Search

Background:It was previously demonstrated that drinking water significantly elevates the resting energy expenditure (REE) in adults, and that low water intake is associated with obesity and lesser success in weight reduction. This study addressed the potential of water drinking to increase the REE in children, as an additional tool for weight management.Objective:To examine the effect of drinking water on the REE of overweight children.Design:A total of 21 overweight, otherwise-healthy children (age 9.9±1.4 years, 11 males) drank 10 ml kg−1 cold water (4 °C). REE was measured before and after water ingestion, for 66 min. The main outcome measure was the change in mean REE from baseline values.Results:Immediately after drinking water, there was a transient decrease in REE, from a baseline value of 3.32±1.15 kilojoule (kJ) per min to 2.56±0.66 kJ per min at minute 3 (P=0.005). A subsequent rise in REE was then observed, which was significantly higher than baseline after 24 min (3.89±0.78 kJ/min (P=0.021)), and at most time points thereafter. Maximal mean REE values were seen at 57 min after water drinking (4.16±1.43 kJ per min (P=0.004)), which were 25% higher than baseline. REE was significantly correlated with age, height, weight and fat-free mass; the correlations with maximal REE values after water drinking were stronger than with baseline REE values.Conclusions:This study demonstrated an increase of up to 25% in REE following the drinking of 10 ml kg−1 of cold water in overweight children, lasting for over 40 min. Consuming the recommended daily amount of water for children could result in an energy expenditure equivalent to an additional weight loss of about 1.2 kg per year. These findings reinforce the concept of water-induced REE elevation shown in adults, suggesting that water drinking could assist overweight children in weight loss or maintenance, and may warrant emphasis in dietary guidelines against the obesity epidemic. [ABSTRACT FROM AUTHOR]

Psychiatric neurosurgery teams in the United States and Europe have studied deep brain stimulation (DBS) of the ventral anterior limb of the internal capsule and adjacent ventral striatum (VC/VS) for severe and highly treatment-resistant obsessive-compulsive disorder. Four groups have collaborated most closely, in small-scale studies, over the past 8 years. First to begin was Leuven/Antwerp, followed by Butler Hospital/Brown Medical School, the Cleveland Clinic and most recently the University of Florida. These centers used comparable patient selection criteria and surgical targeting. Targeting, but not selection, evolved during this period. Here, we present combined long-term results of those studies, which reveal clinically significant symptom reductions and functional improvement in about two-thirds of patients. DBS was well tolerated overall and adverse effects were overwhelmingly transient. Results generally improved for patients implanted more recently, suggesting a ‘learning curve’ both within and across centers. This is well known from the development of DBS for movement disorders. The main factor accounting for these gains appears to be the refinement of the implantation site. Initially, an anterior–posterior location based on anterior capsulotomy lesions was used. In an attempt to improve results, more posterior sites were investigated resulting in the current target, at the junction of the anterior capsule, anterior commissure and posterior ventral striatum. Clinical results suggest that neural networks relevant to therapeutic improvement might be modulated more effectively at a more posterior target. Taken together, these data show that the procedure can be successfully implemented by dedicated interdisciplinary teams, and support its therapeutic promise. [ABSTRACT FROM AUTHOR]

Psychobiologic models of obsessive-compulsive disorder (OCD) have focused on cortico-striatal-thalamic-cortical (CTSC) circuits, noting normal function in cognitive and motoric procedural strategies. Such models have relied on the classification of OCD as an anxiety disorder, seldom exploring other relevant emotions. Based on the hypothesis that a central emotion in OCD is disgust, the authors review the literature on its psychobiology and its relevance to current models of OCD. There are important parallels between the psychobiology of OCD and that of disgust. Obsessive- compulsive disorder may be conceptualized in terms of a false contamination alarm in which disgust plays a crucial organizing or embodying role, not only at a basic brain level, but also in terms of the psychosocial aspects of the disorder. Just as psychobiologic models of panic disorder and post- traumatic stress disorder have been strengthened by the inclusion of preclinical work on amygdala-mediated fear conditioning, so findings on disgust and its mediating CSTC circuits may generate useful hypotheses for OCD research. [ABSTRACT FROM AUTHOR]