Psychiatric Annals

CME Article 

Metabolic Syndrome in Child and Adolescent Psychiatry

Hyun Jung Kim, MD; Cynthia Wilson, MD; Timothy Van Deusen, MD; Hun Millard, MD; Zheala Qayyum, MD, MMSc; Susan Parke, MD

Abstract

In adults, metabolic syndrome (MetS) is defined as a constellation of at least 3 of 5 cardiometabolic risk factors: central obesity, hyperglycemia, elevated blood pressure, elevated triglycerides, and decreased high-density lipoprotein cholesterol. In pediatric populations, MetS remains a controversial topic due to lack of clear consensus regarding the definition, clinical utility, and lack of standardized guidelines. Despite these controversies, pediatric MetS is receiving increasing clinical and research attention due to the growing obesity epidemic and a substantial increase in the use of second-generation antipsychotics in recent years. Clinicians should be familiar with prevention, early identification, and management of obesity and metabolic derangements while working with youth with psychiatric disorders. [Psychiatr Ann. 2020;50(8):326–333.]

Abstract

In adults, metabolic syndrome (MetS) is defined as a constellation of at least 3 of 5 cardiometabolic risk factors: central obesity, hyperglycemia, elevated blood pressure, elevated triglycerides, and decreased high-density lipoprotein cholesterol. In pediatric populations, MetS remains a controversial topic due to lack of clear consensus regarding the definition, clinical utility, and lack of standardized guidelines. Despite these controversies, pediatric MetS is receiving increasing clinical and research attention due to the growing obesity epidemic and a substantial increase in the use of second-generation antipsychotics in recent years. Clinicians should be familiar with prevention, early identification, and management of obesity and metabolic derangements while working with youth with psychiatric disorders. [Psychiatr Ann. 2020;50(8):326–333.]

Metabolic syndrome (MetS) in adults is defined as a person having at least 3 of 5 cardiometabolic risk factors: (1) central obesity, (2) hyperglycemia, (3) elevated blood pressure, (4) elevated triglycerides, and (5) decreased high-density lipoprotein cholesterol.1 Adults with MetS are known to be at increased risk of diabetes, cardiovascular disease (CVD), and early death. MetS remains a topic of discussion in children and adolescents because there is lack of consensus regarding its definition and clinical utility. MetS in children and adolescents is a topic of clinical attention because of its rising prevalence and the increasing obesity epidemic in this population.2 Recent literature suggests that having MetS as a child or adolescent increases the risk of having the syndrome, as well as type 2 diabetes mellitus (T2DM), and possibly CVD, in adulthood.3 In youth with psychiatric disorders, severe mental illness, and unhealthy lifestyles, the use of antipsychotic medication can increase the risk of MetS. Over the past decade, there has been a substantial increase in the use of second-generation antipsychotics (SGAs) for a number of pediatric psychiatric disorders, often off-label. This article discusses the definition, epidemiology, pathogenesis, contributing factors, and clinical implications of MetS in child and adolescent psychiatry.

Definition

In 1923, Eskil Kylin, a Swedish physician, described a syndrome characterized by hypertension, hyperglycemia, obesity, and hyperuricemia, which today is known as MetS.4 The concept of MetS has evolved since then and various diagnostic criteria have been proposed by several health organizations. In 2009, the International Diabetes Federation (IDF) and American Heart Association (AHA) in conjunction with the National Heart, Lung, and Blood Institute (NHLBI) and other medical organizations published a Joint Task Force statement to reach a consensus regarding the definition of MetS in adults.1

Definitions of MetS in children and adolescents have varied. To date, more than 40 different pediatric definitions have been reported, all using elements of adult definitions with variations in the cutoff values. In 2007, the IDF brought together an international group of experts and developed a consensus definition5 (Table 1). In 2009, the AHA published its statement on MetS in children and adolescents, emphasizing the importance of identifying pediatric cardiometabolic risk factors, only some of which are associated with the current proposed definitions of MetS.6 The AHA declined to provide a definition of, or specific criteria for, MetS in children given the limitations of adapting definitions derived from adult populations.6 Currently, there remains no clear consensus on whether MetS should be defined in pediatric populations and, if defined, which definition to use.

The International Diabetes Foundation Consensus Definition of the Metabolic Syndrome in Children and Adolescentsa,b

Table 1.

The International Diabetes Foundation Consensus Definition of the Metabolic Syndrome in Children and Adolescents

Epidemiology

Epidemiological studies about the baseline prevalence of MetS in children and adolescents have been complicated by a variety of factors. The aforementioned lack of consensus guidelines for the diagnosis of pediatric MetS and the use of adult definitions has led to significant discrepancies in prevalence.7 Prevalence data in the pediatric population can vary from 0% to 19.2% depending on the criteria applied.8 Goodman et al.9 compared prevalence of adolescents using the World Health Organization (WHO) and the National Cholesterol Education Program Adult Treatment Panel III (ATP III) criteria and found a prevalence of 4.3% with ATP III criteria versus 8.4% with WHO criteria. When comparing adolescents with obesity, the prevalence of MetS was 19.5% with ATP III criteria versus 38.9% with WHO criteria.9 It is clear that the prevalence of MetS varies widely depending on the criteria used, and pediatric prevalence is higher when age-specific criteria are applied. Childhood prevalence differs again when child and adolescent criteria are applied.10 The definition is further complicated by the lack of normative values by age for many components of MetS, such as high-density lipoproteins, triglycerides, waist circumference, and blood pressure.11

The prevalence of MetS in pediatric patients is strongly influenced by the prevalence of obesity. One systematic review found that the median prevalence for the entire pediatric population was 3.3%, with 11.9% of children who are overweight and 29.2% of children who are obese meeting criteria of MetS.11 It also demonstrated higher rates in boys and older children.10 MetS may develop progressively with age due to pubertal changes and obesity. Ethnicity is also an important consideration because African American and Hispanic children experience insulin resistance more than White children.11

Further studies are needed to determine the baseline prevalence of MetS in children and adolescents with various underlying psychiatric disorders, as there is evidence that having a psychiatric disorder can increase the risk of developing metabolic disorder through a variety of biological and psychosocial pathways. There is then the additional burden of many psychiatric medications that increase this risk further, which is a topic that warrants further epidemiological study.

Pathogenesis

The pathogenesis of MetS remains unclear, but it is widely thought to be multifactorial and is the subject of ongoing research with environmental, nutritional, and genetic influences. Prevailing theories of the physiologic pathogenesis of MetS include an association with obesity, insulin resistance, adipokine dysregulation, and inflammatory processes (Figure 1). Triglycerides or body fat is ideally stored in peripheral adipose tissue; however, in obesity there is an excess of adipocytes and triglycerides, which are stored in the liver, skeletal muscle, and as visceral adipose tissue. Excess triglycerides and the increase of free fatty acids into the portal and plasma circulation leads to hepatic, other organ, and muscular insulin resistance. Reduced insulin response leads to an increase in lipolysis, which results in further increase of free fatty acids. Insulin resistance leads to impairments in compensatory mechanisms meant to sustain euglycemia as pancreatic beta cells chronically over-secrete, leading to hyperglycemia, glucose intolerance, and diabetes.12 Adipokine dysregulation, which is an increase in inflammatory peptides/proteins, and a decrease in anti-inflammatory peptides/proteins, is also theorized to have an impact on MetS pathogenesis.

Obesity leads to increase in free fatty acids, oxidative stress, and adipokine dysregulation (increase in inflammatory and decrease in anti-inflammatory peptides/proteins), affecting multiple organ systems, which can ultimately can lead to insulin resistance, diabetes, hyperlipidemia, and cardiovascular disease.

Figure 1.

Obesity leads to increase in free fatty acids, oxidative stress, and adipokine dysregulation (increase in inflammatory and decrease in anti-inflammatory peptides/proteins), affecting multiple organ systems, which can ultimately can lead to insulin resistance, diabetes, hyperlipidemia, and cardiovascular disease.

Contributing Factors

The US Food and Drug Administration's (FDA) indications for the use of antipsychotics in children and adolescents are limited to the treatment of adolescent schizophrenia, bipolar mania, irritability associated with autism, and Tourette syndrome.13 Off-label use of SGAs is commonly prescribed in disruptive behavioral disorders and other disorders involving behavioral disturbance such as attention-deficit/hyperactivity disorder.13,14 SGAs are also increasingly prescribed to younger children and disproportionately more frequently to boys, children in foster care, and children insured with Medicaid insurance.

SGAs have been shown to contribute to weight gain, dyslipidemia, and insulin resistance.15 Youth in general appear more vulnerable to these effects. Specifically, children have a higher risk of SGA-induced weight gain compared to adolescents and young adults.16 Also, youth undergoing puberty are particularly vulnerable to the weight-inducing effects of SGAs because of the hormonally driven distribution of body fat that occurs.16 Children and adolescents who take SGAs and are admitted to a hospital have been shown to have a 3-fold increase in the prevalence of obesity (defined as sex-specific body mass index for age ≥95th percentile).17 A recent meta-analysis found that compared to youth who are SGA-naive, youth exposed to SGAs had a significantly greater risk of developing T2DM.15 In the antipsychotic-exposed sample, most had disruptive behavior disorder (DBD) or attention-deficit/hyperactivity disorder (ADHD) (46.9%) or a mood spectrum disorder, including mood disorder not otherwise specified (22.8%), depression (26.9%), bipolar disorder (BPD) (16.2%), and BPD or psychosis (5.1%).15 Less commonly observed were anxiety disorders (7.9%), psychosis (5.7%), pervasive developmental disorder or autism (5.3%), substance abuse disorder (4.6%), and tic disorders (0.0003%).15 In the psychiatric control group, there were DBD or ADHD (51.8%), mood spectrum disorder (34.1%), anxiety disorders (8.7%), pervasive developmental disorder or autism (5.4%), psychosis (0.3%), and substance use disorders (0.2%).

In multivariable analyses, one study showed a significantly elevated risk for patients with BPD and either conduct disorder or ADHD. Other diagnoses associated with T2DM were autism, DBD, and mood disorders, although one study did not find any significant effects of psychiatric diagnoses on the risk of or time until developing T2DM.15 In addition, SGAs' antidopaminergic effect peripherally can increase prolactin, an effect that may be more pronounced in postpubertal youth.18

Besides the adverse effects of SGAs and other weight-inducing psychotropics (such as valproic acid and lithium), a sedentary lifestyle, an unhealthy diet, and/or smoking also contribute to the development of MetS.19

A sedentary lifestyle, even in youth, emerges as a significant environmental risk factor for developing MetS and adiposity. Lack of appropriate physical activity has been found in youth who are overweight, contributing to risk for MetS. This is compounded by increased screen time, particularly excessive television viewing and electronic games. It is important to note that children with mental health conditions have been found to consume diets high in sugar, saturated fat, and sodium. However, rather than individual dietary components, it is the overall poor quality of food that is associated with MetS exerting an influence on waist circumference and systolic blood pressure.20 A youth's socioeconomic status can affect accessible food options. Healthy food choices such as fresh fruits and vegetables may not be readily available and are often more costly than energy-dense foods and sugar-sweetened beverages. Parent-child dyads with parents who are obese also impart a genetic risk toward the development of cardiometabolic abnormalities. Additionally, smoking, including passive smoking, has been associated with an increased risk of developing MetS. Psychosocial factors such as trauma and other childhood adversities that contribute to lack of safety in the home environment, family instability, or out-of-home placements have significant impact on many health domains during childhood and throughout the lifespan.21

Clinical Implications

Screening and Assessment

Concerns about weight gain and metabolic changes associated with the use of SGAs should prompt careful consideration for indications supported by scientific evidence. In 2011, the American Academy of Child and Adolescent Psychiatry provided practice guidelines regarding use of SGAs in youth with psychiatric conditions22 (Table 2). The Canadian Alliance for Monitoring Effectiveness and Safety of Antipsychotics in Children has developed evidence-based recommendations for monitoring safety of SGAs in youth23 (Table 3). Clinicians should identify children who are overweight and obese who are at risk for T2DM and CVD by screening for behavioral and medical risks, including persistent obesity and associated comorbidities. Parental obesity is a major risk factor for childhood obesity and should be included in screening evaluations.

American Academy of Child and Adolescent Psychiatry Practice Parameter for the Use of Second-Generation Antipsychotics in Children and Adolescents

Table 2.

American Academy of Child and Adolescent Psychiatry Practice Parameter for the Use of Second-Generation Antipsychotics in Children and Adolescents

Metabolic Monitoring of Children and Adolescents Treated with Second-Generation Antipsychotics

Table 3.

Metabolic Monitoring of Children and Adolescents Treated with Second-Generation Antipsychotics

Behavioral Interventions

Lifestyle modification is the cornerstone of pediatric obesity treatment. Lifestyle modification entails promoting a healthy diet and increasing physical activity by adopting behavioral change strategies24,25 (Table 4). Dietary interventions were recommended in the recent Endocrine Society guidelines,25 which are based on the American Academy of Pediatrics and the US Department of Agriculture guidelines. A meta-analysis found that lifestyle modification had a positive effect on reducing sedentary behavior in long-term trials, and reduced unhealthy dietary habits were more effective when directed toward children compared to adolescents, with even better results achieved when involving the whole family.26 Physical activity is helpful in improving lipid profile and insulin resistance, and it is correlated with lower fasting insulin levels. Exercise may result in anti-inflammatory effects, improvement of endothelial function with reduction in systolic and diastolic blood pressure, and abdominal fat reduction.

Behavioral Interventions for Prevention of Metabolic Syndrome in Children and Adolescents

Table 4.

Behavioral Interventions for Prevention of Metabolic Syndrome in Children and Adolescents

Pharmacological Interventions

A comprehensive review of pharmacological interventions for each component of MetS is beyond the scope of this article. Medications to treat T2DM, hypertension, and dyslipidemia should be initiated as appropriate in close collaboration with pediatricians. Pharmacological interventions for obesity in children and adolescents should be considered only after the proved failure of a formal program of lifestyle modification. Lifestyle modification programs should be continued along with pharmacotherapy when possible. Pharmacological interventions should be provided by experienced clinicians, who can offer close monitoring for potential side effects and weight reduction results. Discontinuation of the medications and reevaluation should be considered in those who are unable to achieve >4% reduction in body mass index (BMI)/BMI z-score following 12 weeks of treatment with the use of medication's full dosage.25 In general, FDA-approved medications for obesity in adults are used for adolescents older than age 16 years with a BMI of 30 kg/m2 or more, or in those with a BMI of 27 kg/m2 or more associated with at least one obesity-related comorbidity. The field of pharmacotherapy for pediatric obesity is still in its infancy. In adolescents, there is limited evidence regarding the safety and efficacy of anti-obesity medications, especially in the long term.

Metformin is known to decrease hepatic gluconeogenesis and improve insulin sensitivity in the liver and muscle. It is approved by the FDA for the treatment of type 2 diabetes in youth age 10 years old and older. Metformin use in children and adolescents diagnosed with prediabetes can lead to improvement in metabolic parameters such as BMI, body fat composition, fasting glucose and insulin, hemoglobin A1c, insulin resistance index (Homeostatic Model Assessment for Insulin Resistance), blood pressure, and lipid profile. Metformin has been studied the most for weight reduction in youth with psychiatric disorders, and it is often used off-label to treat childhood obesity. Anagnostou et al.27 conducted a randomized controlled trial of metformin with 60 participants, age 6 to 17 years, diagnosed with autistic spectrum disorder and weight gain from atypical antipsychotics. Metformin reduced BMI z-scores from baseline to week 16 significantly more than placebo (difference in 16-week change scores vs placebo, −0.10 [95% CI, −0.16 to −0.04]; P = .003). Statistically significant improvements were also noted in secondary body composition measures (raw BMI, −0.95 [95% CI, −1.46 to −0.45] and raw weight, −2.73 [95% CI, −4.04 to −1.43]) but not in metabolic variables. Ellul et al.28 completed a meta-analysis with 205 children and adolescents treated with second-generation antipsychotics and found a significant weight decrease in the metformin group compared with placebo after 4, 12, and 16 weeks of treatment. The decrease in BMI paralleled that of weight, with a significant effect at weeks 4, 12, and 16. Correll et al.29 conducted a multi-site, randomized, parallel group, 24-week clinical trial that enrolled 127 youth in the US age 8 to 19 years with overweight/obesity who were psychiatrically stable but with Diagnostic and Statistical Manual of Mental Disorders, fourth edition30 diagnoses of severe mental illnesses (schizophrenia spectrum disorder, bipolar spectrum disorder, or psychotic depression). All of them had developed substantial weight gain (>10% of baseline weight) after treatment with a SGA. The study found BMI z-score decreased significantly in the metformin add-on group (week 24: −0.09 ± 0.03, P = .002) and antipsychotic switch group (week 24: −0.11 ± 0.04, P = .003), while it increased nonsignificantly in the control (continued antipsychotic treatment) group (week 24: +0.04 ± 0.03). The authors concluded that pediatric SGA-related obesity can be reduced by adding metformin or switching to a more weight-neutral antipsychotic.29

Orlistat is a gastric and pancreatic lipase inhibitor that decreases triglycerides and cholesterol absorption. It is the only FDA-approved (2003) medication for youth age 12 years and older with obesity. Shin et al.31 conducted a review and found that orlistat appeared to improve weight reduction, fasting insulin, glucose, and lipid profiles when used as an adjunct to lifestyle changes.

A number of weight loss agents are still under investigation for the use in adolescents. These agents include phentermine, topiramate, conjugated linoleic acid, and glucagon-like peptide-1 receptor agonists (liraglutide, exenatide).25

Surgical Interventions

Bariatric surgery can result in significant short-term weight loss in obese children and adolescents. All candidates should undergo psychological evaluation before surgery and during the perioperative period25,32 (Table 5).

Bariatric Surgery for Obesity in Children and Adolescents

Table 5.

Bariatric Surgery for Obesity in Children and Adolescents

Conclusion

Although a lack of consensus exists on whether or how MetS should be defined in youth, pediatric MetS is receiving increasing clinical and research attention due to its rising prevalence and the growing obesity rates. The frequent off-label use of SGAs in children and adolescents has increased dramatically in recent years. Metabolic adverse effects and heightened risk for T2DM are the most frequent and worrisome concerns associated with SGAs. Clinicians should be familiar with prevention, early identification, and management of obesity and metabolic derangements while working with youth with psychiatric disorders. Further studies identifying evidence-based treatments for childhood MetS and understanding the pediatric cardiometabolic risk factors and the interactions of these risk factors from childhood to adulthood are needed.5

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The International Diabetes Foundation Consensus Definition of the Metabolic Syndrome in Children and Adolescentsa,b

Age (years) Obesity (WC) Triglycerides HDL-C Blood pressure Glucose
6 to <10 90th percentile Metabolic syndrome cannot be diagnosed, but further measurements should be made if there is a family history of metabolic syndrome, T2DM, dyslipidemia, cardiovascular disease, hypertension and/or obesity.
10 to <16 90th percentile or adult cut-off if lower 1.7 mmol/L (150 mg/dL) <1.03 mmol/L (<40 mg/dL) Systolic BP 130 or diastolic BP 85 mm Hg FPG 5.6 mmol/L (100 mg/dL) or known T2DM
16 (adult criteria) 94 cm for White men and 80 cm for White women, with ethnic-specific values for other groupsc 1.7 mmol/L (150 mg/dL) or specific treatment for high triglycerides <1.03 mmol/L (<40 mg/dL) for men and <1.29 mmol/L (<50 mg/dL) for women, or specific treatment for low HDL Systolic BP 130 or diastolic BP 85 mm Hg or treatment of previously diagnosed hypertension FPG 5.6 mmol/L (100 mg/dL) or known T2DM

American Academy of Child and Adolescent Psychiatry Practice Parameter for the Use of Second-Generation Antipsychotics in Children and Adolescents

<list-item>

Prior to the initiation of and during treatment with an SGA, the general guidelines that pertain to the prescription of psychotropic medications should be followed

</list-item><list-item>

When selecting any SGAs for use in a child or adolescent, the clinician should follow the most current available evidence in the scientific literature

</list-item><list-item>

Due to the specific risks associated with the use of SGAs, additional factors to address prior to the initiation of treatment with the SGAs include obtaining a personal and family history of diabetes and hyperlipidemia, seizures and cardiac abnormalities, as well as any family history of previous response or adverse events associated with SGAs

</list-item><list-item>

Dosing of the SGAs should follow the “start low and go slow” approach and seek to find the lowest effective dose, recognizing that dosing may differ based on the targeted symptoms and patient diagnosis

</list-item><list-item>

Target dosing should be supported by the current literature and will vary depending on the condition being treated

</list-item><list-item>

If side effects do occur, a trial at a lower dose should be considered; however, certain side effects may preclude further treatment with the specific SGA

</list-item><list-item>

The use of multiple psychotropic medications in refractory patients may, at times, be necessary but has not been studied rigorously and clinicians should proceed with caution

</list-item><list-item>

The simultaneous use of multiple SGAs has not been studied rigorously and generally should be avoided

</list-item><list-item>

After the failure of one SGA the selection of an alternative medication may include consideration of another SGA and/or a medication from a different class of drugs

</list-item><list-item>

The acute and long-term safety of these medications in children and adolescents has not been fully evaluated; therefore, careful and frequent monitoring of side effects should be performed

</list-item><list-item>

BMI should be obtained at baseline and monitored at regular intervals throughout treatment with an SGA

</list-item><list-item>

Careful attention should be given to the increased risk of developing diabetes with the use of SGA, and blood glucose levels and other parameters should be obtained at baseline and monitored at regular intervals

</list-item><list-item>

In those patients with significant weight changes and/or a family history indicating high risk, lipid profiles should be obtained at baseline and monitored at regular intervals.

</list-item><list-item>

Measurements of movement disorders using structured measures, such as the Abnormal Involuntary Movement Scale, should be done at baseline and at regular intervals during treatment and during tapering of an SGA

</list-item><list-item>

Due to limited data surrounding the impact of SGAs on the cardiovascular system, regular monitoring of heart rate, blood pressure, and EKG changes should be performed

</list-item><list-item>

Although there is a relationship between SGA use and elevations of prolactin, the current state of evidence does not support the need for routine monitoring of prolactin levels in asymptomatic youths

</list-item><list-item>

Due to drug-specific risks, additional monitoring should be considered for specific SGAs

</list-item><list-item>

The limited long-term safety and efficacy data warrant careful consideration, before the initiation of medication, of the planned duration of the medication trial

</list-item><list-item>

Abrupt discontinuation of a medication is not recommended

</list-item>

Metabolic Monitoring of Children and Adolescents Treated with Second-Generation Antipsychotics

Measure Baseline 1 Month 2 Months 3 Months 6 Months 9 Months 1 Year
Parameter






  Height, weight, and BMI with age- and sex-specific percentilesa x x x x x x x
  WC with percentilesb x x x x x x x
  BP with percentilesc x x x x x x x

Laboratory tests






  Fasting plasma glucosed x - - x x - x
  Fasting insuline x - - x x - x
  Fasting lipids (total cholesterol, LDL-C, HDL-C, TG) x - - x x - x
  AST and ALT x - - - x - x
  TSH (quetiapine only) x - - - - - x
  Prolactinf x - - - - - x

Behavioral Interventions for Prevention of Metabolic Syndrome in Children and Adolescents

Healthy diet <list-item>

Elimination of sugar-sweetened beverages

</list-item><list-item>

Decreasing consumption of fast food

</list-item><list-item>

Less added table sugar

</list-item><list-item>

Avoidance of high fructose corn syrup

</list-item><list-item>

Less high-sodium processed food

</list-item><list-item>

Less saturated dietary fat in adolescents and children older than 2 age years

</list-item><list-item>

Fruit juice intake should be limited to 4–6 ounces per day for children age 6 months to 6 years and 8–12 ounces per day for older children and try to replace with whole fruits instead

</list-item><list-item>

Increasing consumption of vegetables and dietary fiber is encouraged in addition to portion control education, reading food labels, and encouraging eating regular meals to avoid grazing

</list-item>
Physical activity <list-item>

A minimum of 20 minutes of moderate to vigorous physical activity daily, with a goal of 60 minutes daily is recommended in the context of a calorie-controlled diet

</list-item>
Additional healthy lifestyle modification strategies <list-item>

Adopting healthy sleep habits

</list-item><list-item>

Limiting screen time

</list-item><list-item>

Involving the whole family and community in intervention efforts such as using school-based programs

</list-item>

Bariatric Surgery for Obesity in Children and Adolescents

Bariatric surgery is recommended only if: <list-item>

BMI is >40 kg/m2 and when mild weight-related comorbidities are present (mild comorbidities include hypertension, dyslipidemia, moderate orthopedic problems, mild sleep apnea, NASH, and obesity-related extreme psychological distress)

</list-item><list-item>

BMI is >35 kg/m2 and associated with significant and extreme comorbidities including T2DM, moderate to severe sleep apnea, pseudotumor cerebri, debilitating orthopedic problems, and NASH with advanced fibrosis

</list-item>
Bariatric surgeries are contraindicated in: <list-item>

Preadolescents

</list-item><list-item>

Adolescents who are pregnant or breast-feeding and those who are planning to become pregnant within the next 2 years

</list-item><list-item>

Patients with unresolved substance abuse

</list-item><list-item>

Eating disorders or any other underlying untreated psychiatric illnesses

</list-item><list-item>

Medically correctable causes of obesity

</list-item><list-item>

Disabilities that would impair adherence to postoperative treatment

</list-item>
Authors

Hyun Jung Kim, MD, is a Clinical Instructor in Psychiatry, Harvard Medical School; and the Psychiatrist in Charge, McLean Hospital. Cynthia Wilson, MD, is an Assistant Clinical Professor of Psychiatry, Yale University School of Medicine. Timothy Van Deusen, MD, is an Associate Professor of Psychiatry, Yale University School of Medicine. Hun Millard, MD, is an Assistant Professor of Psychiatry, Yale University School of Medicine. Zheala Qayyum, MD, MMSc, is the Child and Adolescent Psychiatry Fellowship Director, Boston Children's Hospital. Susan Parke, MD, is an Assistant Professor of Psychiatry, Yale University School of Medicine.

Address correspondence to Hyun Jung Kim, MD, McLean Hospital, 115 Mill Street, Mail Stop 108, Belmont, MA 02478; email: hkim@mclean.harvard.edu.

Disclosure: The authors have no relevant financial relationships to disclose.

10.3928/00485713-20200630-01

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