41(2):132-46. Eating disorders: an Indian perspective. Khandelwal SK1, Sharan P, Saxena S.
  • 91. Eating Disorders: New Features and New Treatments  Cognitive Functioning in Anorexia Nervosa  Serotonergic abnormalities
  • 92. Eating Disorders: New Features and New Treatments  Negative results with SSRIs in anorexia nervosa
  • 93. Eating Disorders: New Features and New Treatments  Olanzapine in eating disorders
  • 94. Lisdexamphetamins dimesylate  In February 2015, Vyvanse (lisdexamfetamine dimesylate) became the first and only medication approved to treat moderate to severe Binge Eating Disorder in adults
  • 95. Summary and take home message  Need to focus on individuals meals rather than total calorie intake  Eating behaviour is complex and results from interplay of various neuronal/hormonal/metabolic sugnals  Ghrelin- Important in initiation of feeding  CCK- Satiety signal  Leptins-Adiposity signal-Complex interaction with feeding behaviour  There are various vulnerability, precipitating and sustaining factors leading to the the development of eating disorders
  • 96. Refrences  Kaplan & Sadock's Comprehensive Textbook of Psychiatry, 9th Edition  Murphy, K.G. and Bloom, S.R. (2004), Gut hormones in the control of appetite. Experimental Physiology, 89: 507–516.doi:10.1113/expphysiol.2004.027789  Perry, B., & Wang, Y. (2012). Appetite regulation and weight control: the role of gut hormones. Nutrition & Diabetes, 2(1), e26–. http://doi.org/10.1038/nutd.2011.21  Eating Disorders: New Features and New Treatments;Medscape reference  Banks, C. G. (1992). “Culture” in culture-bound syndromes: The case of  anorexia nervosa. Social Science & Medicine, 34, 867–884.