1,721,092 research outputs found
Metabolic Effects of Progressive Weight Loss
No full textThe weight loss threshold required for improving metabolic outcomes in obesity and the nature of the dose-response relationship varies by endpoint. Fat mass, fat-free mass, and resting energy expenditure decrease linearly with weight loss. Visceral adipose tissue and liver fat content decrease with small reductions in weight (2-5%), and these reductions continue in a dose-dependent manner. Hepatic inflammation, ballooning, and fibrosis require greater weight loss to improve (≥7-10%). Cardiometabolic risk factors including fasting glucose and insulin concentrations, glycated hemoglobin, lipid profile, and blood pressure improve with small reductions in weight (2-5%), and gradually thereafter with more weight loss, particularly in subjects with greater levels of these risk factors at baseline. Skeletal muscle insulin sensitivity increases dose-dependently from 5% to 16% weight loss, whereas adipose tissue and hepatic insulin sensitivity and hepatic triglyceride secretion improve maximally with modest reductions in weight (5-10%) and do not improve further with more weight loss. Insulin clearance increases after weight loss, whereas pancreatic insulin secretion does not change within the range of weight reduction achieved by most hypocaloric diets (≤16%); but decreases with more weight loss (≥18%). Weight loss dose-dependently reduces the risk of diabetes, reduces the need for antidiabetic medications, and increases chances for diabetes remission. Although there are dose-response relationships for most endpoints, the clinical value of even small amounts of weight loss (2-5%) needs to be stressed before advocating for “more is better.”.</p
High-Protein Diets in the Prevention and Treatment of Type 2 Diabetes
No full textHigh-protein diets are being recommended to manage conditions such as obesity and type 2 diabetes (T2D). However, population-based studies strongly suggest that increased dietary protein intake is associated with a greater risk of developing T2D: for every 5% increase in dietary energy from protein (25–30 g/day more), the risk of T2D increases by 20–40%. Nevertheless, for the same total protein intake, replacing animal protein with plant protein generally decreases T2D risk. While weight loss induced by calorie restriction is the cornerstone of T2D management, high-protein diets do not induce greater weight loss in people with T2D, either in the short-term (2–6 months) or the long term (1–2 years), compared with other diets. Ingestion of protein alone, without carbohydrate, acutely increases both insulin and glucagon concentrations and does not affect glucose homeostasis. Ingestion of protein with carbohydrate augments postprandial insulin concentrations and mitigates the rise in postprandial glucose concentrations in people with T2D. However, the effects of chronically consuming high-protein diets on glucose homeostasis are difficult to interpret because of concomitant changes in body weight and differences in other dietary components. Results from meta-analyses indicate no consistent weight-independent effects of higher protein intakes on glucoregulation in T2D, although replacing animal protein with plant protein is likely beneficial. In conclusion, current evidence does not support recommending higher-than-adequate protein intakes for the prevention and treatment of T2D.</p
Protein-rich diets for weight loss maintenance
No full textPurpose of review: High-protein diets in the management of obesity have been around for many years and have been rigorously tested for their ability to induce weight loss. Comparably less is known about their effects on the maintenance of lost weight.Recent findings: Several small and a few large randomized trials have evaluated the efficacy of high-protein diets (20-35% of calories from protein; 1.2-1.9 g/kg∙day) compared with normal-protein diets (10-20% of calories from protein; 0.8-1.3 g/kg∙day), consumed mostly ad libitum during weight loss maintenance, i.e., after clinically significant weight loss. Most of these studies indicate that weight regain in the short term (3-12 months) is lower by 1-2 kg with high-protein diets than low-protein diets. This effect is attenuated with longer periods of observation, likely because of decreasing dietary compliance.Summary: In line with findings during the active weight loss phase, studies assessing the efficacy of protein-rich diets to improve weight loss maintenance report beneficial effects in the short term, which nevertheless dissipate over time.</p
A Hypothesis on the Historical Development of Obesity that is Not Only About Food
No full textPurpose of reviewMany physiological models have been put forth to explain the pathogenesis of obesity. All causes must eventually act by altering energy intake, energy expenditure, or the metabolic handling of ingested nutrients to favor storage over oxidation. These mechanisms culminate in two apparently competing models-the Energy Balance Model (EBM) and the Carbohydrate Insulin Model (CIM). In the EBM, eating more precedes increased adiposity, whereas in the CIM, increased adiposity precedes eating more.Recent findingsEpidemiological observations on energy intake and obesity prevalence during the last 50 years have often become the source of controversy between models. Here, I present a hypothesis, which borrows key elements from the EBM and CIM, and offers a framework that traces the root cause of obesity outside of the modern food environment and aligns with historical, 100-year-long trends in metabolic rate, food intake, physical activity, and adiposity. Body weight has been steadily increasing throughout the previous century, in conjunction with reductions in resting metabolic rate. This, superimposed with varying changes in dietary energy intake and physical activity energy expenditure resulted in an accelerated rise in obesity prevalence after the 1970s.SummaryObesity is a multifactorial disease and alterations in the underlying metabolic pathways that synergize to promote net fat deposition in the body have likely been operating for many decades, if not centuries, and involve both food-related and non-food-related factors
The role of dietary protein in obesity
No full textProtein-rich diets are surging in popularity for weight loss. An increase in diet-induced thermogenesis, better preservation of fat-free mass, and enhanced satiety with greater dietary protein intakes may lead to increased energy expenditure and decreased energy intake; and thus promote a more negative energy balance that facilitates weight loss. Results from large randomized trials and meta-analyses of many smaller trials indicate that high-protein diets typically induce significantly greater amounts of weight loss than conventional low-fat or high-carbohydrate diets during the early, rapid weight loss phase (3-6 months), but differences between diets are attenuated and no longer significant during the late, slow weight loss phase (12-24 months). Gradually decreasing adherence may be responsible for this observation; in fact, dietary adherence, rather than macronutrient composition, is likely the major predictor of long-term weight loss success. Recently, some randomized trials evaluated the efficacy of high-protein (vs. normal-protein) diets consumed ad libitum during weight loss maintenance, i.e. after clinically significant weight loss. Weight regain may be smaller with high-protein diets in the short-term (3-12 months), but longer studies are needed to confirm this. Given the lack of conclusive evidence in favor of high-protein diets, or any other dietary pattern, it is reasonable to conclude that no individual nutrient is a friend or a foe when it comes to weight loss and its maintenance. Therefore, any diet that best suits one's dietary habits and food preferences is likely to be better adhered to, and thus lead to more successful long-term weight loss.</p
Is calorie restriction beneficial for normal-weight individuals? A narrative review of the effects of weight loss in the presence and absence of obesity
No full textCalorie restriction regimens are popular for their purported health-promoting effects. However, it is unclear whether chronic reduction in energy intake and subsequent weight loss have beneficial effects in the absence of obesity. To this end, the results of studies that examined the effects of the same diet-induced weight loss in individuals with and without obesity were reviewed. The contribution of lean mass to the total amount of weight lost is greater in participants without obesity than in those with obesity, but the reductions in resting, nonresting, and total energy expenditure are of similar magnitude. Both in the presence as well as in the absence of obesity, weight loss decreases visceral adipose tissue and liver fat, increases insulin sensitivity in skeletal muscle (insulin-mediated whole-body glucose disposal rate) and in adipose tissue (meal-induced or insulin-induced suppression of plasma free fatty acid concentration), and augments insulin clearance rate, without affecting pancreatic insulin secretion. These effects are of similar magnitude in participants with and without obesity and result in reductions in fasting plasma glucose and insulin concentrations. These data suggest that the same degree of calorie restriction and the same amount of weight loss have multiple beneficial effects on health outcomes in individuals without obesity, similar to those observed in individuals with obesity.</p
Metabolically healthy obesity: what's in a name?
No full textMetabolically healthy obesity refers to an obesity phenotype with no or little evidence of metabolic dysfunction. Lower liver fat content and visceral adipose tissue, greater insulin sensitivity and secretion, greater cardiorespiratory fitness, and a predominantly lower body (i.e., leg) fat deposition are key physiological traits of a metabolically healthy phenotype. About 35% of all subjects with obesity are metabolically healthy. These individuals have approximately half the risk of developing type 2 diabetes and cardiovascular disease compared with metabolically unhealthy subjects with obesity, but they still have a significantly greater risk (by 50-300%) compared with metabolically healthy lean subjects. Therefore, absence of metabolic risk factors in people with obesity should not be a contraindication for weight-loss treatment. Metabolically healthy obesity needs to be treated, and this need is reinforced by the fact that this phenotype is not stable over time, as ∼50% of these subjects will cease being metabolically healthy within ∼10 y. Intervening early is therefore important. Weight loss dose-dependently decreases visceral adipose tissue and liver fat content, and it improves multiorgan insulin sensitivity and β-cell function (i.e., it beneficially affects many of the physiological traits of a metabolically healthy phenotype); however, weight loss is very difficult to maintain. This typically results in disappointment among patients and hinders adherence, which is likely critical for the limited success of most weight-loss treatments in the long term. On the other hand, using ≥1 metabolic health targets in a non-weight-loss-centered treatment paradigm that includes prudent dietary changes and increased physical activity can serve as an appropriate first goal that can help motivate patients toward the long-term goals of obesity treatment.</p
- …
