Anorexia Nervosa History
Recognized in medical literature in late nineteenth century in both France and Britain.
Aware of the psychological or nervous components of the disorder, Gull highlighted to pervision of the will and focused on the role of starvation. Similarly, Lasegue emphasized the social and psychological factors associated with the disorder. Bell (1985) provides vivid accounts of saints who starved themselves pursuing purity or devotion to God.
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Self-starvation mirrors symptoms today. p. 234
Anorexia Nervosa Frequency
0.9 % of women and 0.3 % of men. Many more girls suffer from less severe forms of anorexia nervosa, and individuals with subthreshold conditions can experience significant social and occupational impariment. Prevalence can increase wit the removal of that criterion in DSM-V p. 235
Bulimia Nervosa Frequency
5% of women and 0.5% of men. Despite it’s long history not recognized as a psychological disorder until 1979 p. 235
A serious condition marked by a restriction of energy intake relative to needed energy requirements, resulting in significantly low body weight in the context of age, sex, developmental trajectory, and physical health. Psychologists measure how thin their patients are by calculating BMI.
Visible eating disorder, may conceal their emaciation by wearing layers of clothes or otherwise hiding their bodies. Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, even though at a significantly low weight. Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight, or shape on self-evaluation, or persistent lack of recognition of the serious of the current low body weight. p. 235-236
Anorexia Nervosa Subtypes
Restricting: Patients maintain their low weight only by reducing their caloric intake and increasing their physical activityBinging/Purging: Eating an unusually large amount of food in a short period of time and feeling out of control. Purging, self inducting vomiting using laxatives, diuretics, or enemas.
The absence of mensruation for at least 3 consecutive months. Used to be a requirement for Anorexia diagnosis. A common response to starvation and weight loss as the body shuts down reproductive functioning in the face of famine. Was removed in DSM-5 because no meaningful differences between individuals with anorexia nervosa who do and do not menstruate. Should be assessed as an indicator of severity. p.237
Disorders connected to Anorexia Nervosa
Depression, anxiety, low heart rates, low blood pressure, and lowered body temperature, which could explain their tendency to wear layers of clothes even in warm temperatures.
Anorexia Nervosa in Men/Onset
Typically begins around adolescence, commonly after puberty, but more recently, young children and older adults have been reported to suffer from classic anorexia nervosa. Stable rate of new cases over the last several decades. p. 37
What group has increased diagnoses Anorexia?
Increase in the high risk group of 15-19 year olds.
Whos at Risk anorexia?
Actors, dancers, models, and athletes more than any other group. p. 138
Even after recovery people with Anorexia still have low BMIs and can also suffer from osteoporosis (decreased bone density), difficulties with childbirth. Often includes periods of relapse, remission, and crossover to bulimia nervosa. p.
Anorexia Crossover/mortality rate
Between 8 and 62% of people who start with anorexia nervosa develop bulimic symptoms at some point during the course of their illness, usually during the first 5 years. Highest mortality rate, 5% per decade of follow-up. Causes of death include effects of starvation and suicide p. 238
Personality and Anorexia
Perfectionism: People who develop anorexia are often described as model children and model students who set extremely high standards for themselves. Apply this to their diet. Other personality factors include, obsessionality, and neuroticism (being a worrier and having a difficult time shaking things off) People who are uncomfortable transitions and change can accelerate predisposition to eating disorders. p. 239
Comorbidity and Anorexia
Often suffer from anxiety, depression, and other problems.
Up to 80% will experience major depression at some point during their lives, 75% anxiety disorder. Anxiety disorders often present before anorexia shows up, may increase risk of anorexia. For some, early detection and treatment of anxiety may lower the chance of getting an eating disorder.
Bulimia Nervosa Defined
An invisible eating disorder because patients are of normal weight or overweight. Characterized by recurrent episodes of binge eating in combination with recurrent compensatory behaviors in order to prevent weight gain. NOT LIKE SIMPLE OVEREATING, the hallmark feature of a binge is a lack of control for over eating. p. 240
Bulimia Nervosa (Binging Behavior Characteristics)
The person cannot stop the urge to binge once it has begun or has difficulty ending the eating episode even when long past being full. Some patients talk about a trance or “binge mode”, where everything else melts away during this time. Running out of food, being interrupted by other people, or experiencing an extreme urge to purge usually stop the binge.
Overreating is coupled with lack of self control p. 241
Bulimia Nervosa (Caloric Intake)
Around 1,000 calories is the minimum amount to be considered a binge, but in some cases over 20,000 calories may be consumed. p. 241
Bulimia Nervosa (Subjective Binge)
Defines eating a typical or even small amount of food, coupled with the feeling that the eating is out of control.
Bulimia Nervosa (Objective Binge)
Eating a comparatively large amount of food plus feeling out of control. p. 241
Bulimia Nervosa (Binging Patterns)
Frequency can range from occasionally to a few times a week to 20 or 30 times a day. Once per week for 3 months is the required frequency for a threshold diagnosis of bulimia.
Bulimia Nervosa (Binge/Purge Cycle)
Some become locked in a binge purge cycle which dominates their lives. p. 241
Bulimia Nervosa (Inappropriate Compensatory Behaviors)
Any actions that a person uses to counteract a binge or to prevent weight gain. These behaviors include self-induced vomiting, misuse of laxatives, diurectics, enemas, or other agents; fasting; and excessive exercise. p.
Bulimia Nervosa (Purging)
People can also purge without binging! p.241
Bulimia Nervosa (Calorie Absorption/Danger of laxatives)
Many calories associated with binge are absorbed, and those calories lead to weight gain. Laxatives, which work in the colon, after all of the nutrients have been absorbed in the stomach and the small intestine, are ineffective, but dangerous purge agents. 5% of calories consumed are lost, but losing water and necessary electrolytes (potassium), make abusing laxatives very dangerous.
Bulimia Nervosa (Prevalence)
-Tend to keep behavior secret bc stigma-Prevalence around 1 to 3% of women, 0.1 to 0.5% for men, when subthreshold forms included, 5 to 6%-duration criteria in DSM are really just arbitrary cutoffs, even if a person doesn’t meet all of the diagnostic requirements, engaging in binge eating and purging is unhealthy and potentially dangerous. -Prevalence may increase, w/ new dsm-5 criteria, as the previous criteria was more stringent at twice per week for 3 months p.
Bulimia Nervosa (Men/Women)
Far more common in women than men. p. 243
Bulimia Nervosa (When it starts)
Starts later than anorexia nervosa, usually late adolescence to early adulthood, although even later onset is not uncommon. p. 242
Bulimia Nervosa (Physical Complications)
Also associated with serious physical complications including fatigue, lethargy, bloating, and gastrointestinal problems.
Frequent vomiting leads to erosion of dental enamel, swell of salivary glands. Those who abuse laxatives, can have edema (body swelling), fluid loss, and subsequent dehydration, electrolyte abnormalties, and permanent loss of normal bowel functions. p.
Bulimia Nervosa (Mortality rate)
Around 3.9%. In one 10 year outcome study, 11% of individuals continued to meet full diagnostic criteria for bulimia nervosa and 18.5% met critieria for the DSM -IV-TR residual diagnosis of (eating disorder not otherwise specified). p. 243
Bulimia Nervosa (Personality)
Similar to anorexia, perfectionism, low self esteem, but also some differences including being more impulsive (thinking before eating) and having higher “novelty seeking” (stimulus or sensation seeking) behavior.
Contrasting anorexia nervosa, people with bulimia nervosa are far more erratic and impulsive, conisstent with the impulsive and fluctuating nature of alternating starving, binge eating, and compensatory behaviors p. 243
Bulimia Nervosa (Comorbidity)
Approximately 80% have another psychiatric disorder, some even with several disorders at the same time. Some continue to suffer from disorders even after recovery from bulimia.
These disorders include anxiety disorders, major depression, substance use, and personality disorders. p. 244
Binge Eating Disorder (General Info)
First recognized in a subset of obese individuals. BED is characterized by recurrent binge eating behavior but without the inappropriate compensatory behaviors that are part of bulimia nervosa. Can be chronic, average can be 14.4 years, not necessarily a passing phase. p.245-246
Binge Eating Disorder (Epidemiology and Course of BED, Percentage of people who have it))
5% of women and 2% of men in the general population meet criteria for BED as defined in DSM-IV. May increase due to the change in frequency/duration criteria, gone from twice a week for 6 months to once a week for 3 months in DSM-V. p.246
Binge Eating Disorder (Obese Individuals)
Found in approximately 5 to 8% of obese individuals making it the most common eating disorder with the DSM-V.
Binge Eating Disorder (Morbidity/Mortality)
Little is known so far due to it being recent addition to DSM-V. One study, followed clinical sample for 6 years after treatment to determine their long-term outcome; 57.4% of women had a good outcome, 35.
7% an intermediate outcome, and 5.9% a poor outcome. Only one patient had died. Six years later, 6% still had BED, 7.4 percent had developed Bulimia and 7.4 developed EDNOS.
Binge Eating Disorder (Personality)
They score higher on measures of harm avoidance than healthy control individuals. Anothe stud, which compared obese individuals with BED to both obese individuals with out BED and normal weight controls on a number of personality variables, found no distinct differences
Binge Eating Disorder (Comorbidity)
May experience many of the same forms of comorbidity as those with anorexia and bulimia. In one sample, nearly 74 percent reported at least one additional psychological disorder, with the most common being mood disorders, anxiety disorders, substance use disorders. Also associated with development of metabolic syndrome, including hypertension, dyslipdemia, and type-2 diabetes.
Independent of effects from obesity p. 247
Other specified feeding and Eating Disorders (Atypical Anorexia Nervosa)
A person has all the features of anorexia nervosa, except the person’s weight is within or above the normal range. p. 247
Other specified feeding and Eating Disorders Bulimia Nervosa (Of low frequency and/or limited duration)
A person meets all the criteria for bulmia nervosa, bu the binge eating and purging happen less than once a week and/or less than three months.
Other specified feeding and Eating Disorders (Binge eating-disorder, of low frequency/or limited duration)
A person has all the criteria of binge eating disorder, but binge eating happens less than once a week and/or for less than three months. p. 247
Other specified feeding and Eating Disorders (Purging disorder)
A person uses purging behavior to control their weight or shape, but they are not binge eating. p. 247
Other specified feeding and Eating Disorders (Night eating syndrome)
A person eats after waking up during the night, or eats excessively after the evening meal (and they can recall the eating).
Cause excessive distress or impairment of normal functioning. p.248
Other specified feeding and Eating Disorders (Changes to DSM)
Changes were made because most people who sought treatment for an eating disorder, received a diagnosis of EDNOS. DSM-IV did not adequately capture eating disorders as they exist in the real world. p. 248
Feeding and Eating Disorders of Childhood (Pica what is it, word origin)
The persistent eating of nonnutritive, non-food substance.
Comes from the word “magpie”, bird which consumes food and nonfood substances. p. 249
Feeding and Eating Disorders of Childhood (Pica, who it effects)
Occurs in various socioeconomic groups, both sexes, and all ages, but may be more common among women, children, and people of lower socioeconomic status. p. 249
Feeding and Eating Disorders of Childhood (Pica, Health Effects, Social effects)
Can result in lead poisoning, parasitic infections, malnutrition, dental trauma, oral lacerations, gum diseases, and erosion of tooth enamel. Consuming safety pins, glass, or nails can obstruct or perforate the esophagus, stomach, stomach, or intestines. Finally, the ingestion of certain items may repulse caregivers or peers, leading to social isolation and/or rejection. p.
Feeding and Eating Disorders of Childhood (Cultural Pica)
Some women in India consume oil and it’s byproducts in response to pregnancy cravings. Some East African African women consume soil for purposes of fertility. South American certain cultures, eat clay for its purported medicinal value.
U.S. eating kaolin, occurs in Piedmont region of Georgia and parts of Mississippi. p. 249
Feeding and Eating Disorders of Childhood (Pica Causes)
Iron and Zinc deficiencies may result in the urge to ingest certain foods or substances, but many people without these conditions also engage in pica. Environmental Factors, (stress and impoverished living environments) or developmental disorders are important causal factors, such as surgery or the loss of a family member. p.
Feeding and Eating Disorders of Childhood (Pica, intervention)
Behavioral interventions, such as overcorrection, are also effective for pica. If such procedures are done repeatedly and consistently, pica can be eliminated or greatly reduced. p. 249
Feeding and Eating Disorders of Childhood (Rumination Disorder)
Recently eaten food is effortlessly regurgitated into the mouth, followed by rechewing , reswallowing, or spitting it out. p.250
Feeding and Eating Disorders of Childhood (Rumination disorder, when it occurs,Episodes)
Occurs in both sexes and may begin in infancy, childhood, or adolescence.
Episodes may occur several times per day and may last for over an hour.
Feeding and Eating Disorders of Childhood (Rumination, misdiagnosis)
Because it resembles vomiting, some people are initially diagnosed with bulimia or gastroesophageal reflux disease. They sometimes undergo gastrointestinal surgical procedures and consult several physicians before getting a correct diagnosis. p. 250
Feeding and Eating Disorders of Childhood (Feeding disorder treatment)
Medications don’t work very well. Instead, behavioral interventions such as habit reversal, relaxation training, and cognitive behavioral therapy work better. .p250
Feeding and Eating Disorders of Childhood (Avoidant-restrictive food intake disorder)
Introduced to the DSM-V given the frequency with which children with certain types of presentations were given diagnoses of EDNOS.
Captures the behavior of those children who exhibit restricted or otherwise inadequate eating. Associated with the following, significant weight loss, significant nutritional deficiencies, dependence on enteral feeding or oral nutritional supplements, marked interference with psychosocial functioning. Not better explained by lack of food, or culturally sanctioned practice.
Does not occur exclusively during the course of anorexia , no evidence of a disturbance in the way in which one’s body weight or shape is experienced. Not better explained by another disorder. When in context of disorder, disturbance exceeds that routinely associated with the condition or disorder/requires clinical attention p. 250
Feeding and Eating Disorders of Childhood (Avoidant-restrictive food intake disorder, epidemiology)
Most common in children and adolescents, can persist into adulthood p. 250
Feeding and Eating Disorders of Childhood (ARFID, difference between “picky eating”
Causes functional impairment, medical complications p. 250
Sex, Race, Ethnicity, and Developmental Factors(Eating Disorders in Males and Females)
Occurs more often in women, theorized because of society’s outlook on females to maintain a thin body shape, female objectification. p. 251
Sex, Race, Ethnicity, and Developmental Factors (Bias Diagnosis)
Diagnosis criteria somewhat sex biase bc men tend to rely on nonpurging forms of compensatory behavior after binge eating, such as excessive exercise.
Male athletes are among those who may focus excessive attention on their weight and body shape. Intriguingly, the relation among the component behaviors of eating disorders such as binge eating, exercising, purging, and desire for weight loss may also differ among sexes. p.252
Sex, Race, Ethnicity, and Developmental Disorders (Difference in diagnosis between anorexia, bulimia, and BED)
Unlike anorexia and bulimia, the sex distribution of BED fairly equal and binge eating equal across both sexes.
Sex, Race, Ethnicity, and Developmental Factors (Who has eating disorders, race)
Stereotype: Upper-white middle classRecent study suggested higher rates of anorexia and bulimia in white women than black women.
Same study, no black women diagnosed with anorexia, while 1.5% white women. Not a lot of information connecting race to eating disorders.Another study, binge eating in absence of purging found in more black women.
Vice versa for white women. For BED, fewer differences across ethnic group. May be increased risk, lower socioeconomic class p .252
Sex, Race, Ethnicity, and Developmental Factors (Developmental Factors General, Parents)
In one study, childhood predictors of disordered eating beahviors included the mothers own body dissatisfaction, internalization of the thin body ideal (or how much the person accepted society’s pressure to be thin), bulimic symptoms, and maternal and peternal BMI, which predicted the emergence of childhood eating disorders. Familial/genetic influence unknown p. 253
Sex, Race, Ethnicity, and Developmental Factors (Develop Factors/Family, Anorexia Nervosa)
When anorexia begins in early adolescence, social and emotional development are interrupted, by its medical and psychological consequences. Can lead to isolation from peers and family. Recovery means, establishing independence from family, developing trust in friendships, and establishing romantic relationships.
Family meals can cause tension, parents struggle to understand, as their child becomes unreachable and unable to think rationally about a function. Needs of other siblings become secondary. Can break down even the most functional of families. p.253
Sex, Race, Ethnicity, and Developmental Factors (Develop. Factors, Bulimia)
Girls whose body fat percentage increases more rapidly, and who develop mature figures earlier may experience body satisfaction. Leads to early experimentation behaviors to control eating, can increase risk of developing eating disorders. Families tend to have more problems with drug and alcohol dependence and higher frequency of of sexual abuse than in anorexia.
Sex, Race, Ethnicity, and Developmental Factors (Develop. factors, BED)
Associated with earlier onset of obesisty, dieting, and psychopathology. Begins usually in late adolescence or early adulthood.
Ages 6-12, more body fat than those who do not binge. p. 254
The Etiology of Eating Disorders (Biological Perspectives, Using Animals)
Has helped us understand some of the core symptoms of eating disorders. p. 254
The Etiology of Eating Disorders (Bio perspective Role of the Hypothalamus)
As a result of animal studies, hypothalamus: which controls certain metabolic processes and other autonomic activities, is influential in appetite and weight control. Central to appetite and weight regulation in mice, although not consistent enough to be identified with humans who have eating disorders.
The Etiology of Eating Disorders (Bio Perspective Activity Based Anorexia)
In a rodent model, provided with unlimited access to running wheel and scheduled feeding. Increase in running wheel activity and decreased feeding. p. 255
The Etiology of Eating Disorders (Bio perspective Addiction Model of Binge Eating, Brain)
Some neuropsychological systemsthat are associated with addiction-related process including systems related to impulsivity and the executive (decision making) systems.
May play a role in the development of BED. May involve the reinforcing value of food for indiviudals and whether they experience loss of control over eating. Caudate and putamen areas of brain of obese individuals with BED release more dopamine after exposure to a food stimulus than do the brains of obese indivuals without BED. Important finding bc dopamine regulates our motivation to eat suggesting that obese individuals with BED are getting stronger signals to eat when exposed to food stimuli. Stress reactivity important, similar to drugs and alcohol, food is reinforcing for BED. p. 256
The Etiology of Eating Disorders (Bio perspective Neuroendocrine and Neurohormonal Factors, Serotonin and Dopamine)
Serotonin and Dopamine have been linked to changes in the psychological and behavioral features of eating disorders, such as impulsivity and obsessionality, indeed serotonin is directly related to the development of eating disorders.
Not clear if predisposition, or result of disorder. Serotonin may also contribute to some personality features of eating disorders including, perfectionism, rigidity, and obsessionality in anorexia. Dopamine-related disturbance of reward mechanisms that contributed to their behavioral style of self-denial. p. 256
The Etiology of Eating Disorders (Bio PerspectiveBrain structuring and Functioning Studies)
Structural abnormalities exist within brain, including reduced brain mass, los of gray matter, and brain ventricles that are increased in size, anorexia.
Starvation, or alternating starvation and binge eating, could cause lasting biological “scars”, indicating that these changes were a result of the disorders, not the reason they developed. Individuals with anorexia and bulimia nervosa have globally decreased brain glucose and metabolism at rest. Consistent with rigid, inflexible, overcontrolled, behavior seen in individuals with anorexia nervosa and some forms of bulimia nervosa. p. 257
The Etiology of Eating Disorders (Bio Perspective Family and Genetic Studies)
Family studies show that anorexia, bulimia, and BED clearly run in families. 10 times more likely if family member has had one. BED runs in families independently of obesity.
Heritability of anorexia around 60% and heritability of bulimia 28 and 83%, remaining variance has to to do with environmental factors. For BED, best current estimate around 41%. Eating disorders can be influenced by genetic factors p. 257
The Etiology of Eating Disorders (Family and Genetic Studies, chromosomes)
Chromosome 1, serotonergic function and opiodergic function. Under study for potential role in the development of anorexia nervosa. For bulimia, chormosome 10, hot spot for bulimia. Genetic studies using the association approah have focused on many of the same genes targeted in the study of anorexia nervosa.
Relationship between symptoms of impulsivity, affective instability, and insecure attachment in women with eating disorders. Three studies used genome-wide association approaches to compare people with anorexia nervosa to people with no psych disorders, however no results have met the stringent criteria for genome-wide sig. Genes establish baseline risk, our environment can be protective or triggering. p.
Psychological Perspectives (Psychodynamic Perspectives)
Anorexia was considered an unconscious attempt to reverse or reject adult female sexuality via starvation to a prepubertal state. Explanation shifted from interpersonal relationships and interpersonal context in which these disorders arose.
Psychological Perspectives (Psychodynamic Perspectives, Hilde Bruch)
Published The Golden Cage, illustrated rich clinical descriptions of patients with anorexia. Identified features such as body image distortion and pervasive sense of ineffectiveness as core aspects of anorexic pathology.
Psychological Perspectives (Family Models of eating disorders, Salvatore Minuchin)
Identified four dysfunctional patterns to what he referred to as psychosomatic families. Enmeshment, the overinvolvement of all family members in the affairs of any one member. Rigidity, difficulty families faced in adapting to the changing developmental needs of their children. Overprotectiveness, parents shielded children from age-appropriate experiences.
Poor -conflict resolution, reflected the difficulties these families had in dealing with problematic, negative situations. Studies biased towards folks who could afford treatment, oversimplified families not so homogenous anorexia nervosa. p.260
Psychological Perspectives (Cognitive Behavioral Theories)
The cognitive-behavioral model focuses on distorted cognitions about body shape, weight, eating, and personal control that lead to and maintain unhealthy eating and weight-related behaviors. Proponents of cognitive-behavioral model emphasize the power of thoughts to influence feelings and behaviors. In bulimia nervosa, distored thoughts about food, shape, and weight lead to particular feelings and behaviors that then perpetuate the binge-purge cycle. p.
Psychological Perspectives (Sociocultural Theories, Western Beauty Ideals))
Emphasize the western cultural preoccupation with thinness as beauty. The model follows the path from being exposed to the ideal of thinness, to internalizing this ideal, and then to observing a discrepancy between actual and ideal body to dissatisfaction with one’s body, to dietary restraint, and finally to restriction. Women more likely to internalize this ideal bc valued for their appearance. Can also affect men, emphasis on leanness and muscularity can lead to men turning to unhealthy weight control behaviors and steroids, media images can also affect how they see their bodies. P.
Psychological Perspectives (Sociocultural theories, Fiji Study)
Amount of girls reported self-induced vomiting went up to 15%, after only 3% did before television was on the island. Amount of TV watched by someone’s friends can also affect how they see themselves. p.260
Psychological Perspectives (Sociocultural theories, Lines of evidence)
Includes the imbalanced sex ration in anorexia and bulimia nervosa, increasing incidence of anorexia and bulimia in parallel with the decreasing body size ideal for women, cross-cultural differences in the incidence or prevalence of eating disorders (with higher rates in cultures that value extreme female thinness), and the significant prospective relationship between internalization of the thin ideal and disordered eating. p. 261
Psychological Perspectives (Sociocultural theories, Genetic predisposition)
A genetic predisposition may make an individual more vulnerable to behaviors such as dieting, which are triggered exposure towards thinness. p. 261
The treatment for eating disorders (General)
In anorexia nervosa, the intial goals are to increase caloric intake and weight gain so that later stages of treatment can deal more effectively with the psych aspects of the disorder.
For bulimia, when weight is usually within the healthy range, the focus of treatment is to normalize eating, eliminate binge eating and purging episodes, and to improve psychological aspects of the disorder. In BED, controversy exist over whether weight loss should be a therapeutic outcome for patients who are overweight or obese, as many people argue that repeated attempts to lose weight are often causal of BED. p. 262
The treatment for eating disorders (Inpatient treatment for Anorexia
First and most critical step is restoring weight. Psych therapy difficult to conduct when patients really ill bc starvation impairs ability to think.Psychotherapeutic approaches include individual psychotherapy, (cognitive-behavioral, interpersonal, behavioral, supportive, and psychodynamic) family therapy, especially for younger patients, and group therapy. Besides weight, hospitalization should result when medical complications, suicide attempts, failure to improve outpatient treatments, comorbid psychiatric disorders, interference with school, work or family, poor social support, pregnancy, and the unavailability of other treatment options. Inpatient treatments difficult for both patients and families.
Collaborative relationship critical to decerasing patients anxiety about weight gain. p. 262
The treatment for eating disorders (Ethics and Responsibility)
Involuntary treatment controversial.
Legal committment less controversial when patient is suicidal, clearly intending to harm herself or himself. Legally, self-starvation is generally considered a behaior that endangers life and constitutes a grave disability, thereby allowing civil commitment of patients with sever anorexia who refuse treatment. Involuntary commitment, last resort and if it contains therapeutic gain. p. 262
The treatment for eating disorders (Biological Treatment)
Medications, although none have really been effective for anorexia. For bulimia, antidepressant called fluoextine (Prozac) can reduce symptoms of binge and purge, and features such as depress and anx, short term. BED, some meds target core symptoms of binge eating and weight loss, although none have received FDA approval. p.
The treatment for eating disorders (Nutritional Counseling)
Help to apply nutritional advice to their own eating, help to reclaim appropriate portion sizes, caloric intake. Not effective as a sole therapy. p. 263
The treatment for eating disorders (CBT)
Focus cognitions of body shape, weight, eating, and personal control. Addresses automatic thoughts, evaluative in nature and core beliefs, which are guiding principles. Challenge distorted cognitions about food, eating, and body shape. Recovery rates, 35 to 75 at 5 or more years, however, 33 perc.
relapse bulimia, highest risk during year following treatment. May reduce relapse anorexia when weight has been restored, must use cognitive effort, impairments in acute stage make it not as beneficial. p. 263
The treatment for eating disorders (CBT, Bulimia)
Self-monitoring, can help practitioner identify patterns of unhealthy behavior, including high risk times. Self-monitoring technology, smartphone apps, text messaging beneficial. p. 263
The treatment for eating disorders (CBT, Next steps)
Recognizing cognitions associated with unhealthy eating behave. Recognize cues for disordered eating, control automatic thoughts, restructuring distorted cognitions.
Final goal, prevent relapse.
The treatment for eating disorders (CBT, BED)
Self-help book or behavioral program can be beneficial. At next check-in if doing well, encouraged to continue. If deteriorated, might need a specialist. p.263
The treatment for eating disorders (CBT, DBT)
Focuses on emotional dysregulation as the core problem in eating disorders and views symptoms as attemps to manage unpleasant emotional states.
Effective for bulimia, binging purging eps. p.264
The treatment for eating disorders (Interpersonal Psychotherapy)
Brief, time limited. No matter cause depressive symptoms connected to interpersonal relationships. Goal to reduce depress symptoms and to improve interpersonal functioning enhancing communication skills.
IPT eating disorders, interpersonal disputes, role transitions, abnormal grief, or interpersonal deficits. Anorexia, less effective then psych therapy. Bulimia, as effective as CBT, not as rapid decrease in symptoms. BED, good individual and group therapy, preliminary efficacy in BED.
The treatment for eating disorders (Family Based Interventions, Maudsley, approach)
Work with experts who know how to help, work together as a family, don’t blame your child or yourself, blame illness, focus on problem before you, dont’ debate with child about eating, know when to back off, take care of yourself. Empowers parents to take active role. Less appropriate for adults for anorexia. Promise for bulimia nervosa families.
No clinical trials for BED. p. 266