Recently, ADHD has been associated with body weight dysregulation [4], [5]. Indeed, it has been reported that ADHD subjects show higher than average body mass index standard deviation scores, and have significantly higher percentage of body fat and abdominal circumference compared to controls [6], [7]. Conversely, obese subjects are more likely to present with attention problems [8]. In addition, some evidence suggests that patients with eating disorders tend to have attention problems akin to ADHD [9], [10].

From a psychological point of view, both ADHD and childhood obesity have been conceptualized as disorders of impaired self-regulation [11], [12]. Self-regulation is a psychological construct encapsulating the means by which individuals manage themselves in order to attain adaptative goals [13]. This construct implicates emotional and cognitive, particularly executive function (EF) processes [14], [15]. EF represent the neurocognitive processes important for goal-directed behaviours [16] including planning, sustained attention, cognitive flexibility, working memory, and response inhibition. Deficits in EF are believed to play an important role in ADHD. More specifically, ADHD children have shown significant impairments in different EF domains including response inhibition, vigilance, working memory, and planning [17]. Likewise, extremely obese individuals demonstrate significant differences in performances on tests of executive functioning such as planning, problem solving, and mental flexibility [18]. Similarly, in comparison to their peers, obese children exhibit significant cognitive deficits in their attention shifting abilities [19]. Furthermore, in some studies, adults with elevated BMI display reduced cognitive performance [20]. However, in a recent large longitudinal study, obesity indices were differentially associated with performance on neuropsychological tests; while global cognitive function, memory and language ability were found to be associated with obesity indices, attention and visuospatial ability showed the reverse trends [21].

In addition to EFs, self-regulation depends critically on motivational systems that may be dysregulated in both ADHD and obesity. In this regard, mesolimbic dopaminergic neurotransmission has been firmly implicated in the regulation of saliency of behavioral tasks [22] and food stimuli [23]. It has been proposed that ADHD symptoms may be at least in part the consequence of reduced dopamine (DA) signaling in the mesolimbic system, resulting in reduced saliency of tasks [24] and aversion to delayed gratification [25]. This emotional style may result in preferring immediate rewards and being less sensitive to reinforcement schedules [26], [27], and consequently may contribute to abnormal eating habits [28] and promote inclination towards readily available non-healthy food in patients with ADHD. Similarly, pathological eating behavior (food addiction) in obese individuals has been conceptualized as a reaction compensating for a dampened DA reward system [29], [30]. Under this scenario, excessive food intake may result in elevated dopamine activation in the mesolimbic pathway leading to a rewarding experience [31], [32].

These neurocognitive/emotional parallels between ADHD and obesity are also supported by neuroimaging studies in ADHD and obese subjects [33], [34], [35], [36]. Further, it is also noticeable that psychostimulant medications, used to treat ADHD symptoms, also reduce appetite [37], [38]. These observations taken together suggest that the neurobiological pathways implicated in the regulation of attention and motor control are also important determinants of energy intake and eating behaviors [39], [40]. While the literature linking ADHD to body weight regulation is rich in neuropsychological hypotheses attempting to explain the link between these two complex disorders, the experimental data supporting these theories is very limited. To our knowledge, only one study reported an association between body weight and EF in children with ADHD [12]. In addition, the association between ADHD and body mass dysregulation could be due to many factors shared by these two conditions. Childhood socioeconomic adversity has been shown to impact both ADHD [41], [42] and obesity [43]. More specifically, in a national cohort study with a sample of 7,960 children (aged 6–19 years), familial socioeconomic adversity factors including low maternal education level, single parent status and being recipient of social welfare predicted medicated status in school children with ADHD [42]. Likewise, in developed countries, groups belonging to low socioeconomic status (SES) are more likely to be obese compared to other SES groups [44], [45], [46].

With regards to previous medication status, ADHD children within the obese group were significantly less likely to be previously on medication (20.3%) compared to subjects in the overweight (25.0%), and normal weight (36.1%) groups (Χ²=6.15, df =2, p=0.04; Table 1). This finding is in line with previous data indicating that stimulant medication in ADHD subjects may result in weight loss due to suppression of appetite [68], [69].

All subsequent analyses were conducted while controlling for aforementioned SES factors (parental age at child birth, family income status, and MSDP) and prior history of treatment with psychostimulants.

Additionally, as shown in Table 2, neurocognitive features as assessed by the WISC-III, WCST, TOL, SOPT, FW, CPT, and Stroop were not significantly different between the three groups (all p>0.05). Further, no significant differences between the groups were found in emotional/motivational style as evaluated by the CDT and the RASS respectively (all p>0.05; Table 3). Finally, the three groups were not significantly different with regards to motor activity as evaluated by actigraphy (all p>0.05; Table 3).

Different theoretical models have proposed that ADHD and body mass regulation disorders share common pathophysiological underpinnings. From a neuropsychological point of view, it is suggested that ADHD and obesity stem from impairments in individual's self-regulation [11], [12]. More specifically, deficits in Executive Functions [13], [74], dysfunctional motivational regulation systems [75] and aberrant goal directed motor activity regulated by brain dopamine systems are believed to be implicated in both disorders. Supporting this line of argument, neuroimaging data in ADHD and obese subjects report commonality in brain structural abnormalities, including in the frontal cortex [33], [34], [35], [36], a locus considered to be important for self-regulation and EFs. In addition, ADHD subjects have been shown to have reduced DA receptor binding capacity in the hypothalamus, which controls for satiety and hunger [76].

The primary objective of the present study was to investigate the relation between body weight and cognitive, emotional, and motor activity characteristics in a large sample of children with ADHD. Results from our study do not identify statistically significant differences between weight groups (normal, over, and obese categories) in children with ADHD with respect to neurocognitive measures tapping in executive functions, motivational style indices, and overall motor activity. These findings contrast with the results of the only other study examining the association between EF and weight in children with ADHD [12]. More specifically, Graziano et al (2011) showed that children who performed poorly on a neuropsychological battery had greater BMI z-scores (overweight and obese) compared with children who performed better on the neuropsychological battery. Several factors may explain this discrepancy between the two studies. Compared to Graziano and colleagues, the current study has a much larger sample size (n=80 versus n=284), the participants have a narrower age range (4.5–18 years versus 6–12 years), and the neurocognitive assessment is more comprehensive in the present study. Unlike Graziano and colleagues, our participants were not taking any psychostimulant medication for at least one week prior to the neurocognitive assessments. Further, our statistical analysis model used parental (both mothers and fathers) age at child birth, family income status, MSDP, and prior history of treatment with psychostimulants as covariates to prevent potential confounding effects on the result outcomes, which was not the case in Graziano et al. study. In addition, the use of different neuropsychological tests indexing various EF domains in children with ADHD could also contribute to incongruent results. Contrary to Graziano et al. study where all cognitive domains were reduce into one single factor, in the present study; we elected to explore separately all performances assessed by various tests in order to identify any specific differences between the three groups. These analyses did not identify any significant differences, including in neuropsychological tests common to our study and Graziano and colleagues' work (Color-Word Interference Test).

The present study identified a strong association between socioeconomic (SE) characteristics and overweight and obesity status in children with ADHD, including parental age at child birth, MSDP and annual family income. These results are in line with results of previous reports in children from the general population exploring the role of socioeconomic, geographic and environmental factors in influencing body weight gain and fat distribution [43]. In developed countries, low SES strongly predicts obesity [77], [78] and the largest increase in obesity is observed in individuals living within the defined range of poverty [79]. Further, several lifestyle factors associated with obesity have a strong impact on children and adolescents belonging to low SES [80], [81], [82]. For instance, younger children having limited accesses to healthy foods, recreational venues and safe housing are 20–60% more likely to be obese/overweight compared to others [83], [84], [85], [86]. Due to increased financial burden, low SES families may not be able to afford to pay for their children's involvement in any formal sport/recreation activities, and these children may have limited access to safer parks or recreational facilities because they reside in poor neighborhoods [87]. This activity limitation prevents low SES child's engagement in a healthy, active lifestyle, and thus increases the chances of being overweight relative to their affluent high SES peers. Additionally, a diet with fruits and vegetables is highly recommended as part of a healthy lifestyle for growing children, but this may be less affordable for low SES families, resulting in poor nutrition and unhealthy weight gain. Consequently, it is plausible that lower SES is the main risk factor promoting overweight/obesity in children with ADHD.

Like ADHD [88], [89], weight gain/obesity is a multifaceted phenotype depending on complex interactions between genetic and environmental factors [5], [90]. More research in larger independent samples is recommended to further explore the complex relations between gene-environment-obesity amongst children with ADHD.

Our study has a number of strengths. First, to our knowledge, this is the largest and most comprehensive study examining the relations between weight status/BMI and neurocognitive profiles, motivational status and motor activity in children with ADHD. In addition, all clinical, neurocognitive, motivational and motor activity assessments were carried out while the children were not taking any medication (1 week wash out period).

The main limitations of this study also need to be considered. This study could not investigate the moderating effects of physical activity patterns [91] and eating habits/preferences [92] on the relation between body weight and ADHD due to unavailability of data. Future studies should address this issue, given the link between physical activity, eating preferences, obesity and ADHD. Further, our research design investigated BMI which is a generalized measure of body mass and lacked more direct and objective measures of obesity for example, underwater weighing, skin folds, etc. Finally, a link between altered sleep patterns, obesity and ADHD has been recently suggested [93], [94], given the unavailability of the sleep data in this sample, we could not investigate this potential interaction.