The defence of body weight: a physiological basis for weight regain after weight loss

2012 ◽  
Vol 124 (4) ◽  
pp. 231-241 ◽  
Author(s):  
Priya Sumithran ◽  
Joseph Proietto
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Energy Expenditure ◽  
Weight Regain ◽  
Physiological Changes ◽  
Initial Weight Loss ◽  
Physiological Basis ◽  
Subsequent Discussion ◽  
Short And Long Term

Although weight loss can usually be achieved by restricting food intake, the majority of dieters regain weight over the long-term. In the hypothalamus, hormonal signals from the gastrointestinal tract, adipose tissue and other peripheral sites are integrated to influence appetite and energy expenditure. Diet-induced weight loss is accompanied by several physiological changes which encourage weight regain, including alterations in energy expenditure, substrate metabolism and hormone pathways involved in appetite regulation, many of which persist beyond the initial weight loss period. Safe effective long-term strategies to overcome these physiological changes are needed to help facilitate maintenance of weight loss. The present review, which focuses on data from human studies, begins with an outline of body weight regulation to provide the context for the subsequent discussion of short- and long-term physiological changes which accompany diet-induced weight loss.

scholarly journals MON-LB101 5-Year Data of an Aggressive Pharmacological Approach to Moderate and Morbid Obesity: Is Prevention of Bariatric Surgery Feasible in the Long Run?

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Flavio Cadegiani
Keyword(s):  
Bariatric Surgery ◽  
Morbid Obesity ◽  
Weight Loss ◽  
Body Weight ◽  
Weight Regain ◽  
Morbidly Obese ◽  
Biochemical Profile ◽  
Initial Weight ◽  
Initial Weight Loss

Abstract Background: Maintenance of weight loss in patients that undergo weight loss interventions is highly challenging, irrespective of the type of approach to obesity (whether surgical, pharmacological, or non-pharmacological). We proposed a protocol of an aggressive clinical treatment for obesity aiming to prevent the need of bariatric surgery, in patients unwilling to undergo this procedure, by proposing a protocol that included the combination of different anti-obesity medications and non-pharmacological modalities, for longer duration, and with an active approach to prevent weight regain. Our initial 2-year data showed that 93% (40 of 43 patients) with moderate and morbid obesity were able to avoid the need of bariatric surgery, with concomitant improvements of the biochemical profile. However, whether these patients would maintain their successful rates after five years was uncertain. Our objective is to describe the efficacy and safety of a long term (5-year data) pharmacological and multi-modal treatment for moderate and severe obesity. Methods: The 40 patients that were successful in the two-year approach in our obesity center (Corpometria Institute, Brasilia, DF, Brazil) were enrolled. A long-term anti-obesity protocol was employed, with continuous or intermittent use of anti-obesity drugs, trimestral body composition analysis, psychotherapy, visit to a nutritionist every four months, and both resistance and endurance exercises at least four times a week. Body weight (BW), total weight excess (TWE), body fat, markers of lipid and glucose metabolism, liver function, and inflammation were analyzed. Subjects that dropped out were considered as weight regain. Therapeutic success for the 5-year follow-up included as the maintenance of >20% loss of the initial BW loss, and no weight regain (or < 20% of the initial weight loss). Results: A total of 27 patients (67.5%) were able to maintain the body weight, seven dropped out, and six regained more than 20% of the initial weight loss. Of these, 21 (77.8%) had significant further increase of muscle mass and decrease of fat loss, while 17 (63.0%) had further weight loss (p < 0.05), compared to the 2-year data. Improvements on the biochemical profile persisted in all 27 patients, and had significant further improvements in 24 (88.9%) of these patients. Conclusion: The risk of weight regain five years after a weight loss treatment for obesity was significantly lower compared to previous literature, and comparable to the long-term outcomes of bariatric procedures. An aggressive, structured, and long-term clinical weight loss approach has been shown to be feasible, even for morbidly obese patients.

scholarly journals Increasing Energy Flux to Maintain Diet-Induced Weight Loss

Nutrients ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 2533 ◽  
Author(s):  
Christopher L. Melby ◽  
Hunter L. Paris ◽  
R. Drew Sayer ◽  
Christopher Bell ◽  
James O. Hill
Keyword(s):  
Physical Activity ◽  
Weight Loss ◽  
Body Weight ◽  
Energy Balance ◽  
Energy Expenditure ◽  
Energy Flux ◽  
Weight Maintenance ◽  
High Energy ◽  
Daily Energy

Long-term maintenance of weight loss requires sustained energy balance at the reduced body weight. This could be attained by coupling low total daily energy intake (TDEI) with low total daily energy expenditure (TDEE; low energy flux), or by pairing high TDEI with high TDEE (high energy flux). Within an environment characterized by high energy dense food and a lack of need for movement, it may be particularly difficult for weight-reduced individuals to maintain energy balance in a low flux state. Most of these individuals will increase body mass due to an inability to sustain the necessary level of food restriction. This increase in TDEI may lead to the re-establishment of high energy flux at or near the original body weight. We propose that following weight loss, increasing physical activity can effectively re-establish a state of high energy flux without significant weight regain. Although the effect of extremely high levels of physical activity on TDEE may be constrained by compensatory reductions in non-activity energy expenditure, moderate increases following weight loss may elevate energy flux and encourage physiological adaptations favorable to weight loss maintenance, including better appetite regulation. It may be time to recognize that few individuals are able to re-establish energy balance at a lower body weight without permanent increases in physical activity. Accordingly, there is an urgent need for more research to better understand the role of energy flux in long-term weight maintenance.

Peripheral metabolic responses to prolonged weight reduction that promote rapid, efficient regain in obesity-prone rats

2006 ◽  
Vol 290 (6) ◽  
pp. R1577-R1588 ◽  
Author(s):  
Paul S. MacLean ◽  
Janine A. Higgins ◽  
Matthew R. Jackman ◽  
Ginger C. Johnson ◽  
Brooke K. Fleming-Elder ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Weight Reduction ◽  
Weight Regain ◽  
Energy Gap ◽  
Neural Pathways ◽  
Low Fat ◽  
Cross Sectional ◽  
Low Fat Diet

Weight regain after weight loss is the most significant impediment to long-term weight reduction. We have developed a rodent paradigm that models the process of regain after weight loss, and we have employed both prospective and cross-sectional analyses to characterize the compensatory adaptations to weight reduction that may contribute to the propensity to regain lost weight. Obese rats were fed an energy-restricted (50–60% kcal) low-fat diet that reduced body weight by 14%. This reduced weight was maintained for up to 16 wk with limited provisions of the low-fat diet. Intake restriction was then removed, and the rats were followed for 56 days as they relapsed to the obese state. Prolonged weight reduction was accompanied by 1) a persistent energy gap resulting from an increased drive to eat and a reduced expenditure of energy, 2) a higher caloric efficiency of regain that may be linked with suppressed lipid utilization early in the relapse process, 3) preferential lipid accumulation in adipose tissue accompanied by adipocyte hyperplasia, and 4) humoral adiposity signals that underestimate the level of peripheral adiposity and likely influence the neural pathways controlling energy balance. Taken together, long-term weight reduction in this rodent paradigm is accompanied by a number of interrelated compensatory adjustments in the periphery that work together to promote rapid and efficient weight regain. These metabolic adjustments to weight reduction are discussed in the context of a homeostatic feedback system that controls body weight.

scholarly journals How strongly does appetite counter weight loss? Quantification of the homeostatic control of human energy intake

2016 ◽  
Author(s):  
David Polidori ◽  
Arjun Sanghvi ◽  
Randy Seeley ◽  
Kevin D. Hall
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Feedback Control ◽  
Energy Expenditure ◽  
Energy Intake ◽  
List Type ◽  
Homeostatic Control ◽  
Free Living ◽  
Human Energy

AbstractObjectiveTo quantify the homeostatic feedback control of energy intake in response to long-term covert manipulation of energy balance in free-living humans.MethodsWe used a validated mathematical method to calculate energy intake changes during a 52 week placebo-controlled trial in 153 patients treated with canagliflozin, a sodium glucose co-transporter inhibitor that increases urinary glucose excretion thereby resulting in weight loss without patients being directly aware of the energy deficit. We analyzed the relationship between the body weight time course and the calculated energy intake changes using principles from engineering control theory. ResultsWe discovered that weight loss leads to a proportional homeostatic drive to increase energy intake above baseline by ~100 kcal/day per kg of lost weight – an amount more than 3-fold larger than the corresponding energy expenditure adaptations.ConclusionsWhile energy expenditure adaptations are often thought to be the main reason for slowing of weight loss and subsequent regain, feedback control of energy intake plays an even larger role and helps explain why long-term maintenance of a reduced body weight is so difficult.FundingThis research was supported by the Intramural Research Program of the NIH, National Institute of Diabetes & Digestive & Kidney Diseases, using data from a study sponsored by Janssen Research & Development, LLC.DisclosureD.P. is a full-time employee of Janssen Research & Development, LLC. K.D.H. reports patent pending on a method of personalized dynamic feedback control of body weight (US Patent Application No. 13/754,058; assigned to the NIH) and has received funding from the Nutrition Science Initiative to investigate the effects of ketogenic diets on human energy expenditure. R.S. is a paid consultant for Janssen, Novo Nordisk, Takeda, Daichii Sankyo, Novartis, Pfizer, Nestle, Circuit Therapeutics and Ethicon. R.S., also has received research support from Novo Nordisk, Ethicon, Sanofiand Boehringer Ingelheim. A.S. reports no conflicts of interest.What is already known about this subject?Human body weight is believed to be regulated by homeostatic feedback control of both energy intake and energy expenditure.Adaptations of energy expenditure to weight loss have been well-established, but the homeostatic control of energy intake has yet to be quantified.What this study addsWe provide the first quantification of the homeostatic control of energy intake in free-living humans.The increase in energy intake per kg of weight lost is several-fold larger than the known energy expenditure adaptations.Homeostatic control of energy intake is likely the primary reason why it is difficult to achieve and sustain large weight losses.

scholarly journals Revisiting the Compensatory Theory as an explanatory model for relapse in obesity management

2020 ◽  
Vol 112 (5) ◽  
pp. 1170-1179
Author(s):  
Catia Martins ◽  
Gareth R Dutton ◽  
Gary R Hunter ◽  
Barbara A Gower
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Energy Expenditure ◽  
Weight Regain ◽  
The Body ◽  
Explanatory Model ◽  
Lower Body ◽  
Obesity Management ◽  
Lower Body Weight ◽  
Physiological Adaptations

ABSTRACT Weight regain remains the main challenge in obesity management, and its etiology remains elusive. The aim of the present review was to revise the available evidence regarding the “Compensatory Theory,” which is an explanatory model of relapse in obesity treatment, and to propose alternative mechanisms that can contribute to weight regain. It has been proposed, and generally accepted as true, that when a person loses weight the body fights back, with physiological adaptations on both sides of the energy balance equation that try to bring body weight back to its original state: this is the Compensatory Theory. This theory proposes that the increased orexigenic drive to eat and the reduced energy expenditure that follow weight loss are the main drivers of relapse. However, evidence showing a link between these physiological adaptations to weight loss and weight regain is lacking. Here, we propose that the physiological adaptations to weight loss, both at the level of the homeostatic appetite control system and energy expenditure, are in fact a normalization to a lower body weight and not drivers of weight regain. In light of this we explore other potential mechanisms, both physiological and behavioral, that can contribute to the high incidence of relapse in obesity management. More research is needed to clearly ascertain whether the changes in energy expenditure and homeostatic appetite markers seen in reduced-obese individuals are a compensatory mechanism that drives relapse or a normalization towards a lower body weight, and to explore alternative hypotheses that explain relapse in obesity management.

scholarly journals A review of the short- and long-term impact of weight loss on appetite in youth: what do we know and where to from here?

2020 ◽  
Vol 79 (3) ◽  
pp. 357-366
Author(s):  
Helen Truby ◽  
Christie Bennett ◽  
Catia Martins
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Gut Hormones ◽  
Reduced Body ◽  
Short And Long Term ◽  
Long Term Impact ◽  
Desire To Eat ◽  
Individual Effort

This review seeks to synthesise our knowledge about changes in hunger and satiety that occur during diet-induced weight loss and during weight loss maintenance, with a particular focus on youth with obesity. Mechanisms of appetite responses to weight loss rely heavily on the adult literature. Physiological mechanisms that control appetite and satiety via the gut–brain axis have been elucidated but we have an incomplete picture of changes in gut hormones and peptides in youth with obesity. In adolescents, the role of the brain in long-term sensing of body composition and modifying appetite and satiety changes is easily over-ridden by hedonic influences for the reward of highly palatable sweet foods and encourages over-consumption. Accordingly, reward cues and hyper-responsiveness to palatable foods lead to a pattern of food choices. Different reward systems are necessary that are substantial enough to reward the continued individual effort required to sustain new behaviours, that need to be adopted to support a reduced body weight. Periods of growth and development during childhood provide windows of opportunity for interventions to influence body weight trajectory but long-term studies are lacking. More emphasis needs to be placed on anticipatory guidance on how to manage powerful hedonic influences of food choice, essential to cope with living in our obesogenic environment and managing hunger which comes with the stronger desire to eat after weight has been lost.

scholarly journals Improvements in Long-Term Appetite-Regulating Hormones in Response to a Combined Lifestyle Intervention for Obesity

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A489-A490
Author(s):  
Susanne Kuckuck
Keyword(s):  
Weight Loss ◽  
Lifestyle Intervention ◽  
Weight Regain ◽  
Initial Weight ◽  
Short Term ◽  
Initial Weight Loss ◽  
Hormone Levels ◽  
Adiposity Signals ◽  
Term Energy

Abstract Altered levels of hormonal appetite regulators have been observed in obesity (BMI ≥ 30.0 kg/m2), most prominently increases of insulin and leptin (indicating resistance) as well as decreases of adiponectin - all of which are long-term energy regulators and adiposity signals. Disrupted signaling of these hormones may have detrimental effects on metabolism, but may also promote weight gain. Weight loss is often accompanied by normalizations of long-term adiposity signals, but findings concerning short-term appetite regulators after weight loss vary across interventions (e.g. very low calorie diets vs. exercise). Moreover, it is debated whether such weight-loss-induced hormonal changes may reflect a disposition for weight regain. Here, we investigated changes of long- and short-term appetite signals in response to an intensive 75-week combined lifestyle intervention (CLI) comprising a normocaloric healthy diet, physical activity and psychotherapy to promote improved long-term weight management. For 39 patients, data on fasting serum levels of appetite-regulating hormones (leptin, insulin, adiponectin, GIP, PP, PYY, CCK, FGF21) were available. Hormone levels were correlated to BMI at baseline (T0) and compared across three time points: T0, T1 (after 10 weeks; initial weight loss) and T2 (after 75 weeks; weight loss maintenance). T0-T1 hormone changes were correlated to BMI changes between T1 and T2 to investigate whether hormonal alterations during initial weight loss are associated with weight regain. At T0, hormone levels were not associated with BMI. BMI decreased significantly from T0 (40.13 kg/m2 ± 5.7) to T1 (38.2 ± 5.4, p < .001) which was maintained at T2 (38.2 kg/m2 ± 5.9, p < .001). There were no significant changes in GIP, PP, PYY, CCK and FGF21. Leptin decreased from T0 (44.9 ng/nl ± 15.3) to T1 (33 ng/nl ± 14.8, p < .001) and T2 (38.6 ng/nl ± 16.0, p < .01), just like insulin which was significantly decreased at T1 (123 pmol/l ± 65, p < .05) and T2 (128 pmol/l ± 64, p < .05) compared to T0 (160 pmol/l ± 80). Adiponectin did not change between T0 (3.36 ug/ml ± 2.1) and T1 (3.2 ug/ml ± 2.1), but was increased at T2 (3.7 ug/ml ± 2.9, p < .01) compared to T1. T0-T2 BMI decrease correlated positively with T0-T2 decreases in leptin (r = .667, p < .001), insulin (rho = .535, p < .001) and increases of adiponectin (r = .412, p < .01), but no other hormone. T0-T1 hormone changes did not predict T1-T2 BMI changes. Thus, a 75-week CLI was associated with beneficial changes in the long-term energy regulators adiponectin, leptin and insulin, but no changes in short-term appetite-regulating hormones were observed despite significant weight loss. Initial changes in appetite-regulating hormones were not associated with subsequent weight regain. Overall, our data suggest that a CLI does not lead to adverse changes in appetite regulation, but rather long-term improvements such as e.g. increased leptin and insulin sensitivity.

scholarly journals Weight Maintenance with Litramine (IQP-G-002AS): A 24-Week Double-Blind, Randomized, Placebo-Controlled Study

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Barbara Grube ◽  
Pee-Win Chong ◽  
Felix Alt ◽  
Ralf Uebelhack
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Controlled Trial ◽  
Weight Maintenance ◽  
Body Weight Loss ◽  
Controlled Study ◽  
Serious Adverse Events ◽  
Double Blind ◽  
Initial Weight Loss

Background.Litramine (IQP-G-002AS) was shown to be effective and safe for weight loss in overweight and obese subjects. However, long-term effectiveness on maintenance of body weight loss has yet to be ascertained.Objective.To assess effect of Litramine on maintenance of body weight loss.Methods.A double-blind, randomised, placebo-controlled trial on overweight and obese patients was conducted over two sites in Germany for 24 weeks. Subjects with documented previous weight loss of 3% over the last 3–6 months were randomised to groups given either Litramine (3 g/day) or a matching placebo. Primary endpoints were difference of mean body weight (kg) between baseline and end of study and maintenance of initially lost body weight in verum group, where maintenance is defined as ≤1% weight gain.Results.Subjects who were taking Litramine lost significantly more body weight compared to the subjects taking placebo who gained weight instead (-0.62±1.55 kg versus1.62±1.48 kg,p<0.001). More importantly, 92% of subjects in Litramine group were able to maintain their body weight after initial weight loss, versus 25% in placebo group. No serious adverse events were reported throughout.Conclusion.Litramine is effective and safe for long-term body weight maintenance.Trial Registration.This trial is registered with Clinicaltrials.gov identifier:NCT01505387.

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