Characterizing the Perception of the Placebo Effect in Sports Medicine

Objective: To characterize differences in the perception and understanding of the placebo effect between sports physicians, coaches, athletes, and sports science personnel. Design: A short 11-item questionnaire was administered addressing demographic details, understanding of the placebo effect, and willingness to use the effect in an elite sport setting. Setting: All participants were involved in national level sporting programs. Participants: A total of 187 individuals (17 sports physicians, 44 sports scientists, 30 national-level coaches, and 96 national-level athletes) completed the questionnaire. All participants were contacted and invited to participate voluntarily. INTERVENTIONS/ Assessment of risk factors: Not applicable. Main outcome measurements: Self-reported responses on understanding and use of placebo effect in sport. Results: A total of 94% of physicians and 98% of scientists, but only 44% of athletes, indicated a good understanding of the placebo effect. A majority of scientists (63%) and physicians (59%) administered placebo at least once a year. Most of scientists (95%) and a majority of physicians (71%) either mildly or strongly encouraged use of the placebo in their clinical practice. About 60% of athletes indicated they would not care if they were unknowingly administered a placebo: however, 30% of them would not appreciate being misled. Conclusions: There is a substantial difference in the level of understanding of the placebo effect between physicians and athletes in elite sport. Although athletes are willing to use the placebo effect, physicians need to be mindful of the manner of its implementation

Hepatocyte-specific inhibition of NF-κB leads to apoptosis after TNF treatment, but not after partial hepatectomy

One of the earliest TNF-dependent events to occur during liver regeneration is the activation of the transcription factor NF-κB through TNF receptor type 1. NF-κB activation in the liver can have both antiapoptotic and proliferative effects, but it is unclear which liver cell types, hepatocytes or nonparenchymal cells (NPCs), contribute to these effects. To specifically evaluate the role of hepatocyte NF-κB, we created GLVP/ΔN-IκBα transgenic mice, in which expression of a deletion mutant of IκBα (ΔN-IκBα) was induced in hepatocytes after injection of mifepristone. In control mice, injection of 25 μg/kg TNF caused NF-κB nuclear translocation in virtually all hepatocytes by 30 minutes and no detectable apoptosis, while in mice expressing ΔN-IκBα, NF-κB nuclear translocation was blocked in 45% of hepatocytes, leading to apoptosis 4 hours after TNF injection. In contrast, expression of ΔN-IκBα in hepatocytes during the first several hours after partial hepatectomy did not lead to apoptosis or decreased proliferation. As NF-κB activation was not inhibited in liver NPCs, it is likely that these cells are responsible for mediating the proliferative and antiapoptotic effects of NF-κB during liver regeneration

Peroxisome proliferator-activated receptor-α agonist, Wy 14,643, improves metabolic indices, steatosis and ballooning in diabetic mice with non-alcoholic steatohepatitis

Background and Aims: Lipid accumulation precedes hepatocellular injury and liver inflammation in non-alcoholic steatohepatitis (NASH). The peroxisome proliferator-activated receptor (PPAR)α regulates hepatic lipid disposal. We studied whether pharmacolo

Dietary modification dampens liver inflammation and fibrosis in obesity-related fatty liver disease

Background: Alms1 mutant (foz/foz) mice develop hyperphagic obesity, diabetes, metabolic syndrome, and fatty liver (steatosis). High-fat (HF) feeding converts pathology from bland steatosis to nonalcoholic steatohepatitis (NASH) with fibrosis, which lead

Roles of adipose restriction and metabolic factors in progression of steatosis to steatohepatitis in obese, diabetic mice

Background and Aims: We previously reported that steatohepatitis develops in obese, hypercholesterolemic, diabetic foz/foz mice fed a high-fat (HF) diet for 12 months. We now report earlier onset of steatohepatitis in relation to metabolic abnormalities