scholarly journals The role of low-fat diets in body weight control: a meta-analysis of ad libitum dietary intervention studies

2000 ◽  
Vol 24 (12) ◽  
pp. 1545-1552 ◽  
Author(s):  
A Astrup ◽  
GK Grunwald ◽  
EL Melanson ◽  
WHM Saris ◽  
JO Hill
Keyword(s):  
Body Weight ◽  
Weight Control ◽  
Intervention Studies ◽  
Dietary Intervention ◽  
Meta Analysis ◽  
Low Fat ◽  
Ad Libitum ◽  
Body Weight Control ◽  
Fat Diets

scholarly journals The role of dietary fat in body fatness: evidence from a preliminary meta-analysis of ad libitum low-fat dietary intervention studies

2000 ◽  
Vol 83 (S1) ◽  
pp. S25-S32 ◽  
Author(s):  
Arne Astrup ◽  
Louise Ryan ◽  
Gary K. Grunwald ◽  
Mette Storgaard ◽  
Wim Saris ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Weight Gain ◽  
Total Energy ◽  
Dietary Fat ◽  
Meta Analysis ◽  
Low Fat ◽  
Ad Libitum ◽  
Fat Diets

The role of high-fat diets in weight gain and obesity has been questioned because of inconsistent reports in the literature concerning the efficacy of ad libitum low-fat diets to reduce body weight. We conducted a meta-analysis of weight loss occurring on ad libitum low-fat diets in intervention trials, and analysed the relationship between initial body weight and weight loss. We selected controlled trials lasting more than 2 months comparing ad libitum low-fat diets with a control group consuming their habitual diet or a medium-fat diet ad libitum published from 1966 to 1998. Data were included from 16 trials with a duration of 2–12 months, involving 1728 individuals. No trials on obese subjects fulfilled the inclusion criteria. The weighted difference in weight loss between intervention and control groups was 2.55 kg (95 % CI, 1.5–3.5; P < 0.0001). Weight loss was positively and independently related to pre-treatment body weight (r = 0.52,P < 0.05) and to reduction in the percentage of energy as fat (0.37 kg / %, P < 0.005) in unweighted analysis. Extrapolated to a BMI of about 30 kg/m2 and assuming a 10 % reduction in dietary fat, the predicted weight loss would be 4.4 kg (95 % CI, 2.0 to -6.8 kg). Because weight loss was not the primary aim in 12 of the 16 studies, it is unlikely that voluntary energy restriction contributed to the weight loss. Although there is no evidence that a high intake of simple sugars contributes to passive overconsumption, carbohydrate foods with a low glycaemic index may be more satiating and exert more beneficial effects on insulin resistance and cardiovascular risk factors. Moreover, an increase in protein content up to 25 % of total energy may also contribute to reducing total energy intake. In conclusion, a low-fat diet, high in protein and fibre-rich carbohydrates, mainly from different vegetables, fruits and whole grains, is highly satiating for fewer calories than fatty foods. This diet composition provides good sources of vitamins, minerals, trace elements and fibre, and may have the most beneficial effect on blood lipids and blood-pressure levels. A reduction in dietary fat without restriction of total energy intake prevents weight gain in subjects of normal weight and produces a weight loss in overweight subjects, which is highly relevant for public health.

scholarly journals Body Weight Control by a High-Carbohydrate/Low-Fat Diet Slows the Progression of Diabetic Kidney Damage in an Obese, Hypertensive, Type 2 Diabetic Rat Model

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Shuichi Ohtomo ◽  
Yuko Izuhara ◽  
Masaomi Nangaku ◽  
Takashi Dan ◽  
Sadayoshi Ito ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Control ◽  
Advanced Glycation ◽  
Low Fat ◽  
High Carbohydrate ◽  
Low Fat Diet ◽  
Body Weight Control ◽  
And Oxidative Stress ◽  
Type 2 Diabetic

Obesity is one of several factors implicated in the genesis of diabetic nephropathy (DN). Obese, hypertensive, type 2 diabetic rats SHR/NDmcr-cp were given, for 12 weeks, either a normal, middle-carbohydrate/middle-fat diet (MC/MF group) or a high-carbohydrate/low-fat diet (HC/LF group). Daily caloric intake was the same in both groups. Nevertheless, the HC/LF group gained less weight. Despite equivalent degrees of hypertension, hyperglycemia, hyperlipidemia, hyperinsulinemia, and even a poorer glycemic control, the HC/LF group had less severe renal histological abnormalities and a reduced intrarenal advanced glycation and oxidative stress. Mediators of the renoprotection, specifically linked to obesity and body weight control, include a reduced renal inflammation and TGF-beta expression, together with an enhanced level of adiponectin. Altogether, these data identify a specific role of body weight control by a high-carbohydrate/low-fat diet in the progression of DN. Body weight control thus impacts on local intrarenal advanced glycation and oxidative stress through inflammation and adiponectin levels.

scholarly journals Dietary Intervention for Overweight and Obese Adults: Comparison of Low-Carbohydrate and Low-Fat Diets. A Meta-Analysis

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0139817 ◽  
Author(s):  
Jonathan Sackner-Bernstein ◽  
David Kanter ◽  
Sanjay Kaul
Keyword(s):  
Dietary Intervention ◽  
Meta Analysis ◽  
Low Fat ◽  
Obese Adults ◽  
Low Carbohydrate ◽  
Fat Diets

Chronic intracerebroventricular infusion of MCH causes obesity in mice

2003 ◽  
Vol 284 (3) ◽  
pp. E583-E588 ◽  
Author(s):  
Akira Gomori ◽  
Akane Ishihara ◽  
Masahiko Ito ◽  
Satoshi Mashiko ◽  
Hiroko Matsushita ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Control ◽  
Energy Homeostasis ◽  
The Body ◽  
Intracerebroventricular Infusion ◽  
Melanin Concentrating Hormone ◽  
Important Regulator ◽  
Obesity In Mice ◽  
Body Weight Control

Melanin-concentrating hormone (MCH) is a cyclic amino acid neuropeptide localized in the lateral hypothalamus. Although MCH is thought to be an important regulator of feeding behavior, the involvement of this peptide in body weight control has been unclear. To examine the role of MCH in the development of obesity, we assessed the effect of chronic intracerebroventricular infusion of MCH in C57BL/6J mice that were fed with regular or moderately high-fat (MHF) diets. Intracerebroventricular infusion of MCH (10 μg/day for 14 days) caused a slight but significant increase in body weight in mice maintained on the regular diet. In the MHF diet-fed mice, MCH more clearly increased the body weight accompanied by a sustained hyperphagia and significant increase in fat and liver weights. Plasma glucose, insulin, and leptin levels were also increased in the MCH-treated mice fed the MHF diet. These results suggest that chronic stimulation of the brain MCH system causes obesity in mice and imply that MCH may have a major role in energy homeostasis.

Abstract MP63: Randomized Trials of Low-Fat vs. Other Diet Interventions on Weight Loss: A Meta-Analysis

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Deirdre K Tobias ◽  
Mu Chen ◽  
Walter Willett ◽  
Frank B Hu
Keyword(s):  
Weight Loss ◽  
Randomized Trials ◽  
Dietary Intervention ◽  
Meta Analysis ◽  
Dietary Interventions ◽  
Low Fat ◽  
Intervention Intensity ◽  
Low Carbohydrate ◽  
Fat Diets

Introduction: The effectiveness of low-fat diets for weight loss has been debated for decades. Dozens of randomized control trials (RCTs) have assessed whether decreasing the intake of total fat leads to weight loss, giving mixed results. Hypothesis: We hypothesized that low-fat dietary interventions do not lead to greater weight loss when comparator diet intervention intensity is considered. Methods: We conducted a systematic review and meta-analysis. RCTs were included if they compared a low-fat dietary intervention to any control diet with at least 1 year of follow-up. We estimated the combined fixed effect inverse variance weighted mean difference of low-fat vs. comparison diets. Several a priori stratified analyses were considered to explore heterogeneity. Results: Fifty studies met inclusion criteria, reporting 1-10 years of follow-up on 70,054 participants. Overall, low-fat dietary interventions resulted in 0.51kg greater weight loss compared to other diets (95% CI = -0.62, -0.40, p<0.001; I2 = 83%). However, when trials where greater attention was given to the low-fat group were excluded, comparator diets led to greater weight loss than low-fat diets (n=30; WMD=0.87, 95% CI=0.56, 1.17, p<0.001). Similarly, when the type of comparator diet was considered, low-fat diets were only beneficial compared to control groups who were simply asked to maintain their usual diet (n=18; WMD = -1.03, 95% CI = -1.18, -0.88, p<0.001). When equal attention was given to intervention groups, low-carbohydrate diets (n=15; WMD = 1.13kg, 95% CI = 0.53, 1.73, p<0.001) and other “healthy” diets without a low-fat component (n=20; WMD = 0.77kg, 95% CI = 0.42, 1.13, p<0.001) led to greater weight loss than low-fat diets. Comparison diets, irrespective of type, were associated with 1.30kg greater weight loss than low-fat diets when the interventions were intended to be isocaloric (n=19; 95% CI = 0.92, 1.69, p<0.001). Conclusions: Low-fat dietary interventions are not more effective than other diets for weight loss when differences in intervention intensity between treatment groups are considered. Rather, evidence from long-term (>=1 year) randomized trials indicates low-carbohydrate or other healthful dietary pattern interventions without a low-fat focus may be more effective for weight loss than low-fat dietary interventions. Further evidence is needed to establish the role of these interventions in longer-term weight loss and weight maintenance.

scholarly journals Thermogenesis challenges the adipostat hypothesis for body-weight control

2009 ◽  
Vol 68 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Barbara Cannon ◽  
Jan Nedergaard
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Weight Control ◽  
Dietary Intervention ◽  
Human Subjects ◽  
Brown Adipose ◽  
Body Weight Control

According to the adipostat hypothesis for body-weight control, alterations in body weight should always be compensated by adequate alterations in food intake and thermogenesis. Thus, increased thermogenesis should not be able to counteract obesity because food intake would be increased. However evidence is presented here that thermogenesis in different forms (through artificial uncouplers, exercise, cold exposure) may counteract obesity and is not always fully compensated by increased food intake. Correspondingly, a decreased capacity for metaboloregulatory thermogenesis (i.e. non-functional brown adipose tissue) may in itself lead to obesity. This is evident in mice and may be valid for human subjects, as a substantial proportion of adults possess brown adipose tissue, and those with less or without brown adipose tissue would seem to be more prone to obesity. Thus, increased thermogenesis may counteract obesity, without dietary intervention.

scholarly journals Peripheral signalling involved in energy homeostasis control

2012 ◽  
Vol 25 (2) ◽  
pp. 223-248 ◽  
Author(s):  
Andoni Lancha ◽  
Gema Frühbeck ◽  
Javier Gómez-Ambrosi
Keyword(s):  
Body Weight ◽  
Growth Factor ◽  
Weight Control ◽  
Energy Homeostasis ◽  
Molecular Mechanisms ◽  
Sex Hormone Binding Globulin ◽  
Fibroblast Growth Factor 21 ◽  
Peripheral Tissues ◽  
Body Weight Control

The alarming prevalence of obesity has led to a better understanding of the molecular mechanisms controlling energy homeostasis. Regulation of energy intake and expenditure is more complex than previously thought, being influenced by signals from many peripheral tissues. In this sense, a wide variety of peripheral signals derived from different organs contributes to the regulation of body weight and energy expenditure. Besides the well-known role of insulin and adipokines, such as leptin and adiponectin, in the regulation of energy homeostasis, signals from other tissues not previously thought to play a role in body weight regulation have emerged in recent years. The role of fibroblast growth factor 21 (FGF21), insulin-like growth factor 1 (IGF-I), and sex hormone-binding globulin (SHBG) produced by the liver in the regulation of body weight and insulin sensitivity has been recently described. Moreover, molecules expressed by skeletal muscle such as myostatin have also been involved in adipose tissue regulation. Better known is the involvement of ghrelin, cholecystokinin, glucagon-like peptide 1 (GLP-1) and PYY3–36, produced by the gut, in energy homeostasis. Even the kidney, through the production of renin, appears to regulate body weight, with mice lacking this hormone exhibiting resistance to diet-induced obesity. In addition, the skeleton has recently emerged as an endocrine organ, with effects on body weight control and glucose homeostasis through the actions of bone-derived factors such as osteocalcin and osteopontin. The comprehension of these signals will help in a better understanding of the aetiopathology of obesity, contributing to the potential development of new therapeutic targets aimed at tackling excess body fat accumulation.

scholarly journals The role of low-calorie sweeteners in the prevention and management of overweight and obesity: evidence v. conjecture

2017 ◽  
Vol 77 (3) ◽  
pp. 230-238 ◽  
Author(s):  
Peter J. Rogers
Keyword(s):  
Body Weight ◽  
Energy Intake ◽  
Weight Control ◽  
Intervention Studies ◽  
Sweet Taste ◽  
Overweight And Obesity ◽  
Low Calorie ◽  
Increase Energy Intake ◽  
Dietary Energy Density

By virtue of reducing dietary energy density, low-calorie sweeteners (LCS) can be expected to decrease overall energy intake and thereby decrease body weight. Such effects will be limited by the amount of sugar replaced by LCS, and the dynamics of appetite and weight control (e.g., acute compensatory eating, and an increase in appetite and decrease in energy expenditure accompanying weight loss). Consistent with these predictions, short-term intervention studies show incomplete compensation for the consumption of LCS v. sugar, and longer-term intervention studies (from 4 weeks to 40 months duration) show small decreases in energy intake and body weight with LCS v. sugar. Despite this evidence, there are claims that LCS undermine weight management. Three claims are that: (1) LCS disrupt the learned control of energy intake (sweet taste confusion hypothesis); (2) exposure to sweetness increases desire for sweetness (sweet tooth hypothesis); (3) consumers might consciously overcompensate for ‘calories saved’ when they know they are consuming LCS (conscious overcompensation hypothesis). None of these claims stands up to close examination. In any case, the results of the intervention studies comparing LCS v. sugar indicate that the effect of energy dilution outweighs any tendency LCS might conceivably have to increase energy intake.

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