Do Fructose-Containing Sugars Lead to Adverse Health Consequences? Results of Recent Systematic Reviews and Meta-analyses

Sugars have replaced fat as the dominant public health nutrition concern. A fructose-centric view of cardiometabolic disease has emerged whereby fructose-containing sugars are thought to have deleterious effects on body weight, fasting and postprandial blood lipids, glycemia, blood pressure, uric acid, and markers of nonalcoholic fatty liver disease. Long-term prospective cohort studies have not supported these associations when assessing the relation between total fructose-containing sugars at any amount of intake and incident cardiometabolic disease. Conversely, a consistent signal for harm has been reported for sugary beverages when comparing the highest with the lowest intakes. These associations, however, do not hold at moderate intakes, which are more reflective of real-world intakes, are subject to important collinearity effects, and have small risk estimates with modest population-attributable risk fractions. Higher-level evidence from controlled feeding trials shows that fructose-containing sugars in either liquid or solid form have adverse cardiometabolic effects only when they supplement diets with excess calories compared with the same diets without the excess calories. In the absence of harm when fructose-containing sugars are exchanged for other sources of carbohydrate under energy-matched conditions, excess calories appear to be the dominant consideration. Like with the earlier fat story, it is difficult to separate the contribution of fructose-containing sugars from that of other sources of excess calories in the epidemic of obesity and cardiometabolic disease. Attention needs to remain focused on reducing the overconsumption of all caloric foods associated with obesity and cardiometabolic disease, including sugary beverages and foods, and promoting greater physical activity.     

Enhanced Dopamine-Dependent Hippocampal Plasticity after Single MK-801 Application

Dopaminergic hyperfunction and N-methyl-D-aspartate receptor (NMDAR) hypofunction have both been implicated in psychosis. Dopamine-releasing drugs and NMDAR antagonists replicate symptoms associated with psychosis in healthy humans and exacerbate symptoms in patients with schizophrenia. Though hippocampal dysfunction contributes to psychosis, the impact of NMDAR hypofunction on hippocampal plasticity remains poorly understood. Here, we used an NMDAR antagonist rodent model of psychosis to investigate hippocampal long-term potentiation (LTP). We found that single systemic NMDAR antagonism results in a region-specific, presynaptic LTP at hippocampal CA1-subiculum synapses that is induced by activation of D1/D5 dopamine receptors and modulated by L-type voltage-gated Ca²⁺ channels. Thereby, our findings may provide a cellular mechanism how NMDAR antagonism can lead to an enhanced hippocampal output causing activation of the hippocampus-ventral tegmental area-loop and overdrive of the dopamine system.     

Robotic-assisted mesh pelvic closure for prevention of small bowel descent after surgery for recurrent rectal cancer

Techniques in Coloproctology -     

Detection of antibody against antigen expressed by molecularly cloned hepatitis C virus cDNA: application to diagnosis and blood screening for posttransfusion hepatitis.

A cDNA clone has been derived from the plasma of a chimpanzee with chronic non-A, non-B viral hepatitis (NANBH). We have assayed for antibodies reacting with the encoded antigen in sera from posttransfusion hepatitis patients (643 samples from 23 patients) and their corresponding donors collected during the past 10 years in Japan. The antibody was detected in 15 out of 17 (88.2%) posttransfusion NANBH (PT-NANBH) patients whose sera over time displayed multiple alanine aminotransferase (ALT) peaks. In general, the antibody was detected after several peaks of serum ALT elevations and, once detected, it persisted for years. In contrast to the patients of chronic hepatitis, the antibody was barely detected in patients with a single episode of ALT elevation (1 out of 6). Of the 15 well-defined cases of PT-NANBH that showed multiple ALT peaks and hepatitis C virus seroconversions, 11 (73.3%) were shown to be transfused with at least one unit of blood positive for the antibody. The retrospective analysis showed that all tested donor blood found to be positive for the antibody had been transfused to recipients who afterwards developed NANBH. These data strongly suggest that the cloned cDNA originated from an etiological agent of NANBH termed the hepatitis C virus. Furthermore, the present study demonstrates that had the screening been done with the anti-hepatitis C virus assay, 11 out of 17 (64.7%) cases of chronic PT-NANBH and 1 out of 6 (16.6%) acute PT-NANBH would have been prevented. The antibody assay thus can be used for diagnosis and blood screening for PT-NANBH.