"Food addiction" has become a focus of interest for researchers attempting to explain certain processes and/or behaviors that may contribute to the development of obesity. Although the scientific discussion on "food addiction" is in its nascent stage, it has potentially important implications for treatment and prevention strategies. As such, it is important to critically reflect on the appropriateness of the term "food addiction", which combines the concepts of "substance-based" and behavioral addiction. The currently available evidence for a substance-based food addiction is poor, partly because systematic clinical and translational studies are still at an early stage. We do however view both animal and existing human data as consistent with the existence of addictive eating behavior. Accordingly, we stress that similar to other behaviors eating can become an addiction in thus predisposed individuals under specific environmental circumstances. Here, we introduce current diagnostic and neurobiological concepts of substance-related and non-substance-related addictive disorders, and highlight the similarities and dissimilarities between addiction and overeating. We conclude that "food addiction" is a misnomer because of the ambiguous connotation of a substance-related phenomenon. We instead propose the term "eating addiction" to underscore the behavioral addiction to eating; future research should attempt to define the diagnostic criteria for an eating addiction, for which DSM-5 now offers an umbrella via the introduction on Non-Substance-Related Disorders within the category Substance-Related and Addictive Disorders.

The heritability of attention deficit hyperactivity disorder (ADHD) is approximately 0.8. Despite several larger scale attempts, genome-wide association studies (GWAS) have not led to the identification of significant results. We performed a GWAS based on 495 German young patients with ADHD (according to DSM-IV criteria; Human660W-Quadv1; Illumina, San Diego, CA) and on 1,300 population-based adult controls (HumanHap550v3; Illumina). Some genes neighboring the single nucleotide polymorphisms (SNPs) with the lowest P-values (best P-value: 8.38 × 10(-7)) have potential relevance for ADHD (e.g., glutamate receptor, metabotropic 5 gene, GRM5). After quality control, the 30 independent SNPs with the lowest P-values (P-values ≤ 7.57 × 10(-5) ) were chosen for confirmation. Genotyping of these SNPs in up to 320 independent German families comprising at least one child with ADHD revealed directionally consistent effect-size point estimates for 19 (10 not consistent) of the SNPs. In silico analyses of the 30 SNPs in the largest meta-analysis so far (2,064 trios, 896 cases, and 2,455 controls) revealed directionally consistent effect-size point estimates for 16 SNPs (11 not consistent). None of the combined analyses revealed a genome-wide significant result. SNPs in previously described autosomal candidate genes did not show significantly lower P-values compared to SNPs within random sets of genes of the same size. We did not find genome-wide significant results in a GWAS of German children with ADHD compared to controls. The second best SNP is located in an intron of GRM5, a gene located within a recently described region with an infrequent copy number variation in patients with ADHD.

It has been assumed that overweight individuals show weak inhibitory control capacity leading to a failure to resist external cues for palatable food and that this deficit underlies the recently reported empirical association between obesity and attention deficit/hyperactivity disorder (ADHD). In childhood and adolescence, empirical research on this issue is scarce. Here, the hypothesis is tested that high body weight is associated with weak inhibitory control performance and that this association is moderated by age. The sample included 177 overweight and obese children and adolescents (BMI: M = 29.2, SD = 4.33; BMI-SDS: M = 2.45, SD = 0.43) between 8 and 15 years. Inhibitory control was assessed by a Go/No-Go task and an Interference Task. A principal component analysis yielded two components: impulsivity (fast but invalid responses) and inattention (highly variable reaction times). While controlling for age, gender, and maternal education level, we found that more obese children/adolescents showed more inattention. As indicated by a significant interaction effect, exclusively at younger ages, high impulsivity was associated with high body weight. The results thus confirm a link between low inhibitory control capacity and high body weight and might point to a developmental period with heightened significance of impulsivity for weight gain.

Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder. Genetic loci have not yet been identified by genome-wide association studies. Rare copy number variations (CNVs), such as chromosomal deletions or duplications, have been implicated in ADHD and other neurodevelopmental disorders. To identify rare (frequency ⩽1%) CNVs that increase the risk of ADHD, we performed a whole-genome CNV analysis based on 489 young ADHD patients and 1285 adult population-based controls and identified one significantly associated CNV region. In tests for a global burden of large (>500 kb) rare CNVs, we observed a nonsignificant (P=0.271) 1.126-fold enriched rate of subjects carrying at least one such CNV in the group of ADHD cases. Locus-specific tests of association were used to assess if there were more rare CNVs in cases compared with controls. Detected CNVs, which were significantly enriched in the ADHD group, were validated by quantitative (q)PCR. Findings were replicated in an independent sample of 386 young patients with ADHD and 781 young population-based healthy controls. We identified rare CNVs within the parkinson protein 2 gene (PARK2) with a significantly higher prevalence in ADHD patients than in controls (P=2.8 × 10−4 after empirical correction for genome-wide testing). In total, the PARK2 locus (chr 6: 162 659 756–162 767 019) harboured three deletions and nine duplications in the ADHD patients and two deletions and two duplications in the controls. By qPCR analysis, we validated 11 of the 12 CNVs in ADHD patients (P=1.2 × 10−3 after empirical correction for genome-wide testing). In the replication sample, CNVs at the PARK2 locus were found in four additional ADHD patients and one additional control (P=4.3 × 10−2). Our results suggest that copy number variants at the PARK2 locus contribute to the genetic susceptibility of ADHD. Mutations and CNVs in PARK2 are known to be associated with Parkinson disease.

It has been assumed that inhibitory control capacity might influence the success of overweight or obese subjects in reducing weight. However, empirical research on this association is scarce. The present study, therefore, examines whether success in an outpatient weight-reduction program for children and adolescents can be predicted by pre-intervention inhibitory control capacity. The study sample consisted of 111 overweight and obese children and adolescents (7.5-15 years) who attended an outpatient weight-reduction program of 1 year's duration. Inhibitory control was assessed by two computerized neuropsychological procedures, a Go-NoGo and an interference task. Principal component analysis revealed "impulsivity" (fast but less valid reactions) and "inattention" (slow and highly variable reaction times) component. Those who succeeded in the intervention (losing more than 5% of BMI-SDS; n = 63) scored significantly higher in the first component than those who failed, while controlling for pre-intervention BMI-SDS, age, gender, and maternal education level. The association was moderated by age. Although in younger children no effect was found, in adolescents high "impulsivity" predicted success. Our result supports the scant evidence for a role of inhibitory control. However, further studies are required to substantiate that weak inhibitory control, and thus high reactivity to external cues, entails a better outcome in behavior modification interventions.

Objective: To analyze whether caregiver and family characteristics predict success in a family-based lifestyle intervention program for children and adolescents.Method: Participants were 111 overweight and obese children (7-15 years) who attended a family-based weightreduction program. Body mass index (BMI) and BMI standard deviation scores (BMI-SDS) of index child, and BMI of family members, family adversity characteristics, depression, and attachment attitudes of the primary caregiver were assessed.Results: Risk of nonresponse ( 5% reduction of BMI-SDS or dropout) was elevated in older children, cases with obese sibling(s), maternal depression, and avoidant attachment attitude. In a logistic regression analysis, maternal depression, attachment attitude, and age of index child explained common variance whereas the presence of obese siblings explained unique variance in nonresponding.Discussion: To meet the specific needs of all participating families and to prevent the discouraging experience of failure in weight-control interventions, our data suggest that special support should be provided to adolescents with obese siblings, and cases of maternal depression, and avoidant attachment attitude. V V C 2009 by Wiley Periodicals, Inc.

Substitution of (R,S)-methadone by (R)-methadone reduces the QTc interval value. A safer cardiac profile of (R)-methadone is in agreement with previous in vitro and pharmacogenetic studies. If the present results are confirmed by larger studies, (R)-methadone should be prescribed instead of (R,S)-methadone to reduce the risk of cardiac toxic effects and sudden death.

Children with attention-deficit/hyperactivity disorder (ADHD) have a higher rate of obesity than children without ADHD. Obesity risk alleles may overlap with those relevant for ADHD. We examined whether risk alleles for an increased body mass index (BMI) are associated with ADHD and related quantitative traits (inattention and hyperactivity/impulsivity). We screened 32 obesity risk alleles of single nucleotide polymorphisms (SNPs) in a genome-wide association study (GWAS) for ADHD based on 495 patients and 1,300 population-based controls and performed in silico analyses of the SNPs in an ADHD meta-analysis comprising 2,064 trios, 896 independent cases, and 2,455 controls. In the German sample rs206936 in the NUDT3 gene (nudix; nucleoside diphosphate linked moiety X-type motif 3) was associated with ADHD risk (OR: 1.39; 295 Neuropsychiatric GeneticsP ¼ 3.4 Â 10 À4; P corr ¼ 0.01). In the meta-analysis data we found rs6497416 in the intronic region of the GPRC5B gene (G proteincoupled receptor, family C, group 5, member B; P ¼ 7.2 Â 10 À4 ; P corr ¼ 0.02) as a risk allele for ADHD. GPRC5B belongs to the metabotropic glutamate receptor family, which has been implicated in the etiology of ADHD. In the German sample rs206936 (NUDT3) and rs10938397 in the glucosamine-6-phosphate deaminase 2 gene (GNPDA2) were associated with inattention, whereas markers in the mitogen-activated protein kinase 5 gene (MAP2K5) and in the cell adhesion molecule 2 gene (CADM2) were associated with hyperactivity. In the meta-analysis data, MAP2K5 was associated with inattention, GPRC5B with hyperactivity/impulsivity and inattention and CADM2 with hyperactivity/impulsivity. Our results justify further research on the elucidation of the common genetic background of ADHD and obesity.