Harvard Review of Psychiatry:
Obesity in Children with Autism Spectrum Disorder
Curtin, Carol MSW; Jojic, Mirjana MD; Bandini, Linda G. PhD, RD
From the Eunice Kennedy Shriver Center (Charlestown, MA) (Ms. Curtin and Dr. Bandini) and Department of Psychiatry (Worcester, MA) (Dr. Jojic), University of Massachusetts Medical School.
Original manuscript received 15 February 2013, accepted for publication subject to revision 23 April 2013; revised manuscript received 20 May 2013.
Correspondence: Carol Curtin, MSW, University of Massachusetts Medical School–E.K. Shriver Center, 465 Medford St., Suite 500, Charlestown, MA 02129. Email: firstname.lastname@example.org
Research suggests that the prevalence of obesity in children with autism spectrum disorder (ASD) is at least as high as that seen in typically developing children. Many of the risk factors for children with ASD are likely the same as for typically developing children, especially within the context of today’s obesogenic environment. The particular needs and challenges that this population faces, however, may render them more susceptible to the adverse effects of typical risk factors, and they may also be vulnerable to additional risk factors not shared by children in the general population, including psychopharmacological treatment, genetics, disordered sleep, atypical eating patterns, and challenges for engaging in sufficient physical activity. For individuals with ASD, obesity and its sequelae potentially represent a significant threat to independent living, self-care, quality of life, and overall health.
Obesity in children has become a significant health concern, and the prevalence of childhood obesity has tripled over the last 20 years. Data from the National Health & Nutrition Examination Survey indicate that nearly a third of children ages 2–19 years in the general population are overweight or obese.1 Evidence from clinic-based studies and nationally representative surveys suggests that the prevalence of obesity in children with autism spectrum disorder (ASD) is at least as high as that seen in typically developing (TD) children. While significant efforts are under way to understand and treat obesity in the general pediatric population, relatively little work has focused on children with ASD. In general, children who are obese are likely to remain so as adults, and excess weight substantially increases the risk for chronic diseases such as diabetes, cardiovascular disease, and certain cancers.2 Given the increasing prevalence of ASD, the prevention of secondary conditions associated with obesity in children in this population is a pressing public health issue, with implications for independent living and quality of life.
Research on the prevalence of obesity and associated risk factors in children with ASD remains limited. Many of the risk factors for children with ASD are likely the same as for TD children, especially within the context of today’s obesogenic environment. The unique needs and challenges of this population, however, may render them more susceptible to typical risk factors for obesity, and they may also be vulnerable to additional risk factors not shared by children in the general population, including psychopharmacological treatment, genetics, disordered sleep, atypical eating patterns, and challenges for engaging in physical activity.
The purpose of this article is to summarize the literature on the prevalence of, and risk factors for, obesity in ASD. A literature search was undertaken using electronic databases of PubMed, Google Scholar, Ovid, and MEDLINE to locate relevant literature published in English in the last 25 years. Searches including the population term (e.g., autism, autism spectrum disorder) and keywords reflecting the headings below, such as obesity, overweight, obesity prevalence, weight status, genetics, medications, eating patterns, food selectivity, and physical activity. Additionally, several bibliographies were inspected manually to identify additional relevant articles.
THE PREVALENCE OF OBESITY IN CHILDREN WITH ASD
Overweight and obesity are generally recognized as the presence of excess body fat or adipose tissue. Obesity is classified by body mass index (BMI), which is calculated as weight in kilograms divided by the square of height in meters (kg/m2). For children in the United States, sex-specific BMI-for-age percentiles are calculated based on the 2000 U.S. growth reference.3 Youth who are considered overweight have a BMI-for-age that is greater than or equal to the 85th percentile, and those who would be classified as obese have a BMI-for-age at or above the 95th percentile.4 Countries outside of the United States have used different criteria and cutoff points at different times in the past.
Only a few studies have reported data on weight status of children with ASD. An early Japanese study of 140 school children with ASD ages 7–18 years found that 25% were obese.5 In a second large Japanese study of 20,013 children (6–17 years) with intellectual disability attending special schools, 413 of whom had ASD, Takeuchi6 reported an obesity prevalence of 22% in boys, and 11% in girls, with ASD. Mouridsen and colleagues7 examined the weight status of 117 young children with ASD in Denmark (mean age = 5.5 for boys, 5.2 for girls) and found that BMI for males, but not for females, was significantly lower than in an age-matched reference population. Curtin and colleagues8 conducted a chart review of a small sample of children with ASD from a tertiary care clinic and found that the prevalence of overweight and obesity was 35.7% and 19.0% respectively, and thus as significant a problem in children with ASD as for children in the general population. Xiong and colleagues9 found that among 380 boys and 49 girls in a clinical sample with ASD ages 2–11 years in China, 33% were overweight and 18% were obese. Egan and colleagues10 performed a retrospective chart review of 273 young children (mean age, 3.89 years) with ASD seen by developmental specialists and found a prevalence of overweight and obesity of 39.0% and 23.1% among children with autistic disorder and Asperger’s disorder/pervasive developmental disorder not otherwise specified, respectively. In a study of 111 children with ASD ages 2–9 years seen in a developmental clinic in China, Xia and colleagues11 found that the prevalence of overweight and obesity was 31.5% (total) based on 1995 World Health Organization standards. Curtin and colleagues12 examined the prevalence of obesity in children with ASD using data from the National Study of Children’s Health and found that children with ASD were 40% more likely to be obese than children in the general population. Finally, in a small study of 53 children with ASD and 58 TD children recruited from the community, Evans and colleagues13 found that 17% of the children with ASD met criteria for obesity compared to 9% of TD children. However, this difference reached only borderline significance (p = .09), likely due to the study’s small sample size. Notably, the children with ASD included in the study were not taking medications that would have affected their weight status.
These findings suggest that children with ASD are at risk for obesity at the same or higher rate than children generally. And because of the adverse health consequences associated with obesity, the issue of ASD-related obesity warrants both research and clinical attention. In the next sections we review the current evidence on known and potential risk factors for obesity in children with ASD, and then discuss the implications for future research and clinical management/intervention.
THE GENETICS OF OBESITY AND ASD
Numerous twin and family studies indicate that ASD has a biologic basis, with concordance rates higher for monozygotic twins (70%–90%) than for dizygotic twins (20%–30%).14,15 The specific genetic determinants have not been fully identified.16,17 Both inherited and de novo single-nucleotide polymorphisms (variations occurring in a single nucleotide [A, T, C, or G]) and copy-number variants (CNVs; misplaced or duplicated segments of chromosomes) have been implicated in the causation of ASD.18–20 Although direct cause-and-effect from specific genetic variants has yet to be elucidated, approximately 7%–20% of idiopathic cases of ASD result from CNVs, with both deletions and duplications playing a role.16 Recent studies examining chromosome microarrays have identified approximately ten CNVs associated not only with ASD, but with several psychiatric (schizophrenia, bipolar disorder) and prodromal (congenital heart disease, hypotonia, micro/macrocephaly, seizures) disorders. Most notably, genomic imbalances and high rates of recurrent CNVs are emerging as risk factors for obesity,21,22 suggesting an inherited correlation between obesity and ASD.
Genomic duplications and deletions at 16p11.2 are among the most common ones associated with ASD, and deletions in this region have recently have been shown to play a role in early-onset childhood obesity.23 Zufferey and colleagues24 examined 285 child and adult carriers of a ∼600 kb deletion at the 16p11.2 locus. They found that over 80% of the carriers exhibited psychiatric disorders, including attention-deficit, disruptive-behavior, anxiety, and substance-related disorders, and that 15% of the pediatric carriers were diagnosed with ASD. More than 50% of pediatric carriers were obese, with weight gain starting at 3.5 years and progressing rapidly until age 7. The percentage of carriers who were obese increased to 75% in adulthood. Despite the link between 16p11.2 carriers, ASD, and obesity, the researchers found that obesity occurred independently of ASD.
Smaller studies have examined longer deletion sequences (5–30.1 Mb) on 16p11.2. Yu and colleagues23 found that of 28 individuals identified with the deletion, 9 were classified as obese and 6 as overweight, with excessive weight gain occurring between the age of five and six years, consistent with the findings of Zufferey and colleagues.24 A multiplex family study of three boys—a twin pair and an elder brother—found a similar link between ASD, mild intellectual disability, and early-onset severe obesity, although the elder brother had less severe ASD than the twins. The fact that the gene can be present in individuals who do not manifest with overweight or obesity,23 or who have differing degrees of autistic symptomatology, suggests variability in penetrance and gene expression.25
Although the 16p11.2 gene aberration is the one most commonly associated with ASD, several other loci have been identified as being associated with the disorder. Included is the deletion at 11p14.1, which has been implicated in both obesity and ASD, albeit in a small sample.26 Duplication at 15q11.2, a gene originally thought to be associated solely with Prader-Willi and Angelman syndromes, is also now believed to play a role in other disorders associated with developmental delay, ASD, and obesity.27 MAGED1 (part of the MAGE gene family), also involved in the development of Prader-Willi syndrome, may present as progressive obesity with deficits in social interactions suggestive of ASD symptomatology.28 More recently, a Prader-Willi phenotype of fragile X syndrome, also known to be associated with ASD,29,30 was discovered in 13 patients (ages 5–27)—all of whom were found to have obesity and hyperphagia, and 10 of whom were diagnosed with ASD.31 Overall, 200 ASD susceptibility genes have been identified to date;17 given the significant gene variability and penetrance emerging in both animal and human models of ASD, more work is needed to draw definitive genetic associations between ASD and obesity.
PSYCHOPHARMACOLOGICAL EFFECTS ON OBESITY IN ASD
The adverse effects of psychotropic medication on weight status is likely the best understood risk factor for obesity in both children and adults with ASD. The use of psychotropic medication is common in individuals with ASD. Data obtained from clinical and nationally representative populations of children, including those psychiatrically hospitalized, report that approximately 30%–60% of children with ASD are prescribed at least one psychotropic medication, and that 10% are prescribed more than three medications, with stimulants, antidepressants, and antipsychotics being the most common.32
Typical and atypical antipsychotics are used extensively to treat psychotic disorders and bipolar disorder, and as adjuncts to antidepressants. Most recently, in 2006 and 2009, the Federal Drug Administration approved risperidone and aripiprazole, respectively, for treating irritability associated with ASD.33 Atypical antipsychotics have subsequently come to be widely used in ASD, and studies have shown they are twice as likely as any other medications to be prescribed for children with ASD.34
Atypical antipsychotics (e.g., aripiprazole, clozapine, olanzapine, quetiapine, risperidone, ziprasidone) provide significant benefit in reducing the frequency of extrapyramidal symptoms. However, these second-generation antipsychotics (SGAs) are considerably more apt to cause weight gain.35–38 In addition to weight gain, metabolic syndrome (defined by abdominal obesity, atherogenic dyslipidemia, raised blood pressure, insulin resistance ± glucose intolerance, proinflammatory state, and prothrombotic state) is of major concern with SGAs.39,40 Children appear to be more susceptible than adults to developing obesity and lipid abnormalities associated with SGAs—a finding that is noteworthy, given that SGAs are becoming the first-line treatment in children with ASD-associated irritability.41
Risperidone and aripiprazole have the best evidence for treating ASD-associated irritability and have thus garnered Federal Drug Administration approval for this indication. Risperidone is the most widely studied of the antipsychotics prescribed to children with ASD, and was the first to be studied in the Research Units on Psychopharmacology Autism Network.42 All studies of children with ASD treated with risperidone have found weight gain to be significant in treatment versus placebo groups.39,43 Risperidone was shown to increase appetite in 33% of children with ASD, likely one contributor to the weight increase. Fortunately, weight gain was shown to decelerate with treatment time.44 Aripiprazole has been studied in two randomized, double-blind, placebo-controlled trials funded by pharmaceutical companies.45 The first trial enrolled 98 children ages 6–17,46 and the second, 218 children.47 Marcus and colleagues47 confirmed that all treatment groups prescribed aripiprazole 5–15 mg had significant weight gain over placebo, but no one in the study discontinued the medication as a result. Similar to risperidone, sedation was the most common side effect seen with aripiprazole.
Several other atypical antipsychotics have been studied in the treatment of ASD symptoms. One small randomized, controlled trial (RCT) with olanzapine estimated a weight increase of 7.5 ± 4.8 pounds. In fact, since the risks of weight gain, metabolic syndrome, hyperlipidemia, and diabetes type 2 associated with even short-term use of olanzapine are considerable, most physicians refrain from using olanzapine as the first-line agent for children with ASD.38,45 Ziprasidone is felt to be less obesogenic than other SGASs in adults.48 Although no RCTs of ziprasidone in ASD have been published, a small trial of ten adults suggests that the medication reduced total cholesterol and triglyceride levels in patients, while eight patients lost an average of 13.1 ± 7.1 pounds.49 Another open-label study found the medication to be overall weight neutral, with a BMI reduction that was not statistically significant.50 One small, eight-week, open-label trial of quetiapine in 11 adolescent patients did not find any significant difference in body weight of treated individuals.51 In general, ziprasidone is considered the SGA with the lowest potential for weight gain, followed by aripiprazole, quetiapine, and risperidone with intermediate risk, whereas olanzapine is considered to present a high risk of weight gain and metabolic disturbances.48
The diverse mechanisms by which antipsychotics cause weight gain are not fully understood. It is postulated that weight gain is tied to increased appetite associated with SGAs’ interaction with neuronal dopamine, serotonin, and histamine receptors.52 Atypical antipsychotics target several receptors, including 5HT2cR, 5HT3R, α2R, H1R, and β3R, and scientists have theorized that weight gain is associated with the communal effect of SGAs on these receptors.53 Serotonin and histamine have been most widely implicated in the appetite and metabolic disturbances, and several studies have confirmed an association between the H1 receptor and antipsychotic-induced weight gain.54,55 Although SGAs are more commonly associated with metabolic disturbances, pioneering work by Leibowitz56 revealed that the typical antipsychotics, including haloperidol, chlorpromazine, and fluphenazine, also stunted appetite suppression via endogenous amines in the perifornical lateral hypothalamus. Thus, through interactions with multiple neuronal receptors, both typical and atypical antipsychotics have the propensity to significantly affect patients’ weight and metabolic profile.
The prevalence of antipsychotic-induced weight gain has spurred investigation into pharmacological and behavioral interventions to reduce the impact of these medications on weight and metabolism.57 Topiramate has shown efficacy in limiting weight gain associated with initiation of olanzapine in adult males with schizophrenia.58 One case study further reported efficacy of topiramate in reducing antipsychotic-induced weight gain in a 14-year old female with major depressive disorder with psychotic features.59 More recently, buproprion has been effective in reducing antipsychotic-induced weight gain in seven subjects by an average of 3.4 kg.60
Metformin has also emerged as a safe and effective option in reducing body weight and in improving fasting insulin levels and insulin resistance in adults treated with antipsychotics.61 A placebo-controlled trial examined weight, insulin sensitivity, and development of diabetes in 39 adolescents, ages 10–17, treated with olanzapine, risperidone, or quetiapine. Psychiatric diagnoses varied. Bipolar disorder and attentional disorders were most common, and 12% of the children were diagnosed with either autism or Asperger’s disorder. Over the 16-week study, metformin was effective in stabilizing weight and decreasing insulin sensitivity, with overall good tolerability.62
Although psychopharmacological treatments have shown efficacy in reducing antipsychotic-induced weight gain, behavioral strategies remain important in weight loss and in preventing obesity-associated complications such as hypertension, hyperlipidemia, and diabetes mellitus. Despite the efficacy of metformin as an adjunct to reduce antipsychotic-induced weight gain, Wu and colleagues63 found that metformin alone was inferior to metformin when used with a lifestyle intervention that incorporated dietary education and an exercise regimen. Cognitive-behavioral therapy has also demonstrated efficacy in reducing weight and binge-eating behaviors in individuals treated with chronic antipsychotic therapy.64 No such studies have been carried out in children or adults with ASD, and further investigation into psychopharmacology combined with lifestyle intervention is needed to determine efficacy and feasibility of such treatments in this population.
In lieu of established treatments and preventive measures for antipsychotic-induced weight gain, the American Academy of Child and Adolescent Psychiatry developed a “practice parameter” that addresses some of the risks associated with antipsychotic use in children. The parameter includes (1) obtaining a thorough review of current symptoms, past medical history, and past medication trials, and establishing the need for antipsychotic medication, (2) dosing atypical antipsychotics by the “start low and go slow” method, (3) obtaining baseline BMI and continuing to monitor at regular intervals, and (4) obtaining baseline and ongoing measurements of heart rate, blood pressure, fasting blood glucose, and fasting lipid profiles.65 Children whose weight rises over the 90th percentile of BMI while on atypical antipsychotics should be referred for weight management and have more frequent lipid and blood glucose monitoring. The practice parameter includes complete guidelines and monitoring recommendations for specific antipsychotics.65
Mood stabilizers (e.g., divalproex/valproic acid, lithium, lamotrigine, levitracetam) are generally not supported for treatment in ASD, although they have shown efficacy in patients with mania and conduct disorders.66 The consensus is that most mood stabilizers are associated with weight gain, and studies in bipolar disorder have identified divalproex as the likeliest culprit, with one double-blind, placebo-controlled trial of divalproex in ASD noting increased appetite as a significant side effect.67,68 By contrast, lamotrigine-associated weight gain has been minimal in studies of children with bipolar disorder,69 and one RCT of 27 children with ASD found no significant differences in outcomes or adverse events between treatment groups.70 Levitracetam, with one controlled, double-blind study of 20 children with ASD, also did not reveal significant weight gain, weight loss, or changes in appetite.71 No open-label studies or RCTs of lithium in treating ASD have been published.
Serotonin is postulated to play a key role in aggressive drive; as such, several RCTs have examined the effectiveness of antidepressants on irritability and aggression, as well as on repetitive and other maladaptive behaviors in ASD.66 Selective serotonin reuptake inhibitors have shown variable association with weight disturbances.72 Fluoxetine has been linked with mild anorexia and decreased appetite in individuals with ASD,73 whereas neither citalopram and escitalopram was associated with weight gain.74,75 Fluvoxamine studied in adults with ASD revealed mild sedation; sertraline showed no significant weight gain in a small study and several case studies; and venlafaxine has shown no significant weight gain in the few studies conducted to date.76 By contrast, mirtazapine—a noradrenergic and specific serotonergic antidepressant—contributed to increased appetite and significant weight gain (greater than 7% over baseline) in one study of 26 subjects, ages 3.8 to 23.5 (mean age, 10.1 ± 4.8 years), diagnosed with autism and other pervasive developmental disorders.77 Clomipramine, a tricyclic antidepressant, was associated with fatigue and lethargy, but also decreased appetite,76 and one adult study, albeit of poor quality, showed weight gain in 13 of 33 individuals with ASD.78 Overall, the few studies available provide limited evidence of weight gain associated with antidepressant use in individuals with ASD.
OTHER POTENTIAL RISK FACTORS FOR OBESITY IN CHILDREN WITH ASD
Little research has been done to determine the risk factors associated with obesity in children with ASD—which will require longitudinal prospective studies. Some of the potential risk factors that may be particularly relevant to children with ASD are described below.
Epidemiologic evidence suggests a link between short sleep duration and body weight.79,80 Cross-sectional studies of children and adults have found a link between short sleep duration and overweight,81–84 as have prospective studies.85–87 In children, several studies have documented that longer sleep duration is inversely related to overweight in children.85,88,89 And in a population-based, prospective study in New Zealand, short sleep duration during childhood was found to increase obesity risk in adulthood.86 Thus, in relation to obesity, the aspect of sleep that appears to be most important is sleep duration.80
Sleep problems are common in children with ASD90,91 and are present at similar rates in those with and without co-occurring intellectual disability.91–93 The fluctuation of sleep problems with age is variably reported, but most investigators find that in contrast to TD children, whose early childhood sleep problems often resolve, sleep problems in children with ASD tend to persist.90,91 The specific sleep problems consistently identified include difficulty falling asleep and difficulty staying asleep.94 Children with ASD, ages 5 to 16, studied by polysomnography were found to have shorter sleep times by an average of 43 minutes, compared to TD children matched for age and sex.95,96
Experimental and observational studies have suggested potential direct and indirect pathways to explain the link between short sleep duration and excess weight. Experimental studies in rodents and humans demonstrate sleep-deprivation effects on hyperphagia.96 In a small study of young men,97 sleep restriction increased reports of hunger and appetite. Endocrine effects associated with sleep deficit, including elevated ghrelin and decreased leptin, which together increase hunger and stimulate appetite, were also observed. In the large Wisconsin Sleep Cohort, short sleep duration was associated with low leptin and high ghrelin levels.98 Sleep problems could be expected to influence energy balance by decreasing activity or increasing energy intake in the context of daily family life. Children who are tired during the day may be less likely to engage in active play. On the food-intake side, nighttime snacking may add to caloric intake.
The relationships among sleep disturbances, engagement in physical activity, eating behaviors, and weight status have not been fully elucidated in children with ASD. Given their notable propensity for sleep disturbances, however, research in this area is warranted.
It is frequently reported that children with ASD are highly selective eaters (often referred to as “picky eating”), with aversions to specific textures, colors, smells, temperatures, and brand names of foods. The diets of children with selective eating are characterized by a lack of variety and may be associated with inadequate nutrient intake.98–101 Although picky eating occurs in TD children, it appears to be more prevalent in children with ASD102 and other developmental disabilities.99 Few studies, however, have examined the relationship between food selectivity and overweight.
Schreck and colleagues103 examined food selectivity in 128 children with ASD and TD controls ages 5–12 years. They concluded that children with ASD had a significantly greater degree of food selectivity than TD children. Using the same data set in a subsequent analysis, Schreck and colleagues98 reported that children with ASD preferred energy-dense foods within food groups (e.g., chicken nuggets, hot dogs, and peanut butter in the protein group; cake, French fries, macaroni, and pizza in the starch group; and ice cream in the dairy group). No measures of height and weight were available, however, to examine the relationship of food selectivity to weight status.
In their cross-sectional study of 3- to 11-year-old children with ASD, Bandini and colleagues98 found that children with ASD refused more foods than TD peers and had more limited repertoires of foods. They also found that children with ASD ate significantly fewer fruits and vegetables than TD children and reported more daily servings of sugar-sweetened beverages (SSBs) than did TD children. However, only SSB intake in TD children was associated with BMI z-score. In a multivariate analysis, controlling for age, race, parental weight status, and education, the interaction between ASD and consumption of SSBs as a predictor of BMI z-score was not statistically significant, likely due to limited power.13 In prospective, observational studies of TD children, increased intake of SSBs104–106 and decreased intake of fruits and vegetables107 have been shown to be associated with obesity. Additional research is needed on whether intake of SSBs increases the risk of obesity in children with ASD.
Delayed/Impaired Motor Development
Data from prospective observational studies suggest that increased participation in physical activity and decreased sedentary behavior are two protective factors in the development of obesity in children and adolescents.108 Children with ASD may be particularly challenged to engage in physical activity by virtue of motor-skill difficulties, which have been documented in toddlers109 and school-age children109 with ASD. Motor-function impairments include unevenness of acquiring developmental milestones, low muscle tone, and postural instability.110–113 These impairments may compromise children’s endurance, balance, motor planning, and ability to participate successfully in motor-related activities. The impairments may result in exclusion from activities by peers and reduced motivation to participate in physical activities. The participation of children with ASD in physical activity may also be compromised by their social-skill and communicative difficulties. Dziuk and colleagues114 found that motor-planning difficulties in children with ASD were strongly correlated with the social, communicative, and behavioral impairments that define ASD. The need for close supervision may also hamper these children’s participation.
The data on the extent to which children with ASD engage in physical activity are mixed. Rosser and colleagues115 did not find differences in physical activity between children with ASD and TD children. In a cross-sectional study of 3- to 11-year-old children with and without ASD, Bandini and colleagues116 found that parents of children with ASD reported that their children participated in fewer types of activities and for less time than did TD children. Similar to Rosser’s findings,115 however, when physical activity levels were measured by accelerometry, there were no differences between the two groups.116 The authors speculated that questionnaires may not capture behaviors such as roaming and pacing that are frequently observed in children with ASD. Pan,117 Macdonald,118 Memari,119 and their colleagues have reported declines in physical activity with age in cross-sectional analyses of children and adolescents with ASD. The relationship between weight status and physical activity were not reported in these studies. Additional research is needed to determine whether physical activity levels are related to weight status in children with ASD and whether this relationship is influenced by age.
Increased time spent in sedentary behavior has been shown to increase the risk for obesity.79 As noted, the social, behavioral, or intellectual impairments evidenced by children with ASD may make participation in formal and informal forms of physical activity more difficult, potentially increasing the amount of time spent in sedentary behavior. For example, parents of children with ASD report using television for its calming effect on their children and as a respite from caregiver challenges.120 A recent study by Mazurek and colleagues121 comparing screen time between 202 youth with ASD and 179 TD children found that both males and females with ASD (mean age, 12.1) spent more time watching video games than did TD children (mean age, 12.5). Television time did not differ between ASD boys and TD boys, but was significantly higher among ASD girls than TD boys. Further work is needed to explore the relationship between screen time and weight status in this population.
Dietary, physical activity, and sleep patterns emerge within the context of the family environment; thus, family dynamics are central to any examination of childhood obesity risk factors. Research has documented that parental practices, mealtime routines, and parents’ feeding styles influence children’s feeding patterns.122 A growing body of literature highlights the role that family stress, maternal depression, and family cohesion play in mediating or moderating the development of obesity in children. For example, obese adolescent girls have reported that their families are less cohesive, less expressive, and more authoritarian than non-obese youth.123 Zeller and colleagues124 reported that mothers of obese children ages 8–16 years were more likely to report high levels of emotional distress, more family conflict, greater mealtime problems, and fewer positive family interactions during mealtimes than mothers of children who were not obese. Few disorders pose a greater threat to the psychosocial well-being of family members than ASD; the behaviors associated with ASD can be taxing for even the strongest of families.125 Parents often report social isolation and difficulty managing their children’s temper tantrums, obsessions, and self-injurious behaviors. No research to date has examined the relation of family stress and obesity in children with ASD, but given that these factors have been shown to be associated with obesity in TD children, this line of research warrants future attention.
Myriad other potential risk factors for obesity in children with ASD deserve research attention. For example, many children with ASD receive applied behavior analysis treatment, with food often used as a primary reinforcer. Research is needed to determine whether using food as a reward, including the types and frequency of foods used, affect children’s overall food intake and weight status. Additionally, the extent to which early feeding problems and gastrointestinal problems common to children with ASD are associated with obesity merits future investigation.
While addressing the problem of obesity in children with ASD has implications for their health and well-being, efforts to address obesity should not come at the expense of the important social opportunities that eating with others confers. Mealtimes are a vehicle for conveying social values and expectations for children. Eating meals with others is a major process through which many cultures, including American culture, communicate about social relationships and socialize their children. In fact, it has been argued that “the act of eating is overtly social.”126 Likewise, anthropologists have suggested that “food and eating are not just biologically significant for the reproduction of families and social groups, but are saturated with social import.”127p84 Thus, efforts to address obesity in this population must ensure that the enjoyable and social dimensions of eating and of eating with others are supported.
DISCUSSION AND CONCLUSIONS
Since the extant literature suggests that obesity is at least as high, or even higher, in children with ASD compared to children generally, the comorbidities associated with obesity are likewise a threat to the health and well-being of this population. Current research demonstrates that atypical antipsychotics present a risk for obesity in both children and adults with ASD, but little research exists on how to address this problem. Although some evidence supports the use of psychopharmacological interventions for children with weight gain induced by atypical antipsychotics, research in children with autism is sparse. Furthermore, given the increase in use of medications in this population and the concern for long-term consequences, more research is needed to determine safer alternatives to combat weight gain, such as lifestyle interventions. In the meantime, if the use of atypical antipsychotic medications is indicated for ASD children, prescribers should provide anticipatory guidance to patients and families around the likelihood of weight gain and should discuss strategies for managing hunger and increased appetite, and for engaging children in physical activity. Families may also benefit from a referral to a registered dietician, who can assist them in identifying preferred foods lower in caloric content.
Increasingly, community organizations are expressing an interest in, and willingness to include, children with ASD in recreational programming, which families should be encouraged to pursue. Very recently, the Office for Civil Rights in the U.S. Department of Education128 clarified the obligations of schools to provide students with disabilities an equal opportunity to participate alongside their peers in after-school athletics and clubs. This is good news for children with ASD and other disabilities, though additional research and professional training will be needed to understand how children with ASD can be engaged successfully in physical activity and extramural sports. Involvement in physical activity may improve children’s sleep, which would address one of the risk factors believed to be associated with obesity and may also bring about improved behavioral control.
As noted, research suggests that children with ASD have higher levels of food selectivity and that their diets may be characterized by calorically dense foods low in nutrients. Whether these eating patterns contribute to the development of obesity is a topic worthy of future research. Children with ASD, whose eating patterns are selective for foods such as sugar-sweetened beverages, cookies/cakes, and savory snacks, may benefit from the input of a registered dietitian, occupational therapist, and behavioral psychologist. A dietitian can assess the child’s eating patterns and assist with devising a nutritionally sound eating plan. Because sensory issues are so common in children with ASD and may be an underlying factor in selective eating patterns, an occupational therapist may be able to assess sensory-processing difficulties and suggest sensory-desensitization strategies to help the child to accept new foods. It is likely that the eating patterns seen in children with ASD are associated with core features of ASD itself, including the rigidity and insistence on sameness. Behavioral approaches that are considered the gold-standard treatments for ASD, such as applied behavior analysis, may prove useful in increasing children’s eating repertoires and acceptance of a healthy diet.
In sum, the prevalence of obesity is at least as high, if not higher, in children with ASD compared to other children. Research has documented that atypical antipsychotic medication is a clear risk for weight gain in this clinical population. Studies on diet, physical activity, and sleep in TD children have shown positive associations with obesity, but this work remains to be done in children with ASD, as do other investigations on the implications of gastrointestinal disorders and using food as a reward for learning and behavior management. Obesity and its associated sequelae represent significant threats to independent living, self-care, quality of life, and long-term health outcomes for individuals with ASD. Information about risk factors for developing obesity in children with ASD is needed so that obesity prevention and intervention strategies may be developed that are both appropriate and effective for this population.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the article.
1. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity and trends in body mass index among US children and adolescents, 1999–2010. JAMA 2012; 307: 483–90.
2. Must A, Strauss RS. Risks and consequences of childhood and adolescent obesity. Int J Obes Relat Metab Disord 1999; 23 suppl 2: S2–11.
3. Kuczmarski RJ, Ogden CL, Guo SS, et al. 2000 CDC Growth Charts for the United States: methods and development. Vital Health Stat 11 2002; (246): 1–190.
4. Krebs NF, Himes JH, Jacobson D, Nicklas TA, Guilday P, Styne D. Assessment of child and adolescent overweight and obesity. Pediatrics 2007; 120 suppl: S193–228.
5. Sugiyama T. A research of obesity in autism. Jpn J Dev Disabil 1991; 13: 53–8.
6. Takeuchi E. Incidence of obesity among school children with mental retardation in Japan. Am J Ment Retard 1994; 99: 283–8.
7. Mouridsen SE, Rich B, Isager T. Body mass index in male and female children with infantile autism. Autism 2002; 6: 197–205.
8. Curtin C, Bandini LG, Perrin EC, Tybor DJ, Must A. Prevalence of overweight in children and adolescents with attention deficit hyperactivity disorder and autism spectrum disorders: a chart review. BMC pediatr 2005; 5: 48.
9. Xiong N, Ji C, Li Y, He Z, Bo H, Zhao Y. The physical status of children with autism in China. Res Dev Disabil 2007; 30: 70–6.
10. Egan AM, Dreyer ML, Odar CC, Beckwith M, Garrison CB. Obesity in young children with autism spectrum disorders: prevalence and associated factors. Child Obes 2013; 9: 125–31.
11. Xia W, Zhou Y, Sun C, Wang J, Wu L. A preliminary study on nutritional status and intake in Chinese children with autism. Eur J Pediatr 2010; 169: 1201–6.
12. Curtin C, Anderson SE, Must A, Bandini L. The prevalence of obesity in children with autism: a secondary data analysis using nationally representative data from the National Survey of Children’s Health. BMC Pediatr 2010; 10: 11.
13. Evans EW, Must A, Anderson SE, et al. Dietary patterns and body mass index in children with autism and typically developing children. Res Autism Spectr Disord 2012; 6: 399–405.
14. Hallmayer J, Cleveland S, Torres A, et al. Genetic heritability and shared environmental factors among twin pairs with autism. Arch Gen Psychiatry 2011; 68: 1095–102.
15. Sharma JR, Arieff Z, Sagar S, Kaur M. Autism and obesity: prevalence, molecular basis and potential therapies. Autism Insights 2012; 4: 1–13.
16. Heil KM, Schaaf CP. The genetics of autism spectrum disorders—a guide for clinicians. Curr Psychiatry Rep 2013; 15: 334.
17. Pinto D, Pagnamenta AT, Klei L, et al. Functional impact of global rare copy number variation in autism spectrum disorders. Nature 2010; 466: 368–72.
18. Anney R, Klei L, Pinto D, et al. A genome-wide scan for common alleles affecting risk for autism. Hum Mol Genet 2010; 19: 4072–82.
19. Luo R, Sanders SJ, Tian Y, et al. Genome-wide transcriptome profiling reveals the functional impact of rare de novo and recurrent CNVs in autism spectrum disorders. Am J Hum Genet 2012; 91: 38–55.
20. Sanders SJ, Murtha MT, Gupta AR, et al. De novo mutations revealed by whole-exome sequencing are strongly associated with autism. Nature 2012; 485: 237–41.
21. Bochukova EG, Huang N, Keogh J, et al. Large, rare chromosomal deletions associated with severe early-onset obesity. Nature 2010; 463: 666–70.
22. Walters RG, Jacquemont S, Valsesia A, et al. A new highly penetrant form of obesity due to deletions on chromosome 16p11.2. Nature 2010; 463: 671–5.
23. Yu Y, Zhu H, Miller DT, et al. Age- and gender-dependent obesity in individuals with 16p11.2 deletion. J Genet Genomics 2011; 38: 403–9.
24. Zufferey F, Sherr EH, Beckmann ND, et al. A 600 kb deletion syndrome at 16p11.2 leads to energy imbalance and neuropsychiatric disorders. J Med Genet 2012; 49: 660–8.
25. Tabet A-C, Pilorge M, Delorme R, et al. Autism multiplex family with 16p11.2p12.2 microduplication syndrome in monozygotic twins and distal 16p11.2 deletion in their brother. Eur J Hum Genet 2012; 20: 540–6.
26. Shinawi M, Sahoo T, Maranda B, et al. 11p14.1 microdeletions associated with ADHD, autism, developmental delay, and obesity. Am J Med Genet A 2011; 155A: 1272–80.
27. Kitsiou-Tzeli S, Tzetis M, Sofocleous C, et al. De novo interstitial duplication of the 15q11.2-q14 PWS/AS region of maternal origin: clinical description, array CGH analysis, and review of the literature. Am J Med Genet A 2010; 152A: 1925–32.
28. Dombret C, Nguyen T, Schakman O, et al. Loss of Maged1 results in obesity, deficits of social interactions, impaired sexual behavior and severe alteration of mature oxytocin production in the hypothalamus. Hum Mol Genet 2012; 21: 4703–17.
29. Gabis LV, Baruch YK, Jokel A, Raz R. Psychiatric and autistic comorbidity in fragile X syndrome across ages. J Child Neurol 2011; 26: 940–8.
30. Goldfine PE, McPherson PM, Heath GA, Hardesty VA, Beauregard LJ, Gordon B. Association of fragile X syndrome with autism. Am J Psychiatry 1985; 142: 108–10.
31. Nowicki ST, Tassone F, Ono MY, et al. The Prader-Willi phenotype of fragile X syndrome. J Dev Behav Pediatr 2007; 28: 133–8.
32. Siegel M. Psychopharmacology of autism spectrum disorder: evidence and practice. Child Adolesc Psychiatr Clin N Am 2012; 21: 957–73.
33. Seida JC, Schouten JR, Boylan K, et al. Antipsychotics for children and young adults: a comparative effectiveness review. Pediatrics 2012; 129: e771–84.
34. Tyler CV, Schramm SC, Karafa M, Tang AS, Jain AK. Chronic disease risks in young adults with autism spectrum disorder: forewarned is forearmed. Am J Intellect Dev Disabil 2011; 116: 371–80.
35. Basile V, Masellis M, McIntyre R, Meltzer H, Liberman A, Kennedy J. Genetic dissection of atypical antipsychotic-induced weight gain: novel preliminary data on the pharmacogenetic puzzle. J Clin Psychiatry 2001; 62( suppl 23): 45–66.
36. Crilly J. The history of clozapine and its emergence in the US market: a review and analysis. Hist Psychiatry 2007; 18: 39–60.
37. Simpson MM, Goetz RR, Devlin MJ, Goetz SA, Walsh BT. Weight gain and antipsychotic medication: differences between antipsychotic-free and treatment periods. J Clin Psychiatry 2001; 62: 694–700.
38. Scheltema Beduin A, De Haan L. Off-label second generation antipsychotics for impulse regulation disorders: a review. Psychopharmacol Bull 2010; 43: 45–81.
39. Maayan L, Correll CU. Weight gain and metabolic risks associated with antipsychotic medications in children and adolescents. J Child Adolesc Psychopharmacol 2011; 21: 517–35.
40. Grundy SM, Brewer HB, Cleeman JI, Smith SC, Lenfant C. Definition of metabolic syndrome: report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Circulation 2004; 109: 433–8.
41. McDougle CJ, Stigler KA, Erickson CA, Posey DJ. Atypical antipsychotics in children and adolescents with autistic and other pervasive developmental disorders. J Clin Psychiatry 2008; 69 suppl 4: 15–20.
42. McDougle CJ, Scahill L, McCracken JT, et al. Research Units on Pediatric Psychopharmacology (RUPP) Autism Network. Background and rationale for an initial controlled study of risperidone. Child Adolesc Psychiatr Clin N Am 2000; 9: 201–24.
43. Posey DJ, Stigler KA, Erickson CA, McDougle CJ. Antipsychotics in the treatment of autism. J Clin Invest 2008; 118: 6–14.
44. Aman MG, Arnold LE, McDougle CJ, et al. Acute and long-term safety and tolerability of risperidone in children with autism. J Child Adolesc Psychopharmacol 2005; 15: 869–84.
45. Siegel M, Beaulieu AA. Psychotropic medications in children with autism spectrum disorders: a systematic review and synthesis for evidence-based practice. J Autism Dev Disord 2012; 42: 1592–605.
46. Owen R, Sikich L, Marcus RN, et al. Aripiprazole in the treatment of irritability in children and adolescents with autistic disorder. Pediatrics 2009; 124: 1533–40.
47. Marcus RN, Owen R, Kamen L, et al. A placebo-controlled, fixed-dose study of aripiprazole in children and adolescents with irritability associated with autistic disorder. J Am Acad Child Adolesc Psychiatry 2009; 48: 1110–9.
48. De Hert M, Dobbelaere M, Sheridan EM, Cohen D, Correll CU. Metabolic and endocrine adverse effects of second-generation antipsychotics in children and adolescents: a systematic review of randomized, placebo controlled trials and guidelines for clinical practice. Eur Psychiatry 2011; 26: 144–58.
49. Cohen SA, Fitzgerald BJ, Khan SRF, Khan A. The effect of a switch to ziprasidone in an adult population with autistic disorder: chart review of naturalistic, open-label treatment. J Clin Psychiatry 2004; 65: 110–3.
50. Malone RP, Delaney MA, Hyman SB, Cater JR. Ziprasidone in adolescents with autism: an open-label pilot study. J Child Adolesc Psychopharmacol 2007; 17: 779–90.
51. Golubchik P, Sever J, Weizman A. Low-dose quetiapine for adolescents with autistic spectrum disorder and aggressive behavior: open-label trial. Clin Neuropharmacol 2011; 34: 216–9.
52. Baptista T. Body weight gain induced by antipsychotic drugs: mechanisms and management. Acta Psychiatr Scand 1999; 100: 3–16.
53. Panariello F, De Luca V, De Bartolomeis A. Weight gain, schizophrenia and antipsychotics: new findings from animal model and pharmacogenomic studies. Schizophr Res Treatment 2011; 2011: 459284.
54. Kroeze WK, Hufeisen SJ, Popadak BA, et al. H1-histamine receptor affinity predicts short-term weight gain for typical and atypical antipsychotic drugs. Neuropsychopharmacology 2003; 28: 519–26.
55. Matsui-Sakata A, Ohtani H, Sawada Y. Receptor occupancy-based analysis of the contributions of various receptors to antipsychotics-induced weight gain and diabetes mellitus. Drug Metab Pharmacokinet 2005; 20: 368–78.
56. Leibowitz S. Neurochemical systems of the hypothalamus: control of feeding and drinking behavior and water electrolyte excretion. In: Morgan P, Panksepp J, eds. Handbook of the hypothalamus, vol. 3. New York: Marcel Dekker, 1980: 299–437.
57. Kapoor S. Strategies to control antipsychotic-induced weight gain. Psychoneuroendocrinology 2008; 33: 1171.
58. Kim JH, Yim SJ, Nam JH. A 12-week, randomized, open-label, parallel-group trial of topiramate in limiting weight gain during olanzapine treatment in patients with schizophrenia. Schizophr Res 2006; 82: 115–7.
59. Lessig MC, Shapira NA, Murphy TK. Topiramate for reversing atypical antipsychotic weight gain. J Am Acad Child Adolesc Psychiatry 2001; 40: 1364.
60. Gadde KM, Zhang W, Foust MS. Bupropion treatment of olanzapine-associated weight gain: an open-label, prospective trial. J Clin Psychopharmacol 2006; 26: 409–13.
61. Wang M, Tong J, Zhu G, Liang G, Yan H, Wang X. Metformin for treatment of antipsychotic-induced weight gain: a randomized, placebo-controlled study. Schizophr Res 2012; 138: 54–7.
62. Klein DJ, Cottingham EM, Sorter M, Barton BA, Morrison JA. A randomized, double-blind, placebo-controlled trial of metformin treatment of weight gain associated with initiation of atypical antipsychotic therapy in children and adolescents. Am J Psychiatry 2006; 163: 2072–9.
63. Wu R-R, Zhao J-P, Jin H, et al. Lifestyle intervention and metformin for treatment of antipsychotic-induced weight gain: a randomized controlled trial. JAMA 2008; 299: 185–93.
64. Khazaal Y, Fresard E, Rabia S, et al. Cognitive behavioural therapy for weight gain associated with antipsychotic drugs. Schizophr Res 2007; 91: 169–77.
65. American Academy of Child and Adolescent Psychiatry. Practice parameter for the use of atypical antipsychotic medications in children and adolescents. http://http://www.aacap.org
66. Nazeer A. Psychopharmacology of autistic spectrum disorders in children and adolescents. Pediatr Clin North Am 2011; 58: 85–97.
67. Coryell W. Maintenance treatment in bipolar disorder: a reassessment of lithium as the first choice. Bipolar Disord 2009; 11 suppl 2: 77–83.
68. Hellings JA, Weckbaugh M, Nickel EJ, et al. A double-blind, placebo-controlled study of valproate for aggression in youth with pervasive developmental disorders. J Child Adolesc Psychopharmacol 2005; 15: 682–92.
69. Biederman J, Joshi G, Mick E, et al. A prospective open-label trial of lamotrigine monotherapy in children and adolescents with bipolar disorder. CNS Neurosci Ther 2010; 16: 91–102.
70. Belsito KM, Law PA, Kirk KS, Landa RJ, Zimmerman AW. Lamotrigine therapy for autistic disorder: a randomized, double-blind, placebo-controlled trial. J Autism Dev Disord 2001; 31: 175–81.
71. Wasserman S, Iyengar R, Chaplin WF, et al. Levetiracetam versus placebo in childhood and adolescent autism: a double-blind placebo-controlled study. Int Clin Psychopharmacol 2006; 21: 363–7.
72. Jaselskis CA, Cook EH, Fletcher KE, Leventhal BL. Clonidine treatment of hyperactive and impulsive children with autistic disorder. J Clin Psychopharmacol 1992; 12: 322–7.
73. Hollander E, Soorya L, Chaplin W, et al. A double-blind placebo-controlled trial of fluoxetine for repetitive behaviors and global severity in adult autism spectrum disorders. Am J Psychiatry 2012; 169: 292–9.
74. Canitano R, Scandurra V. Psychopharmacology in autism: an update. Prog Neuropsychopharmacol Biol Psychiatry 2011; 35: 18–28.
75. Owley T, Walton L, Salt J, et al. An open-label trial of escitalopram in pervasive developmental disorders. J Am Acad Child Adolesc Psychiatry 2005; 44: 343–8.
76. Dove D, Warren Z, McPheeters ML, Taylor JL, Sathe NA, Veenstra-Vanderweele J. Medications for adolescents and young adults with autism spectrum disorders: a systematic review. Pediatrics 2012; 130: 717–26.
77. Posey DJ, Guenin KD, Kohn AE, Swiezy NB, McDougle CJ. A naturalistic open-label study of mirtazapine in autistic and other pervasive developmental disorders. J Child Adolesc Psychopharmacol 2001; 11: 267–77.
78. Remington G, Sloman L, Konstantareas M, Parker K, Gow R. Clomipramine versus haloperidol in the treatment of autistic disorder: a double-blind, placebo-controlled, crossover study. J Clin Psychopharmacol 2001; 21: 440–4.
79. Must A, Parisi SM. Sedentary behavior and sleep: paradoxical effects in association with childhood obesity. Int J Obes (Lond) 2009; 33 suppl 1: S82–6.
80. Chen X, Beydoun MA, Wang Y. Is sleep duration associated with childhood obesity? A systematic review and meta-analysis. Obesity (Silver Spring) 2008; 16: 265–74.
81. Eisenmann JC, Ekkekakis P, Holmes M. Sleep duration and overweight among Australian children and adolescents. Acta Paediatr 2006; 95: 956–63.
82. Gupta NK, Mueller WH, Chan W, Meininger JC. Is obesity associated with poor sleep quality in adolescents? Am J Hum Biol 2002; 14: 762–8.
83. Sekine M, Yamagami T, Handa K, et al. A dose-response relationship between short sleeping hours and childhood obesity: results of the Toyama Birth Cohort Study. Child Care Health Dev 2002; 28: 163–70.
84. von Kries R, Toschke AM, Wurmser H, Sauerwald T, Koletzko B. Reduced risk for overweight and obesity in 5- and 6-y-old children by duration of sleep—a cross-sectional study. Int J Obes Relat Metab Disord 2002; 26: 710–6.
85. Agras WS, Hammer LD, McNicholas F, Kraemer HC. Risk factors for childhood overweight: a prospective study from birth to 9.5 years. J Pediatr 2004; 145: 20–5.
86. Landhuis CE, Poulton R, Welch D, Hancox RJ. Childhood sleep time and long-term risk for obesity: a 32-year prospective birth cohort study. Pediatrics 2008; 122: 955–60.
87. Reilly JJ, Armstrong J, Dorosty AR, et al. Early life risk factors for obesity in childhood: cohort study. BMJ 2005; 330: 1357.
88. Lumeng JC, Somashekar D, Appugliese D, Kaciroti N, Corwyn RF, Bradley RH. Shorter sleep duration is associated with increased risk for being overweight at ages 9 to 12 years. Pediatrics 2007; 120: 1020–9.
89. Snell EK, Adam EK, Duncan GJ. Sleep and the body mass index and overweight status of children and adolescents. Child Dev 2007; 78: 309–23.
90. Wiggs L, Stores G. Sleep patterns and sleep disorders in children with autistic spectrum disorders: insight using parent report and actigraphy. Dev Med Child Neurol 2004; 46: 372–80.
91. Gail Williams P, Sears LL, Allard A. Sleep problems in children with autism. J Sleep Res 2004; 13: 265–8.
92. Allik H, Larsson J-O, Smedje H. Sleep patterns of school-age children with Asperger syndrome or high-functioning autism. J Autism Dev Disord 2006; 36: 585–95.
93. Oyane NMF, Bjorvatn B. Sleep disturbances in adolescents and young adults with autism and Asperger syndrome. Autism 2005; 9: 83–94.
94. Elia M, Ferri R, Musumeci SA, et al. Sleep in subjects with autistic disorder: a neurophysiological and psychological study. Brain Dev 2000; 22: 88–92.
95. Rechtschaffen A, Bergmann BM, Everson CA, Kushida CA, Gilliland MA. Sleep deprivation in the rat: X. Integration and discussion of the findings. Sleep 1989; 12: 68–87.
96. Spiegel K, Tasali E, Penev P, Van Cauter E. Brief communication: sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med 2004; 141: 846–50.
97. Taheri S, Lin L, Austin D, Young T, Mignot E. Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Med 2004; 1: e62.
98. Bandini LG, Anderson SE, Curtin C, et al. Food selectivity in children with autism spectrum disorders and typically developing children. J Pediatr 2010; 157: 259–64.
99. Schreck KA, Williams K, Smith AF. A comparison of eating behaviors between children with and without autism. J Autism Dev Disord 2004; 34: 433–8.
100. Cermak SA, Curtin C, Bandini LG. Food selectivity and sensory sensitivity in children with autism spectrum disorders. J Am Diet Assoc 2010; 110: 238–46.
101. Ahearn WH, Castine T, Nault K, Green G. An assessment of food acceptance in children with autism or pervasive developmental disorder–not otherwise specified. J Autism Dev Disord 2001; 31: 505–11.
102. Williams K, Gibbons B, Schreck K. Comparing selective eaters with and without developmental disabilities. J Dev Phys Disabil 2005; 17: 299–309.
103. Schreck KA, Williams K. Food preferences and factors influencing food selectivity for children with autism spectrum disorders. Res Dev Disabil 2006; 27: 353–63.
104. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet 2001; 357: 505–8.
105. Phillips SM, Bandini LG, Naumova EN, et al. Energy-dense snack food intake in adolescence: longitudinal relationship to weight and fatness. Obes Res 2004; 12: 461–72.
106. Tam CS, Garnett SP, Cowell CT, Campbell K, Cabrera G, Baur LA. Soft drink consumption and excess weight gain in Australian school students: results from the Nepean study. Int J Obes (Lond) 2006; 30: 1091–3.
107. Must A, Phillips S, Bandini L. Longitudinal fruit and vegetable consumption, fiber, and glycemic load as predictors of fatness and relative weight change over adolescence in girls. Obes Res 2005; 13: A152–3.
108. Must A, Tybor DJ. Physical activity and sedentary behavior: a review of longitudinal studies of weight and adiposity in youth. Int J Obes (Lond) 2005; 29 suppl 2: S84–96.
109. Provost B, Lopez BR, Heimerl S. A comparison of motor delays in young children: autism spectrum disorder, developmental delay, and developmental concerns. J Autism Dev Disord 2007; 37: 321–8.
110. Dewey D, Cantell M, Crawford SG. Motor and gestural performance in children with autism spectrum disorders, developmental coordination disorder, and/or attention deficit hyperactivity disorder. J Int Neuropsychol Soc 2007; 13: 246–56.
111. Minshew NJ, Sung K, Jones BL, Furman JM. Underdevelopment of the postural control system in autism. Neurology 2004; 63: 2056–61.
112. Molloy CA, Dietrich KN, Bhattacharya A. Postural stability in children with autism spectrum disorder. J Autism Dev Disord 2003; 33: 643–52.
113. Klin A, Volkmar FR, Sparrow SS. Autistic social dysfunction: some limitations of the theory of mind hypothesis. J Child Psychol Psychiatry 1992; 33: 861–76.
114. Dziuk MA, Gidley Larson JC, Apostu A, Mahone EM, Denckla MB, Mostofsky SH. Dyspraxia in autism: association with motor, social, and communicative deficits. Dev Med Child Neurol 2007; 49: 734–9.
115. Rosser Sandt D, Frey G. Comparison of physical activity levels between children with and without autistic spectrum disorder. Adapt Phys Activ Q 2005; 22: 146–59.
116. Bandini LG, Gleason J, Curtin C, et al. Comparison of physical activity between children with autism spectrum disorders and typically developing children. Autism 2013; 17: 44–54.
117. Pan C-Y, Tsai C-L, Hsieh K-W. Physical activity correlates for children with autism spectrum disorders in middle school physical education. Res Q Exerc Sport 2011; 82: 491–8.
118. Macdonald M, Esposito P, Ulrich D. The physical activity patterns of children with autism. BMC Res Notes 2011; 4: 422.
119. Memari AH, Ghaheri B, Ziaee V, Kordi R, Hafizi S, Moshayedi P. Physical activity in children and adolescents with autism assessed by triaxial accelerometry. Pediatr Obes 2013; 8: 150–8.
120. Nally B, Houlton B, Ralph S. Researches in brief: the management of television and video by parents of children with autism. Autism 2000; 4: 331–7.
121. Mazurek MO, Shattuck PT, Wagner M, Cooper BP. Prevalence and correlates of screen-based media use among youths with autism spectrum disorders. J Autism Dev Disord 2012; 42: 1757–67.
122. Davison KK, Birch LL. Childhood overweight: a contextual model and recommendations for future research. Obes Rev 2001; 2: 159–71.
123. Mendelson BK, White DR, Schliecker E. Adolescents’ weight, sex, and family functioning. Int J Eat Disord 1995; 17: 73–9.
124. Zeller MH, Reiter-Purtill J, Modi AC, Gutzwiller J, Vannatta K, Davies WH. Controlled study of critical parent and family factors in the obesigenic environment. Obesity (Silver Spring) 2007; 15: 126–36.
125. Abbeduto L, Seltzer MM, Shattuck P, Krauss MW, Orsmond G, Murphy MM. Psychological well-being and coping in mothers of youths with autism, Down syndrome, or fragile X syndrome. Am J Ment Retard 2004; 109: 237–54.
126. Rozin P. The socio-cultural context of eating and food choice. In: Meiselman HL, MacFie HJH, eds. Food choice, acceptance, and consumption. London: Springer, 1996.
127. Ochs E, Shohet M. The cultural structuring of mealtime socialization. New Dir Child Adolesc Dev 2006;( 111): 35–49.
autism spectrum disorder; children; eating patterns; genetics; obesity; physical activity; psychopharmacology; sleep
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