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