Eating Disorder and Obesity
Eating Disorders: Involve persistent disturbances in eating behavior that impair health and daily functioning.
Common disorders: Anorexia nervosa, Bulimia nervosa, Binge-eating disorder.
Obesity: Not classified as a psychiatric disorder in the DSM but is rising at alarming rates and contributes to significant morbidity and mortality.
Connection: Disordered eating patterns often coexist with obesity.
Anorexia Nervousa
Definition: Not simply a “lack of appetite” but a relentless pursuit of thinness leading to a significantly low body weight.
DSM-5 Criteria:
A: Restriction of energy intake resulting in significantly low body weight.
B: Intense fear of gaining weight or becoming fat.
C: Disturbance in body weight/shape perception.
Subtypes:
Restricting Type: Extreme limitation of food intake.
Binge-Eating/Purging Type: In addition to restriction, includes bingeing and/or purging behaviors.
Bulimia Nervousa
Definition: Characterized by recurrent binge eating followed by inappropriate compensatory behaviors.
DSM-5 Criteria Highlights:
Recurrent episodes of binge eating (eating an unusually large amount of food in a short time with a loss of control).
Inappropriate compensatory behaviors (self-induced vomiting, misuse of laxatives, fasting, or excessive exercise).
Occurs at least once a week over 3 months.
Clinical Notes:
Typically, individuals are within a normal weight range or slightly overweight.
Often accompanied by feelings of shame and guilt.
Comparing Eating Disorder
Anorexia Nervosa:
Weight: Markedly low.
Atypical anorexia: despite extreme weight loss, bmi remains in the “normal” range
Behavior: Restrictive intake (or binge/purge in one subtype).
Body Image: Distorted perception; intense fear of weight gain.
Bulimia Nervosa:
Weight: Normal or slightly overweight.
Behavior: Binge eating with compensatory behaviors.
Body Image: Overconcern with weight; feelings of shame.
Binge-Eating Disorder:
Weight: Often overweight or obese.
Behavior: Binge eating without compensatory measures.
Body Image: Concerns present, though less rigid dietary restraint compared to other disorders.
Risk Factor and Demographics
Age of Onset:
Most eating disorders begin in adolescence.
Binge-eating disorder often develops between ages 30–50.
Gender Differences:
Historically seen as predominantly affecting females; current ratio is about 3:1 (female:male).
Men’s body dissatisfaction may focus on muscularity.
High-Risk Groups:
Individuals in professions emphasizing thinness (e.g., models, ballet dancers).
Athletes in sports with weight restrictions.
Sociocultural pressures and media influence play significant roles.
Medical Complication of Eating Disorders
Anorexia Nervosa:
Heart arrhythmias and risk of cardiac arrest.
Electrolyte imbalances leading to kidney damage.
Osteoporosis due to low bone density.
Other signs: dry skin, brittle hair, lanugo (fine hair growth).
Bulimia Nervosa:
Dental erosion and mouth ulcers from repeated vomiting.
Swollen salivary glands (“chipmunk cheeks”).
Electrolyte disturbances impacting heart and muscle function.
General Issues:
Chronic malnutrition may lead to organ damage and increased risk for self-injury or suicide.
Course and Outcomes
Anorexia Nervosa:
Mortality rate is high; complications (e.g., heart arrhythmias, suicide) are common.
Recovery is possible even after prolonged illness.
Long-term studies indicate about 51–63% eventual recovery.
Bulimia Nervosa:
Prognosis is generally good with approximately 70% of patients achieving remission.
Some continue to struggle with bingeing, shape concerns, and substance-abuse issues.
Binge-Eating Disorder:
High rates of clinical remission after intensive treatment.
Note: Early detection and treatment are critical for improved outcomes.
Association with Other Psychopathology
High Rates of Comorbidity:
Depression: ~68% in anorexia nervosa, 63% in bulimia nervosa, nearly 50% in binge-eating disorder.
Obsessive-Compulsive Disorders: Common in anorexia and bulimia nervosa.
Personality Disorders: Approximately 58% of women with eating disorders may have a personality disorder.
Substance Abuse: Frequently co-occurs in binge-eating/purging subtypes.
Risk and Causal Factors: An Overview
Multifactorial Etiology:
Biological Factors: Genetic predisposition, brain structure and neurotransmitter imbalances.
Sociocultural Influences: Western media, internalization of the thin ideal, family influences.
Individual Variables: Personality traits (e.g., perfectionism), negative emotionality, dieting behaviors.
Conceptual Model:
Best understood via the diathesis–stress model where genetic factors heighten sensitivity to environmental pressures.
Biological Factors in Eating Disorders
Genetics:
Family and twin studies indicate high heritability for anorexia and bulimia nervosa.
Recent GWAS found a genetic locus on chromosome 12 linked to anorexia nervosa and metabolic factors.
Brain and Neurotransmitters:
Hypothalamus Role:
Lateral hypothalamus stimulation promotes appetite.
Serotonin:
Abnormalities (such as altered 5-HIAA levels) suggest disrupted serotonergic function.
Set Points & Reward Sensitivity:
The body’s “set point” resists significant weight changes.
Differences in reward processing (e.g., response to food cues) may predispose to binge eating or restrictive behaviors.
Sociocultural Factors Influencing Eating Disorders
Media and Cultural Ideals:
Exposure to Western media (TV, magazines) is linked to body dissatisfaction.
Studies (e.g., in Fiji) show that media can shift local attitudes toward thinness.
Icons like Twiggy and Kate Moss have influenced the “thin ideal.”
Internalization of the Thin Ideal:
Believing that thinness equals beauty and success increases risk.
Social comparisons and peer evaluation reinforce these beliefs.
Family Influences:
Families of patients often exhibit rigid attitudes, high expectations, and focus on dieting.
Parental preoccupation with appearance may contribute to the development of eating disorders.
Individual Risk Factors and Psychological Influences
Personality Traits:
Perfectionism: An enduring trait linked to rigid dieting and excessive self-criticism.
More pronounced in women; men with eating disorders tend to be less perfectionist.
Body Dissatisfaction:
A powerful predictor of eating disorder onset.
Distorted self-perceptions lead to chronic dieting and negative self-evaluation.
Dieting and Negative Emotionality:
Dieting is common and can trigger or worsen disordered eating.
Negative moods and depression are predictive of binge eating and dietary restriction.
Treatment of Eating Disorders – Anorexia Nervosa
Medical Stabilization & Refeeding:
Hospitalization and measures like intravenous feeding to restore weight.
Aggressive refeeding protocols may be successful short term, yet without addressing psychological issues, gains are often temporary.
Medications:
Antidepressants have limited evidence.
Olanzapine (an antipsychotic) may benefit by addressing distorted beliefs and promoting weight gain.
Treatment of Anorexia Nervosa – Family Therapy & CBT
Family Therapy:
Maudsley Model is the treatment of choice for adolescents.
Involves 10–20 sessions over 6–12 months with phases:
Refeeding and re-establishing healthy eating habits.
Negotiating new patterns of family relationships.
Termination with focus on long-term support.
Cognitive-Behavioral Therapy (CBT):
Aims to modify dysfunctional beliefs about food, weight, and self.
Often used for both anorexia and bulimia, though success in anorexia may be limited due to cognitive rigidity.
Treatment of Bulimia Nervosa
Cognitive-Behavioral Therapy (CBT):
Leading treatment; focuses on normalizing eating patterns and challenging dichotomous food beliefs.
Controlled studies show elimination of binge–purge cycles in 30–50% of cases.
Medications:
Antidepressants (with a positive response often seen within the first 3 weeks) reduce binge frequency and improve mood.
Interpersonal Psychotherapy (IPT):
An alternative focusing on improving interpersonal functioning.
Treatment of Binge-Eating Disorder (BED)
Pharmacological Options:
Use of antidepressants, appetite suppressants, and anticonvulsants (especially given high comorbidity with depression).
Psychotherapeutic Approaches:
Randomized trials comparing IPT, guided self-help CBT, and behavioral weight loss:
At 6 months, remission rates were similar.
At 2-year follow-up, IPT and guided CBT outperformed behavioral weight loss.
Emerging & Transdiagnostic Treatments
Enhanced Cognitive-Behavior Therapy (CBT-E):
A transdiagnostic approach targeting eating pathology regardless of specific diagnosis.
Two forms:
Default (focused): Targets disordered eating, extreme dieting, purging, and binge eating.
Broad: Also addresses perfectionism, low self-esteem, and relationship issues.
Studies show higher remission rates compared with IPT, with benefits maintained at follow-up.
New Options for Adults with Anorexia Nervosa:
Multiple approaches (CBT, psychodynamic, treatment as usual) yield similar clinical benefits.
No single superior treatment yet—patient preferences and clinician expertise are key.
Defining Obesity & Its Medical Impact
Definition Using BMI:
Underweight: BMI < 18.5
Normal: BMI 18.5–24.9
Overweight: BMI 25.0–29.9
Obese: BMI ≥ 30; Morbid obesity: BMI ≥ 40 or >100 lbs over ideal weight.
Medical Issues:
Increased risk for heart disease, hypertension, diabetes, and certain cancers.
Obesity is linked with a reduction in life expectancy by 5–20 years.
Prevalence:
In the U.S., approximately 36% of adults are obese and 34% are overweight.
Significant state-by-state and demographic variations exist.
Weight Stigma & Sociocultural Influences on Obesity
Weight Stigma:
Obese individuals often face harsh judgment and discrimination.
Bias exists even among health care professionals, affecting treatment quality.
Media & Cultural Portrayals:
Negative stereotypes in media perpetuate biased perceptions.
Weight-based discrimination can affect legal outcomes and social interactions.
Risk and Causal Factors in Obesity – Genetics & Hormones
Genetic Influences:
BMI is polygenic; GWAS studies have identified many genetic regions (e.g., 97 regions related to BMI and fat distribution).
Specific genetic mutations (found in a subset) are linked to binge eating.
Hormonal Regulation:
Leptin: Produced by fat cells; signals fat reserves to the brain. Obesity often involves leptin resistance.
Ghrelin: Produced by the stomach; stimulates appetite. Elevated in conditions like Prader–Willi syndrome
Environmental & Family Influences, & Pathways to Obesity
Environmental Factors:
Easy access to hyperpalatable foods engineered with high fat and sugar.
Large portion sizes and aggressive food marketing contribute to overeating.
Time pressures and convenience drive choices toward fast food and prepackaged meals.
Family Influences:
Early overfeeding and family eating habits may predispose to more adipose cells.
Family behaviors around food and emotional support can have long-term impacts.
Social Contagion:
Close social ties may influence weight gain; obesity can be “socially contagious.”
Stress & Comfort Food:
Chronic stress and negative emotional states can trigger consumption of high-calorie comfort foods.
Summary & Key Takeaways
Eating Disorder Treatments:
Emphasis on medical stabilization, refeeding, and addressing psychological issues.
Family therapy and CBT remain central for anorexia and bulimia.
Emerging transdiagnostic approaches (CBT-E) show promise across disorders.
Obesity Overview:
Defined by BMI, obesity is a major global health issue with significant medical and social impacts.
Multifactorial causes include genetic predisposition, hormonal regulation, environmental factors, and sociocultural influences.
Integrated Perspective:
Both eating disorders and obesity require comprehensive, individualized treatment strategies.
Overview of Obesity Treatment Challenges
Modest Weight Loss:
Typical sustained weight loss of ~7 pounds is common.
Even small reductions can yield health benefits.
Treatment Complexity:
Biological defenses (set-point, hormonal changes) make weight loss difficult.
Prevention is Key:
Preventing weight gain may be easier than achieving and maintaining weight loss.
Metabolic & Hormonal Challenges in Weight Loss
Set-Point Theory:
The body defends a specific weight range through hormonal and metabolic adaptations.
Physiological Responses to Weight Loss:
Increased hunger, slower metabolic rate, and reduced satiety.
Energy expenditure decreases with weight loss, making maintenance challenging.
Implication:
Relapse rates are high due to these built-in biological defenses.
Strategies & Simple Behavioral Changes
Individual Strategies:
Reduce daily caloric intake by 100 calories (e.g., three fewer bites per meal).
Increase physical activity (e.g., taking the stairs, walking an extra mile).
Improve sleep quality (adults sleeping 7–8 hours tend to maintain healthier weights).
Key Message:
Small, consistent changes can help prevent and reduce gradual weight gain over time.
Public Policy Approaches to Obesity Prevention
Calorie Labeling:
NYC’s mandate for chain restaurants to post calorie information reduced average calorie consumption by 14%.
Regulatory Actions:
Attempts to ban large sugary drinks (though legal challenges may arise).
Implementation of the Healthy, Hunger-Free Kids Act to improve school food standards.
Additional Measures:
Better regulation of food advertising to children.
Subsidizing healthier foods and increasing taxes on sugar-sweetened beverages (e.g., a 20% tax could lead to nearly 4 pounds weight loss per year).