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Background: An increasing body of research points to a significant association of obesity to Attention-Deficit/Hyperactivity Disorder (ADHD) and deficits in executive functions. There is also preliminary evidence suggesting that children with ADHD may be at risk of obesity in adulthood., Discussion: In this article, we discuss the evidence showing that ADHD and/or deficits in executive functions are a barrier to a successful weight control in individuals enrolled in weight loss programs. Impairing symptoms of ADHD or deficits in executive functions may foster dysregulated eating behaviors, such as binge eating, emotionally-induced eating or eating in the absence of hunger, which, in turn, may contribute to unsuccessful weight loss. ADHD-related behaviors or neurocognitive impairment may also hamper a regular and structured physical activity. There is initial research showing that treatment of comorbid ADHD and executive functions training significantly improve the outcome of obesity in individuals with comorbid ADHD or impairment in executive functions., Summary: Preliminary evidence suggests that comorbid ADHD and deficits in executive functions are a barrier to a successful weight loss in individuals involved in obesity treatment programs. If further methodologically sound evidence confirms this relationship, screening and effectively managing comorbid ADHD and/or executive functions deficits in individuals with obesity might have the potential to reduce not only the burden of ADHD but also the obesity epidemics.

Although quite overlooked, increasing evidence points to a significant association between attention-deficit/hyperactivity disorder (ADHD) and obesity. Here, we present an updated systematic review and a critical discussion of studies on the relationship between ADHD and obesity, with a particular emphasis on the possible behavioral, neurobiological, and genetics underlying mechanisms. Available empirically based studies indicate that the prevalence of ADHD in clinical samples of patients seeking treatment for their obesity is higher than that in the general population. Moreover, although still limited, current evidence shows that individuals with ADHD have higher-than-average body mass index z-scores and/or significantly higher obesity rates compared with subjects without ADHD. Three mechanisms underlying the association between ADHD and obesity have been proposed: (1) obesity and/or factors associated with it (such as sleep-disordered breathing and deficits in arousal/alertness) manifest as ADHD-like symptoms; (2) ADHD and obesity share common genetics and neurobiological dysfunctions, involving the dopaminergic and, possibly, other systems (e.g., brain-derived neurotropic factor, melanocortin-4-receptor); and (3) impulsivity and inattention of ADHD contribute to weight gain via dysregulated eating patterns. With regards to the possible clinical implications, we suggest that it is noteworthy to screen for ADHD in patients with obesity and to look for abnormal eating behaviors as possible contributing factors of obesity in patients with ADHD. If further studies confirm a causal relationship between ADHD and obesity, appropriate treatment of ADHD may improve eating patterns and, as a consequence, weight status of individuals with both obesity and ADHD.

Recent studies suggest a possible comorbidity between Attention-Deficit/Hyperactivity Disorder (ADHD) and obesity. To gain insight into this potential association, we performed a systematic review of the literature excluding case reports, non-empirical studies, and studies not using ADHD diagnostic criteria. Empirically based evidence suggests that obese patients referred to obesity clinics may present with higher than expected prevalence of ADHD. Moreover, all reviewed studies indicate that subjects with ADHD are heavier than expected. However, data on the prevalence of obesity in subjects with ADHD are still limited. As for the mechanisms underlying the potential association between ADHD and obesity, ADHD might lead to obesity via abnormal eating behaviors, impulsivity associated with binge eating might contribute to ADHD in obese patients, or, alternatively, both obesity and ADHD might be the expression of common underlying neurobiological dysfunctions, at least in a subset of subjects. In patients with obesity and ADHD, both conditions might benefit from common therapeutic strategies. Further empirically based studies are needed to understand the potential comorbidity between obesity and ADHD, as well as the possible mechanisms underlying this association. This might allow a more appropriate clinical management and, ultimately, a better quality of life for patients with both obesity and ADHD.

Objective: Recent evidence suggests an association between obesity and Attention Deficit/Hyperactivity Disorder (ADHD) or ADHD traits. The characteristics of obese subjects with a higher probability of ADHD symptoms are still unclear. We explore the hypothesis that obese adolescents with sleep/alertness problems represent a subgroup at high risk for ADHD traits, independently from associated symptoms of anxiety/depression. The aim of this study was to assess the relationship between parent reports of sleep/alertness problems and ADHD traits in a clinical sample of obese adolescents, controlling for symptoms of anxiety/depression., Methods: Seventy obese subjects (age range, 10-16 years) were included. The parents filled out the Sleep Disturbance Scale for Children (SDSC), the Conners Parents Rating Scale-Revised (Short Version) (CPRS-R:S), and the Child Behavior Checklist (CBCL). The ADHD Rating Scale (ADHD-RS) was completed by a child psychiatrist., Results: Using multiple regression models controlling for symptoms of anxiety/depression, scores of excessive daytime sleepiness on the SDSC were significantly associated with ADHD traits on the CPRS-R:S as well as on the ADHD-RS., Conclusions: Obese adolescents described as excessively sleepy by their parents may be at higher risk of ADHD symptoms, independently from symptoms of anxiety/depression. Although the clinician may overlook a potential diagnosis of ADHD in obese adolescents described as sleepy, the results of this study suggest to systematically look for symptoms of ADHD in this subgroup of obese patients. Further studies using objective methods to assess sleep/alertness disturbances are needed to gain insight into the relationship between sleep/alertness disturbances and ADHD in obese individuals.

• ADHD and obesity are significantly associated. • The characteristics of individuals with obesity at increased risk of ADHD need to be elucidated. • We found a significant correlation between inflammatory cytokines and ADHD symptoms severity. • These results pave the way for further role on the role of inflammatory mechanisms in the link between obesity and ADHD. Whilst the association between Attention-Deficit/Hyperactivity Disorder (ADHD) and obesity is supported by meta-analytic evidence, the mechanisms underpinning this link need to be further elucidated. Inflammatory processes may increase the risk of ADHD symptoms in individuals with obesity. This pilot study set out to start testing this hypothesis by assessing the correlation between serum levels of inflammatory cytokines and ADHD symptoms severity in a sample of children and adolescents with obesity. We measured ADHD symptoms severity in 52 children/adolescents with obesity (BMI > 95th centile) with the Conners questionnaire, revised, short version, parent (CPRS-R:S) and teacher (CTRS-R:S) versions. Additionally, a categorical diagnosis of ADHD was established using the Kiddie-SADS-PL. Serum levels of IL-6, Il-10, and TNF-alpha were also obtained. The prevalence of ADHD was 9.6%. We found a significant correlation between IL-6, as well as TNF-alpha, and hyperactivity/impulsivity subscores of the CPRS-R:S and CTRS-R:S, that held even after controlling for BMI and oppositional symptoms. This study provides a rationale for larger, longitudinal studies to gain insight into inflammatory processes underpinning the link between obesity and ADHD. This line of research has the potential to lead to novel, pathophysiologically-based management strategies for individuals with obesity and ADHD. [ABSTRACT FROM AUTHOR]