Eating disorders Flashcards
What is Other specified feeding or eating disorder?
*This is the diagnostic category for individuals who do not fit the criteria for AN or BN, but who have characteristics of one or both conditions (Bariatric surgery patients)
What is binge eating disorder?
Characterised by repeated overeating, no compensation, it is estimated to be present in 9-18% of obese individuals, mainly female
Probably the most common eating disorder, shares characteristics of
BN
What is night eating disorder?
(a putative diagnostic category)
*Again linked to obesity, the persons circadian rhythm is abnormal and this may be linked to leptin dysfunction
What is rumination disorder?
Repeated regurgitation & re-chewing of food (more in children, especially with Int. Dis.)
What is Avoidant/Restrictive food intake disorder?
*Like anorexia, but withoutfear of weight gain, fat or body distortions (more in children)
Inability to eat a wide range of foods, characterised by weight loss
What is child pica?
*Often associated with developmental disorders
*Can include paint, plastics, animal droppings, sand etc
What is adult pica?
*Iron deficiency (anaemia) –pagophagia (ice eating) and consumption of soil
*Psychiatric conditions
What is Prader-Willi?
Developmental disorder
*1:20,000, rare genetic condition, with compulsive overeating, many die from obesity related conditions
Disregulation of capacity to feel full (feel hungry all the time)
What eating disorders are sequelae of brain injury?
*Gourmand syndrome–MCA stroke, frontal damage
*Hyperphagia–Amygdala lesion, Kluver-Bucy syndrome
What is Klein-Levine syndrome?
(1:1000000), autoimmune triggered sleep disorder after a cold or flu, sleep for 15-20 h a
day and when wake up, are completely preoccupied with sex of eating so all they do when they’re awake is eat
What is the clinical definition of AN?
*Restriction of energy intake relative to requirements, leading to significant low body weight (as judged by BMI relative to age, gender and health expectations)
*Intense fear of gaining weight or becoming fat, or persistent behaviour that interferes with weight gain, even though at a significantly low weight
*Disturbance of perception of shape or bodyweight, undue influence of of body weight or shape on self-evaluation or denial of the seriousness of current low body weight
What are the 2 subtypes of AN?
*Restricting –dieting, fasting and exercise (often early presentation)
*Binge-eating/purging –vomit, laxatives, diuretics & enemas (often later presentation)
What is the prevalence of AN? (5)
*Lifetime prevalence of AN is 0.5-2% in women
*AN is primarily a disorder of women, with a sex ratio of between 10-20 to 1
*AN occurs in all races, cultures and classes, but is predominantly found in middle or upper middle class Caucasian women
*Higher rates of AN are observed in those participating in dance, fashion and elite sport
*AN typically appears at around 12/13 years (i.e., post menarche) with a range of around 10-60 years
What is the onset of AN? (10)
*Starts with minor changes in diet
–Desserts are abandoned, then meat, then all fat containing food
–Vegetarianism may be used to justify this transition
*Increasing focus on “safe-foods”(e.g., lettuce, fruit)
–Restriction of fluid intake
–Decreased eating speed
–Longer intervals between meals
–Progressive reduction in caloric intake
–May be well disguised from family (e.g., baggy clothes)
*Thinness starts to become the only salient goal
What are the medical consequences of AN? (8)
*Overactivity (peculiar to AN) and cold sensitivity
- Can include fidgeting, excess walking and prolonged standing
*Multiple endocrine abnormalities (e.g., Type 1 diabetes)
*Low blood pressure and slow HR
*Diminished libido and amenorrhea
*Osteoporosis (post-recovery)
*Neuropsychological impairments in learning and memory and reduction in hippocampal volume
*Anxiety and depression (estimated range 21-91%)
*Lifetime mortality 5-10% (from starvation and suicide –with a 56x greater risk for the latter, relative to norms). This makes it the most lethal of all psychiatric disorders
What is the cause of AN?
*Even with over a 100 years of accumulated research there is no clearly identified single cause for AN
*The best supported models suggest multiple interacting factors, that include genetic, biological, psychological, social and cultural variables
What are the genetics like in AN? (4)
*There is a significant genetic component to AN
*Female relatives of someone with AN are between 7-20x’s more likely to develop AN
*This is likely to reflect genetic factors as MZ twins have a higher concordance of AN than DZ twins
*Estimates based upon such twin studies suggest that 58-76% of the variance in who has (vs who doesn’t have) AN results from genetics alone
What are the traits in AN? (caused by genetics) (7)
*Serotonin metabolism appears abnormal in AN and in recovered individuals too -this is associated with three heritable traits
–OCD-like personality characteristics such as ‘perfectionism’, ‘inflexibility’ and ‘restraint’
*Hence, desire to have perfect body and ability to rigidly (inflexibly) restrain food intake
–Abnormal satiety (role of serotonin in modulating appetite)
–Chronic anxiety (serotonin modulates the HPA axis)
*Other heritable behavioural traits include
–Diminished sensitivity to hunger cues
–Heightened sensitivity to reinforcing effects of hunger/starvation
–Tendency towards excessive exercise
*These three traits can be modeled in animals using a food deprivation schedule with free access to wheel running –these animals run to death
What is development like in AN? (5)
*25% of parents of a child who goes on to develop AN have experienced majorobstetric difficulty and loss, compared with only 7.5% of matched controls (overprotective?)
*Parents of children with AN also report significantly higher levels of anxiety during pregnancy than controls (affects foetal HPA)
*The incidence of prematurity and birth trauma is 2-3x’s higher for those with AN than matched controls (hypoxia produces hippocampal damage which can dysregulates HPA)
*Parents of children with AN are also more controlling and overprotective too (as a result of the above or the AN?)
*Parents of children with AN have a higher incidence of abnormal attachment styles (dismissive [minimising emotional expression] & insecure [attaches to stranger as easily as to mother])
What are developmental consequences that lead to AN?
*Abnormal attachment, maternal stress during pregnancy, birth trauma and serotonergic abnormalities have similar psychobiological consequences
*They impact particularly on the HPA axis and thus on the way that the body (and mind) deal with stress
What is the HPA axis?
*The HPA axis is composed of 3 components
*The Hypothalamus (PVN –paraventricular nucleus)
*It releases Vasopressin (AVP) & Corticotrophin Releasing Hormone (CRH)
*These hormones affect the Pituitary gland (anterior lobe)
*It then releases adrenocorticotropic hormone
*This hormone then affects the Adrenal gland which releases cortisol which then acts to suppress release of hormones from the PVN (negative feedback)
*The hypothalamus is also regulated by serotonergic pathways and by feedback from the Hippocampus
How does stress affect the HPA? (7)
*Stress -psychological or physiological -results in activation of the HPA and the release of cortisol
*Cortisol raises blood glucose, increases blood pressure and down-regulates immune function (allied to the fight or flight response)
*Problems arise when cortisol levels are chronically high which produces:
*Muscle wasting
*High blood glucose
*Immune suppression
*Hippocampal damage
How is the HPA linked to AN? (11)
*HPA function is abnormal in AN and following recovery and there are multiple biological causes of this (e.g., abnormal feedback from the PVN)
*HPA abnormalities can overtly manifest under conditions of acute stress
–A severe life event preceded the onset of AN in 67% of a clinical sample of AN sufferers
*Profound changes occur during puberty to the HPA axis which may provide a window of vulnerability (these may also combine with fears arising from the start of menarche)
–This occurs because of looser control of body weight during menarche resulting from changes in fat distribution in the body & from concurrent hormonal changes
*The hypothalamus is involved in central appetite regulation
*Chronic release of CRH from the PVN can significantly affect appetite regulation in other hypothalamic nuclei
–CRH is a powerful inhibitor of Neuropeptide Y (NY)
–NY acts to increase appetite and its suppression results in loss of appetite and weight loss (useful in an emergency, but not all the time)
*Chronic CRH release also leads to
–Suppression of reproductive hormones
–Hypotension and bradycardia
–Altered locomotion (overactivity)
–Delayed gastric emptying
*These are all significant features of AN
What is the causal synthesis of AN? (6)
*Predisposing individual factors:
*Abnormal HPA axis
*Increased serotonin availability associated with OCP traits, chronic anxiety and enhancedsatiety
*Situational factors:
*Biological window of sensitivity during menarche (HPA axis)
*Acute stressors (life events, psychosocial transition to adulthood)
*Chronic stressors (family and social influences)
*Culture of weight loss
*Results in the manifestation of AN
How is AN maintained? (8)
Sufferers deny having a problem
*As AN develops in severity the following pattern typically manifests
*Various measures of body weight (& loss) are taken, often several times daily
*Complex rituals may evolve around these measures
*Weight loss results in profound (but short lived) satisfaction
*Increasingly punitive measures are taken if weight loss is not observed (purging, further dietary restriction)
*Highly stylised rituals may evolve around eating and the types of food eaten may become extremely restricted
*Social avoidance occurs (although not in the early stages where weight loss may be reinforced by friends and family)
*Investment is gradually withdrawn from all other activities until pursuit of further weight loss becomes the only meaningful goal
What biological factors are at work to keep this highly maladaptive fasting behaviour (AN) going? (5)
–Some have suggested that the process of weight loss itself may become physically addictive
–Indeed there is evidence of heightened b-endorphin levels in AN
–This addiction model suggests that the person may experience
*An affective high (from endogenous opioids) -problems with this version due to inconsistent data on the role of endorphins in AN
*An avoidance of dysphoria (by avoiding eating)
*A reduction in anxiety/stress (from not eating tryptophan the precursor for serotonin, thus lowering abnormally high serotonin levels)
What is the outcome and treatment of AN? (5)
*As noted earlier there is a 5-10% lifetime mortality rate
*Approximately 50% never fully recover and experience repeated periods of recovery and then relapse (of varying severity)
*Treatment
–The first goal is refeeding which usually takes place in hospital (2000-4000Kcal/day) under strict supervision
–This is usually combined with some form of on-going psychotherapy (various)
–Additional treatments include the use of certain anti-depressants but these are only effective after refeeding and may assist in preventing relapse
What is the clinical definition of BN? (7)
*Recurrent episodes of binge eating. An episode of binge eating is characterised by both of the following:
–Eating in a discrete period of time (a 2 hour block) an amount of food larger than what most people would eat under similar circumstances
–A sense of lack of control (a feeling that one can’t stop eating)
*Recurrent inappropriate compensatory behaviour to avoid weight gain (e.g., laxatives, diuretics, fasting or excessive exercise)
*Binge eating and inappropriate compensatory behaviours both occur, on average, at least once per week for 3 months
*Self-evaluation unduly influenced by body weight and shape
*Occurs independently of any episodes of AN
What is the prevalence of BN? (4)
–Lifetime prevalence is 1-3% in women
–Predominantly a female disorder with 1 male case to every 10 female
–BN typically develops in late adolescence or early adulthood
–BN is most common in the same cultural and social groups as AN
What are the medical consequences of BN? (4)
–Benign relative to AN and includes
*Dental erosion
*Swelling of the parotid glands (with characteristic ‘Chipmunk’face)
*Electrolyte abnormalities
*Rare complications from oseophageal tear/gastric rupture
What is the cause of BN? (9)
*Predisposing factors
–A history of AN
*Some studies suggest 20-30% of people with BN met the criteria for AN earlier in their lives
*May share certain common genetic traits with AN
–Childhood and parental obesity
–A history of dieting (prior to onset -in many cases)
–Family environment
*Critical comments about weight during adolescence
*Sexual abuse -incidence is higher than for controls, but this is true for all psychiatric disorders (as with AN)
–Higher rates of anxiety and depression -75% life time risk -(and in family members too)
–Higher rates of personality disorders, substance abuse and self harming, which along with traits of impulsivity may combine towards self-harm behaviour such as BN
*Instigation
–One possible model of how BN may get started has been suggested
*The person diets
*They are preoccupied with their weight (cultural influence)
*They discover (from media, friend, teammate) a method for ‘quick weight loss’(typically vomiting or laxatives)
*This is then coupled with the discovery that palatable food may be eaten without consequences
*As the condition develops perceived control over eating and purging is gradually lost
*Frequency and duration of binges increases
*The range of triggers increases
–Dysphoria -which it may temporarily relieve
–Certain foods (sight or smell)
*Binged foods are highly idiosyncratic and binges can vary from intakes of 700-10000+Kcal
How is BN maintained? (7)
*The development of BN is accompanied by various physiological changes related to abnormal satiety
*Enlarged gastric capacity »Water filled balloon into stomach
*Delayed gastric emptying »General digestive slowing throughout GI tract
*Reduced gastric elasticity »Disturbed sensation of gastric fullness
*Impaired CCK release »Correlates with diminished subjective post-meal satiety
*Reduced vagal information flow »Associated with increased pain threshold observed in BN
*Abnormal serotonergic function & serum leptin levels
*All of these changes are perhaps adaptations to binges, although some maybe predispositions -it is hard to tell as prospective studies are rare
What is the prognosis of BN? (3)
*50% appear to make a full recovery
*30% experience occasional relapse
*20% exhibit chronic BN
How do we treat BN? (3)
–This is usually a combination of CBT (4-6M) and antidepressants which together appear quite successful
*CBT identifies cues to bingeing and how to deal with them
*Antidepressants work even if the patient is not depressed
–BN is far more easily treated than AN
