Psychiatric Aspects of Child and Adolescent Obesity: A Review of the Past 10 Years

Body mass index (BMI) is the simplest and most common assessment tool for categorizing childhood obesity and is calculated by dividing weight (kg) by height (m²). BMI charts for boys and girls can be found at www.cdc.gov/growthcharts. BMI accurately reflects the proportion of excess body fat and correlates with markers of secondary complications of obesity and long-term mortality (Barlow and Dietz, 1998). An expert panel on obesity evaluation and treatment recommends that a BMI greater than the 95th percentile for age and sex should be used as a cutoff for medical evaluation of obesity (Barlow and Dietz, 1998). In older adolescents, a BMI in the 95th percentile is associated with elevated blood pressure and lipid profiles, increasing risks of obesity-related disease and mortality (Barlow and Dietz, 1998). A patient with a BMI above the 85th percentile or a large increase in BMI should be observed closely for secondary complications. To maintain consistency with the existing literature, this review will use the term “obesity” to describe a BMI greater than or equal to the 95th percentile and “overweight” for BMI greater than or equal to the 85th percentile.

Rates of childhood and adolescent obesity have increased dramatically in the past decade. According to a recent article in the Journal of the American Medical Association based on results from the 1999–2000 National Health and Nutrition Examination Survey (NHANES), more than 15% of youths ages 6 through 19 were obese, and more than 10% of children ages 2 through 5 were obese (Ogden et al., 2002). The percentages of obese children and adolescents were relatively stable over NHANES I (1971–1974) and II (1976–1980) but doubled to 11% during NHANES III (1988–1994) and then increased again by 4% during NHANES IV (1999–2000) (National Center for Health Statistics [NCHS], 1999).

This recent increase is particularly evident among non-Hispanic black and Mexican-American adolescents. For youths in these groups, the prevalence of obesity increased more than 10% between 1988 to 1994 and 1999 to 2000. As a result, more than 23% of non-Hispanic black and Mexican-American adolescents were obese in 1999 to 2000 (Ogden et al., 2002). African-American girls ages 6 to 19 have the highest rates of obesity, slightly higher than Native Americans and Hispanics (NCHS, 1999). These figures merit further research into cultural and racial influences on the prevalence of childhood obesity.

Although many of the effects of childhood obesity do not manifest themselves until adulthood, the obese child may suffer immediate consequences from his or her condition. The medical sequelae that threaten the young obese child include cardiovascular disease, endocrine and pulmonary problems, and orthopedic, gastroenterological, and neurological difficulties (Strauss, 1999).

A 40-year follow-up study revealed a twofold increase in the rate of cardiovascular disease and hypertension and a threefold increase of diabetes in obese children compared with normal-weight children (Mossberg, 1989). A 50-year follow-up to the Harvard Growth Study of 1922 to 1935 showed that obese adolescent boys ages 13 to 18 experienced twice the mortality rate from cardiovascular disease in adulthood. Being obese as an adolescent was a better predictor of overall mortality than being obese as an adult (Strauss, 1999).

Endocrine malfunction caused by obesity results in insulin resistance, associated with the onset of type 2 diabetes mellitus. The number of children with type 2 diabetes mellitus increased 10-fold between 1982 and 1992, and more than 90% of these patients had a BMI above the 90th percentile (Pinhas-Hamiel et al., 1996). It is noteworthy that most of these patients exhibited no symptoms or unrelated symptoms of type 2 diabetes mellitus. Data from the Bogalusa Heart Study showed the development of type 2 diabetes mellitus in 2.4% of the obese adolescents by age 30 compared to none in the lean population (Srinivasan et al., 1996).

Recent research on asthma and child obesity has demonstrated mixed results, and most findings suggest no correlation between the two disorders (Brenner et al., 2001; Chinn and Rona, 2001; Von Kries et al., 2001; Von Mutius et al., 2001). Multiple studies of obese children have shown that as many as 94% suffer from a sleep abnormality, most often sleep apnea (Mallory et al., 1989; Marcus et al., 1996; Silvesti et al., 1993). Obese children with obstructive sleep apnea demonstrate clinically significant decrements in learning and memory function compared with obese children without obstructive sleep apnea (Rhodes et al., 1995).

Orthopedic problems, such as slipped capital epiphyses and Blount’s disease, occur in obese children. Approximately 50% to 70% of patients with slipped capital epiphyses are obese. Hip pain, knee pain, or altered gait in an obese child could result from this event (Kelsey et al., 1972; Strauss, 1999). Blount’s disease involves bowing of the legs and tibial torsion from bearing unequal or early excess weight, and one study reported that up to 80% of children with Blount’s disease were obese (Dietz et al., 1982). Obesity accounts for 8% to 33% of cases of gallstones observed in children, and it has been estimated that the risk of gallstone formation is approximately 4.2 times greater in 14- to 20-year-old obese girls than in their peers of normal weight (Friesen and Roberts, 1989; Halcomb et al., 1980; Honore, 1980). Studies have also shown a positive correlation between obesity and pseudotumor cerebri (Corbett et al., 1982; Durcan et al., 1988; Scott et al., 1997; Sugerman et al., 1997).

No data suggest that childhood obesity contributes directly to an increased risk of cancer in adulthood. However, a high-fat childhood diet may increase long-term cancer risks, because excess fat intake in adults correlates with an increased risk of breast, uterine, cervical, colon, prostate, and pancreatic cancer (Deslypere, 1995; Weisburger, 1997).

During young adulthood, the psychosocial consequences of obesity can include fewer years of education, lower family income, higher poverty rates, and lower marriage rates (Dietz, 1997; Maffeis and Tato, 2001). The challenge of preventing such sequelae is similar to that associated with youth smoking. In both cases, health care professionals must consider how to persuade youths to change their behavior even though the negative physical consequences are so distant.

Obese children are at great risk for adulthood obesity. Leading predictors are parental weight status and the child’s adiposity (amount of fatty tissue) after age 10. Both obese and nonobese children have twice the risk of adulthood obesity when at least one parent is obese (NCHS, 1999; Whitaker et al., 1997). For children ages 3 to 9 years, both their BMIs and their parents’ BMIs are predictors of later obesity. Furthermore, 80% of obese adolescents ages 10 to 14 with at least one obese parent remain obese (Whitaker et al., 1997). Although a high percentage of obese children become obese adults, this does not mean that most obese adults were obese as children.

As children mature, their own adiposity and BMI become more accurate predictors of future obesity than parental weight. Klish (1998) reports that 25% of obese 6-year-olds become obese adults and 75% of obese 12-year-olds remain obese. Other studies supporting these data, such as Whitaker et al. (1997) and Styne (2001), estimate that one third to one half of obese 6-year-olds become obese adults.

Gestational events and the adiposity rebound period (see below) may influence childhood-onset obesity leading to adult obesity. Studies have observed that famine during gestation can either increase or decrease later obesity prevalence, and “infants with higher neonatal amniotic fluid concentrations of insulin show significantly increased obesity at age 6 years” (Strauss, 1999, p. 8). Infants whose mothers had gestational diabetes have a 50% greater risk of obesity at age 10 (French et al., 1995; Styne, 2001). Although some studies indicate that breast-feeding protects against obesity, others indicate either no influence or an increased risk of becoming obese (Ebbeling et al., 2002; Parsons et al., 1999; Strauss, 1999). Parsons et al. (1999) found a strong correlation between low socioeconomic status during early life and adult obesity.

Many studies on childhood obesity causes have focused on adiposity rebound, a normal childhood developmental event. Rebound is the increase of BMI that occurs after the normal decrease in adiposity between infancy and approximately age 5 to 7. Some studies identify early adiposity rebound in childhood (before age 5) as an obesity predictor (French et al., 1995; Styne, 2001). Parsons et al. (1999) and Strauss (1999) discuss early maturation, noted in several studies, as an increased obesity risk. However, no clear consensus exists concerning how early adiposity rebound or early maturation influences obesity.

Researchers cannot reliably predict which obese children will become obese adults. Intervention studies are needed in high-risk early childhood populations, and pinpointing responsible factors should be a national priority.

Obesity-associated annual hospital costs, the only U.S. cost data available that isolate childhood obesity, have more than tripled in the past 20 years, from $35 million in 1979 to 1981 to $127 million in 1997 to 1999 (Wang and Dietz, 2002). These data reflect an increase in the percentage of discharges with obesity-related diseases, particularly obesity (197% increase), gallbladder disease (228% increase), and sleep apnea (436% increase). The increased incidence of hospital stays related to obesity-associated diseases serves as further evidence of the increasing prevalence of obesity in children and adolescents.

There are no published reports on the national costs of childhood obesity. However, in 1995, the total cost of health care attributed to adult obesity was $99.2 billion, $51.64 billion of which involved direct medical costs for obesity-related diseases (Wolf and Colditz, 1998).

The median reimbursement rate for pediatric obesity treatment is estimated to be 11%. This rate varies greatly among different types of insurance policies, although there are no significant variations based on a child’s sex, race, or degree of obesity (Tershakovec et al., 1999).

Obesity stigmatizes young children even before adolescence, placing them outside the social norms. When shown drawings of children of different sizes, children rank obese classmates as the least desirable playmates.

Studies on self-esteem in obese children report inconsistent results. Many indicate that obese children and adolescents have moderately lower self-esteem than nonobese peers (French et al., 1995; Manus and Killeen, 1995; Pesa et al., 2000; Stradmeijer et al., 2000; Strauss, 2000). However, other studies reveal no differences in self-esteem between population-based groups of obese children and adolescents and nonobese controls (Gortmaker, 1993; Renman et al., 1999; Rumpel and Harris, 1994). Furthermore, studies finding lower self-esteem report that self-esteem is not significantly lower in obese populations once body image is controlled for (French et al., 1995; Pesa et al., 2000). The most consistently replicated finding is that obese children and adolescents have a more negative body image than their peers (Buddeburg-Fisher et al., 1999; French et al., 1995; Israel and Ivanova, 2002; Manus and Killeen, 1995; Pesa et al., 2000; Renman et al., 1999; Rumpel and Harris, 1994). Overweight children as young as age 5 can develop low self-esteem and negative body image (Ebbeling et al., 2002). A study completed by Grilo et al. (1994) demonstrated that “the greater the frequency of being teased about weight and shape while growing up, the more negative one’s appearance is regarded, and the greater the degree of body dissatisfaction in adulthood” (p. 448).

Self-esteem in obese children varies with gender and age. Females are at greater risk for self-esteem problems because body image is an important component of their self-esteem (Manus and Killeeen, 1995; Pesa et al., 2000). Some obese females develop lower self-esteem as they go through puberty into adolescence (Israel and Ivanova, 2002; Stradmeijer et al., 2000). Some studies report that severely obese females express lower self-esteem than moderately obese females, which suggests that self-esteem relates to the severity of obesity (Israel and Ivanova, 2002). In female adolescents and children, dieting is associated with lower self-esteem (Pesa et al., 2000). The frustrating dieting cycle of losing and regaining weight may itself contribute to lower self-esteem. In addition, dieting correlates with perceived, not actual, body weight. Therefore, although some studies show that an adolescent female’s severity of obesity is correlative with lower self-esteem, dieting behavior, regardless of the severity of obesity, is an indicator of lower self-esteem.

Few studies have examined relationships between self-esteem and race and culture in obese individuals. One study did report that whereas obese white and Latin American females had significantly lower levels of self-esteem than age- and race-matched controls, obese and nonobese African-American girls did not differ significantly on this construct (Strauss, 2000).

Another factor influencing self-esteem is parental concern for the child’s well-being. For 5-year-old obese girls, the mothers’ restriction of food and the fathers’ opinion of the child’s obesity were significantly associated with the child’s negative self-perception (Davison and Birch, 2001). Stradmeijer et al. (2000) found that parental concern in obese 10- to 16-year-olds more significantly correlated with self-esteem problems than did BMI. Parental acceptance or lack of concern may be a protective factor for self-esteem.

Clinical populations show a clear relationship between lower self-esteem and obesity (Rumpel and Harris, 1994). Obesity in children seeking clinical treatment is often more severe than in children in the general population and may correlate with lower self-esteem. However, no data are available to support this relationship in community samples because subjects with obesity as severe as that seen in clinically referred patients are rare. Therefore, associations between the severity of obesity and low self-esteem may be more difficult to assess in a population-based study. One hypothesis is that clinically referred children represent a subgroup of obesity associated with especially low self-esteem. In addition, parents who seek clinical treatment for their child’s obesity may exhibit more concern, an indicator for negative self-esteem in children as described above.

Manus and Killeen (1995) and Israel and Ivanova (2002) indicate that some obese children and adolescents with normal self-esteem use compensatory methods to protect themselves from lower self-esteem. Manus and Killeen suggest that obese children use discounting (diminishing the importance of domains in which they are less competent) as a coping mechanism. For instance, such children may view their physical appearance as unimportant and place more importance on other domains in which they excel. They also use distortion (enhancing their perception of competence) by underestimating their actual body size or weight. Similarly, Israel and Ivanova suggest that both obese girls and boys place decreased emphasis on their physical self-esteem and increased emphasis on other self-esteem dimensions to maintain general self-esteem. Further research is needed on why some obese children are more susceptible than others to low self-esteem.

For a complete review of the neuroscience and neuroendocrinology involved in eating, see Schwartz (2001) and Lustig (2001).

The hypothalamus regulates energy balance and food intake. Leptin, an adipocyte (fat cell) hormone, and insulin, both present in proportion to fat stores in the body, have a high density of receptors in the hypothalamus. The presence of leptin and insulin activates the anorectic branch of the hypothalamus (which decreases food intake) and inhibits the orexigenic branch (which stimulates food intake) (Fig. 1).

Conversely, the absence of these hormones activates the orexigenic branch and inhibits the anorectic branch, increasing food intake. In addition, peripherally generated signals such as low plasma glucose, cortisol, and the recently discovered hormone ghrelin also increase food intake. A detailed description of these processes is beyond the scope of this review.

Irregular hypothalamus development or damage to hypothalamic neurons may cause some rare cases of obesity, generally before age 10. Certain disorders causing abnormal hypothalamus development, such as Prader-Willi, Bardet-Biedl, Cohen, or Carpenter syndrome, may predispose children to obesity (Lustig, 2001). Tumors may also damage the hypothalamus. Diencephalic tumors, more common in children than adults, are associated with early-onset childhood obesity (Lustig, 2001).

Other brain regions influence hypothalamic control and food intake through projections to the ventral medial hypothalamus (VMH). Dopaminergic brain areas affect eating behavior and motivation. In the 1960s doctors treated weight problems with stimulants such as dextroamphetamine, which have subsequently been shown to alter intrasynaptic dopamine levels (Towell et al., 1988). Further implicating dopamine in obesity, Wang et al. (2001), in a positron emission study, found that adults with fewer dopamine (DA2) brain receptors had greater BMIs. Identifying abnormalities in brain receptors or function in obese children and adolescents could lead to earlier, more precise identification of susceptible individuals. Surprisingly, there are few brain imaging studies on idiopathic obese adults and none on children.

Other important neurotransmitters controlling eating and weight include serotonin (5-HT) and norepinephrine (NE). Serotonergic neurons, which project to areas of the VMH, originate in the raphe nuclei. Studies on 5-HT reuptake inhibitors reveal that serotonin induces satiety and decreases food intake. The role of NE in food regulation is not completely understood. However, studies report that noradrenergic alpha-2 receptor agonists induce food intake, while alpha-1 receptor agonists reduce food intake (Lustig, 2001). Understanding how neurotransmitters and the hypothalamus regulate food intake will permit research into more specialized obesity treatments.

Farooqi and O’Rahilly (2000) provide a complete review of the molecular genetics of childhood obesity.

Twin studies estimate that genetic factors account for 50% to 90% of the variance in BMI. Estimates from numerous adoption, parent–offspring, and sibling studies indicate that genetic factors account for 20% to 80% of the variance in factors associated with obesity development. Such factors include energy intake and expenditure (Klish, 1998; Maes et al., 1997). Maes et al. (1997) examined more than 25,000 twin pairs and 50,000 biological and adoptive relatives and found the strongest BMI correlations among children range from 0.74 for monozygotic twins and 0.32 for dizygotic twins to 0.25 for siblings. The wide range (20%–80%) of estimated influence of genetic factors is due to the large number of studies and very divergent methodologies used.

Several family studies have provided evidence for the role of genetics in obesity, suggesting that 30% to 50% of obesity phenotypes are inherited (Pérusse and Bouchard, 1999a). In mouse and human models, researchers have identified over 200 genes that affect metabolism, food intake, energy expenditure, and other weight-related functions. Mouse models of obesity resulting from environmental factors also exist (Yager, 2000).

Although genes may set biological limits for metabolism and other weight-related mechanisms, behavior and environment influence variations within these limits.

Genes may affect behavior, such as calorie expenditure, by influencing the amount someone moves or fidgets (Levine et al., 1999). Specific genes and mechanisms underlying such behaviors have not been identified, but genetic and familial patterns have been examined. Pérusse and Bouchard (1999a) cited one family study showing that children of active parents tended to be more active, while children of less active parents were less active. This study did not parse out genetic and environmental effects. Another study that Pérusse and Bouchard (1999a) cited found that parents who tended to eat carbohydrates and fatty foods had children who desired similar diets.

Gene–environment interactions are an important aspect of obesity genetics. Intra-twin studies show that similar genotypes respond with little variance to the environment, while inter-twin studies show that dissimilar genotypes vary greatly in environmental response (Pérusse and Bouchard, 1999b). For example, infant biological twins have more similar overfeeding responses than comparisons across twin pairs, who display a large variation in response (Strauss, 1999).

The most common genetic cause of human obesity is mutations in the melanocortin 4 receptor (MC4R) coding region. Whereas most genetic forms of obesity are rare recessive disorders, mutations in the MC4R gene cause dominant and recessive obesity (Lubrano-Berthelier et al., 2003). In some studies, mutations in this gene have accounted for up to 6% of all cases of severe obesity.

Although rare in the population at large, systemic medical conditions can result in obesity. Table 1 lists most of the medical causes. However, fewer than 10% of the child obesity cases seen have endogenous causes; more than 90% are idiopathic (Moran, 1999). This large idiopathic percentage is responsible for the child obesity epidemic of the past 30 years (Strauss, 1999).

Overeating, the chronic inability to control how much is eaten, results in obesity and causes suffering, stigmatization, and social cost, but it is not classified as a behavioral or psychiatric disorder. The International Classification of Diseases (ICD) categorizes obesity as a general medical condition. DSM-IV does not characterize it as a psychiatric disorder “because it has not been established that obesity is consistently associated with a psychological or behavioral syndrome” (American Psychiatric Association, 1994, p. 539). However, binge-eating disorder, seen in high numbers of obese individuals, is a separate proposed DSM-IV disorder (Yanovski et al., 1993).

For obese children and adolescents, who are commonly teased and bullied, obesity is often associated with psychological and behavioral symptoms (see below). Whether pediatric obesity should be labeled a psychiatric disorder is debatable and requires empirical/epidemiological studies. “Compulsive eating” as a symptom has received very little attention in published studies and also merits further research.

Obese patients should be thoroughly evaluated to identify any medical or psychiatric conditions that may affect the course of treatment.

Weight gain is an adverse side effect of many psychiatric medications and a leading cause of noncompliance in adults taking psychotropics. Psychiatric disorders usually require long-term treatment. Hence, medications that cause weight gain can lead to the serious adverse effects of obesity (Malhi et al., 2001). Little research is available on the ramifications of psychiatric treatment and weight gain in children. However, studies on adults reveal findings that may apply to children.

Psychiatric drugs that cause weight gain include certain classes of antidepressants, antipsychotics, and mood stabilizers. Lithium leads to weight gain in up to two thirds of adults, especially those who are already overweight (Devlin et al., 2000). Other antidepressants associated with weight gain are tricyclics and monoamine oxidase inhibitors (MAOIs). The antiepileptic drugs valproate, gabapentin, carbamazepine, and vigabatrin have been shown to cause weight gain, while lamotrigine, levetiracetam, and phenytoin have no effect on weight (Asconapé, 2002). Clozapine, olanzapine, and risperidone are antipsychotics associated with significant weight gain (Bryden and Kopala, 1999; Martin et al., 2000; Ratzoni et al., 2002). Although few studies document the effects of these medications on children, Bryden and Kopala (1999) reported a 58% increase in BMI in one adolescent patient treated with olanzapine, while Horrigan et al. (2001) described an adolescent boy with attention-deficit/hyperactivity disorder (ADHD) who experienced weight gain of approximately 0.4 kg/week from olanzapine treatment. The patient lost weight by taking Adderall before meals. Other medications associated with weight gain are drugs that block histamine H1, serotonin 5-HT2, and dopamine D2 receptors (Devlin et al., 2000). Gothelf et al. (2002) found that BMI increased significantly in schizophrenic adolescent inpatients treated with olanzapine, but not those given haloperidol. A recent study by Morrison et al. (2002) assessed metformin, an antidiabetic therapy, as a treatment for weight gain in children taking olanzapine, risperidone, quetiapine, or valproate. The majority of the subjects lost weight, and the mean changes in weight and BMI at 12 weeks were highly significant. In a letter to the editor, Lessig et al. (2001) describe patients who were given topiramate to counteract weight gain caused by atypical antipsychotics with significant success.

Clinicians should consider the implications of psychiatric medications for weight gain. According to Devlin et al. (2000) and Masand (1999), patients should be informed that weight gain is possible, monitored closely, and given a prevention and weight-management program. If weight gain occurs, one must consider alternative medications not associated with weight gain (for alternative medications see Cheskin et al., 1999). In addition, in adults “the use of weight loss medications must be carefully considered in populations already being treated with psychotropic (and perhaps other) drugs” (Masand, 1999, p. 3). As noted above, weight-loss medications are not approved by the Food and Drug Administration and cannot be considered for routine use in children.

Child and adolescent psychiatrists face a range of ethical dilemmas. Some are specific to certain genetic conditions (e.g., Prader-Willi syndrome). Others are more general and pertain to the classification and proper treatment of obesity, which can be especially complicated in cases involving comorbid psychological disorders. Five recent publications address ethical issues and pediatric obesity; two of these (Holland and Wong, 1999; Kodish and Cuttler, 1996) focus on the issues surrounding Prader-Willi syndrome, a genetic condition associated with a known mutation and mental retardation. Fatal overeating conditions in Prader-Willi individuals present difficult management issues.

More germane to clinicians seeing idiopathic obesity are ethical/legal issues raised by several other authors. Kuss (1996) raises medical and legal arguments for including obesity as a disability under the Americans With Disabilities Act.

One ethical issue confronting clinicians is “cosmetic psychopharmacology,” in which parents pressure providers to prescribe anorectic agents. Another common ethical decision occurs in treating seriously depressed adolescents or psychotic teenagers who resist medication because of concerns over weight gain. Is it ethical to minimize or not mention the weight-gain effects of taking psychotropic medications if noncompliance may have lethal consequences?

Financial conflicts of interest should be avoided with unproven weight-loss approaches. Practitioners should steer their patients away from therapies that could be expensive, prone to failure, or physically harmful.

Finally, psychiatrists should understand and deal with countertransference. “Fat-ism,” like sexism and racism, may contaminate the development of appropriate therapeutic relationships. This is particularly true in working with younger obese patients, where parent-bashing or blaming is common.

Wigton and Mcgaghie (2001) document medical students’ increased pessimism and decreased expectations of compliance while working with obese versus nonobese simulated patients, although the same medical tests and treatments were recommended for both. Clinicians need to confront their own belief systems in order to treat or refer these patients.

Ethical issues are common for researchers studying obese children. Considerable debate exists in academic circles about whether obese children without medical complications have a “condition” that would allow them to participate in studies where no direct benefit may result. Finally, does having merely a risk factor (e.g., two obese parents) permit more invasive or preventive/proactive types of intervention in research settings?

Targeted research to combat childhood obesity will need to focus on several specific areas. Few empirical data exist regarding prevention. For a comprehensive and extensive prevention literature review, see the Cochrane Review by Campbell et al. (2002). School-based intervention programs have been shown to be ineffective (Story, 1999). Approaches to avoid first episodes of obesity must be developed. High-risk and minority populations need to be oversampled and much earlier interventions need to be used. Public policy must support environmental changes (Devlin et al., 2000).

A second important area that needs research is the involvement of parents in the treatment of preadolescents. Collaborations among pediatricians, behaviorally oriented psychologists, and child and adolescent psychiatrists are needed to target behavior change beyond “diet and exercise.” Research is needed on how to modify activity levels and food choices permanently before trying to impose reduced-calorie regimens. Overeating should be conceptualized as a result of combined behaviors that can be targeted for individual study. Behavioral therapy should be integrated with pharmacological interventions and identification of genetic predispositions (Epstein et al., 2001). Long-term studies on the maintenance phase are needed to avoid the relapses seen among adults. Research is also needed on the factors that promote long-term maintenance and the best ways parents can help a child progress successfully (Jelalian and Saelens, 1999; Robinson, 1999a).

Many questions remain regarding effective styles of treatment for short- and long-term success. Research must explore speculation that group treatment for teens is the most effective method because it facilitates social skills and reduces psychosocial morbidity. Practitioners, parents, and investigators must consider the psychosocial outcomes of treatment—and its possible failure. Will weight-loss intervention improve a child’s overall quality of life (Jelalian and Saelens, 1999)?

A final area for research efforts is molecular biology and neuroendocrinolgy. Although a safe and effective long-term pharmacological treatment is the goal of intense industry-based research, a more pressing and realistic goal is the search for biological markers that confer risk. The discovery of a single gene responsible for obesity is unlikely, but discoveries in animal models eventually will prove clinically useful. In humans, imaging studies of receptors (e.g., dopamine and serotonin) that regulate hunger and satiety will be particularly informative. Only through sustained research efforts in the neurobiology of feeding and satiation will the neural circuitry of this behavior eventually become clear enough to inform more successful treatment strategies.

It has been proposed that we abandon traditional weight-loss goals based on tables in favor of “reasonable weight” (Devlin et al., 2000, p. 862). Significant health benefits are associated with modest weight losses that fall short of healthy and aesthetic ideals. Despite the lack of genetic markers or predictors of who will be successful candidates for significant weight-loss maintenance, features to maximize success are known. Obesity will remit in some individuals. Few empirical data exist from rigorously controlled research studies on the psychiatric (as opposed to pediatric) management of obese children with psychiatric disorders. Child and adolescent psychiatrists play a critical role in treating obese children with classic psychiatric disorders. Care and ingenuity must be used to avoid exacerbating weight problems in children with psychiatric disorders.

In September 2003, the Food and Drug Administration formally requested that the makers of all atypical antipsychotic medications change the “Warnings” of the product labeling of antipsychotic medications to include baseline and periodic glucose monitoring. The letter stated, “epidemiological studies suggest an increased risk of treatment emergent hyperglycemia-related adverse events in patients treated with the atypical antipsychotics” (Rosack, 2003).

(Reprinted with permission from the Journal of the American Academy of Child and Adolescent Psychiatry 2004; 43:134–150)