SummaryBackgroundThe increasing prevalence of overweight and obesity needs effective approaches for weight loss in primary care and community settings. We compared weight loss with standard treatment in primary care with that achieved after referral by the primary care team to a commercial provider in the community.MethodsIn this parallel group, non-blinded, randomised controlled trial, 772 overweight and obese adults were recruited by primary care practices in Australia, Germany, and the UK. Participants were randomly assigned with a computer-generated simple randomisation sequence to receive either 12 months of standard care as defined by national treatment guidelines, or 12 months of free membership to a commercial programme (Weight Watchers), and followed up for 12 months. The primary outcome was weight change over 12 months. Analysis was by intention to treat (last observation carried forward [LOCF] and baseline observation carried forward [BOCF]) and in the population who completed the 12-month assessment. This trial is registered, number ISRCTN85485463.Findings377 participants were assigned to the commercial programme, of whom 230 (61%) completed the 12-month assessment; and 395 were assigned to standard care, of whom 214 (54%) completed the 12-month assessment. In all analyses, participants in the commercial programme group lost twice as much weight as did those in the standard care group. Mean weight change at 12 months was −5·06 kg (SE 0·31) for those in the commercial programme versus −2·25 kg (0·21) for those receiving standard care (adjusted difference −2·77 kg, 95% CI −3·50 to −2·03) with LOCF; −4·06 kg (0·31) versus −1·77 kg (0·19; adjusted difference −2·29 kg, −2·99 to −1·58) with BOCF; and −6·65 kg (0·43) versus −3·26 kg (0·33; adjusted difference −3·16 kg, −4·23 to −2·11) for those who completed the 12-month assessment. Participants reported no adverse events related to trial participation.InterpretationReferral by a primary health-care professional to a commercial weight loss programme that provides regular weighing, advice about diet and physical activity, motivation, and group support can offer a clinically useful early intervention for weight management in overweight and obese people that can be delivered at large scale.FundingWeight Watchers International, through a grant to the UK Medical Research Council.

A significant contributor to the rising rates of human obesity is an increase in energy intake. The ‘protein leverage hypothesis’ proposes that a dominant appetite for protein in conjunction with a decline in the ratio of protein to fat and carbohydrate in the diet drives excess energy intake and could therefore promote the development of obesity. Our aim was to test the ‘protein leverage hypothesis’ in lean humans by disguising the macronutrient composition of foods offered to subjects under ad libitum feeding conditions. Energy intakes and hunger ratings were measured for 22 lean subjects studied over three 4-day periods of in-house dietary manipulation. Subjects were restricted to fixed menus in random order comprising 28 foods designed to be similar in palatability, availability, variety and sensory quality and providing 10%, 15% or 25% energy as protein. Nutrient and energy intake was calculated as the product of the amount of each food eaten and its composition. Lowering the percent protein of the diet from 15% to 10% resulted in higher (+12±4.5%, p = 0.02) total energy intake, predominantly from savoury-flavoured foods available between meals. This increased energy intake was not sufficient to maintain protein intake constant, indicating that protein leverage is incomplete. Urinary urea on the 10% and 15% protein diets did not differ statistically, nor did they differ from habitual values prior to the study. In contrast, increasing protein from 15% to 25% did not alter energy intake. On the fourth day of the trial, however, there was a greater increase in the hunger score between 1–2 h after the 10% protein breakfast versus the 25% protein breakfast (1.6±0.4 vs 25%: 0.5±0.3, p = 0.005). In our study population a change in the nutritional environment that dilutes dietary protein with carbohydrate and fat promotes overconsumption, enhancing the risk for potential weight gain.

Objective: There are limited controlled data for intragastric balloons (IGB) in obesity treatment. This randomized, controlled study evaluated the efficacy and safety of an IGB in obese individuals with metabolic syndrome (MS). Design and Methods: Sixty-six adults (BMI: 30-40 kg/m 2 ) were randomized to IGB for 6 months, with a 12 month behavioral modification (IGB Group; ''IGBG''), or 12 month behavioral modification alone (Control Group; ''CG''). The primary outcome was percentage change in body weight. Results: Thirty-one subjects (female: 68%; mean age: 43; mean BMI: 36.0) were randomized to IGBG and 35 (66%; 48; 36.7) to CG. At 6 months, there was a significantly greater weight loss in the IGBG: À14.2 vs. À4.8; P < 0.0001. This was associated with a significantly greater reduction in waist circumference, and an improvement in quality of life, with a trend for a larger %MS remission (50% vs. 30%; n.s.). At month 12, the differences in weight loss were enduring: À9.2 vs. À5.2; P ¼ 0.007. Gastrointestinal-related adverse events were common in the IGBG, resolving predominantly within two weeks. The IGB was removed prematurely in three subjects (one for refractory gastrointestinal symptoms). Conclusions: Statistically significant and clinically relevant improvements in weight loss and health outcomes were observed with the IGBG at 6 months versus behavioral modification alone. The differential weight loss was still evident 6 months after IGB removal.

High egg consumption did not have an adverse effect on the lipid profile of people with T2D in the context of increased MUFA and PUFA consumption. This study suggests that a high-egg diet can be included safely as part of the dietary management of T2D, and it may provide greater satiety. This trial was registered at the Australia New Zealand Clinical Trials Registry (http://www.anzctr.org.au/) as ACTRN12612001266853.