▪ Abstract Obesity is now recognized as a serious chronic disease, but there is pessimism about how successful treatment can be. A general perception is that almost no one succeeds in long-term maintenance of weight loss. To define long-term weight loss success, we need an accepted definition. We propose defining successful long-term weight loss maintenance as intentionally losing at least 10% of initial body weight and keeping it off for at least 1 year. According to this definition, the picture is much more optimistic, with perhaps greater than 20% of overweight/obese persons able to achieve success. We found that in the National Weight Control Registry, successful long-term weight loss maintainers (average weight loss of 30 kg for an average of 5.5 years) share common behavioral strategies, including eating a diet low in fat, frequent self-monitoring of body weight and food intake, and high levels of regular physical activity. Weight loss maintenance may get easier over time. Once these successful main...

Successful weight loss maintenance

The incidence of obesity is increasing rapidly. Research efforts for effective treatment strategies still focus on diet and exercise programmes, the individual components of which have been investigated in intervention trials in order to determine the most effective recommendations for sustained changes in bodyweight. The foremost objective of a weight-loss trial has to be the reduction in body fat leading to a decrease in risk factors for metabolic syndrome. However, a concomitant decline in lean tissue can frequently be observed. Given that fat-free mass (FFM) represents a key determinant of the magnitude of resting metabolic rate (RMR), it follows that a decrease in lean tissue could hinder the progress of weight loss. Therefore, with respect to long-term effectiveness of weight-loss programmes, the loss of fat mass while maintaining FFM and RMR seems desirable. Diet intervention studies suggest spontaneous losses in bodyweight following low-fat diets, and current data on a reduction of the carbohydrate-to-protein ratio of the diet show promising outcomes. Exercise training is associated with an increase in energy expenditure, thus promoting changes in body composition and bodyweight while keeping dietary intake constant. The advantages of strength training may have greater implications than initially proposed with respect to decreasing percentage body fat and sustaining FFM. Research to date suggests that the addition of exercise programmes to dietary restriction can promote more favourable changes in body composition than diet or physical activity on its own. Moreover, recent research indicates that the macronutrient content of the energy-restricted diet may influence body compositional alterations following exercise regimens. Protein emerges as an important factor for the maintenance of or increase in FFM induced by exercise training. Changes in RMR can only partly be accounted for by alterations in respiring tissues, and other yet-undefined mechanisms have to be explored. These outcomes provide the scientific rationale to justify further randomised intervention trials on the synergies between diet and exercise approaches to yield favourable modifications in body composition.

/pdf/the-role-of-diet-and-exercise-for-the-maintenance-of-fat-5cmsxw17ue.pdf

The role of diet and exercise for the maintenance of fat-free mass and resting metabolic rate during weight loss.

The availability of mice lacking the mitochondrial uncoupling protein UCP1, has provided an opportunity to analyze the relationship between the capacity for energy expenditure and the development of obesity in response to a high-fat, high-sucrose diet. Congenic UCP1-deficient mice on a C57BL/6J genetic background show a temperature-dependent resistance to diet-induced obesity when compared with wild-type mice. This resistance, which occurs at 20 degrees C, is quickly reversed when the ambient temperature is increased to 27 degrees C. At 20 degrees C, total oxygen consumption and physical activity of mutant and wild-type mice are indistinguishable; however, body temperature is higher in UCP1-deficient mice by 0.1-0.3 degrees C, and respiratory quotient is slightly reduced. A reduced respiratory quotient, together with elevated beta-hydroxybutyrate and reduced plasma fatty acid levels, suggests that the mutants oxidize a greater proportion of fat than wild-type mice, and that this possibly accounts for the resistance to diet-induced obesity. Although shivering is one alternative mechanism of thermogenesis that is probably used in UCP1-deficient mice, whether there are others remains to be determined. Nevertheless, our study underscores the paradox that elimination of the major thermogenic mechanism in the animal reduces rather than increases metabolic efficiency. We propose that in the absence of nonshivering thermogenesis, alternative, calorically more costly pathways of metabolism must be used to maintain body temperature.

/pdf/paradoxical-resistance-to-diet-induced-obesity-in-ucp1-2xdwq8fkf7.pdf

Paradoxical resistance to diet-induced obesity in UCP1-deficient mice

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.

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

The prevalence of obesity is increasing in both developed and developing countries, with rates reaching approximately 10-35% among adults in the Euro-American region. Obesity is associated with increased risks of cardiovascular diseases, type 2 diabetes, arthritis, and some type of cancers. Obesity significantly affects the quality of life and reduces the average life expectancy. The effective treatment of obesity should address both the medical and the social burden of this disease. Obesity needs to be treated within the health care system as any other complex disease, with empathy and without prejudice. Both health care providers and patients should know that the obesity treatment is a lifelong task. They should also set realistic goals before starting the treatment, whereas keeping in mind that even a modest weight loss of 5-15% significantly reduces obesity-related health risks. Essential treatment of obesity includes low-calorie low-fat diets, increased physical activity, and strategies contributing to the modification of lifestyle. Anti-obesity drugs facilitate weight loss and contribute to further amelioration of obesity-related health risks. A short-term weight loss, up to 6 months, is usually achieved easily. However, the long-term weight management is often associated with a lack of compliance, failures, and a high dropout rate. Regular physical activity, cognitive behavioral modification of lifestyle, and administration of anti-obesity drugs improve weight loss maintenance. Bariatric surgery is an effective strategy to treat severely obese patients. Bariatric surgery leads to a substantial improvement of comorbidities as well as to a reduction in overall mortality by 25-50% during the long-term follow-up. Obesity treatment should be individually tailored and the following factors should be taken into account: sex, the degree of obesity, individual health risks, psychobehavioral and metabolic characteristics, and the outcome of previous weight loss attempts. In the future, an evaluation of hormonal and genetic determinants of weight loss could also contribute to a better choice of individual therapy for a particular obese patient. A multilevel obesity management network of mutually collaborating facilities should be established to provide individually tailored treatment. Centers of excellence in obesity management represented by multidisciplinary teams should provide comprehensive programs for the treatment of obesity derived from evidence-based medicine.

https://care.diabetesjournals.org/content/diacare/31/Supplement_2/S269.full.pdf

Treatment Modalities of Obesity: What fits whom?

Objective: A low resting metabolic rate for a given body size and composition, a low rate of fat oxidation, low levels of physical activity, and low plasma leptin concentrations are all risk factors for body weight gain. The aim of the present investigation was to compare resting metabolic rate (RMR), respiratory quotient (RQ), levels of physical activity, and plasma leptin concentrations in eight post-obese adults (2 males and 6 females; 48.9 ± 12.2 years; body mass index [BMI]: 24.5 ± 1.0 kg/m2; body fat 33 ± 5%; mean ± SD) who lost 27.1 ± 21.3 kg (16 to 79 kg) and had maintained this weight loss for ≥2 months (2 to 9 months) to eight age- and BMI-matched control never-obese subjects (1 male and 7 females; 49.1 ± 5.2 years; BMI 24.4 ± 1.0 kg/m2; body fat 33 ± 7%).



Research Methods and Procedures: Following 3 days of weight maintenance diet (50% carbohydrate and 30% fat), RMR and RQ were measured after a 10-hour fast using indirect calorimetry and plasma leptin concentrations were measured using radioimmunoassay. Levels of physical activity were estimated using an accelerometer over a 48-hour period in free living conditions.



Results: After adjustment for fat mass and fat-free mass, post-obese subjects had, compared with controls, similar levels of physical activity (4185 ± 205 vs. 4295 ± 204 counts) and similar RMR (1383 ± 268 vs. 1430 ± 104 kcal/day) but higher RQ (0.86 ± 0.04 vs. 0.81 ± 0.03, p < 0.05). Leptin concentration correlated positively with percent body fat (r = 0.57, p < 0.05) and, after adjusting for fat mass and fat-free mass, was lower in post-obese than in control subjects (4.5 ± 2.1 vs. 11.6 ± 7.9 ng/mL, p < 0.05).



Discussion: The low fat oxidation and low plasma leptin concentrations observed in post-obese individuals may, in part, explain their propensity to relapse.

Low plasma leptin concentration and low rates of fat oxidation in weight-stable post-obese subjects.

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Low plasma leptin concentration and low rates of fat oxidation in weight-stable post-obese subjects.