Weight reduction in obese adolescents with and without binge eating

Little is known about binge eating (BE) in adolescents. The primary aim of the present study was to examine the relationship between BE and weight loss in adolescents (BMI ≥95th percentile) enrolled in a randomized controlled trial of behavioral and pharmacologic treatment of obesity. Participants were 82 treatment-seeking adolescents (BMI = 37.9 ± 3.8 kg/m(2); age = 14.1 ± 1.2 years; 67% females; 42% African American, 55% white). Participants completed the Children's Depression Inventory (CDI), the Piers Harris Self-Esteem Questionnaire, and the Eating Inventory (including cognitive restraint, disinhibition, and hunger scales). BE was assessed by a questionnaire and a confirmatory interview. At baseline, 24% of participants met criteria for BE (N = 13 met full BE disorder (BED) criteria; N = 7 met subthreshold BE). There were no significant differences in percentage reduction in initial BMI between participants with or without BE at month 6 (-7.0 ± 1.6 vs. -6.9 ± 0.9%) or month 12 (-8.8 ± 2.4 vs. -8.3 ± 1.3%) (omnibus main effect BE P = 0.89, interaction BE × time P = 0.84, interaction BE × drug P = 0.61). The rate of BE declined significantly over time from 24% (n = 20) at baseline to 8% (n = 6) at month 6 and 3% (n = 2) at month 12 (P = 0.003). There were significant decreases in hunger and disinhibition as well as an increase in cognitive restraint over time (all P ≤ 0.0001). Findings suggest a combination of behavioral and pharmacologic therapy may produce both weight loss and improvement in BE.     

Reductions in Internal Disinhibition During Weight Loss Predict Better Weight Loss Maintenance

The construct of disinhibition, as measured by the Eating Inventory, was recently found to have two factors: internal disinhibition (eating in response to cognitive and emotional cues) and external disinhibition (eating in response to environmental cues). This study examined whether early changes in disinhibition that occurred during a weight loss program predicted later weight loss maintenance. Participants were adults enrolled in a weight loss treatment study (n = 81, 16% men, BMI = 38.4 ± 6.5 kg/m²). Two‐thirds of participants were African Americans. Participants received a uniform, meal‐replacement‐based weight loss program in months 1–3 and one of four nutritionally focused programs for weight loss maintenance in months 4–12. Disinhibition and weight were assessed at clinic visits. Change in internal disinhibition from months 1–3 (i.e., the weight loss period) significantly predicted change in weight from month 4 to 12 (i.e., the weight maintenance period); this remained significant when treatment group, age, gender, ethnicity, baseline weight, baseline depression, baseline internal disinhibition, and initial weight loss were controlled for (P = 0.03). A comparable analysis examining change in external disinhibition found that it was not a significant predictor of weight maintenance (P = 0.43). Participants who experienced the biggest decreases in internal disinhibition during the initial phase of treatment had the most success maintaining their weight loss in the next phase of treatment. Long‐term weight loss outcomes may be improved by spending sufficient treatment time teaching strategies for reducing eating in response to internal cues.     

Implantable gastric stimulator does not prevent the increase in plasma ghrelin levels that occurs with weight loss

The SHAPE (Screened Health Assessment and Pacer Evaluation) trial was a 24 month randomized multicenter placebo-controlled study to determine the efficacy of an implantable gastric stimulator (IGS) for weight loss. This report is an investigator-initiated sub-study at one site designed to assess whether IGS affects plasma levels of ghrelin and peptide YY (PYY). The device was implanted in all subjects but was activated in the Treatment group (n = 7, BMI = 41.5 ± 2.0 kg/m2) and remained inactive in the Control (n = 6, BMI = 39.5 ± 1.7 kg/m2) during the first 12 months. IGS was activated in both groups during months 12-24. Fasting venous blood was drawn at months 0, 12, and 24 and an oral glucose tolerance test (OGTT) was performed at month 12. Although there was no difference in weight loss at 6 months (Control: -6.6 ± 1.5% vs. Treatment: -6.2 ± 1.4%), at 24 months the Control group exhibited weight gain from baseline (+2.2 ± 1.5%) that was significantly different from the weight loss in the Treatment group (-1.9 ± 1.4%; P < 0.05). At 12 months, fasting ghrelin was significantly increased (P < 0.05) in the Treatment group (285 ± 35 to 336 ± 35 pg/ml; weight change, -4.9 ± 1.4%), but not in the Control (211 ± 36 to 208 ± 35 pg/ml; weight change, -3.4 ± 1.5%). No significant change was observed in postprandial suppression of plasma ghrelin or in fasting and postprandial PYY levels. In conclusion, IGS does not prevent the increase in fasting plasma ghrelin levels associated with weight loss. Further studies are needed to determine whether changes in technology can improve weight loss and maintenance, perhaps using gut hormones as biomarkers of possible efficacy.     

Psychosocial Functioning Improves Following Adolescent Bariatric Surgery

The aims of the present study were to examine changes in health‐related quality of life (HRQOL) and depressive symptoms in adolescents with extreme obesity undergoing Roux‐en‐Y gastric bypass (RYGBP) across the first postoperative year. A prospective longitudinal observational study of 31 adolescent patients undergoing RYGBP at a pediatric medical center (mean = 16.4 years; 64.5% females, mean BMI 63.5; 97% of study eligible and consecutive patients) was conducted. Participants completed two adolescent HRQOL measures, the PedsQL (generic) and the IWQOL‐Kids (weight‐related), the Beck Depression Inventory (BDI), and height and weight were measured at three time points: baseline, and 6 and 12 months following RYGBP. Prior to RYGBP, significant impairments in HRQOL were documented and 38.7% reported depressive symptomatology in the clinical range. As expected, BMI and depressive symptoms decreased and HRQOL improved from baseline to 12 months post‐RYGBP. Linear mixed modeling analyses detected several nonlinear slopes in BMI, depressive symptoms, and the majority of HRQOL domains over time with deceleration in these postoperative changes beginning at the 6th month time point. In contrast, the rate of change in weight‐related social relations was linear (e.g., no deceleration), indicating continued improvement across the first postoperative year. Adolescent RYGBP results in significant improvement in HRQOL and depressive symptomatology over the first postoperative year. Longer‐term follow‐up will be critical to determine adolescent weight and psychosocial trajectories, their interrelations, and what role psychosocial status plays in continued weight loss, maintenance, and regain.     

Effect of weight loss on the rate of muscle protein synthesis during fasted and fed conditions in obese older adults

Although weight loss ameliorates many of the metabolic abnormalities associated with obesity, there has been reluctance to prescribe weight loss in obese, older individuals because of the fear that it will cause debilitating loss of muscle mass and impair physical function. To gain insight into the mechanisms responsible for the weight loss-induced changes in muscle mass, we measured the rate of muscle protein synthesis (by using stable isotope labeled tracer methodology) during basal, postabsorptive conditions and during mixed meal ingestion in eight obese, older adults: (i) before weight loss therapy, (ii) ~3 months after starting the weight loss intervention (i.e., during the active weight loss phase), when subjects had lost ~7% of their initial body weight, and (iii) after they had lost ~10% of their body weight and maintained this new body weight for ~6 months (~12 months after starting the weight loss intervention). The basal muscle protein fractional synthesis rate (FSR) was not affected by weight loss. Mixed meal ingestion stimulated the rate of muscle protein synthesis, and the anabolic response (i.e., increase in the protein synthesis rate above basal values) was greater (P < 0.05) during negative energy balance and active weight loss at 3 months (0.033 ± 0.012%·per hour, mean ± s.e.m.) than during weight maintenance before and at 12 months of weight loss therapy (0.003 ± 0.003 and 0.008 ± 0.012%·per hour, respectively). We conclude that during dietary calorie restriction and weight loss in older adults, the rate of muscle protein synthesis is not impaired. Thus, the loss of muscle mass must be mediated predominately by adverse effects of dietary calorie restriction on muscle proteolysis.     

Potentiation of the early-phase insulin response by a prior meal contributes to the second-meal phenomenon in type 2 diabetes

Improved glucose tolerance following a sequential meal is known as the second-meal phenomenon. We aimed to investigate its extent and underlying mechanisms in patients with type 2 diabetes. Metabolic responses after lunch in 12 diabetic patients were compared on two separate days: one with (Day BL) and another without (Day FL) breakfast. The responses of hormones were calculated by the incremental area under the curve (iAUC) values for 180 min after each meal. Indexes of early-phase insulin secretion were assessed, and β-cell function was estimated by mathematical modeling. [iAUC(glucose(180-360 min))] was significantly lower on Day BL than on Day FL (181 ± 43 vs. 472 ± 29 mmol·liter(-1)·min, P = 0.0005). The magnitude of the The second-meal phenomenon [iAUC(glucose(180-360 min)) on Day BL/Day FL] was 35 ± 9%. The peak levels of insulin and C-peptide were attained 45 min earlier after the second meal than after the first meal. iAUC(glucose(180-360 min)) correlated negatively with iAUC(insulin(180-210 min)) (r = -0.443, P = 0.0300), insulinogenic index (r = -0.769, P < 0.0001), acute C-peptide response (r = -0.596, P = 0.0021), and potentiation factor [i.e., potentiation effect on insulin secretion] ratio (180-360)/(0-20) (r = -0.559, P = 0.0045), while correlated positively with free fatty acid level before lunch (r = 0.679, P = 0.0003). The second-meal phenomenon was evident in patients with type 2 diabetes. Potentiation of the early-phase insulin response by a prior meal contributes to this phenomenon in type 2 diabetes.     

Randomized controlled trial of chewing gum for weight loss

The possible effects on body weight of chewing gum on a regular schedule have not been tested in a randomized controlled trial (RCT). We conducted an 8-week RCT in 201 overweight and obese adults to test the hypothesis that receiving printed material on good nutrition and chewing gum for a minimum of 90 min/day (n = 102) would lead to greater weight loss than receiving printed nutrition information only (n = 99). Changes in BMI, waist circumference, and blood pressure were secondary outcomes. Adherence to the gum-chewing protocol in the intervention group was >95%. In the intention-to-treat analysis, there were virtually no changes in weight or BMI in either group between baseline and the end of the intervention at 8 weeks. Waist circumference decreased significantly in the intervention group between baseline and 8 weeks (mean ± SD change = -1.4 ± 5.3 cm; P = 0.0128); however, there was no significant difference in change in waist circumference comparing the groups. Similarly, systolic and diastolic blood pressure decreased significantly in the intervention group between baseline and 8 weeks (-3.0 ± 9.9 mm Hg; P = 0.0032 and -3.2 ± 7.3 mm Hg; P = 0.0001, respectively); however, there were no significant differences in the changes in systolic or diastolic blood pressure between the groups. Analyses including completers only produced essentially the same results. We conclude that chewing gum on a regular schedule for 8 weeks did not facilitate weight loss in these overweight and obese adults.     

Exenatide as a weight-loss therapy in extreme pediatric obesity: a randomized, controlled pilot study

The objective of this pilot study was to evaluate the effects of exenatide on BMI (primary endpoint) and cardiometabolic risk factors in nondiabetic youth with extreme obesity. Twelve children and adolescents (age 9-16 years old) with extreme obesity (BMI ≥1.2 times the 95th percentile or BMI ≥35 kg/m(2)) were enrolled in a 6-month, randomized, open-label, crossover, clinical trial consisting of two, 3-month phases: (i) a control phase of lifestyle modification and (ii) a drug phase of lifestyle modification plus exenatide. Participants were equally randomized to phase-order (i.e., starting with control or drug therapy) then crossed-over to the other treatment. BMI, body fat percentage, blood pressure, lipids, oral glucose tolerance tests (OGTT), adipokines, plasma biomarkers of endothelial activation, and endothelial function were assessed at baseline, 3-, and 6-months. The mean change over each 3-month phase was compared between treatments. Compared to control, exenatide significantly reduced BMI (-1.7 kg/m(2), 95% confidence interval (CI) (-3.0, -0.4), P = 0.01), body weight (-3.9 kg, 95% CI (-7.11, -0.69), P = 0.02), and fasting insulin (-7.5 mU/l, 95% CI (-13.71, -1.37), P = 0.02). Significant improvements were observed for OGTT-derived insulin sensitivity (P = 0.02) and β-cell function (P = 0.03). Compliance with the injection regimen was excellent (≥94%) and exenatide was generally well-tolerated (the most common adverse event was mild nausea in 36%). These preliminary data suggest that exenatide should be evaluated in larger, well-controlled trials for its ability to reduce BMI and improve cardiometabolic risk factors in youth with extreme obesity.     

Water Consumption Increases Weight Loss During a Hypocaloric Diet Intervention in Middle‐aged and Older Adults

Water consumption acutely reduces meal energy intake (EI) among middle‐aged and older adults. Our objectives were to determine if premeal water consumption facilitates weight loss among overweight/obese middle‐aged and older adults, and to determine if the ability of premeal water consumption to reduce meal EI is sustained after a 12‐week period of increased water consumption. Adults (n = 48; 55–75 years, BMI 25–40 kg/m²) were assigned to one of two groups: (i) hypocaloric diet + 500 ml water prior to each daily meal (water group), or (ii) hypocaloric diet alone (nonwater group). At baseline and week 12, each participant underwent two ad libitum test meals: (i) no preload (NP), and (ii) 500 ml water preload (WP). Meal EI was assessed at each test meal and body weight was assessed weekly for 12 weeks. Weight loss was ～2 kg greater in the water group than in the nonwater group, and the water group (β = ?0.87, P < 0.001) showed a 44% greater decline in weight over the 12 weeks than the nonwater group (β = ?0.60, P < 0.001). Test meal EI was lower in the WP than NP condition at baseline, but not at week 12 (baseline: WP 498 ± 25 kcal, NP 541 ± 27 kcal, P = 0.009; 12‐week: WP 480 ± 25 kcal, NP 506 ± 25 kcal, P = 0.069). Thus, when combined with a hypocaloric diet, consuming 500 ml water prior to each main meal leads to greater weight loss than a hypocaloric diet alone in middle‐aged and older adults. This may be due in part to an acute reduction in meal EI following water ingestion.     

A 6-month supervised employer-based minimal exercise program for police officers improves fitness

The purpose of the study was to determine the effects of a 6-month supervised, job-specific moderate exercise program in police officers on body composition, cardiovascular and muscular fitness. Body weight (BW), body mass index (BMI), and cardiovascular and muscular fitness were assessed at baseline, after a 6-month supervised fitness program and at 12-month follow-up (18 months). One hundred sixty-five (n = 131 men and n = 34 women) young (mean ± SEM, 26.4 ± 1.9 years), overweight (BMI = 26.2 ± 1.2 kg·m) police officers participated. Aerobic exercise progressed from 3 d·wk, 20 minutes per session at 60% of the heart rate reserve (HRR) to 5 d·wk, 30 minutes per session at 75% of HRR at 3 months, and this level was maintained until 6 months. Muscular strength training progressed using 8 different calisthenics exercises from 3 d·wk, 2 sets of 5 repetitions using the participant's own BW to 5 d·wk, 3 sets of 15 repetitions of the participant's own BW at 3 months, and this level was maintained until 6 months. Cardiovascular and muscular fitness was measured using a 0.25-mile obstacle course incorporating various job-specific exercises and expressed as the physical abilities test (PAT) time. There was a significant reduction in BMI (-0.6 ± 0.2 kg·m, p < 0.001) and BW (-2.8 ± 2.3 kg) and reduction in PAT time (-11.9 ± 2.1%, p < 0.01) from baseline to 6 months. However, BMI (1.4 ± 1.1 kg·m, p < 0.001), BW (5.1 ± 3.0 kg, p < 0.01), and PAT time significantly increased (12.8 ± 2.2%, p < 0.01) from 6 to 18 months. There were no sex by time differences. The practical applications of this study indicate that a supervised, job-specific exercise program for police officers improves fitness and body composition after 6 months in both men and women, but continued supervision of exercise program may be necessary for maintenance of health benefits.     

Approaches for quantifying energy intake and %calorie restriction during calorie restriction interventions in humans: the multicenter CALERIE study

Calorie restriction (CR) is a component of most weight loss interventions and a potential strategy to slow aging. Accurate determination of energy intake and %CR is critical when interpreting the results of CR interventions; this is most accurately achieved using the doubly labeled water method to quantify total energy expenditure (TEE). However, the costs and analytical requirements of this method preclude its repeated use in many clinical trials. Our aims were to determine 1) the optimal TEE assessment time points for quantifying average energy intake and %CR during long-term CR interventions and 2) the optimal approach for quantifying short-term changes in body energy stores to determine energy intake and %CR during 2-wk DLW periods. Adults randomized to a CR intervention in the multicenter CALERIE study underwent measurements of TEE by doubly labeled water and body composition at baseline and months 1, 3, and 6. Average %CR achieved during the intervention was 24.9 ± 8.7%, which was computed using an approach that included four TEE assessment time points (i.e., TEE(baseline, months 1, 3, and 6)) plus the 6-mo change in body composition. Approaches that included fewer TEE assessments yielded %CR values of 23.4 ± 9.0 (TEE(baseline,) months 3 and 6), 25.0 ± 8.7 (TEE(baseline,) months 1 and 6), and 20.9 ± 7.1% (TEE(baseline, month 6)); the latter approach differed significantly from approach 1 (P < 0.001). TEE declined 9.6 ± 9.9% within 2-4 wk of CR beginning and then stabilized. Regression of daily home weights provided the most reliable estimate of short-term change in energy stores. In summary, optimal quantification of energy intake and %CR during weight loss necessitates a TEE measurement within the first month of CR to capture the rapid reduction in TEE.     

Obesity negatively impacts aerobic capacity improvements both acutely and 1-year following cardiac rehabilitation

Cardiac rehabilitation (CR) produces a host of health benefits related to modifiable cardiovascular risk factors. The purpose of the present investigation was to determine the influence of body weight, assessed through BMI, on acute and long-term improvements in aerobic capacity following completion of CR. Three thousand nine hundred and ninety seven subjects with coronary artery disease (CAD) participated in a 12-week multidisciplinary CR program. Subjects underwent an exercise test to determine peak estimated metabolic equivalents (eMETs) and BMI assessment at baseline, immediately following CR completion and at 1-year follow-up. Normal weight subjects at 1-year follow-up demonstrated the greatest improvement in aerobic fitness and best retention of those gains (gain in peak METs: 0.95 ± 1.1, P < 0.001). Although the improvement was significant (P < 0.001), subjects who were initially classified as obese had the lowest aerobic capacity and poorest retention in CR fitness gains at 1-year follow-up (gain in peak eMETs: 0.69 ± 1.2). Subjects initially classified as overweight by BMI had a peak eMET improvement that was also significantly better (P < 0.05) than obese subjects at 1-year follow-up (gain in peak eMETs: 0.82 ± 1.1). Significant fitness gains, one of the primary beneficial outcomes of CR, can be obtained by all subjects irrespective of BMI classification. However, obese patients have poorer baseline fitness and are more likely to "give back" fitness gains in the long term. Obese CAD patients may therefore benefit from additional interventions to enhance the positive adaptations facilitated by CR.     

Sex hormones in postmenopausal women receiving low-dose hormone therapy: the effect of BMI

The aim of our study was to evaluate the effect of BMI on the change in circulating sex hormone in postmenopausal women during 6 months of oral continuous combined low-dose hormone therapy (HT). Fifty postmenopausal women were allocated to receive daily one tablet containing combination of 17β-estradiol (1 mg)/norethindrone acetate (0.5 mg) for 6 months. Serum levels of follicle-stimulating hormone (FSH), estradiol, total testosterone, sex hormone-binding globulin (SHBG), free androgen index (FAI), free estrogen index (FEI), Δ4-androstendione (Δ4A), and dehydroepiandrosterone sulfate were assessed at baseline and at the end of 6 months. Mean absolute values and percent changes from baseline were compared between lean and overweight women. Mean FSH decreased and mean 17β-estradiol increased significantly in both groups (FSH lean: 82.3 ± 26.7 decreased to 45.0 ± 17.0 mIU/ml, P = 0.0001; FSH overweight: 85.5 ± 22.1 decreased to 52.3 ± 23.8 mIU/ml, P = 0.003; P between groups = 0.661; E2 lean: 23.24 ± 12.55 increased to 53.62 ± 28.29 pg/ml, P = 0.006; E2 overweight: 24.17 ± 10.88 increased to 68.36 ± 53.99 pg/ml, P = 0.0001; P between groups = 0.619). Lean individuals had statistically significant higher increments of FAI and specifically FEI compared to overweight (FEI lean; 0.14 ± 0.09 increased to 0.29 ± 0.14, P = 0.009; overweight 0.23 ± 0.18 increased to 0.52 ± 0.40, P = 0.126; P between groups = 0.034). Although BMI does not affect total 17β-estradiol changes, free sex steroid concentrations increase more steeply in lean compared to overweight women receiving oral low-dose HT.     

Short-term regional meal fat storage in nonobese humans is not a predictor of long-term regional fat gain

Although body fat distribution strongly predicts metabolic health outcomes related to excess weight, little is known about the factors an individual might exhibit that predict a particular fat distribution pattern. We utilized the meal fatty acid tracer-adipose biopsy technique to assess upper and lower body subcutaneous (UBSQ and LBSQ, respectively) meal fat storage in lean volunteers who then were overfed to gain weight. Meal fatty acid storage in UBSQ and LBSQ adipose tissue, as well as daytime substrate oxidation (indirect calorimetry), was measured in 28 nonobese volunteers [n = 15 men, body mass index = 22.1 ± 2.5 (SD)] before and after an ～8-wk period of supervised overfeeding (weight gain = 4.6 ± 2.2 kg, fat gain = 3.8 ± 1.7 kg). Meal fat storage (mg/g adipose tissue lipid) in UBSQ (visit 1: 0.78 ± 0.34 and 1.04 ± 0.71 for women and men, respectively, P = 0.22; visit 2: 0.71 ± 0.24 and 0.90 ± 0.37 for women and men, respectively, P = 0.08) and LBSQ (visit 1: 0.60 ± 0.23 and 0.48 ± 0.29 for women and men, respectively, P = 0.25; visit 2: 0.62 ± 0.24 and 0.65 ± 0.23 for women and men, respectively, P = 0.67) adipose tissue did not differ between men and women at either visit. Fractional meal fatty acid storage in UBSQ (0.31 ± 0.15) or LBSQ (0.19 ± 0.13) adipose tissue at visit 1 did not predict the percent change in regional body fat in response to overfeeding. These data indicate that meal fat uptake trafficking in the short term (24 h) is not predictive of body fat distribution patterns. In general, UBSQ adipose tissue appears to be a favored depot for meal fat deposition in both sexes, and redistribution of meal fatty acids likely takes place at later time periods.     

Tissue-specific responses of lipoprotein lipase to dietary macronutrient composition as a predictor of weight gain over 4 years

This study evaluated if the effect of dietary macronutrient composition on adipose tissue lipoprotein lipase (ATLPL) and skeletal muscle lipoprotein lipase (SMLPL) predicted the long-term (over 4 years) changes in body weight and composition in free-living adults. Using a crossover design, 39 healthy subjects (n = 24 normal weight, n = 7 overweight, n = 8 obese) each followed a 2-week isocaloric high-carbohydrate (HC; 55% CHO:25% fat) and high-fat (HF; 30% CHO:50% fat) diet. On day 15 of each diet, biopsies were performed in the fasted state and 6 h after a meal. Body weight and composition were measured annually over 4 years. The outcomes for body weight, fat mass and % body fat were assessed using a linear two-stage mixed model. The mean (±SEM) increase in body weight and fat mass over 4 years was 0.29 ± 0.15 kg/year (P = 0.063) and 0.31 ± 0.15 kg/year (P = 0.051), respectively. The most consistent predictors of future body weight and fat changes were the ΔATLPL and ΔSMLPL responses (0-6 h) to a HC diet/meal. For the HC diet/meal, the subjects who had an increase in ATLPL activity/cell gained more % body fat over 4 years (P = 0.006) whereas subjects who had a decrease in SMLPL activity/g also had an increase in fat mass (P = 0.021). No significant relationships were observed between fasting ATLPL and SMLPL or enzyme responses to meals and any of the outcomes following the HF diet. In free-living adults the variability in tissue-specific lipoprotein lipase (LPL) responsiveness to a HC diet/meal predicts longitudinal changes in body composition.     

Meal replacements and fibre supplement as a strategy for weight loss. Proprietary PGX® meal replacement and PGX® fibre supplement in addition to a calorie-restricted diet to achieve weight loss in a clinical setting

Meal replacements and viscous soluble fibre represent safe and sustainable aids for weight loss. Our purpose was to determine if PGX® meal replacements and PGX^® fibre complex in combination with a calorie-restricted diet would aid in weight loss in a clinical setting. Fifty-two overweight and obese participants (49 women, 3 men; average age 47.1 years) with a mean body mass index (BMI) of 33.8 ± 6.4 kg/m² consumed 57 g of proprietary PGX® meal replacement product at breakfast and another 57 g at lunch for 12 weeks. In addition to the meal replacements, they were also asked to consume 5 g/day of PGX® fibre in the form of granules, powder or capsules together with 250 mlwater. A registered dietician recommended low-fat, low-glycaemic-index foods for snacks and the dinner menus such that each volunteer was consuming a total of 1200 kcal/day. All participants (n = 52) lost a significant amount of weight from baseline (?4.69 ± 3.73 kg), which was further reflected in the reductions in their waist (?7.11 ± 6.35 cm) and hip circumference (?5.59 ± 3.58 cm) over the 12-week study (p < 0.0001). BMI scores (n = 51) were reduced by 1.6 ± 1.4 kg/m². The use of PGX® meal replacements and PGX^® fibre along with a controlled dietary caloric intake is of benefit for short-term weight loss.     

Dietary adherence during weight loss predicts weight regain

This study examined the relationship between previous dietary adherence during a low-calorie diet weight loss intervention and subsequent weight change during a 2-year follow-up for weight maintenance. One hundred and sixteen healthy, recently weight reduced (lost ~12 kg, BMI 22-25 kg/m2) premenopausal women were studied. Dietary adherence was assessed by doubly labeled water (DLW) and body composition change. Comparisons were made between the upper and lower tertiles for previous dietary adherence and subsequent weight change at 1- and 2-year follow-up. Percent weight regained was significantly lower (30.9 ± 6.7% vs. 66.7 ± 9.4%; P < 0.05) in the upper compared to the lower adherence tertile for previous weight loss dietary adherence (49.9 ± 8.8% vs. 96.8 ± 12.8% P < 0.05) at 1- and 2-year follow-up, respectively. This difference was partly explained by increases in daily activity-related energy expenditure (AEE) (+95 ± 45 kcal/day vs. -44 ± 42 kcal/day, P < 0.05) and lower daily energy intake (2,066 ± 71 kcal/day vs. 2,289 ± 62 kcal/day, P < 0.05) in the higher tertile for previous dietary adherence, compared to the lower. These findings suggest that higher adherence (i.e., higher tertile) to the previous low-calorie diet predicts lower weight regain over 2-year follow-up for weight maintenance, which is explained by lower energy intake and higher physical activity. Finally, how well an individual adheres to a low-calorie diet intervention during weight loss may be a useful tool for identifying individuals who are particularly vulnerable to subsequent weight regain.     

Effects of maintained weight loss on sleep dynamics and neck morphology in severely obese adults

The goals of the study were to determine if moderate weight loss in severely obese adults resulted in (i) reduction in apnea/hypopnea index (AHI), (ii) improved pharyngeal patency, (iii) reduced total body oxygen consumption (VO(2)) and carbon dioxide production (VCO(2)) during sleep, and (iv) improved sleep quality. The main outcome was the change in AHI from before to after weight loss. Fourteen severely obese (BMI > 40 kg/m(2)) patients (3 males, 11 females) completed a highly controlled weight reduction program which included 3 months of weight loss and 3 months of weight maintenance. At baseline and postweight loss, patients underwent pulmonary function testing, polysomnography, and magnetic resonance imaging (MRI) to assess neck morphology. Weight decreased from 134 +/-6.6 kg to 118 +/- 6.1 kg (mean +/- s.e.m.; F = 113.763, P < 0.0001). There was a significant reduction in the AHI between baseline and postweight loss (subject, F = 11.11, P = 0.007). Moreover, patients with worse sleep-disordered breathing (SDB) at baseline had the greatest improvements in AHI (group, F = 9.00, P = 0.005). Reductions in VO(2) (285 +/- 12 to 234 +/-16 ml/min; F = 24.85, P < 0.0001) and VCO(2) (231 +/- 9 to 186 +/- 12 ml/min; F = 27.74, P < 0.0001) were also observed, and pulmonary function testing showed improvements in spirometry parameters. Sleep studies revealed improved minimum oxygen saturation (minSaO(2)) (83.4 +/- 61.9% to 89.1 +/- 1.2%; F = 7.59, P = 0.016), and mean SaO(2) (90.4 +/- 1.1% to 93.8 +/- 1.0%; F = 6.89, P = 0.022), and a significant increase in the number of arousals (8.1 +/- 1.4 at baseline, to 17.1 +/- 3.0 after weight loss; F = 18.13, P = 0.001). In severely obese patients, even moderate weight loss (approximately 10%) boasts substantial benefit in terms of the severity of SDB and sleep dynamics.     

Fueling the Obesity Epidemic? Artificially Sweetened Beverage Use and Long‐term Weight Gain

We have examined the relationship between artificially sweetened beverage (ASB) consumption and long-term weight gain in the San Antonio Heart Study. From 1979 to 1988, height, weight, and ASB consumption were measured among 5,158 adult residents of San Antonio, Texas. Seven to eight years later, 3,682 participants (74% of survivors) were re-examined. Outcome measures were incidence of overweight/obesity (OW/OB(inc)) and obesity (OB(inc)) (BMI > or = 25 and > or = 30 kg/m(2), respectively), and BMI change by follow-up (DeltaBMI, kg/m(2)). A significant positive dose-response relationship emerged between baseline ASB consumption and all outcome measures, adjusted for baseline BMI and demographic/behavioral characteristics. Consuming >21 ASBs/week (vs. none) was associated with almost-doubled risk of OW/OB (odds ratio (OR) = 1.93, P = 0.007) among 1,250 baseline normal-weight (NW) individuals, and doubled risk of obesity (OR = 2.03, P = 0.0005) among 2,571 individuals with baseline BMIs <30 kg/m(2). Compared with nonusers (+1.01 kg/m(2)), DeltaBMIs were significantly higher for ASB quartiles 2-4: +1.46 (P = 0.003), +1.50 (P = 0.002), and +1.78 kg/m(2) (P < 0.0001), respectively. Overall, adjusted DeltaBMIs were 47% greater among artificial sweetener (AS) users than nonusers (+1.48 kg/m(2) vs. +1.01 kg/m(2), respectively, P < 0.0001). In separate analyses--stratified by gender; ethnicity; baseline weight category, dieting, or diabetes status; or exercise-change category--DeltaBMIs were consistently greater among AS users. These differences, though not significant among exercise increasers, or those with baseline diabetes or BMI >30 kg/m(2) (P = 0.069), were significant in all 13 remaining strata. These findings raise the question whether AS use might be fueling--rather than fighting--our escalating obesity epidemic.