The Magenstrasse and Mill procedure is the simplest and most physiological gastroplasty yet described. Many of the drawbacks of vertical banded gastroplasty, adjustable banding and gastric bypass are avoided. It is safe, has few side-effects and leads to major and durable weight losses, similar to those produced by other types of gastroplasty.

Loperamide hydrochloride (4 mg t.d.s.) was compared with codeine phosphate (60 mg t.d.s.) in a double blind crossover study of patients with loose output from their ileostomies. Both drugs significantly decreased the daily output and water content of ileostomy fluid. Daily losses of sodium and potassium were less when the patients were treated with loperamide. Loperamide was also associated with less side effects. It is concluded that loperamide hydrochloride was more effective in the treatment of ileostomy diarrhoea than codeine phosphate. In this group of patients those with the highest outputs from their ileostomies benefited most from this treatment.

short communications nature publishing group intervention and PreventionSummer weight-loss camps for overweight and obese children are increasing in number and reaching beyond North America. When evaluated, they share with residential school programmes impressive weight-loss outcomes (1-3). Although weight loss is a desirable product of negative energy balance, there may be less desirable consequences. In adults, there are many examples of acute energy restriction leading to increases in hunger ratings and food intake, a compensatory effect that demonstrates the powerful mechanisms defending against under-eating (4). In a weight-loss camp setting, we previously measured diurnal profiles of hunger motivation and fullness in a group of 38 children at the start and end of camp. They lost >8 kg in 6 weeks but had significantly higher daily hunger ratings and lower fullness at the end of camp (5). There is value in knowing how to moderate this change in experience, especially given its potential to undermine eating control outside of a managed environment.Accordingly, evidence that high-protein diets increase satiety and reduce energy intake (6,7) led us to report on a trial increasing the amount of protein in campers' daily diet. Disappointingly, 22.5 and 15% protein energy diets were indistinguishable in their effects on hunger motivation and weight loss (8). This dietary manipulation requires replication. This study, therefore aimed to evaluate the weight loss and hunger motivation effects of a further increased level of daily dietary protein. We also included methodological refinements such as weekly hunger motivation monitoring, and added precision to measurement by monitoring food consumption and urinary protein excretion. Methods And Procedures Participants and designA total of 103 children attending the Carnegie International Weightloss camp, a residential camp for overweight and obese children, were eligible, and had parental consent for the study. Three were excluded before randomization and a further five withdrew during the camp. Ethical approval was by Leeds West NHS Research Ethics Committee. the programme and dietary manipulation Children were divided by age and sex into four groups for all aspects of the camp programme (9-14 and 15-18 year olds, girls and boys). The schedule of the camp programme included six 1-h sessions of physical activity each day and four educational sessions per week (2). Children were assigned to one of four daily energy intakes according to their basal metabolic rate (5.44, 7.54, 9.63, or 11.72 MJ/day). Mean caloric deficit was 9.8% based on estimated average requirements. The standard (SP) diet was 15% protein, 30-35% fat, and 50-55% carbohydrate; the high-protein (HP) diet was 25% protein, 30-35% fat, and 40-45% carbohydrate. Treatment randomization was by stratified This study aimed to evaluate the weight loss and hunger motivation effects of an energy-restricted high-protein (HP) diet in overweight and obese children. In total, 95 overweight and obese children attended an ...

This study investigated the effect of carbohydrate (CHO) dose and composition on fuel selection during exercise, specifically exogenous and endogenous (liver and muscle) CHO oxidation. Ten trained males cycled in a double‐blind randomized order on 5 occasions at 77% normalV˙normalO2max for 2 h, followed by a 30‐min time‐trial (TT) while ingesting either 60 g·h−1 (LG) or 75 g·h−1 13C‐glucose (HG), 90 g·h−1 (LGF) or 112.5 g·h−1 13C‐glucose‐13C‐fructose ([2:1] HGF) or placebo. CHO doses met or exceed reported intestinal transporter saturation for glucose and fructose. Indirect calorimetry and stable mass isotope [13C] tracer techniques were utilized to determine fuel use. TT performance was 93% “likely/probable” to be improved with LGF compared with the other CHO doses. Exogenous CHO oxidation was higher for LGF and HGF compared with LG and HG (ES > 1.34, P < 0.01), with the relative contribution of LGF (24.5 ± 5.3%) moderately higher than HGF (20.6 ± 6.2%, ES = 0.68). Increasing CHO dose beyond intestinal saturation increased absolute (29.2 ± 28.6 g·h−1, ES = 1.28, P = 0.06) and relative muscle glycogen utilization (9.2 ± 6.9%, ES = 1.68, P = 0.014) for glucose‐fructose ingestion. Absolute muscle glycogen oxidation between LG and HG was not significantly different, but was moderately higher for HG (ES = 0.60). Liver glycogen oxidation was not significantly different between conditions, but absolute and relative contributions were moderately attenuated for LGF (19.3 ± 9.4 g·h−1, 6.8 ± 3.1%) compared with HGF (30.5 ± 17.7 g·h−1, 10.1 ± 4.0%, ES = 0.79 & 0.98). Total fat oxidation was suppressed in HGF compared with all other CHO conditions (ES > 0.90, P = 0.024–0.17). In conclusion, there was no linear dose response for CHO ingestion, with 90 g·h−1 of glucose‐fructose being optimal in terms of TT performance and fuel selection.

Diabetes is associated with the development of premature cardiovascular disease (CVD), which relates to the clustering of risk factors such as dyslipidaemia, hypertension, obesity and hyperglycaemia in the presence of insulin resistance. In addition, diabetes is associated with an inflammatory and pro-thrombotic environment, exacerbating the development of atherothrombosis. Insulin resistance and hyperglycaemia both contribute to the development of endothelial cell dysfunction and increased oxidative stress, culminating in accelerated atherosclerosis. Clot formation and function are also directly affected by insulin resistance and hyperglycaemia, with increased levels of coagulation factors and anti-fibrinolytic proteins and a fibrin network that is more resistant to lysis, coupled with increased platelet activation.It is well recognised that the intensification of glycaemic control leads to a reduction in microvascular complications in type 1 and type 2 diabetes; however, the same is less clear with macrovascular disease. Several randomised studies have attempted to address the effect of short-, medium- and long-term glycaemic control on cardiovascular outcomes, with mixed results. The overall interpretation of these trials suggests that intensive glycaemic control in patients with a relatively short duration of diabetes, without very poor control and with no CVD, might be safe and associated with fewer cardiovascular events.This review will summarise the effects of hyperglycaemia on the development of atherothrombosis and examine key cardiovascular outcome trials following intensive glucose control.

Criterion data for total energy expenditure (TEE) in elite rugby are lacking, which prediction equations may not reflect accurately. This study quantified TEE of 27 elite male rugby league (RL) and rugby union (RU) players (U16, U20, U24 age groups) during a 14-day in-season period using doubly labelled water (DLW). Measured TEE was also compared to estimated, using prediction equations. Resting metabolic rate (RMR) was measured using indirect calorimetry, and physical activity level (PAL) estimated (TEE:RMR). Differences in measured TEE were unclear by code and age (RL 4369 ± 979; RU 4365 ± 1122; U16, 4010 ± 744; U20, 4414 ± 688; U24, 4761 ± 1523 Kcal day− 1). Differences in PAL (overall mean 2.0 ± 0.4) were unclear. Very likely differences were observed in RMR by code (RL 2366 ± 296; RU 2123 ± 269 Kcal day− 1). Differences in relative RMR between U20 and U24 were very likely (U16, 27 ± 4; U20, 23 ± 3; U24, 26 ± 5 Kcal kg− 1 day− 1). Differences were observed between measured and estimated TEE, using Schofield, Cunningham and Harris–Benedict equations for U16 (187 ± 614, unclear; − 489 ± 564, likely and − 90 ± 579, unclear Kcal day− 1), U20 (− 449 ± 698, likely; − 785 ± 650, very likely and − 452 ± 684, likely Kcal day− 1) and U24 players (− 428 ± 1292; − 605 ± 1493 and − 461 ± 1314 Kcal day− 1, all unclear). Rugby players have high TEE, which should be acknowledged. Large inter-player variability in TEE was observed demonstrating heterogeneity within groups, thus published equations may not appropriately estimate TEE.

This study compared the effects of coingesting glucose and fructose on exogenous and endogenous substrate oxidation during prolonged exercise at altitude and sea level, in men. Seven male British military personnel completed two bouts of cycling at the same relative workload (55% W max) for 120 min on acute exposure to altitude (3375 m) and at sea level (~113 m). In each trial, participants ingested 1.2 g·min−1 of glucose (enriched with 13C glucose) and 0.6 g·min−1 of fructose (enriched with 13C fructose) directly before and every 15 min during exercise. Indirect calorimetry and isotope ratio mass spectrometry were used to calculate fat oxidation, total and exogenous carbohydrate oxidation, plasma glucose oxidation, and endogenous glucose oxidation derived from liver and muscle glycogen. Total carbohydrate oxidation during the exercise period was lower at altitude (157.7 ± 56.3 g) than sea level (286.5 ± 56.2 g, P = 0.006, ES = 2.28), whereas fat oxidation was higher at altitude (75.5 ± 26.8 g) than sea level (42.5 ± 21.3 g, P = 0.024, ES = 1.23). Peak exogenous carbohydrate oxidation was lower at altitude (1.13 ± 0.2 g·min−1) than sea level (1.42 ± 0.16 g·min−1, P = 0.034, ES = 1.33). There were no differences in rates, or absolute and relative contributions of plasma or liver glucose oxidation between conditions during the second hour of exercise. However, absolute and relative contributions of muscle glycogen during the second hour were lower at altitude (29.3 ± 28.9 g, 16.6 ± 15.2%) than sea level (78.7 ± 5.2 g (P = 0.008, ES = 1.71), 37.7 ± 13.0% (P = 0.016, ES = 1.45). Acute exposure to altitude reduces the reliance on muscle glycogen and increases fat oxidation during prolonged cycling in men compared with sea level.

The potential for imprecision in the estimation of hydration status from changes in body mass has been outlined previously but the equations derived from these derivations appear inconsistent. Reconciliation of body mass loss in terms of sweat loss and effective body water loss is possible from specific equation sets provided that gains and losses of both body mass and water used in the derivation of sweat loss and to derive effective body water loss are in inclusive equation sets. This is obligatory so that mass and water changes as quantifiable determinants are consistent with both internal processes and external gains and losses. Thus, body mass loss, substrate oxidation, metabolic water, and all the terms used in simultaneous equation sets have to be reconciled not only as identical variables but mathematically balance exactly. The revised equation for effective body water loss given here is different from that originally proposed. Metabolic water is part of body mass loss corrected for substrate oxidation, fluid ingestion, and respiratory water to derive sweat loss and it may not be justified to also include water associated with glycogen as releasable bound water. Accordingly, our calculated effective body water loss is substantially a greater loss than originally supposed but clearly still less than the simple balance between mass loss and fluid ingested.