Baseline weight loss expectations are independent cognitive predictors of attrition in obese patients entering a weight-losing program; the higher the expectations, the higher attrition at 12 months. Unrealistic weight goals should be tackled at the very beginning of treatment.

CMF therapy apparently has no effect on REE either acutely or during a 6-month-period; the increased REE observed in the long-term is likely due to the concomitant increase in FFM. The lack of evidence of sarcopenic obesity, at variance with previous literature, is likely due to different patient selection.

No abstract

The reduction in resting metabolic rate (RMR) during weight loss exceeds that accounted for by changes in body composition by 15%, suggesting that factors other than fat-free mass (FFM) explain the metabolic adaptation during food restriction in obesity. Our study aimed to establish if changes in the sympathoadrenal system activity, as inferred from an integrated measure such as 24 h urinary excretion of catecholamines, may play a role in the RMR adaptation observed during dietary restriction in obese patients. Ninety-three obese female subjects consumed a low-energy diet (LED) (2930 kJ/d (700 kcal/d)) for a 3-week period. At the beginning and at the end of the study, 24 h urinary excretion of catecholamines, FFM and RMR were measured. The LED induced a significant reduction in body weight (-3·3 (SEM 0·4) KG; P < 0·01), FFM (-1·9 (sem 0·7) kg; P < 0·01) and in the fat mass (-1·2 (sem 0·5) kg; P < 0·01). Noradrenalin excretion (24 h) decreased during the LED from 264 (sem 26) during a weight-maintenance period to 171 (sem 19) nmol/24 h after consumption of the LED for 3 weeks (P < 0·001); mean 24 h adrenalin excretion did not change during the LED (22 (sem 3) during the weight-maintenance period v. 21 (sem 3) nmol/24 h after consumption of the LED for 3 weeks; NS). The LED induced a significant decrease in RMR (7300 (sem 218) v. 6831 (sem 138) kJ/24 h; P < 0·001). The only independent variable that significantly explained variations in RMR both before and after consumption of the LED for 3 weeks, was FFM (r2 0·79 and r2 0·80 respectively). Urinary noradrenalin excretion explained a further 4 % of the variability in RMR, but only before the diet, so that a role of sympathoadrenal system on RMR seems to be present in obese patients in basal conditions but not at the end of the LED.

Summary.  Despite widespread use of laparoscopic procedures, no adequate data are available to support specific recommendations for venous thromboprophylaxis in patients undergoing laparoscopic surgery. This prospective, randomized trial is the first to be designed to evaluate a regimen of out‐of‐hospital thromboprophylaxis after laparoscopic surgery. Consecutive patients admitted for laparoscopic surgery were considered for the study. The thromboprophylaxis regimen used for each patient was based on a risk score. Possible thromboprophylactic measures included elastic stockings and pre‐ and postoperative Dalteparin or early ambulation. At discharge, patients were randomly allocated either to continue Dalteparin for 1 week, or to receive no further prophylaxis. Patients judged to be at low risk were not randomized. Compression ultrasound of the leg veins was performed in all patients 4 weeks after hospital discharge. Fifty‐three patients, all with acute appendicitis, were judged to be at low risk of deep vein thrombosis and were not included in the randomized study. The remaining 209 patients fell into two groups: 104 patients received postdischarge Dalteparin and 105 patients did not. The incidence of deep vein thrombosis was 0% (0 of 104) vs. 0.95% (one of 105), respectively (P = 1.00). The risk of postdischarge venous thromboembolism is low in patients undergoing laparoscopic surgery who receive in‐hospital thromboprophylaxis. Given this low risk, a clinical trial powered to determine if extending prophylaxis in such patients reduces the risk of clinically apparent deep vein thrombosis would be unfeasibly large.