Manualised Cognitive Remediation Therapy for adult obesity: study protocol for a randomised controlled trial

Background: Research has shown that obese individuals have cognitive deficiencies in executive function, leading to poor planning and impulse control, and decision-making difficulties. An intervention that could help reduce these deficits and in turn help weight loss maintenance is Cognitive Remediation Therapy for Obesity (CRT-O). We aim to examine the efficacy of manualised CRT-O, which is intended to improve executive function, enhance reflective practice and help weight loss maintenance. \ud \ud Methods/Design: A randomised controlled trial (registered with the Australian New Zealand Clinical Trials Registry) will be conducted. First, 90 obese adults (body mass index >30 kg/m2) in the community will receive three weekly sessions of a group Behaviour Weight Loss Treatment (BWLT), and then will be randomised either to receive CRT-O or to enter a no-treatment control group. CRT-O training will comprise twice-weekly sessions of 45 minutes over a 4 to 6 week period, for a total of eight sessions. Measurement points will be at baseline, post CRT-O (or 4 to 6 weeks after BWLT for the no-treatment control), 3 months post treatment and 1 year post treatment. The primary outcome will be executive function and secondary outcome measures will include participants' body mass index, hip to waist ratio, eating behaviours and quality of life. \ud \ud Discussion: This is the first study of its kind to examine the efficacy of Cognitive Remediation Therapy for obese adults through a randomised controlled trial

Case-control genome-wide association study of persistent attention-deficit hyperactivity disorder identifies FBXO33 as a novel susceptibility gene for the disorder

Attention-deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder with high heritability. At least 30% of patients diagnosed in childhood continue to suffer from ADHD during adulthood and genetic risk factors may play an essential role in the persistence of the disorder throughout lifespan. To date, genome-wide association studies (GWAS) of ADHD have been completed in seven independent datasets, six of which were pediatric samples and one on persistent ADHD using a DNA-pooling strategy, but none of them reported genome-wide significant associations. In an attempt to unravel novel genes for the persistence of ADHD into adulthood, we conducted the first two-stage GWAS in adults with ADHD. The discovery sample included 607 ADHD cases and 584 controls. Top signals were subsequently tested for replication in three independent follow-up samples of 2104 ADHD patients and 1901 controls. None of the findings exceeded the genome-wide threshold for significance (PGC<5e-08), but we found evidence for the involvement of the FBXO33 (F-box only protein 33) gene in combined ADHD in the discovery sample (P=9.02e-07) and in the joint analysis of both stages (P=9.7e-03). Additional evidence for a FBXO33 role in ADHD was found through gene-wise and pathway enrichment analyses in our genomic study. Risk alleles were associated with lower FBXO33 expression in lymphoblastoid cell lines and with reduced frontal gray matter volume in a sample of 1300 adult subjects. Our findings point for the first time at the ubiquitination machinery as a new disease mechanism for adult ADHD and establish a rationale for searching for additional risk variants in ubiquitination-related genes