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Anorexia Nervosa Tran Huynh, Kristina Nguyen, Jake McGrane, Taylor Minckley Video Importance 95% of those who have eating disorders are between the ages of 12 and 25.8 What is Anorexia Nervosa • DSM-IV Criteria o Intense fear of gaining weight o Distorted view of body o Loss of menstrual cycle o Body weight 85% or below normal for age/ height • 2 Types: o Restricting o Binge/Purge Statistics • Average American woman: o 5’4” and 140 lbs • Average American model: o 5’11” and 117 lbs • 80% American women dissatisfied with • their appearance Highest mortality rate of psychiatric disorder Behaviors and Symptoms • Behaviors o Unusual eating habits, rituals o Compulsive, punishing exercise • o Cycles of hyperactivity and fatigue Symptoms o Isolation from friends/family o Dry skin, shallow complexion o Brittle hair, nails, purple nail beds o Sensitivity to/intolerance of cold Anorexic personalities • Exhibit high levels of: o low self-esteem o obsessionality o perfectionism o anxiety o harm avoidance o drive for thinness o dietary preoccupation Clicker question Based on the behaviors, symptoms, and personalities of patients with anorexia nervosa, what do you think would be a comorbid psychiatric disorder of anorexia? A) Schizophrenia B) Insomnia C) Obsessive-compulsive disorder D) Munchausen Syndrome Comorbidity • Depression • Phobias • Anxiety disorder • Obsessive-compulsive disorder • Panic attacks • Post-traumatic stress disorder • Substance abuse • Body dysmorphic disorder Models of Anorexia Through Time 1300's - Anorexia was motivated by religious conviction or illness, often confabulated with consumption St. Catherine of Siena (1347-80) 1689 - Dr. Richard Morton gives first case studies. He described AN as "a nervous consumption" 1874 - Sir William Gull publishes "Anorexia Nervosa", coining the term. He prescribed bicholoride of mercury, syrup of iodide of iron, and citrate of quinine Catherine of Siena died at the age of 33. Catherine herself described her inability to eat as an infermita (illness). Eating Disorders in the 20th Century 1940's1973 - Freudian psychoanalytic interpretations. Origins of AN were sexual Hilde Bruch's working Eating Disorders considered the seminal work on AN. - Identified three pathognomonic psychological factors in AN 1. Disturbance of Body Image 2. Disturbance of Perception 3. Sense of Ineffectiveness - Also associates AN with schizophrenia - Created the idea of the "anorexigenic family" - On the surface, family life is perfect, BUT underneath the family was riddled with secrecy, and followed a similar pattern in case studies The Role of the Media 1980s - The rise of feminism brought attention to body image 1940 Ideals of body image in the media changed greatly between and 1970. 1960's 1940's Laurette Luez 1950's Bunny Yeager Twiggy The Role of the Media Whilst women models were getting thinner,the incidence of anorexia was increasing This supported the theory that AN was a sociocultural phenomenon. The fact that dancers and models have the highest prevalence of AN would appear to support this assertion. Clicker question What do you think is a possible predisposition to anorexia nervosa? A) Environmental factors B) Personality traits C) Neurotransmitters D) All of the above Predisposition • Genetic factors o ~50-80% heritability rate o not linked to single gene o possible linkage at chromosome 1, 2, 13 • Personality traits o obsession o perfectionism o finding little rewards in life • Neurotransmitter system o dopamine and serotonin Dopamine and ABA • Involved in major symptoms of AN o repulsion to food o weight loss o hyperactivity o menstrual abnormalities (amenorrhea) o distortion of body image o OCD behavior • Non Selective DA antagonist = reduces ABA behavior o cis-flupenthixol Reward Pathway: Dopamine • Disruption = sensitization/desensitization o reinforces behavior/addiction • Food restriction = heightened dopamine response o Sensitive to dopamine • AN: Significantly increase brain reward response in orbitofrontal cortex o Limbic system: Decision making Dopamine: Brain Region • Ventral Striatum • Midbrain • Insula • Anterior Cingulate Cortex • Orbitofrontal* o Impulse Control o High food-intake control • Increase in brain regions = high ability to discriminate rewards Dopamine: Animal Studies • Does not affect preference, but desire o "wanting" not "liking" • Damage to dopamine innervation of forebrain = no hedonic effect, only motivational signals Recovered AN Studies • Reduced D2/D3 receptor binding o Linking to Ventral Striatum • Dopaminergic Drugs promote weight loss o methylphenidate o antidepressants bupropion Serotonin: 5-HT pathway • 5-HT pathway o modulates appetite, body weight regulation o motor activity o mood o obsessive compulsive behavior (OCD) • 5-HT2A - restricting o link between OCD and AN • 5-HT1A - bulimic o harm avoidance AN and the Brain -A cross-sectional and follow-up voxel-based morphometric MRI study in adolescent anorexia nervosa (2009) +Josefina Castro-Fornieles, et. al. -12 children & adolescents -9 control subjects -Follow up test 7 months later (after AN weight recovery) -Weight recovery procedure -MRI procedure +MRI volume calculation +VBM analysis 2009 Results (VBM MRI) 2009 Results (VBM MRI) cont'd The Comprehensive Model! The Neurobiological Substrate Noradrenergic Dysregulation - Noradrenaline is a neurotransmitter that has multiple functions, including: 1. Regulating sympathetic arousal 2. The regulation of cerebral blood flow 3. The mediation of cortical neuroplasticity - Premorbidly, there is increased noradrenergic activity due to genetic predisposition - This leads to an increased resting sympathetic tone, which increases the likelihood of high-arousal and highsensitivity states - The result ANXIETY However, Once Dieting Starts... Early Stages (days to weeks): There is a depletion of noradrenaline and its precursors. This reduces noradrenergic activity, which reduces stress and reinforces dieting. Medium Term (weeks to months): The noradrenergic system adjusts to lack of neurotransmitter, and anxiety re-emerges. After Refeeding: When the patient begins eating, there is a repletion of noradrenaline, and the activity of the noradrenergic system increases, leading back to anxiety and re-starting the cycle. Chronic AN: Eventually, if AN persits and refeeding is resisted, over time the noradrenergic system becomes so severely compromised that the capacity for anxiety is lost, and the patient often will become depressed and apathetic. Impaired Neuroplasticity - Dysregulation of any neurotransmitter system can impair cortical neuroplasticity. - Specifically, impairment of neuroplasticity in the insula has been implicated in AN. - Reduced capacity to respond to demands for neuroplasticity during puberty, the cortical pruning of adolescence, and the effects of dieting on neuromodulatory system leads to AN Insula Dysfunction -The insular cortex is involved with several functions 1. Interoceptive Awareness - Pain, temperature, itch, tickle, sensual touch - Provides link between perceptive and cognitive brain regions 2. Bridge between left and right hemispheres 3. Social emotion and the sense of self. -Sensory homunculi - Every person has somatotopic representation of a body map in their mind. This is called a sensory homunculi. Sensory homunculi have three overlapping components. 1. Primary (anterior parietal lobe), Sensory and Perceptual 2. Secondary (anterior parietal lobe), Interpretive 3. Tertiary (insula), Integration and meaning - Each homunculus provides "representational space" for each body part - These homuncular representations change throughout life due to Neuroplasticity! Bringing it all together - Puberty is the most crucial time for neuroplascity. - The growth spurt experiences creates competition -In normal children, neuroplasticity will allow the insula to create a homunculi that represents their new bodies post-puberty. In AN, the insula is dysfunction due to impaired neuroplasticity created through noradrenergic dysregulation. Thus, a major discrepancy between actual body size and the homunculi occurs, creating a distorted body image (DBI) -The parts of the body most commonly misrepresented in AN are those parts that grow fastest in puberty and have the least volume in the somatotopic map -Given that puberty has an earlier onset and shorter duration in girls vs boys, this could explain why prevalence of AN is higher in girls vs boys. Works Cited: Bruch, Hilde. "Anorexia Nervosa: Therapy and Theory." The American Journal of Psychiatry 139.12 (1982): 1531-538. PsychiatryOnline. Web. 21 Nov. 2012. <http://www.neuro.psychiatryonline.org/data/Journals/AJP/3299/1531.pdf>. Bruch, Hilde. "Family Transactions in Eating Disorders." Comprehensive Psychiatry12.3 (1971): 238-48. SciVerse. Web. 22 Nov. 2012. <http://www.sciencedirect.com/science/article/pii/0010440X71900216#>. Castro-Fornieles, J., N. Bargallo, L. Lazaro, S. Andres, C. Falcon, M. Plana, and C. Junque. "A Cross-sectional and Follow-up Voxel-based Morphometric MRI Study in Adolescent Anorexia Nervosa." Journal of Psychiatric Research 43.3 (2009): 331-40. Print. Castro-Fornieles, Josefina, Xavier Caldú, Susana Andrés-Perpiñá, Luisa Lázaro, Nuria Bargalló, Carles Falcón, Maria Teresa Plana, and Carme Junqué. "A Cross-sectional and Follow-up Functional MRI Study with a Working Memory Task in Adolescent Anorexia Nervosa." Neuropsychologia 48.14 (2010): 4111-116. Print. Lask, Bryan; Frampton, Ian. Eating Disorders and the Brain. Wiley, 2011. 6 December 2012 < http://lib.myilibrary.com?ID=317799> Lucas, Alexander R., C. M. Beard, Michael O'Fallon, and Leonard T. Kurland. "50-Year Trends in the Incidence of Anorexia Nervosa in Rochester, Minn.: A Population-Based Study." American Journal of Psychiatry 148.7 (1991): 917-22. Web. 26 Nov. 2012. <http://www.focus.psychiatryonline.org/data/Journals/AJP/3558/917.pdf>. Schmidt, Ulrike. "Aetiology of Eating Disorders in the 21st Century. New Answers to Old Questions." European Child and Adolescent Psychiatry 12.Suppl 1 (2003): 30-37. Web. 21 Nov. 2012. <http://link.springer.com/article/ 10.1007%2Fs00787-003-1105-9?LI=true>. The Anorexigenic Family The Idea 1. Feeding in the human infant ALWAYS demands the cooperation of another person. 2. The interaction between infant and food giver is accompanied by emotional and affectional experience with surround eating and food intake forever 3. Non-normal interaction could lead to later inability to characterize hunger correctly, leading to disturbances in perception.