یک مطالعه روانی ژنتیکی برای ارتباط بین نشانه های اختلال تغذیه ای مفرط و کسانی که اختلال کمبود توجه (بیش فعالی) دارند
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|31007||2009||10 صفحه PDF||سفارش دهید||7416 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Journal of Psychiatric Research, Volume 43, Issue 7, April 2009, Pages 687–696
Objective Some recent studies have reported intriguingly strong correlations between ADHD and obesity. This study examined whether ADHD symptoms were more pronounced in adults with symptoms of binge eating disorder (BE) than in their non-binging obese counterparts, and whether the links were stronger with inattentive vs impulsive/hyperactive symptoms. We also assessed the role of the dopamine D3 receptor in ADHD symptoms since the DRD3 gene has been associated with impulsivity and drug addiction – both relevant features of ADHD. Methods A case (BE: n = 60) double-control (normal weight: n = 61 and obese: n = 60) design was employed. Assessments of both childhood and adults ADHD symptoms were made, as well as genotyping of seven markers of DRD3 including the functional Ser9Gly polymorphism. Results Three DRD3 genotypes, including Ser/Ser, had significantly elevated scores on the hyperactive/impulsive symptom scale. In turn, the four ADHD symptom scales were all significantly elevated in the BE and obese groups, who did not differ from each other, compared to those with normal weight. Conclusions Results indicated a role for the D3 receptor in the manifestation of the hyperactive/impulsive symptoms of ADHD, and that symptoms of ADHD are significantly, but not differentially, elevated in obese adults with and without binge eating. Our findings suggest that ADHD screening in adults seeking treatment for obesity, including those with BE, may be warranted as methods used to treat ADHD may help some to better manage overeating and other factors contributing to weight gain.
Attention deficit/hyperactivity disorder (ADHD) was initially seen as a childhood disorder that typically remitted with puberty (Mayes and Rafalovich, 2007). Views changed with the evidence that 70–80% of children with ADHD retain some of their symptoms in adolescence, and that in a substantial number of cases, one or more disabling features of the disorder persist into adulthood (Biederman et al., 1996 and Mannuzza et al., 1998). However, the quality of the core characteristics tends to change with maturity. For example, the overt and extreme restlessness seen in children is usually channeled into more socially appropriate behaviours (Weiss et al., 1999). There is a wealth of research demonstrating an association between ADHD and addiction disorders – a co-morbidity that is both robust and bi-directional (e.g. Fuemmeler et al., 2007, Ohlmeier et al., 2007 and Tang et al., 2007). Moreover, the conclusions from a recent familial-risk analysis are that ADHD and drug dependence share a common vulnerability profile rather than present with independent modes of transmission (Biederman et al., 2008). Since both disorders have strong links to the dopamine (DA) system, Biederman and his colleagues propose the conjoint involvement of DA genes that regulate arousal, attention, and the common reward pathway. 1.1. ADHD and obesity In recent years, we have also become aware of strong links between ADHD and obesity (e.g. Agranat-Meged et al., 2005, Altfas, 2002 and Fleming et al., 2005) – an association of particular interest because of their individual connectedness to addictive behaviours. First, there is some evidence that highly palatable food can be an addictive substance, and that compulsive overeating can be modelled as an addictive behaviour (Avena et al., 2008, Davis et al., 2008, Trinko et al., 2007 and Volkow and O’Brien, 2007). Second, is the compelling that body weight and food intake are regulated – perhaps at least in part – by the same DA brain reward mechanisms as pharmacologic agents like cocaine and nicotine (Hoebel et al., 2007, Kenny, 2007 and Campbell and Eisenberg, 2007). Therefore, some cases of obesity may be the consequence of a food addiction (see Cassin and von Ranson, 2007) that occurs – like drug dependence – with greater prevalence in those with ADHD. Another unifying thread in these syndromes is the centrality of impulsivity – a personality trait characterized by the diminished ability to inhibit behaviour when restraint is the most advantageous and appropriate response in a particular situation. Converging evidence suggests that DA pathways play an important role in the expression of this endophenotype, which varies widely in the general population (e.g. Eisenberg et al., 2007, Limosin et al., 2005 and Ondo and Lai, 2008). Impulsivity correlates positively and consistently with drug use and abuse ( Verdejo-Garcia et al., 2007), with compulsive overeating ( Steiger and Bruce, 2007), and with ADHD, where it serves as one of the diagnostic criteria for this disorder ( American Psychiatric Association, 1994; Drechsler et al., 2008). To date, the research linking obesity and ADHD has focused largely on co-morbidity prevalence data. For example, in a sample of morbidly obese adults recruited from a bariatric clinic, almost half met diagnostic criteria for ADHD (Altfas, 2002). Only a handful of studies has examined mechanisms underlying the ADHD/obesity association. The principal finding is that measures of hedonic eating1 – including binge eating – may mediate the relationship in adults and adolescents (Cortese et al., 2007 and Davis et al., 2006).