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Audio-Digest FoundationFamily Practice


Volume 55, Issue 10
March 14, 2007

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CONSEQUENCES OF TOO LITTLE AND TOO MUCH FOOD

EATING DISORDERS Shirah Vollmer, MD, Associate Clinical Professor of Psychiatry and Family Medicine, David Geffen School of Medicine at the University of California, Los Angeles
Eating disorders: disorder of mind that affects body; anorexia nervosa—affects 0.5% to 1.0% of population; 10:1 ratio of women to men; bulimia nervosa—more common than anorexia; 1% to 3% of population; more common in women; binge eating disorder (BED)—affects 1% to 4% of population; similar rate in women and men; new to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV); diagnosis questionable

Anorexia
Anorexia: definition—<85% of ideal body weight; amenorrhea for 3 mo; psychopathologic attitude—belief that every morsel of food harmful; obsession with food but no desire to eat; premenarchal anorexia—anorexia in girls 10 yr of age uncommon; onset usually insidious; fear of changes in body shape and of sexual development; way to avoid sexuality and interaction with opposite sex; sometimes associated with sexual abuse; anorexia in boys—uncommon; can be caused by preoccupation with certain weight (eg, wrestlers) or excessive exercise
Distorted body image: “every time they look in the mirror, they’re seeing a different thing than what other people are looking at”; positive responses from others about weight loss may encourage patients to lose more weight (“they don’t know when to stop”; patients continue to see overweight image in mirror)
Types of anorectics: restricting—excessive dieter; eats 500 to 600 calories daily; binge eating and purging—relies on purging; eats small amounts and purges; aversion to food leads to overwhelming urge to purge
Etiology: psychodynamic view—association with family relationships; history of sexual abuse; means of compensating for self-defects; classic anorectic from perfectionistic family (eg, does well in school) but never feels self-confident or valued; unable to express feeling of worthlessness and stops eating to gain attention; family therapy useful
Psychologic processes: isolation; avoidance of social activities that involve food; depression; alienation from family (family often does not take responsibility); lack of preparation to cope with adulthood (onset commonly at age 13-14 yr or before going to college); anxiety; fear of sexuality; attitudes of boys and girls in grades 5 to 8—42% wanted to lose weight; 41% thought they looked fat; 33% exercised to lose weight; 31% had dieted; 23% had fear of eating due to weight gain; 16% reported binge eating; 4% vomited to lose weight; 5% used diuretics, diet pills, or laxatives; difficult to distinguish eating disorder from substance abuse (eg, cocaine, ipecac syrup)
Heritability: positive family history of eating disorder in 29%; dizygotic twins have 7% concordance rate, monozygotic twins, 53%; greater degree of affective illness in first-degree relatives (environmental?); no significant relationship between serotonin genes and eating disorders; uncoupling protein (UCP-2/UPC-3 gene) or estrogen gene may be related; “basically we don’t know”; activation of genes during puberty may predispose people to eating disorders
Progression of disease: self-starvation; dieting begins after comment about weight (“you’ve put on a few”); pubertal changes raise concerns about weight; restriction begins subtly (eg, with desserts); warning signs—obsession with food; excessive exercise; amenorrhea or irregular menstruation; fainting or dizziness; perfectionist attitude; tooth decay from vomiting
Clinical description: onset at puberty or before leaving home for college (17-18 yr of age); personality traits include serious-minded, intense, high standards, sensitive and empathic, fear of criticism, obsessive, overcompliant and duty- bound, limited autonomy, feelings of helplessness, overly rigid (“I can’t eat any carbs”); denial of illness; adolescents “very guarded”; physiologic changes—decreased heart rate, respiratory rate, and body temperature (cold intolerance); increased obsession with food; episodic binging; irritability and anger; depression, anxiety, tiredness; decreased libido; decreased concentration; electrocardiographic changes include low voltage and arrhythmias (particularly from ipecac syrup); low blood pressure (BP); heart failure; anemia; delayed gastric motility (refeeding process complicated); osteoporosis (long-term consequence of lack of estrogen); hypothyroid state
Differential diagnosis: pituitary tumors, gastrointestinal (GI) disorders, and malabsorption syndromes less common than anorexia; conversion disordereg, patient’s anxiety converts to belief he or she cannot swallow; no desire to be thin; no body image distortion; hypomania—patients have high mental energy and creativity, compared to anorectic patients; schizophrenia—delusion, eg, belief that bug in throat prevents swallowing
Treatment: some patients improve without intervention; developing relationship with patient difficult and takes time; address nutritional needs (eg, recommend calcium) and psychologic needs; engage patient in treatment; psychiatric hospital (patients given 3 meals per day); behavioral program that rewards patients for eating (“they get more privileges the more they eat”)
Prognosis: 5% to 20% of patients die; 6% commit suicide; deaths occur after 7 yr (prognosis worse after 5-7 yr)

Bulimia
Bulimia: recurrent binge eating—eating 1200 calories in 1 sitting (usually high carbohydrate items, eg, cookies) 2 times per week for 3 mo; eating alone; secret habit; later onset than anorexia; extreme concern with weight and shape; may be habit; skipping meals leads to hunger and binging; most bulimics normal weight; borderline personality; affective instability; impulse-control disorder; socially outgoing; comorbid substance abuse common; cycle of binge eating—1) low self-esteem; overconcern about shape and weight; 2) dieting leads to hunger, resulting in binge eating; 3) compensatory purging with vomiting, laxatives, or diuretics
Physical examination: Russell’s sign (teeth marks on hand); erosion of dental enamel; large parotids; electrolyte imbalance (hypokalemia; bupropion [Wellbutrin] contraindicated due to high risk for seizure); gastric rupture; cardiomyopathy; cardiac arrhythmias; relapse; psychologic morbidity; may be lifelong disorder (some patients do not want treatment)
Binge eating disorder: recurrent binge eating for 6 mo; eating rapidly until uncomfortably full; eating when not hungry; patients not responsive to bodies; eat to self-soothe and to deal with anxiety
Eating disorder not otherwise specified: sometimes restrict, sometimes binge, and sometimes vomit; do not meet criteria for anorexia or bulimia
Treatment: fluoxetine (Prozac) approved by Food and Drug Administration (FDA) for bulimia; effective 40% to 50% of time; decreases binging; cognitive behavioral therapy—probably best approach; helps patients become aware of motivation and feelings experienced; self-monitoring report (eg, journal) helpful; explain that behavior prompted by psychologic trigger (helps patients regain control); discuss physical consequences of vomiting, ineffectiveness of vomiting, and adverse effects of dieting; thought-recording and developing rational thoughts
MORBID OBESITY Richard E. Pratley, MD, Professor of Medicine, University of Vermont College of Medicine, Burlington, and Director, Diabetes and Metabolism Translational Medicine Unit, Fletcher Allen Health Care, Burlington
Definitions of obesity: chronic, lifelong, genetically related, life-threatening disease with highly significant medical, psychologic, social, physical, and economic comorbidities; condition of abnormal or excessive fat accumulation in adipose tissue to extent that health may be impaired; complex multifactorial chronic disease that develops from interaction between genotype and environment; understanding of how and why obesity develops incomplete, but involves integration of social, behavioral, cultural, physiologic, metabolic, and genetic factors
Body mass index (BMI): weight (kg)/height (m2 ); normal—BMI <25; overweight—BMI 25 to 30; obese—BMI >30; BMI >40 classified as obese class III (morbid obesity; risk severe); recognize BMI as “index” of obesity; 64% of population overweight or obese; obesity disproportionately affects women, minorities, and people of low income; morbid obesity 15% in black women, 6% in Hispanic women, 5% in white women; 4% of population has morbid obesity
Conditions associated with obesity: pulmonary disease; nonalcoholic steatohepatitis (NASH); gallbladder disease; gynecologic abnormalities; arthritis; skin problems; gout; lobitis; cancers (breast, uterus, colon, esophageal, pancreas); stroke; dyslipidemia; high risk for diabetes, hypertension, insulin resistance, and heart disease; asthma; gastroesophageal reflux disease (GERD); incontinence; depression; nephropathy; poor physical functioning (decreased activities of daily living [ADL]); psychologic consequences—stigma of overweight (negative response from others); shame; guilt; self- blame; social and economic consequences—completing less school; less likely to be married; less income
Risk for comorbidities: type 2 diabetes—42-fold increase in relative risk of developing diabetes in men with BMI >35, 93-fold increase in women; hypertension—risk 2 to 3 times higher in obese men, 2 times higher in women; high blood cholesterol—50% increased risk; coronary risk factors include low high-density lipoprotein (HDL; 3 times higher risk); 10% of morbidly obese men diabetic (higher in women), 10% have gallbladder disease (higher in women), 14% have coronary heart disease, 36% have high blood cholesterol, 66% have high BP, 10% have osteoarthritis; asthma—study following children 11 yr of age found 5- to 7-fold higher incidence of asthma in obese girls; disability— among women 50 to 69 yr of age with BMI >35, 40% report poor health, 20% report limitations in ADL, and 45% report health and weight affect ability to work; disability age-dependent, but amplified in obese patients
Causes of death in United States: obese men at 3-fold higher risk of dying from cardiovascular disease, 2-fold higher risk in women; heart disease, cancer, and stroke among leading causes of death in United States; diabetes; tobacco smoking; poor diet; lack of exercise
Costs: in 1998, direct costs of type 2 diabetes $53 million; direct costs of obesity $51 million; current total annual cost of obesity and diabetes $120 to $130 billion; costs include medications, physician visits, hospitalizations, time off from work, and disability
Pathophysiology: fat cells produce leptin, cytokines, inflammatory factors, elements of complement system, acute- phase reactants (eg, C-reactive protein), and proteins that affect glucose metabolism and hemostasis; BP regulation, renin-angiotensin system, and lipid metabolism dysregulated in obesity; fat cells attract monocytes that differentiate into macrophages that contribute to proinflammatory state
Benefits of weight loss: insulin sensitivity—moderate and mild weight loss (2%-7%) associated with improvement; greater improvement with greater weight loss; insulin sensitivity can be normalized in many patients with substantial weight loss; reduces risk of developing diabetes; diabetes prevention—walking 30 min/day for 5 days/week recommended; study saw weight loss of 3.5 to 7.0 kg and 58% reduction in new cases of diabetes in high-risk group; lipids— weight loss beneficial for lowering total cholesterol, low-density lipoprotein (LDL), and triglycerides; weight loss raises HDL; weight loss lowers BP; in patients with diabetes, 5% reduction in weight associated with lowering hemoglobin A1c, BP, total cholesterol, and increase in HDL cholesterol (improving triglycerides may require greater weight loss)
Management: system must support patients; clinical information, decision support, and self-management support needed; support from community; education about obesity; supportive environment (eg, chairs that have no arms in waiting room; larger gowns, BP cuffs, and scales); use educational materials; be empathic, respectful, and supportive
Initial office evaluation: focus on weight history, eating and activity habits, triggers, and medications; calculate BMI; stratify risks; determine whether patient ready to change; initiate treatment plan involving other professionals; discuss goals and expectations; arrange follow-up and support; evaluate and encourage methods that were successful in past; medications that cause weight gain include psychotropic agents, atypical antipsychotics, and diabetes drugs; HIV associated with weight gain (peculiar pattern of distribution); measure waist circumference; identify risks (eg, coronary heart disease) and other obesity-associated diseases; look at cardiovascular risk factors, level of physical activity, and diet; ask about patient’s view on weight (eg, “do you think your weight is affecting your health?”)
Therapy: goals—prevent further weight gain; encourage healthy rather than “ideal” body weight; help patients accept slow incremental progress (loss of 1-2 lb per week); maintenance long-term goal; choosing therapy—diet, exercise, and behavioral therapy for all patients; pharmacotherapy and surgical treatment appropriate for patients with comorbidities and increasing BMI; weight loss cannot be achieved without restriction of energy intake; exercise painful and difficult for morbidly obese patients (start with slow interventions); encourage exercising (eg, walking) for 30 to 45 min daily; consider referral for behavioral therapy; drugs difficult to tolerate; pharmacologic therapy should not be tried unless patient committed to diet and exercise; evaluate patients to determine whether pharmacotherapy appropriate; orlistat—fat blocker; study showed, after 4 yr, weight loss benefit of 2.5 kg more than with diet and exercise program alone; side effects include fatty oily stools; to be released over-the-counter; sibutramine—nonselective monoamine blocker; blocks uptake of serotonin, norepinephrine, and dopamine; causes 3.5 to 4.0 kg greater weight loss after 1 yr, compared to placebo; side effects include headache, dry mouth, constipation, insomnia, dizziness, and hypertension (monitor BP); combining medication, behavioral modification, meal replacement, and exercise can result in 15% to 20% weight loss

Educational Objectives

The goal of this program is to educate the listener about eating disorders and the management of obesity. After hearing and assimilating this program, the participant will be better able to:
1. List criteria for diagnosis of anorexia nervosa.
2. Describe psychologic and physiologic changes in patients with anorexia and bulimia.
3. Use cognitive behavioral therapy to help patients control binge eating and purging.
4. Identify risks in overweight and obese patients.
5. Counsel patients about lifestyle modification and long-term goals of losing weight.

Suggested Reading

American Dietetic Association: Position of the American Dietetic Association: Nutrition intervention in the treatment of anorexia nervosa, bulimia nervosa, and other eating disorders. J Am Diet Assoc 106:2073, 2006; American Psychiatric Association: Treatment of patients with eating disorders, third edition. American Psychiatric Association. Am J Psychiatry 163:4, 2006; Blackburn G: Effect of degree of weight loss on health benefits. Obes Res 3 Suppl 2:211s, 1995; Bowers WA: Basic principles for applying cognitive-behavioral therapy to anorexia nervosa. Psychiatr Clin North Am 24:293, 2001; Casiero D et al: Cardiovascular complications of eating disorders. Cardiol Rev 14:227, 2006; Dattilo AM et al: Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis. Am J Clin Nutr 56:320, 1992; Ditschuneit HH et al: Lipoprotein responses to weight loss and weight maintenance in high-risk obese subjects. Eur J Clin Nutr 56:264, 2002; Fairburn C: Overcoming Binge Eating. New York: The Guilford Press; 1995; Foster GD et al: What is a reasonable weight loss? Patients' expectations and evaluations of obesity treatment outcomes. J Consult Clin Psychol 65:79, 1997; Halmi KA: The multimodal treatment of eating disorders. World Psychiatry 4:69, 2005; Kondo DG et al: Eating disorders in primary care. A guide to identification and treatment. Postgrad Med 119:59, 2006; Mertens IL et al: Overweight, obesity, and blood pressure: the effects of modest weight reduction. Obes Res 8:270, 2000; Padwal R et al: Long-term pharmacotherapy for overweight and obesity: a systematic review and meta-analysis of randomized controlled trials. Int J Obes Relat Metab Disord 27:1437, 2003; Pope HG Jr et al: Binge eating disorder: a stable syndrome. Am J Psychiatry 163:2181, 2006; Siegel M: Surviving an Eating Disorder. New York: HarperCollins Publishers, Inc.; 1997; Stevens VJ et al: Long-term weight loss and changes in blood pressure: results of the Trials of Hypertension Prevention, phase II. Ann Intern Med 134:1, 2001; Wadden TA et al: Benefits of lifestyle modification in the pharmacologic treatment of obesity: a randomized trial. Arch Intern Med 161:218, 2001; Waller G et al: The psychopathology of bulimic women who report childhood sexual abuse: the mediating role of core beliefs. J Nerv Ment Dis 189:700, 2001; Wing RR et al: Long-term effects of modest weight loss in type II diabetic patients. Arch Intern Med 147:1749, 1987; Wirth A et al: Long-term weight loss with sibutramine: a randomized controlled trial. JAMA 286:1331, 2001; Zerbe K: The Body Betrayed: A Deeper Understanding of Women, Eating Disorders, and Treatment. Carlsbad, CA: Gurze Books; 1993.

Faculty Disclosure

In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, the faculty reported nothing to disclose.


Dr. Vollmer spoke in Beverly Hills, CA, at the 33rd Annual UCLA Family Practice Refresher Course, presented June 5- 9, 2006, by the David Geffen School of Medicine at the University of California, Los Angeles. Dr. Pratley was recorded in Burlington, VT, at the 32nd Annual Vermont Family Medicine Review Course, presented June 13-16, 2006, by the University of Vermont College of Medicine. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.


Reproduction of this summary in whole or in part in any form or medium without express written permission is prohibited.

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