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The accuracy of 24-hour dietary recall of patients with bulimia nervosa was examined by comparing the actual intake of subjects in a laboratory meal with their reported intake in a 24-hour dietary recall interview. The mean caloric intake of the 15 patients who participated in the study was 1,088 (SD 1,335) kilocalories. There were significant positive correlations between actual and recalled kilocalories (r2 = .97, p < .001), total grams (r2 = .92, p < .001), and grams of macronutrients consumed (protein r2 = .96; fat r2 = .97; carbohydrate r2 = .94; p < .001). However, there was a tendency for patients to overestimate the amount of food they had eaten when actual intake was large.

The present investigation examined the significance of a past history of substance abuse on treatment outcome for bulimia nervosa. Seventy-five women with bulimia nervosa participated in a 6-week double-blind outpatient trial of desipramine; 19 patients had a history of substance abuse and 56 did not. Although patients with a history of substance abuse reported higher levels of anxiety and depression at presentation for treatment than patients without such histories, the two groups reported a similar age of onset of their bulimia nervosa and similar severity of eating pathology with regards to binge and vomit frequencies and measures of concern about body shape and weight. On all outcome measures, the improvement of the substance abuse group was equal to or greater than that in the group without a history of substance abuse. Results suggest that a past history of substance abuse has no implication regarding response to pharmacological treatment for bulimia nervosa.

The current DSM-Ill-R psychiatric diagnostic system recognizes only one disorder of overeating, bulimia nervosa. Our clinical work has led us to believe that there are a number of individuals who believe that they have a serious overeating problem, but do not meet criteria for bulimia nervosa. We surveyed the literature for studies pertaining to overeating among individuals not meeting criteria for bulimia nervosa. Studies of obese binge eaters and of binge eating among young women suggest the existence of a significant proportion of obese and non-obese individuals with such a problem. However, the limitations in the existing data for addressing this question preclude definitive conclusions. Further work is needed to establish the defining features of an additional binge eating syndrome, to assess the reliability and validity of such a syndrome, and to determine its clinical utility.

Diagnostic criteria have been developed for a new eating disorder, binge eating disorder (BED), to describe the many individuals who have problems with recurrent binge eating but do not engage in the characteristic compensatory behaviors of bulimia nervosa, vomiting, or use of laxatives. The results of a multisite field trial involving 1,984 subjects indicate that the disorder is common (30.1%) among subjects attending hospital-affiliated weight control programs, but is relatively rare in the community (2.0%). The disorder is more common in females than in males and is associated with severity of obesity and a history of marked weight fluctuations. Based on these results, the DSM-IV Work Group on Eating Disorders has recommended that the disorder be considered for inclusion in DSM-IV, either as an official category or in an appendix of categories requiring further study.

Background: Body image distortions are a core feature of anorexia nervosa (AN). We, and others, previously reported abnormalities in adipose tissue distribution after acute weight restoration in adult women with AN compared with body mass index–matched healthy control women. Whether these abnormalities persist over time remains unknown. Objectives: We aimed to 1) replicate previous findings that showed preferential central accumulation of adipose tissue in recently weight-restored AN women compared with control subjects, 2) describe the change within patients with longer-term (1-y) weight maintenance, and 3) compare adipose tissue distribution after 1-y maintenance with that of control subjects. Design: Body composition and adipose tissue distribution were assessed by whole-body magnetic resonance imaging in women with AN shortly after weight normalization (n = 30) and again 1 y after hospital discharge (n = 16) and in 8 female control subjects at 2 time points. Results: With acute weight restoration, AN patients had significantly greater visceral and intermuscular adipose tissue compared with control women [visceral: 0.75 ± 0.26 compared with 0.51 ± 0.26 kg in AN patients and controls, respectively (P = 0.02); intermuscular: 0.46 ± 0.17 compared with 0.29 ± 0.13 kg in AN patients and controls, respectively (P = 0.01)]. With maintenance of normal weight for ≈1 y, visceral adipose tissue distribution in AN patients was not different from that in healthy control subjects. Conclusions: In adult women with AN, normalization of weight in the short term is associated with a distribution of adipose tissue that is consistent with a central adiposity phenotype. This abnormal distribution appears to normalize within a 1-y period of weight maintenance. This research was registered at clinicaltrials.gov as {"type":"clinical-trial","attrs":{"text":"NCT 00271921","term_id":"NCT00271921"}}NCT 00271921 and {"type":"clinical-trial","attrs":{"text":"NCT 00368667","term_id":"NCT00368667"}}NCT 00368667.

Overconcern with shape and weight is considered a primary feature of the psychopathology of bulimia nervosa and was included as a diagnostic criterion in DSM-III-R. In order to test the significance of shape and weight concern in bulimia nervosa, we administered the Body Shape Questionnaire (BSQ) to 78 outpatients with bulimia nervosa and three comparison groups: 14 women with seasonal affective disorder (SAD), 10 acquaintances of patients, and 32 normal controls

Objective: Amenorrhea is a DSM-IV criterion for the diagnosis of anorexia nervosa (AN). Several studies have reported few differences between patients who meet the full DSM-IV criteria for AN and those who meet all but the amenorrhea criterion. Although this suggests that the absence of menses does not provide critical diagnostic information, many of these studies are limited by small sample sizes. This study aims to examine the clinical utility of amenorrhea as a criterion for the diagnosis of AN. Method: A chart review was conducted of 240 consecutive patients admitted for inpatient treatment at the NY State Psychiatric Institute from 1993 to 2006. Menstrual data were collected from the Eating Disorder Examination conducted upon admission. Independent samples t-tests were performed to evaluate differences in clinical variables, including age, lifetime lowest body mass index (BMI), admission and discharge BMI, previous number of hospitalizations, duration of illness, Beck Depression Inventory total score, Beck Anxiety Inventory total score, and Eating Disorder Examination subscale scores. Results: The amenorrheic and menstruating groups differed significantly only on lowest lifetime BMI and admission BMI, with individuals with amenorrhea having lower BMIs on both measures. Conclusion: These results indicate that amenorrhea does not distinguish between groups on a number of important measures of clinical severity. It may be that amenorrhea reflects weight and nutritional status, rather than providing useful diagnostic information. Future studies are needed to examine the potential prognostic value of menstrual status. © 2008 by Wiley Periodicals, Inc. Int J Eat Disord 2008

Background Prior studies suggest that certain psychiatric and medical disorders co-occur with binge eating disorder (BED). However, there has been no large, community-based study with diagnoses made by clinician interviewers. We used data from that type of study to assess the co-occurrence of various psychiatric and medical disorders with DSM-IV BED and with subthreshold BED. Method From October 2002 to July 2004, we interviewed 150 probands with BED, 150 probands without BED, and 888 of their first-degree relatives (135 of whom had BED, and 54 of whom met specific partial criteria for BED that we defined as subthreshold BED). Study participants were interviewed using the Structured Clinical Interview for DSM-IV to assess BED and other psychiatric disorders and a supplemental structured interview to assess certain medical disorders; participants also completed a self-report questionnaire, the Bad Things Scale. For each psychiatric and medical disorder, we calculated the age- and sex-adjusted co-occurrence odds ratio: the odds of having that disorder in one's lifetime among individuals with (full or subthreshold) lifetime BED compared to individuals without lifetime BED. We also used subjects' responses to the Bad Things Scale to adjust for adversity over-reporting, a type of response bias that could result in spurious findings of co-occurrence. Results Full BED co-occurred significantly with bipolar disorder, major depressive disorder, bulimia nervosa but not anorexia nervosa, most anxiety disorders, substance use disorders, body dysmorphic disorder, kleptomania, irritable bowel syndrome, and fibromyalgia. These results changed little after correcting for adversity over-reporting. Subthreshold BED co-occurred significantly with many, but not all, of the significantly co-occurring disorders for full BED. Conclusion BED and, to a lesser degree, subthreshold BED exhibit substantial lifetime co-occurrence with psychiatric and medical disorders.

The article by Von Holle et al. in this issue is one of a series of reports emerging from a large and impressive group of investigators assembled to collect information on the genetics of eating disorders [1]. Having rigorously obtained an extensive array of information from a large number of probands and family members, the investigators are appropriately mining the data in numerous ways. In this paper they turn their attention to temporal patterns of recovery among 901 women with anorexia nervosa and bulimia nervosa. The retrospective data were collected from subjects at the time of their assessment and entry into the genetics studies. The investigators report what appears to be, at first blush, a remarkably low rate of improvement: fewer than 20% of participants reported recovery at the time of assessment. However, this observation must be interpreted in light of the study’s definitions and methods. The investigators chose to rate as recovered only those individuals who denied being below normal weight, as well as reporting no behavioural symptoms suggestive of an eating disorder, for a full 3 years. While the investigators’ rationale for this very conservative criterion is solid, it obviously reduced the fraction of subjects who had recovered. For example, because the average time between reported onset of the disorder and the assessment was 12 years, individuals, on average, had to begin their full recovery no more than 9 years after onset. Other studies of recovery from eating disorders have generally utilized less stringent criteria, making comparisons across studies difficult. In addition, as noted by the authors, most reports of recovery are derived from clinical populations, and examine time to recovery from entry into treatment. In the current report, duration is measured from the time of reported onset. Furthermore, individuals were recruited expressly to participate in a genetics study, and were at various stages of illness and recovery at the time of their assessment. Conceivably, individuals with more chronic courses may have been more motivated to participate. In any case, it is very difficult to apply these estimates of time to recovery to patients presenting for treatment. As the authors emphasize, both the conduct of their study and the interpretation of their results are limited by the lack of a consensus in the eating disorders field on precisely what constitutes recovery. Unfortunately, this is not a newly recognized problem, nor is it confined to eating disorders [2]. Because of the multifaceted nature of psychiatric disorders, and the paucity of objective, easily obtained markers of illness, it has proven difficult for consensus to form around definitions of relapse, recovery and remission. In the eating disorders field, the wide range of definitions limits the ability to pool data across studies, much less to have confidence about comparisons between studies. However, within the Von Holle et al. study the interpretation of different temporal patterns of recovery between eating disorders is more straightforward and of interest. In the early years after onset, the odds of recovering from anorexia nervosa were greater than those of recovering from bulimia nervosa but, over time, the probabilities of recovery shifted to favour bulimia nervosa. This pattern is consistent with the results of other types of studies, such as those based on follow up of clinical samples, and echo the anecdotal reports of many clinicians. These varied sources of information suggest that an adolescent B. Timothy Walsh, Professor of Psychiatry, College of Physicians & Surgeons, Columbia University, Director, Division of Clinical Therapeutics, New York State Psychiatric Institute

Preliminary evidence suggests that the antiobesity agent sibutramine is effective in the treatment of binge eating disorder, impacting both binge eating and weight. This study is the first large-scale, multisite, placebo-controlled trial to test the efficacy of sibutramine in binge eating disorder.Participants (N=304) who met DSM-IV criteria for binge eating disorder were randomly assigned to 24 weeks of double-blind sibutramine (15 mg) or placebo treatment. The outcome measures included the frequency of eating binges (primary outcome), binge day frequency, body mass index, body weight, global improvement, response categories, associated eating pathology, and quality of life. The primary analysis for continuous measures was the difference between groups in the change from baseline to endpoint using analysis of variance (ANOVA) with the last observation carried forward.Compared with subjects receiving placebo, participants who received sibutramine had a significantly greater reduction in weekly binge frequency (sibutramine group mean=2.7 [SD=1.7], placebo group mean=2.0 [SD=2.3]); weight loss (sibutramine group mean=4.3 kg [SD=4.8], placebo group mean=0.8 kg [SD=3.5]); reduction in frequency of binge days; reduction in body mass index; global improvement; level of response, including the percentage of abstinence from binge eating (sibutramine group: 58.7%; placebo group: 42.8%); and reduction in eating pathology (cognitive restraint, disinhibition, and hunger). The change in quality of life scores was not significant. Sibutramine was associated with significantly higher incidence of headache, dry mouth, constipation, insomnia, and dizziness.This trial demonstrated the efficacy of sibutramine in reducing binge eating, weight, and associated psychopathology.

Objective: Cognitive behavioral therapy (CBT) is efficacious for the treatment of bulimia nervosa (BN) and binge-eating disorder (BED). As a number of factors limit the availability of CBT, self-help manuals have been developed to make the treatment more widely available. Method: Published studies evaluating the efficacy of self-help programs in the treatment of BN and BED were reviewed. Results: Controlled studies of self-help programs for BN and BED have often employed a waiting list control group, and indicate that self-help provides more benefit than remaining on a waiting list. However, fewer studies have utilized a more active control group, and these studies have not been as positive. Conclusion: In general, open and wait-list trials indicate that self-help is helpful in treating BN and BED, but there is little evidence for the specific efficacy of self-help in comparison to other treatments. Additional studies of self-help are needed to determine the specific utility of self-help interventions for BN and BED.

BACKGROUND Recovery from osteoporosis in anorexia nervosa (AN) is uncertain. OBJECTIVE The purpose of this study was to understand the changes in bone mineral density (BMD) in women with AN and the mechanisms of recovery from osteopenia. DESIGN We studied BMD and markers of bone formation and resorption, osteocalcin and N-telopeptide (NTX), in patients with AN (n=28) who were following a behavioral weight-gain protocol. RESULTS Anorexic patients experienced significant percentage increases in BMD (4.38 +/- 7.48% for spine; 3.77 +/- 8.8% for hip; P

Objective: This article provides a brief overview of the development of the diagnostic criteria for eating disorders in DSM-IV. Method: The process by which DSM-IV was developed is reviewed, including perspectives on what constitutes diagnostic validity and clinical utility, and their importance in assessing proposed changes in diagnostic criteria. Results: The question of whether alterations in diagnostic criteria would clearly improve clinical utility was a major consideration in the DSM-IV process. Because of concerns that changes in diagnostic criteria would be disruptive and might entail loss of established knowledge, the DSM-IV Task Force assumed a generally conservative stance vis-a-vis change. Conclusion: The process of developing DSM-V is just beginning, and it is far from clear what alterations in diagnostic criteria for eating disorders will occur. However, the evolution of DSM-IV may provide a useful perspective on the development of DSM-V. © 2007 by Wiley Periodicals, Inc. Int J Eat Disord 2007.

Objective: This study sought to quantify, among patients hospitalized for the treatment of anorexia nervosa (AN), the reinforcing value of exercise, defined as the amount of work a patient would expend for the opportunity to exercise. Method: Sixteen inpatients with AN performed a computerized progressive ratio (PR) task for the opportunity to exercise for either 15 or 30 min, or a monetary voucher. Exercise “breakpoint” was calculated and compared with clinical measures. Results: Patients performed an average of 1134.4 (±751.2) button presses for exercise. Exercise breakpoint was significantly correlated with the Beck Depression Inventory (BDI; r = .728, p = .001), and there was a trend toward a correlation with the Commitment to Exercise Scale (CES; Davis, 1993; r = .490, p = .054). Conclusion: Results support the feasibility and potential utility of this novel application of the PR task to quantify the reinforcing value of exercise in AN. The association between exercise and depression is consistent with some prior studies in AN. The trend toward an association with CES scores suggests that breakpoint captures an aspect of the motivation for exercise in this population. © 2007 by Wiley Periodicals, Inc. Int J Eat Disord 2007

Elevated physical activity is commonly observed among patients with Anorexia Nervosa (AN) and can manifest in several forms. While elevated physical activity may play a key role in the pathophysiology of this disorder, much remains unknown about it, including the relationship among its various manifestations, and their underlying mechanism(s). The purposes of the current study were to (1) quantify locomotor activity in inpatients with AN using an accelerometer, (2) determine the association between locomotor activity and exercise history and (3) determine the association between urinary cortisol and physical activity. Thirty-six women hospitalized with AN wore activity armbands for 48 h during the first 2 weeks of hospitalization, collected 24-h urine to measure cortisol, and completed rating forms. Activity counts varied more than four-fold among individuals but were consistent within individuals over the 2 monitoring days (p

This study investigated the relationship between self-reported dietary restraint and expectancies about caloric content on test meal consumption among undergraduate women. Participants completed two test meal sessions during which they were asked to consume as much milkshake from a covered opaque container as they wished. In one session, participants were instructed that the milkshake was made with high-calorie ingredients, and in the other that the milkshake was made with low-calorie ingredients. The milkshakes in both sessions were actually made with the same ingredients. Participants’ mean consumption was less on the low-calorie instruction day (402 g) than on the high-calorie instruction day (382 g), but the difference was not statistically significant. In addition, few significant relationships were observed between dietary restraint measures and total intake on either the low- or high-calorie instruction days. Thus, this study supports a growing body of literature indicating that scores on measures of dietary restraint are not related to the actual restriction of food intake.

ContextAntidepressant medication is frequently prescribed for patients with anorexia nervosa.ObjectiveTo determine whether fluoxetine can promote recovery and prolong time-to-relapse among patients with anorexia nervosa following weight restoration.Design, Setting, and ParticipantsRandomized, double-blind, placebo-controlled trial. From January 2000 until May 2005, 93 patients with anorexia nervosa received intensive inpatient or day-program treatment at the New York State Psychiatric Institute or Toronto General Hospital. Participants regained weight to a minimum body mass index (calculated as weight in kilograms divided by the square of height in meters) of 19.0 and were then eligible to participate in the randomized phase of the trial.InterventionsParticipants were randomly assigned to receive fluoxetine or placebo and were treated for up to 1 year as outpatients in double-blind fashion. All patients also received individual cognitive behavioral therapy.Main Outcome MeasuresThe primary outcome measures were time-to-relapse and the proportion of patients successfully completing 1 year of treatment.ResultsForty-nine patients were assigned to fluoxetine and 44 to placebo. Similar percentages of patients assigned to fluoxetine and to placebo maintained a body mass index of at least 18.5 and remained in the study for 52 weeks (fluoxetine, 26.5%; placebo, 31.5%; P = .57). In a Cox proportional hazards analysis, with prerandomization body mass index, site, and diagnostic subtype as covariates, there was no significant difference between fluoxetine and placebo in time-to-relapse (hazard ratio, 1.12; 95% CI, 0.65-2.01; P = .64).ConclusionsThis study failed to demonstrate any benefit from fluoxetine in the treatment of patients with anorexia nervosa following weight restoration. Future efforts should focus on developing new models to understand the persistence of this illness and on exploring new psychological and pharmacological treatment approaches.Trial Registrationclinicaltrials.gov Identifier: NCT00288574

Anorexia nervosa (AN) is a severe mental illness characterized in part by rigid thinking and ritualized behaviors involving eating and weight. Cognitive rigidity may play a role in the perpetuation of symptoms, and may provide information as to important brain-based abnormalities. Neuropsychological studies of patients with AN have shown cognitive dysfunction, but few have focused on cognitive flexibility. This study assessed set shifting in patients with AN, as a measure of cognitive flexibility. In this study, 15 patients with AN were compared with 11 healthy controls using a neuropsychological battery including the Wisconsin Card Sort Test (WCST). While patients with AN did not differ from controls on 5 measures of neuropsychological function, they made significantly more perseverative errors on the WCST, indicating a problem in set shifting. This finding suggests that patients with AN have a specific neurocognitive abnormality that may play a role in the development and persistence of this disorder.

Binge-eating disorder (BED)-a syndrome that only recently has attracted scientific attention-is often seen in obese individuals, especially those with severe obesity. However, it remains unclear whether BED represents an etiologically distinct behavioral phenotype of obesity or simply a nonspecific eating pattern sometimes seen in obese individuals.To test whether BED aggregates in families independently of obesity, and if so, whether familial factors for BED also independently increase the risk of obesity.Blinded family interview study of overweight or obese probands with (n = 150) and without (n = 150) BED, and their first-degree relatives (n = 888) in a community setting evaluated between October 2002 and July 2004.Lifetime diagnosis of BED; current and highest lifetime body mass index (calculated as the weight in kilograms divided by the square of the height in meters).Binge-eating disorder aggregated strongly in families independently of obesity (odds ratio, 2.2; 95% confidence interval, 1.4-3.6; P.001). Furthermore, relatives of probands with BED displayed a markedly higher prevalence of severe obesity in adulthood (body mass index/=40) than relatives of probands without BED even when controlling for proband body mass index (odds ratio, 2.5; 95% confidence interval, 1.4-4.4; P = .002).Binge-eating disorder is a familial disorder caused in part by factors distinct from other familial factors for obesity. Furthermore, these BED-specific familial factors may independently increase the risk of obesity, especially severe obesity. It follows that targeted interventions capable of preventing or treating traits influenced by these BED-specific familial factors could reduce the public health burden of obesity.

Objective Numerous trials have demonstrated the efficacy of antidepressant medications for the treatment of bulimia nervosa (BN). The current study examined whether early response to medication predicted response to medication at the end of a controlled trial. Method Data from two previously published studies of desipramine (DMI) were used. Seventy-seven patients with BN were included in the analysis. Receiver operating characteristic (ROC) curves were constructed to examine the relation between the percentage reduction in symptoms at each week and failure to respond to antidepressant medication at the end of the trial. Results Eventual nonresponders to DMI could be reliably identified in the first 2 weeks of treatment. Conclusion The current study provides preliminary evidence that patients with BN who will not respond to antidepressant medication can be identified in the first 2 weeks of treatment. © 2005 by Wiley Periodicals, Inc.

An occasion of drug taking may be a passing indulgence of an adolescent, perhaps initiated in a moment of immature judgment. All too often, the drug taking can become repetitive and may lead to a syndrome of abuse or addiction, possibly in an interaction of inherited vulnerability traits with environmental conditions and processes. The development of addiction and the dependence syndrome in adolescents are emotion-laden, controversial, and often misunderstood topics. Public opinion leaders often do not appreciate the scientific evidence that tends to favor a disease concept of addiction or dependence on alcohol, tobacco, and other drugs such as cocaine or cannabis. This evidence includes a neuronal basis for many of the prominent clinical features of dependence, genetic vulnerability, and a characteristic chronic, relapsing course that resembles that of many medical illnesses. Unfortunately, these biological bases of addiction are often forgotten or misunderstood by a nonetheless opinionated American public that can view adolescent drug problems as purely behavioral and morally objectionable. Consequently, many affected adolescents end up being managed by their parents, school authorities, or the judicial system rather than being treated in specialized adolescent treatment programs. Even those seeking treatment often discover that appropriate programs do not exist in their geographic region or are difficult to access because of low capacity or managed care policies. While there would be a public uproar if treatment were not available to adolescents with head injuries, diabetes, or cancer, obvious disparities in addiction treatment have been tolerated for decades and may well reflect public skepticism about the biological bases of drug dependence and addiction. Unfortunately,we have much to learn about the onset, nature, and treatment of these conditions in adolescents. It is our contention that gaps in our knowledge should be addressed with research and clinical experience, and not cited to justify an inadequate treatment infrastructure.

This chapter on the research agenda for anxiety disorders in adolescents consists of a summary of what is currently known, what is currently not known and what further research is needed on the subject, including how they can be treated, and how they can be prevented.

ajp.psychiatryonline.org In any case, as I read chapter after chapter I began to discover a different perspective about this book. While there is no longer a need to prove that homosexuality is not a mental disorder or that Dr. Spitzer’s study of 2001 lacked scientific rigor, this compendium of papers/chapters permitted the review of this historical series of events together rather than separately. This historical and comprehensive approach has some value when seen in this context. However, for the reader who might want to examine both sides of this issue for the purpose of deciding who was right or who was wrong on this topic, reading this book will serve no purpose whatsoever, since that type of decision has no validity in the 21st century. In terms of the book itself, it has 37 chapters, divided into four sections. The first section lays out an introduction to the topic of this book and the book itself. The second section focuses on the concept of “changing sexual orientation.” The third section is comprised of a series of commentaries about Dr. Spitzer’s controversial study of the early 2000s and his response to them. Both sides attempt to explain how right or wrong Dr. Spitzer’s study was. The fourth section includes commentaries on the Spitzer study as well as an interview with Dr. Spitzer conducted by Dr. Jack Drescher. In summary, despite its shortcomings, this compendium of previously published papers offers a unique opportunity to review and understand the historical perspective of “homosexuality” as perceived by the profession and society at large during the last several decades. From this viewpoint, I strongly recommend this book to those interested in this historical perspective.

The purpose of this chapter is to discuss an additional complicating factor that impacts adolescent treatment and goes beyond the individual youth and his or her family: the service delivery system. These systems (e.g., educational institutions, health care, juvenile justice, and mental health systems) are complex environments that offer opportunities to identify, treat, and monitor adolescent substance abusers. However, the architecture and operating procedures of these systems often serve to inhibit access to needed services and to confuse or confound coordination of complementary service delivery across systems. The result can be formidable challenges to the identification and subsequent intervention and treatment of the adolescent who uses, abuses, or is dependent upon substances. In the text that follows, we identify problems within the current “standard” system of care leading to failure to identify these adolescents, inadequate access to even basic substance abuse intervention for those identified, and failure to provide adequate amounts or types of services to those who do access the care system. We also present mechanisms for enhancements and conclude with a summary of three innovative approaches targeted to systems improvement.

The prevention of an individual's first episode of depression is worthy of greater study among investigators concerned with mood disorders. Not only is the first episode devastating for individuals and those around them but it is a major burden within our health system and society. Once the first episode of major depressive disorder (MDD) occurs, the sequelae are substantial. Following an episode of MDD, the probability of subsequent episodes is significantly increased, even to the point that many now consider MDD to be a chronic disease. The sequelae to MDD are numerous and include poorer social relationships, increased substance abuse, increased use of medical services, interference with long-term cognitive functioning, significant comorbidity with major health problems, and younger ages of death (even when deaths by suicide are taken into account). Most investigators of mood disorders believe that the first episode lays down neural pathways that are difficult to overcome and, without modification via medications or psychosocial interventions or their combination, are likely to be lasting pathways that impact individuals' lives. Even though prevention of MDD is an important topic, empirical work in this area is difficult and has been slow to progress. Some recent work has been conducted on the prevention of second and subsequent episodes, but the work designed to prevent the first episode of MDD has been meager. Before addressing the empirical work on prevention of MDD, it is important to note again the conceptual and historical context in which general prevention research has been defined.

There are no scientific studies to indicate the optimal treatment of eating disorders for adolescents, in terms of when treatment should begin, where that treatment should be delivered, or who should provide the treatment. The consensus view is that therapy should begin as soon as possible after a clinically significant eating problem has been identified, with the treatment provider, parents, and patient working to individualize treatment. The setting for the treatment is partially determined by availability, but the severity and duration of illness, especially with regard to medical complications, must also be considered. The optimal professional to treat an adolescent with an eating disorder is again determined in part by availability. Eating disorders can be effectively managed by a variety of different professionals, including physicians (psychiatrists, primary care providers, or adolescent medicine specialists), psychologists, social workers, and nutritionists who are familiar with efficacious treatment of eating disorders.

This chapter on the research agenda for depression and bipolar disorders consists of a summary of what is currently known, what is currently not known and what further research is needed on the subject of major depressive disorder (MDD) and bipolar disorder, including how they can be treated, and how they can be prevented.

The purpose of this chapter is to outline these challenges to improving delivery of effective treatments for adolescents and their families and to define a set of research and policy directions that may help improve delivery. In particular, a number of major multisite studies supported by several foundations and federal agencies are currently under way to examine contextual influences on delivery of youth mental health services. These studies will very likely lead to new ways of thinking about implementation and dissemination of effective practices.

Our primary goal in this section of the book is to examine youth suicide prevention strategies and interventions with an eye toward identifying what works, what does not appear to work, and what research needs to be undertaken to move the field forward. We begin with a review of the multiple factors that have been suggested to put youth at risk for suicide.

This chapter reviews the epidemiology and definitions of mood disorders in children and adolescence. The psychological, social, and biological factors that have been shown to increase the risk of mood disorders in children and adolescents are also discussed.

In this chapter, we focus on suicide prevention programs that have taken a universal approach, targeting youth in specific settings regardless of individual risk factors. One particularly widespread approach targets youth where they are most accessible–in the schools. Although the ultimate goal of all suicide prevention programs is to reduce death by suicide, school-based programs typically focus on more proximal outcomes. Two broad types of universal prevention programs have been especially common. The first includes educational programs that aim to increase students' knowledge and awareness about suicidal behavior, encourage troubled students to seek help, and improve recognition of at-risk students by teachers, counselors, and other “gatekeepers” within the school or community settings. In the second category are screening programs that seek to identify and refer to treatment youth who are at risk for suicidal behavior. In each category, suicide prevention efforts have been separately designed for high school and college students. In the following pages, we summarize these universal programs, identifying for each broad type the underlying assumptions and specific program examples, and providing a summary critique of the approach.

There are currently recognized precursors of schizophrenia that are apparent during adolescence. A wide variety of early-intervention techniques have been developed that draw on the knowledge of these precursors to identify individuals at risk for the illness and to prevent the predisposition toward schizophrenia from developing into the full disorder. Unfortunately, most of the research that has enabled the identification of these precursors and the development of these intervention techniques has been performed retrospectively in adults with schizophrenia, with little specific research attention directed toward forms of schizophrenia that manifest during adolescence. In addition, prevention efforts have necessarily lagged behind studies of the risk factors, detection, and early intervention of the disease. Yet, a great deal has already been learned about risk-profiling and early intervention in schizophrenia generally, and those aspects that may be useful in understanding the adolescent forms of the illness are discussed below.

This chapter on the prevention of anxiety disorders in adolescents considers intervention studies, but before this it is important to briefly consider what is known about risk and protective factors at the individual, familial, and societal level, because it is knowledge of these factors and their interrelations that should inform the development of specific intervention strategies. Unfortunately, knowledge of such factors is limited, and perhaps the paucity of prevention studies in anxiety disorders is a direct result of this limited knowledge. Of particular concern is the absence of evidence about protective factors that are specific to anxiety disorders. That is, although the youth resilience literature has generally underscored the importance of factors such as high IQ, selfesteem, social support, and positive coping in serving to protect young people from the development of psychopathology in general, there is a paucity of literature regarding whether any protective factor(s) may serve to protect against anxiety disorders in particular. Certainly, development of effective prevention programs will continue to be hampered until evidence-based knowledge has accumulated in this area. The summary below is thus reflective of this in proportion to the literature; that is, considerable more coverage is paid to risk factors than to protective factors.

We have learned a great deal about the early course of schizophrenia during the past two decades, leading to therapeutic optimism. However, several key areas of research continue to be a priority. First, we need to identify specific clinical characteristics in the premorbid and prodromal phases that can help us predict the individuals at a high risk for developing psychosis. Second, we do not know how to prospectively identify the early beginnings of the psychotic illness with an adequate degree of reliability to be able to intervene early. We also need to better understand the pathways to care for these patients. Educating the public and health care providers in early signs and symptoms can reduce the delay in care. Third, we need to further clarify the clinical features in the first psychotic episode that can help us predict subsequent illness course. Finally, we need to better understand the neurodevelopmental and neurodeteriorative processes that may underlie both the emergence and the subsequent course of the first psychotic episode.

Concurrent with the emergence of a growing psychopathology literature, child and adolescent clinical psychology and psychiatry have moved away from nonspecific interventions toward problem-focused treatments keyed to specific diagnoses and, within diagnoses, targets. The past 40 years have seen the emergence of diverse, sophisticated, empirically supported, cognitivebehavioral and pharmacological therapies that cover the range of childhood-onset anxiety disorders). Before reviewing what is known about the treatment of anxiety disorders in adolescence, we first provide a brief overview of the history and rationale for cognitive-behavioral therapy (CBT), for pharmacotherapy, and for the combination of the two in the treatment of youth with anxiety disorders. Because of increasing emphasis in the field on evidence-based approaches, those interventions that have not been subjected to treatment outcome study by means of accepted research methodology, such as psychodynamic approaches, “play therapy,” and other approaches, are not reviewed in this chapter.

This chapter presents research conducted as part of the Sunnylands Adolescent Mental Health Initiative (SAMHI) to determine primary care provider practices in identifying and referring adolescents for treatment of mental health problems.

Although it is clear that adolescent mood disorders exist and lead to significant immediate and lifelong impairment for the child, there exists limited treatment research in this special population. This has led clinicians to consult with the adult literature to provide guidance in their treatment approaches. In fact, the adult research studies have provided the template for the present interventions being explored in adolescent treatment studies. To appreciate how the adult literature informs the field of adolescent mood disorder treatments, the current status of the adult literature for both psychosocial and psychopharmacologic treatments will be reviewed. This will be followed by an appraisal of the same treatment areas for adolescents.

In this chapter we review examples of selective suicide prevention programs that have been developed for youth identified or presumed to be at increased risk for suicidal behavior. Although the youth targeted by such programs are considered to be particularly vulnerable to suicide, in most cases they have not yet exhibited specific signs of suicidality. Discussed here are programs for three specific groups, each of which has shown elevated rates of suicidal behavior: Native American youth, youth with recent exposure to a suicide in the school or community, and youth who have access to firearms in the home. While there has been considerable research suggesting that adolescents and young adults in these groups are at greater risk for suicide, relatively few intervention programs for these populations have been developed to date.

The effective prevention and treatment of adolescent substance abuse, like that for any public health problem, require a clear understanding of causes and the context in which these causes operate. Research on the origins of adolescent substance abuse is asking many important questions: How do different drugs affect the brains of different adolescents at different stages of maturation? How do environmental conditions increase or decrease the probability of substance abuse? Are there individual sensitivities to drugs of abuse that increase the risk of a substance use disorder? How do social factors produce contagion of drug abuse among adolescents? Are there specific treatments or prevention interventions for specific types of adolescent substance abuse? How do biological, psychological, and social factors account for failed prevention efforts or drug treatment relapse, and how common is it? This promising body of research carries with it the potential to create more effective approaches to the prevention of adolescent substance abuse as well as guiding treatment efforts.

The research of the past few decades has expanded our understanding of the phenomena linked to the concepts of anxiety and anxiety disorder. A comparison of contemporary reports with those of the last half century provides reason for optimism, for we have learned several important facts. First, the state we call anxiety in humans is not unitary in origin or consequence and can be the result of living with realistic threat, past history, conditioning, or a temperamental bias for unexpected somatic sensations that are interpreted as meaning one is anxious. Second, epidemiological and genetic data imply distinct biological profiles for the varied anxiety disorders, many of which implicate neurochemical processes. Finally, clinicians and investigators now have an initial set of cognitive and biological procedures that promise to aid differential diagnosis of individuals who report anxiety. Major advances will occur when investigators and clinicians add these procedures to their interview data. The results of this work will permit the parsing of individuals who have a particular diagnosis into subgroups with more homogeneous biological and psychological features. This knowledge should lead to a more fruitful set of psychiatric classifications.

Interest in psychological treatments for schizophrenia has increased in recent years, particularly in Europe and Australia, driven by understandable patient dissatisfaction with purely pharmacological approaches. The recognition that 40% of patients do not achieve symptom resolution with drug treatment has added impetus to the search for alternatives and adjuncts. Unfortunately, the paucity of data concerning the application of such approaches to adolescents suffering from schizophrenia means that, at least for the time being, inferences have to be drawn mainly from studies of adult populations. Nevertheless, the similar lack of data regarding efficacy and safety of antipsychotic drug treatment in adolescents and the observation that adolescents may be especially sensitive to the adverse effects of typical antipsychotics (e.g., extrapyramidal side effects) and clozapine (e.g., neutropenia and seizures) mean that there is a real need for alternative or supplementary interventions. Indeed, one could hypothesize that psychological treatments might be more effective in adolescents than in adults. This is a group with a greater degree of neural plasticity and a still evolving personality, and who are especially likely to have an ongoing system of support in the form of family and educational input. Furthermore, the latter presents opportunities for early detection. Alongside early treatment with antipsychotics, there is potential for psychotherapeutic interventions to lessen the impact of positive symptoms, improve coping strategies, and potentially to reduce the cognitive deficits, which so impair psychosocial function.

For any disorder, understanding the risk factors, or variables that predict the development of the disorder, is vital to prevention efforts. In eating disorders, considerable progress has been made in identifying risk factors for the development of the syndrome of bulimia nervosa and for a number of the behavioral and psychological symptoms of eating disorders; however, much less is know about risk factors for anorexia nervosa. Through recent efforts we have begun to identify risk factors and to examine how they increase the probability that an eating disorder will develop. This information is being used to inform rational prevention efforts.

For a variety of reasons, little research has been conducted among adolescents with substance abuse problems. We operate as though data obtained from studies in adults applies to adolescents, but we know that there are critical differences. Thus assumptions about adolescents must be empirically tested. The following are a series of questions compiled by the Commission on Abuse of Alcohol and Other Drugs that we believe should be given high priority.

The high rate of adolescent substance abuse in the United States makes the identification of effective treatment approaches a significant priority. Effective early intervention is crucial. Adolescents who initiate alcohol use by age 14 are significantly more likely to develop alcohol dependence as adults than those who initiate use by age 20, with significant reductions in the odds of developing dependence for each year of delayed initiation. Effective early intervention is also crucial with substance-abusing adolescents because it can play a preventive role in later years. Treatment of substance-abusing adolescents is complicated by a number of factors that appear to be particularly prevalent or problematic among adolescents. First, adolescents in treatment samples usually use multiple substances. Second, substance-using adolescents have very high rates of comorbid psychiatric disorders, which can greatly complicate treatment delivery and outcome. Treatment of substance-abusing adolescents is also complicated by high rates of substance abuse in their immediate families. Another obstacle to treatment for adolescents is that adolescents rarely seek treatment voluntarily but are usually coerced at some level after experiencing school, legal, or medical problems. Treatment is also complicated by their involvement in the multiple systems in which their legal, school, and medical problems are being addressed, as these problems may be identified prior to recognition of the presence of a substance use disorder. Finally, high attrition from treatment is a particular problem among adolescents, with treatment completion rates for adolescents in therapeutic communities estimated at less than 20%. Completion rates for outpatient programs are generally estimated at 50%.