Energy expenditure of obese, overweight, and normal weight females during lifestyle physical activities

To quantify energy expenditure of various lifestyle physical activities of obese, overweight, and normal-weight girls. In total, fifty-five girls participated in six activities: a treadmill walk at 4.0 km·hr-1, run, football throw, walk in open area, cycle, and riding a scooter. Intensities for all activities except the treadmill walk were self-selected. Energy expenditure was measured using the COSMED K4b2 portable metabolic system. Analyses of variance were used to compare the three groups (obese n=11, overweight n=16, and normal weight n=28) on relative ./SPOB_A_287654_O_XML_IMAGES/SPOB_A_287654_O_ILM0001.gif (ml·kg-1·min-1 and ml·FFM-1·min-1), and absolute energy expenditure (kJ·min-1). Magnitudes of the mean differences were examined using Cohen's delta (ES). Relative ./SPOB_A_287654_O_XML_IMAGES/SPOB_A_287654_O_ILM0002.gif (ml·FFM-1·min-1) was not significantly different (p>0.05) among the groups for any activity. Obese girls expended more energy (p<0.05) than normal-weight girls on all weight bearing activities. These differences were large (ES≥0.91). The differences in kJ·min-1 between the obese and normal weight groups for the bicycle and scooter activities were moderate to large (ES≥0.56), although not statistically significant. The overweight group expended more energy than the normal weight group and less energy than the obese group on all activities (ES=0.17 to 1.82), although these differences were generally not statistically significant. The oxygen costs of various activities are similar among obese, overweight, and normal-weight girls when expressed relative to fat-free mass. When engaging in self-selected levels of activity, obese girls have a higher absolute energy expenditure than normal-weight girls

Antiinflammatory therapy with canakinumab for atherosclerotic disease

BACKGROUND: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. METHODS: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P=0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P=0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P=0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P=0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P=0.31). CONCLUSIONS: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. Copyright © 2017 Massachusetts Medical Society