Eating Disorders (PDF)

Eating disorders Appetite: The psychology of eating and drinking 1 1 Overview • In this lecture we will focus on two eating disorders – Anorexia nervosa (AN; DSM V) – Bulimia nervosa (BN; DSM V) • Unfortunately, we do not have the time to cover these other less well studied conditions – Other sp...

Eating disorders Appetite: The psychology of eating and drinking 1 1 Overview • In this lecture we will focus on two eating disorders – Anorexia nervosa (AN; DSM V) – Bulimia nervosa (BN; DSM V) • Unfortunately, we do not have the time to cover these other less well studied conditions – Other specified feeding or eating disorder (DSM V) • 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) – Binge eating disorder (new to DSM V) • Characterised by repeated overeating, no compensation, it is estimated to be present in 918% of obese individuals, mainly female – Night eating disorder (a putative diagnostic category) • Again linked to obesity, the persons circadian rhythm is abnormal (see earlier lecture) and this may be linked to leptin dysfunction – Rumination disorder (DSM V) • Repeated regurgitation & re-chewing of food (more in children, especially with Int. Dis.) – Avoidant/Restrictive food intake disorder (DSM V) • Like anorexia, but without fear of weight gain, fat or body distortions (more in children) 2 2 Overview II – Pica (DSM V) • Often associated with developmental disorders • Can include paint, plastics, animal droppings, sand etc – Pica (Adults) • Iron deficiency (anaemia) – pagophagia (ice eating) and consumption of soil • Psychiatric conditions – see left - “A 62 year old French man is rushed to ER with severe stomach pains. At first the doctors are not sure what the problem is, so they x-ray his stomach and find a mass there, heavy enough to push his stomach downwards. They operate and are ʻsurprisedʼ to find more than 5 Kg of coins worth $650 in total” – Developmental disorders (e.g. Prader-Willi) • 1:20,000, rare genetic condition, with compulsive overeating, many die from obesity related conditions – Sequelae of brain injuries (Research) • Gourmand syndrome – MCA stroke, frontal damage • Hyperphagia – Amygdala lesion, Kluver-Bucy syndrome 3 3 Anorexia nervosa (AN) • Clinical definition: • 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 • Sub-types: • Restricting – dieting, fasting and exercise (often early presentation) • Binge-eating/purging – vomit, laxatives, diuretics & enemas (often later presentation) • Specification: • Full, partial or in remission, and severity (based on BMI; Mild, BMI = 17, to Extreme, BMI < 15) 4 4 Prevalence • 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 5 5 Onset • 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 6 6 Medical consequences • 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 7 7 Cause • Earliest documentation of AN is in the 15th and 16th Centuries (female saints?), with the earliest formal medical report dating back to the 19th Century (1870 - William Gull) • 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 • We will start by looking at various individual risk factors and then examine how these might interact to produce AN 8 8 Genetics • There is a significant genetic component to AN • Female relatives of someone with AN are between 7-20xʼs 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 doesnʼt have) AN results from genetics alone • So what traits are underpinned by these genetic vulnerabilities? 9 9 Traits • Serotonin metabolism appears abnormal in AN and in recovered individuals too - this is associated with three heritable traits – OCD-like personality characteristics such as ʻperfectionismʼ, ʻinflexibilityʼ and ʻrestraintʼ • Hence, desire to have perfect body and ability to rigidly (inflexibly) restrain food intake – Abnormal satiety (recall the role of serotonin in modulating appetite) – Chronic anxiety (and 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 *Hypothalamic-Pituitary-Adrenal axis 10 10 Development • 25% of parents of a child who goes on to develop AN have experienced major obstetric 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 2-3xʼs 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]) 11 11 Developmental consequences • 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 • We will start by looking (briefly) at the HPA axis - what is it and what is known about it in relationship to AN 12 12 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 13 13 Stress and the HPA • 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 14 14 HPA and AN - 1 • 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 – Stress related anorexiaʼs, resulting from HPA dysfunction, have been observed in animals (lean sow disease) • 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 15 15 HPA and AN - 2 • The hypothalamus is involved in central appetite regulation (recall our earlier lectures) • Chronic release of Corticotrophin Releasing Hormone (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 16 16 Causal synthesis (one of many possibilities) • Predisposing individual factors • Abnormal HPA axis • Increased serotonin availability associated with OCP traits, chronic anxiety and enhanced satiety • 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 (note Fiji data on Western Media; little exposure prior to 1980, post 1980 big increase in body dissatisfaction) • Results in the manifestation of AN 17 17 Maintenance 1 • Whilst the types of factors we have just been examining may initiate AN, what factors seek to maintain it? • AN is widely regarded by psychiatrists as being highly treatment resistant (egosyntronic), indeed a diagnostic feature of the disease is that sufferers themselves may deny there is a problem • So what factors might keep a person on a near starvation diet and how does it affect their life? 18 18 Maintenance 2 • 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 19 19 Maintenance 3 • So what biological factors are at work to keep this highly maladaptive fasting behaviour going? – 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) 20 20 Outcome & Treatment of AN • 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 • Why? - Bread & butter (stuck under table), hair conditioner (to induce vomiting), water loading & weights (prior to weighing) are examples – 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 21 21 Bulimia nervosa (BN) • First medically described by Russell in 1973, but anecdotal accounts date back 100ʼs of years • Clinical definition: • 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 • Specification: • Full or partial remission, and degree of severity (defined by frequency of inappropriate compensatory behaviours) 22 22 Prevalence & medical consequences • Prevalence – – – – 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 • Medical consequences – Benign relative to AN and includes • • • • Dental erosion Swelling of the parotid glands (with characteristic ʻChipmunkʼ face) Electrolyte abnormalities Rare complications from oseophageal tear/gastric rupture • An example – Tall and normal weight for height at 18. Entered teacher training college, but felt unhappy and started dieting. First enforced vomit after Xmas lunch. Cycles of overeating/vomiting continued for 3 years. Vomiting became routine, like ‘having a cigarette’ or ‘cleaning teeth’. Used laxatives where social restriction prevented vomiting. 23 23 Cause • 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 24 24 Cause • 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 ʻquick weight lossʼ (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 25 25 Maintenance • 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 may be predispositions - it is hard to tell as prospective studies are rare 26 26 Prognosis & Treatment • Prognosis • 50% appear to make a full recovery • 30% experience occasional relapse • 20% exhibit chronic BN • Treatment – 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 27 27 Conclusion • AN and BN are the most commonly encountered eating disorders • Both have complex causation, which is still not fully understood • Whilst BN is relatively amenable to treatment AN is difficult to treat and has one of the highest mortality rates of any psychiatric condition 28 28