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Eating Disorders and Substance Abuse. November 8, 2006. James M. Greenblatt, M.D. Chief Medical Officer. Walden Behavioral Care. Anorexia – A Life Threatening Illness.
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Eating Disorders and Substance Abuse November 8, 2006 James M. Greenblatt, M.D. Chief Medical Officer Walden Behavioral Care
Anorexia – ALife Threatening Illness • Anorexia Nervosa has the highest mortality rate of any psychiatric disorder. The most common causes of death are complications of starvation and suicide. • The mortality rate at five years is 5%, increasing to 20% at 20 years F/U (APA 2000) • The highest predictor of mortality is?
Eating Disorders and Substance Abuse • One of the strongest and most consistent predictors of fatal outcome for patients with Anorexia Nervosa was severity of alcohol abuse during follow-up!
The highest rates of suicide attempts are reported among bulimic individuals who have co-morbid alcohol abuse (54%). (Eating Disorders 2002; 10:205)
Eating Disorders and Substance Abuse The National Center on Addiction and Substance Abuse (CASA) • between 30 and 50% of individuals with Bulimia Nervosa abuse or are dependent on drugs or alcohol • 12-18% with Anorexia Nervosa abuse or are dependent on drugs or alcohol • compared with 9% of the general population
Eating Disorders and Substance Abuse • 35% of people who abuse drugs and alcohol have an eating disorder, compared to 3% of the general population.
Similarities Between ED and SUD • Life Threatening • Chronic Relapsing Course • Long Term • Compulsiveness • Ritualistic Behaviors • Resistant to Treatment • Begin with experimentation; only a small percentage lose control • Lead to chronic compromised nutritional and medical complications
Eating Disorders and Substance Abuse Drugs that Decrease Eating Alcohol Amphetamine Cocaine Diet Pills Caffeine Nicotine Drugs that Increase Eating Marijuana
Eating Disorders and Substance Abuse Drugs that Increase Purging • Alcohol • Caffeine • Ipecac • Laxatives • Diuretics
The lack of awareness and understanding of the link between eating disorders and substance abuse has led to limited treatment options for patients. Despite their high rates of co-occurrence few treatment programs exist that address both eating disorders and substance abuse simultaneously and effectively.
While substance abuse and eating disorders have much in common, their treatment is based on very different philosophical approaches.
DIFFERENCES – RECOVERY Alcohol/Drugs Restrict or abstain from substance. Abstinence – external imposed structures of control. Eating Disorders Food as ally to sustain life. Inner Strengths with little external controls. CONTROL
Treatment of one disorder often leads to exacerbation of the other. Is it not uncommon for patients being treated for bulimia to increase the use of alcohol or drugs as they decrease binging and purging. Likewise, patients might find it harder to curb a binge eating disorder or a restrictive eating disorder after substance abuse treatment.
A majority of young woman diet at some point in time yet only a small fraction develop eating disorders. Why?
Misplaced Blame • Eating disorders have traditionally been viewed as psychiatric illnesses that are strongly influenced by social pressures towards thinness. • Recent research suggests a substantial influence of genetic factors on the development of an eating disorder. • Family Twin and molecular genetic studies support substantial genetic influences on eating disorders
Family Studies • 7 – 12x increase in the prevalence of Anorexia and Bulimia in relatives of eating disorder patients • Personality traits & genetic susceptibility Perfectionistic, Obsessional, Meticulous
Twin Studies • 58 – 76% of the variance in the liability to AN and 54 – 83% of the variance in the liability to BN can be accounted for by genetic factors. • No genetic factors in weight preoccupation and eating pathology in 11 year old twins • 52 – 57% variance in eating pathology in 17 year old twins
Twin Studies Prevalence, Heretability and Prospective Risk Factors for Anorexia Nervosa 31, 406 twins born between 1935-1958 Arch Gen Psychiatry. 2006;63:305-312
Twin Studies • No genetic factors in weight preoccupation and eating pathology in 11 year old twins • 52 – 57% variance in eating pathology in 17 year old twins
Twin Studies • 11 year old twins were divided into a pre- and post-pubertal group • Genetic factors accounted for 0% of variance in weight preoccupation and overall eating pathology in pre-pubertal twins • Genetic factors accounted for 26 – 35% of the variance in post-pubertal twins
The Genetics of Eating Disorders • Activation of the heritability of eating pathology may be mediated by hormones in puberty. • Cultural attitudes toward thinness have relevance to the psycho-pathology of eating disorder, but they are unlikely to be sufficient to account for the pathogenesis of these disorders
Puberty and Onset of Anorexia Nervosa “My childhood was perfection. It was full of vacations and love and family time. Something must have been lacking that no one was aware of. Something must have gone wrong. Maybe it was puberty.”
Genetics Candidate genes for AN has been found on chromosome 1 in an area that controls Serotonin and opiate receptor genes. A susceptibility gene for BN was recently found on chromosome 10. Both AN ad BN are complex and likely caused by multiple genes.
Serotonin Metabolites • Under weight malnourished Anorexia Nervosa patients have significant decreased levels of CSF 5-H1AA • Recovered Anorexia Nervosa patients have increased CSF 5-H1AA • PET imaging has shown recovered Anorexia Nervosa patients have changes in 5-HT1A and 5-HT2A receptors actively consistent with increased serotonin activity
Tryptophan Availability and Serotonin Synthesis Rats fed a corn diet for 5 weeks had reduced plasma tryptophan and reduced brain tryptophan serotonin levels Wurtman (1971)
Starvation as a form of Self Medication • Starvation produces a reduction of extracellular 5-HT concentration in Anorexia Nervosa
Starvation as a form of Self Medication Patients with Anorexia may discover that restricted eating by its effects on availability of plasma tryptophan as a means by which they can crudely reduce extracellular 5-HT concentrations and thus briefly reduce a dysphoric state Refeeding consistently results in depressive symptoms and suicidal ideation is not uncommon
Genetics of Anorexia Nervosa • Individuals with Anorexia Nervosa may have altered sequence and gene polymorphisms for 5-HT receptors • Anorexia Nervosa patients may have a trait related increase in serotonin neurotransmission that occur in the premorbid state and persists after recovery • Increased 5-HT neurotransmission contributes to core symptoms of obsessionality, perfectionism, harm avoidance and anxiety
“Pharmacotherapy is …ancillary in Eating Disorder Treatment.” S. Crow, MD President Academy for Eating Disorders (2006)
Psychotropic Medication in the Treatment of Eating Disorders
Comorbidity of Anorexia Nervosa • The lifetime rates of psychiatric comorbidity among patients with Anorexia are approximately 80% • Affective disorders • Anxiety disorders • Substance use disorders • Personality disorders
Comorbidity of Bulimia Nervosa • The lifetime rates of psychiatric comorbidity among patients with Bulimia are approximately 83% • Affective disorders • Anxiety Disorder • Substance Abuse • ADHD • Personality Disorder
Bulimia Nervosa: A Chronic Persistent Illness Approximately 50% of bulimic patients including those who have been treated continue to show eating disorder features on long term follow up.
Bulimia Nervosa DrugFindingsEvidence Fluoxetine ↓BE/P + + + SSRI’s Fluoxetine Prevent Relapse + Fluvoxamine No evidence o Imipramine ↓BE/P + + TCAs Desipramine ↓BE/P + + Amitriptyline +/- ↓BE/P + MAOI’s ↓BE/P + +
Treatment Recommendations • Antidepressants: SSRI’s: Higher than “usual” antidepressant dosage may be required. - Prozac 60mg/day considerably more effective than 20mg/day for reducing binge eating behavior and vomiting frequency. - Celexa 40-60mg, Zoloft 100 – 200 mg. - The only medicine approved by the FDA for BN is Fluoxetine.
Persistence and Patience • Study of 36 Bulimic Patients • 26 Patients who tried 2nd or 3rd antidepressants - 17 patients 65% remission on follow-up - 10 patients refused another med trial
Binge Eating Disorder – Pharmacologic Treatment Celexa 20-60 mg x 6 weeks Prozac 20-80 mg x 6 weeks Luvox 50-300 mg x 9 weeks Zoloft 50-200 mg x 6 weeks All medication resulted in significant reduction in binge eating and body weight.
Augmenting Agents • Antidepressants alone rarely lead to complete remission of Bulimic symptoms. 1. T3 25mg/day 2. Topamax – 75-200mg/day 3. Lithium – below therapeutic blood levels 4. Naltrexone – 200 mg 5. Ondonsetron – (Zofran) 6. Inositol – 12-18 gms 7. Strattera
Topamax • Most patients tolerate Topamax without difficulties. • Common side effects include: • Sedation, paresthesia, cognitive impairment • Side effects avoided by • Titrating dose slowly • May need only 50-75 mg • Average dose 100-200 mg
Topamax McElroy et al., 2003, Am J Psychiatry • 14 week placebo controlled study • 61 patients with BED • Topamax median dose 212 mg/day (50-600 mg) • Significantly reduced binge eating frequency and body weight vs placebo. • 64% of patients on Topamax vs 3% on placebo.
Bulimia • Bulimic patients with comorbid disorders may need a rational systematic regimen of multiple psychotropic medications. • Treatment failures usually result from not treating all comorbid psychiatric disorders.
Bulimia Nervosa/Binge Eating Disorder • Genetic, biological and psychosocial factors involved • Psychosocial Interventions critical component of treatment • Pharmacological treatments appear effective – although little long term data available
Multimodal Treatment for Bulimia Nervosa is Effective! 1. Psychopharm 2. Nutrition 3. Psychologic Treatments (CBT)
Psychopharmacology of Anorexia Nervosa
Anorexia Nervosa THE LITERATURE……… • Medications are used after weight restoration and normalized eating behaviors to maintain weight and treat Co-Morbid Psych illness