Prevention of Overweight/Obesity as a Strategy to Optimize Cardiovascular Health

Abstract

HomeCirculationVol. 124, No. 7Prevention of Overweight/Obesity as a Strategy to Optimize Cardiovascular Health Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBPrevention of Overweight/Obesity as a Strategy to Optimize Cardiovascular Health Marc-Andre Cornier, Julie A. Marshall, James O. Hill, David M. Maahs and Robert H. Eckel Marc-Andre CornierMarc-Andre Cornier From the Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine (M.C., R.H.E.), Department of Epidemiology (J.A.M.), Anschutz Health and Wellness Center (J.O.H.), and Barbara Davis Center for Childhood Diabetes, The Children's Hospital Denver (D.M.M.), University of Colorado Denver, Aurora. Search for more papers by this author , Julie A. MarshallJulie A. Marshall From the Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine (M.C., R.H.E.), Department of Epidemiology (J.A.M.), Anschutz Health and Wellness Center (J.O.H.), and Barbara Davis Center for Childhood Diabetes, The Children's Hospital Denver (D.M.M.), University of Colorado Denver, Aurora. Search for more papers by this author , James O. HillJames O. Hill From the Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine (M.C., R.H.E.), Department of Epidemiology (J.A.M.), Anschutz Health and Wellness Center (J.O.H.), and Barbara Davis Center for Childhood Diabetes, The Children's Hospital Denver (D.M.M.), University of Colorado Denver, Aurora. Search for more papers by this author , David M. MaahsDavid M. Maahs From the Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine (M.C., R.H.E.), Department of Epidemiology (J.A.M.), Anschutz Health and Wellness Center (J.O.H.), and Barbara Davis Center for Childhood Diabetes, The Children's Hospital Denver (D.M.M.), University of Colorado Denver, Aurora. Search for more papers by this author and Robert H. EckelRobert H. Eckel From the Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine (M.C., R.H.E.), Department of Epidemiology (J.A.M.), Anschutz Health and Wellness Center (J.O.H.), and Barbara Davis Center for Childhood Diabetes, The Children's Hospital Denver (D.M.M.), University of Colorado Denver, Aurora. Search for more papers by this author Originally published16 Aug 2011https://doi.org/10.1161/CIRCULATIONAHA.110.968461Circulation. 2011;124:840–850IntroductionThe prevalence of obesity in the United States and the world has risen to epidemic/pandemic proportions. This increase has occurred despite efforts by healthcare providers and consumers alike to improve the health-related behaviors of the population and a tremendous push from the scientific community to better understand the pathophysiology of obesity. This epidemic is all the more concerning given the clear association between excess adiposity and adverse health consequences such as cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). These risks associated with overweight/obesity are primarily related to the deposition of excess adiposity or body fatness. Weight loss, specifically loss of body fat, is associated with benefits in all of the obesity-related comorbidities, but, unfortunately, most weight loss interventions are associated with weight regain and are therefore not successful in the long term. It is for these reasons that efforts to prevent weight gain and overweight/obesity are necessary. This is especially important when one considers younger individuals, who have even more to lose as a consequence of a longer duration of excess adiposity.After a brief review of the epidemiology of obesity, this statement will make the case for the importance of weight gain prevention. This argument will first include a review of the complications of overweight and obesity in both adults and children, including the future CVD risks of obesity in early life. Energy balance dysregulation and adaptations to the weight-reduced state, favoring weight regain, will then be reviewed as further argument for the need for obesity prevention. This will be followed by a discussion on the goals and strategies for accomplishing the difficult task of the prevention of weight gain and obesity.Scope of the ProblemClassification of Overweight and ObesityThe body mass index (BMI) is the most widely used and accepted method for the assessment and classification of excess adiposity or body fatness. Overweight and obesity are classified according to BMI for adults.1 A BMI <18.5 kg/m2 is considered underweight, between 18.5 and 24.9 kg/m2 corresponds to a healthy weight, between 25.0 and 29.9 kg/m2 is overweight, and ≥30.0 kg/m2 is obese. Obesity is further classified as stage I or mild (BMI of 30.0 to 34.9 kg/m2), stage II or moderate (BMI of 35.0 to 39.9 kg/m2), and stage III or severe (BMI of ≥40.0 kg/m2). In children, BMI percentiles adjusted for age and sex and calculated on the basis of a compilation of national survey data collected over a 30-year period are used. In children aged 2 to 19 years, overweight is defined as a BMI between the 85th and 95th percentiles, and obesity is defined as a BMI ≥95th percentile.2Epidemiology of Overweight and ObesityThe prevalence of overweight and obesity in the United States and the world has risen dramatically over the last 4 to 5 decades and has been summarized.3,4 In the most recent US population estimates based on data from the 2007–2008 National Health and Nutrition Examination Survey (NHANES), 34% of adults in the United States were obese, and 68% were either overweight or obese.5 Although obesity prevalence appears to have stabilized to some degree over the past few years, the prevalence of severe obesity has continued to increase.6 The overall prevalence of overweight and obesity in children and adolescents has also increased dramatically over the last 4 decades, with rates of obesity now approaching 17%. Approximately 10% of preschool children, 20% of those aged 6 to 11 years, and 18% of adolescents are obese. As in adults, however, trends over the last decade have not shown a further increase in childhood obesity except in the heaviest boys.7Despite the apparent stabilization of obesity prevalence, there continue to be significant racial and ethnic, as well as geographic and socioeconomic, disparities. Hispanics and non-Hispanic blacks have a significantly higher prevalence of both overweight and obesity compared with non-Hispanic whites. Forty-four percent of non-Hispanic blacks are obese, and 80% of Hispanics are overweight or obese.5 Similar racial and ethnic disparities are seen in children, especially among Hispanic boys and non-Hispanic black girls. The prevalence of obesity is 17% in non-Hispanic white boys, 20% in non-Hispanic black boys, and 27% in Hispanic boys. In girls, the prevalence is 14% in non-Hispanic whites, 29% in non-Hispanic blacks, and 17% in Hispanics. In addition, the prevalence of obesity is highest among low-income children.7 Geographic disparities are also evident, with the highest rates of obesity seen in the Southeast, Appalachia, and tribal lands in the West and Northern Plains.8These changes in the prevalence of overweight and obesity have occurred over a relatively short period of time, suggesting that genetics, although important, are not the primary cause of this epidemic. Most agree that the epidemic is primarily due to changes in the environment that promote reduced energy expenditure and increased energy intake in “at-risk” individuals; however, environmental influences on gene expression or epigenetic effects remain possible.The Case for PreventionIt seems obvious that preventing a disorder or disease makes more sense than treating one; this concept holds especially true for obesity. As will be discussed in this section, the “case” for obesity prevention will be centered on 2 key premises. The first is that obesity is associated with many “downstream” complications and costs that can and need to be prevented. The second is that although treating obesity is associated with improvements in all obesity-related comorbidities (reviewed elsewhere),9 the long-term success of obesity treatment is fraught with difficulties, primarily because of the biological and behavioral impetus to regain weight.Complications Associated With Overweight and ObesityComorbidities of Obesity in AdultsObesity has been consistently shown to be associated with an increased risk of all-cause mortality.10–13 The data are conflicting, however, for the effects of overweight on mortality, with some studies showing no increased and even reduced mortality with overweight, which is known as the “obesity paradox.”10,12 The effects of excess adiposity on mortality appear to be most apparent in adults during midlife compared with older adults and in healthy nonsmokers. The association between BMI and mortality has also been shown to vary by cause of death. Obesity, for example, has been shown to be associated with increased CVD and obesity-related cancer mortality11 but not with mortality due to other causes. Obesity has been shown to be independently associated with CVD, specifically coronary heart disease14–16 and stroke,17 which prompted the American Heart Association to adopt obesity as a major CVD risk factor in 1998.18 Weight gain independent of obesity status is also associated with increased risk of CVD.19 These associations appear to be especially true for those with central obesity, a core component of the metabolic syndrome (defined as ≥3 of the following: central obesity, elevated blood pressure, low high-density lipoprotein cholesterol, elevated triglycerides, impaired fasting glucose).20 Markers of central obesity such as waist circumference and waist-to-hip ratio have been shown to be independently associated with CVD risk.21–24 Furthermore, obesity has been shown to be associated with the development of T2DM, with excess adiposity being a key contributor to the development of insulin resistance.25,26 In fact, the significant rise in the prevalence of diabetes mellitus is thought to be primarily due to the obesity epidemic. Overweight and obesity are also associated with other CVD risk factors such as systemic hypertension, metabolic dyslipidemia, inflammation, and thrombosis. Finally, obesity has also been associated with many other non–CVD-related health complications, including osteoarthritis, obstructive sleep apnea, polycystic ovarian syndrome, depression, gastrointestinal diseases, and cancer, to name a few.27–38Comorbidities of Obesity in Children and AdolescentsObesity in childhood and adolescence is associated with a variety of concurrent metabolic and CVD risk factor derangements such as insulin resistance and T2DM, systemic hypertension, dyslipidemia, and inflammation. Worldwide, T2DM has increased in adolescents in the past few decades in parallel with the obesity pandemic,39 suggesting an impending earlier onset of diabetic vascular complications.40,41 Although numerous definitions of the metabolic syndrome exist in pediatrics,42 obesity is a key component, and the Princeton Lipids Clinic Follow-Up Study reported that for every 10-point increase in childhood BMI percentile, metabolic syndrome increased by 24%.43 Systemic hypertension,44 low high-density lipoprotein cholesterol, and elevated triglycerides45,46 are common CVD abnormalities seen with pediatric obesity. Childhood obesity is also associated with inflammation, as measured by elevated C-reactive protein, an important component of atherosclerosis.47In addition to the metabolic derangements of obesity in children and adolescents, other associated comorbidities have been reviewed recently48 and include psychological (depression and decreased quality of life), pulmonary (asthma and obstructive sleep apnea), orthopedic (slipped capital femoral epiphysis and Blount's disease), renal (increased proteinuria), hepatic (nonalcoholic fatty liver disease and steatohepatitis), and neurological (pseudotumor cerebri) disorders, among others. Finally, Franks et al49 recently found that obesity in childhood is strongly associated with increased rates of premature death from endogenous causes.Cardiovascular Disease Risk in Adulthood of Obese ChildrenAs discussed above, increases in the prevalence and degree of obesity in childhood and adolescence have been well documented in the United States and worldwide over the past several decades. Numerous epidemiological studies worldwide demonstrate that childhood obesity is strongly correlated with or tracks into adulthood.50 Recently, data analyzed from the US National Longitudinal Study of Adolescent Health found that over a 13-year period between adolescence (1996) and adulthood (2007–2009), obese adolescents (>95th percentile) were 16 times more likely to develop severe obesity than normal-weight or overweight (85th to 95th percentile) adolescents.51 Studies performed in a longitudinal cohort in Minnesota have demonstrated that BMI at 13 years of age predicted BMI and insulin sensitivity at age 22 years52 and that adiposity and insulin sensitivity each independently predicted CVD risk factors, but they synergistically predicted increased CVD risk factors.53 The Bogalusa Heart Study reported that childhood BMI and age of obesity onset predict adult systemic hypertension, although not independent of adult obesity.54 Results from the Young Finns, Bogalusa Heart, and the Childhood Determinants of Adult Health studies concluded that adolescent lipid levels are more strongly associated with adult carotid intima-media thickness than change in lipid levels and that dyslipidemia combined with high BMI is associated more strongly with increased carotid intima-media thickness than either factor.55 Compelling data also exist on the association of obesity with atherosclerosis in autopsy specimens in adolescents and young adults in the Bogalusa Heart Study56 and the Pathobiologic Determinants of Atherosclerosis in Youth study.57 Currently, however, the precise mechanism for increased CVD in adulthood due to pediatric obesity is uncertain (Figure 1). Further data are needed on whether childhood obesity increases adulthood CVD risk simply because of the tracking of obesity from childhood to adulthood or via increases in CVD risk factors in childhood and young adulthood such as dysregulated glucose metabolism (insulin resistance/T2DM), systemic hypertension, dyslipidemia, and inflammation or via multiple pathways.Download figureDownload PowerPointFigure 1. Temporal association of childhood and adulthood obesity with cardiovascular disease. IR/DM indicates insulin resistance/diabetes mellitus.Acknowledgment of the need for surrogate markers detectable early in the natural history of CVD to study the effect of childhood obesity on adulthood CVD is another important consideration.58,59 Few cardiovascular events occur in young adulthood, and investigation of the association of childhood risk factors with adult disease requires following these cohorts for years to monitor change in surrogate markers and even longer, often many decades, for hard outcomes such as myocardial infarction or death. Although longitudinal cohorts have demonstrated that childhood obesity is associated with adulthood CVD as measured by surrogate markers,60,61 the Young Finns Study has also demonstrated that improvement of obesity from childhood to young adulthood can reverse the effect of childhood obesity on adult CVD risk factors and future atherosclerosis.62,63 This suggests that although primary prevention of obesity in childhood will reduce CVD risk factor burden over time, a window of opportunity exists in which efforts to reduce obesity in young adulthood can reduce adulthood CVD risk factors. Moreover, it has been suggested that prevention goals should be refocused from decreasing risk for future CVD events to preventing development of atherosclerotic plaques.64Other Contributing IssuesPregnancyWomen who gain excessive weight during pregnancy have an increased risk of complications of pregnancy and babies with a greater chance of developing obesity. In addition, excessive weight gain increases the risk of postpartum obesity, with the failure to lose weight after gestation predictive of a higher likelihood of overweight or obesity to follow.65–67 At present, however, targeted interventions to reduce the amount of weight gain during pregnancy have been variably successful.68 To improve outcomes of pregnancy for both the mother and baby and reduce the risk of excessive weight gain to follow, revised gestational weight gain guidelines have been published recently by the Institute of Medicine.69 For women whose BMI is <18.5 kg/m2 before pregnancy, a weight gain of 13 to 18 kg during pregnancy is recommended; for women whose BMI is 18.5 to 24.9 kg/m2 prepartum, 11 to 16 kg of weight gain should ensue; women who are overweight with a BMI of 25 to 29.9 kg/m2 should gain 7 to 11 kg; for obese women whose BMI is >30 kg/m2, only a weight gain of 5 to 9 kg is recommended. In the environment of increasing overweight/obesity that currently exists, however, it remains doubtful that these recommendations will be immediately successful.AgingIn general, aging is associated with a plateau in body weight or even modest weight loss in the elderly.70 This loss in part relates to unintentional weight loss as an indicator of undiagnosed disease.71 Even if weight is stabilized, however, body composition changes unfavorably with an increase in fat mass, including intra-abdominal fat, and loss in lean tissue.72,73 These changes in body composition result in limitations of BMI as a surrogate marker of adiposity. With the decrease in lean body mass with aging, a reduction in basal/resting metabolic rate is expected. However, with aging there appears to be a protective effect of higher body weight on survival.74 This obesity paradox in the overweight/obese elderly is noteworthy in that despite an increased risk of CVD, there is decreased mortality from related diseases.75 Thus, unless obesity-related comorbidities that are known to affect the quality of life and/or limit life expectancy exist, weight loss is not recommended. Nevertheless, there is no evidence that overfeeding in the elderly will increase survival.CostThe costs, both direct and indirect, of overweight and obesity are substantial and have been reviewed recently elsewhere.76–79 The direct cost of medical care for overweight/obesity is 5% to 10% of healthcare spending in the United States.76 Obese individuals have direct medical costs ≈30% greater than normal-weight individuals.77 Overweight and obesity in younger adults are associated with significantly greater healthcare expenditures later in life.80,81 This is especially concerning for obese children, who already at a young age have greater direct medical costs.82 Waist circumference, a surrogate marker of abdominal obesity, further predicts healthcare costs beyond BMI.83 Obesity is also associated with significant increases in indirect costs such as missed time from work, increased disability, and reduced compensation78 as well as reduced education and job and insurance discrimination.84 The data supporting the cost-effectiveness of interventions to reduce overweight and obesity, however, are less clear. Although bariatric surgery has been shown to be cost-effective at a number of levels,85 the impact of behavioral and pharmacological interventions is more variable.86–88 Modeling of prevention polices, however, has shown favorable cost-effectiveness.89,90Adaptations to Weight LossObesity is a metabolic condition best described as a defense of an expanded adipose tissue mass.91 In a recent report from the Coronary Artery Risk Development in Young Adults (CARDIA) study, among the 1869 overweight/obese individuals without major disease in 1995, only 29% lost ≥5% between 1995 and 2000, and among those who lost weight, only 34% maintained at least 75% of their weight loss between 2000 and 2005.92 NHANES also examined weight data from 14 306 participants (aged 20 to 84 years) in the interval 1999–2006.93 Weight loss maintenance was defined, however, as weight loss maintained for a minimum of 1 year. Among US adults who had ever been overweight or obese, 36.6%, 17.3%, 8.5%, and 4.4% reported weight loss maintenance of only 5%, 10%, 15%, and 20% of their initial weight loss, respectively. This effect was more evident among adults aged 75 to 84 years versus those aged 20 to 34 years, in non-Hispanic whites versus Hispanics, and in women versus men. However, when NHANES and CARDIA are compared, the interval of 5 years versus 1 year is critically important. Overall, <10% of obese subjects are successful at maintaining weight loss for ≥5 years,94 and the percentage is perhaps far lower because studies in which weight loss was not maintained may be less likely to be reported. Thus, the case for prevention can be more than made and needs to be the focus of everyone, including patients, their families, friends, workplace, primary care physician, subspecialist, third-party payers, school systems, local communities, and beyond.Brief Review of Energy Balance RegulationEnergy balance is defined as a homeostatic yet dynamic environment wherein energy intake (food) matches energy expenditure. Energy expenditure has 3 basic components: basal/resting metabolic rate, energy expended in the form of physical activity, and thermogenesis (Figure 2). All components of energy expenditure can be measured in humans with a whole room calorimeter (almost always indirect calorimetry)95 and/or doubly labeled water.96 In general, the majority of energy expenditure is accounted for by the basal/resting metabolic rate (55% to 70%), with the smallest contribution from thermogenesis (5% to 10%) and the most variable form from physical activity (20% to 40%).97Download figureDownload PowerPointFigure 2. Adaptations to the weight-reduced state. The weight-reduced state is associated with increased energy intake and reduced energy expenditure, resulting in a net positive energy balance and a milieu favoring weight regain.Adaptations to Weight-Reduced StateChanges in Energy ExpenditureIn general, weight loss is associated with a reduction in total energy expenditure, including reductions in basal/resting metabolic rate and nonresting energy expenditure (Table 1).98 Reductions in resting metabolic rate best reflect the expected loss in lean body mass that accompanies weight reduction and is one of the opposing forces against the maintenance of weight reduction. Weight reduction also affects the energy cost of low levels of physical activity.98 Weight loss also leads to a decrease in nonresting energy expenditure.98,99 Moreover, the energy cost of walking is significantly reduced below that predicted solely on the basis of weight loss,100 and, after weight reduction, skeletal muscle work efficiency changes in a manner that opposes the maintenance of an altered body weight.101 At the reduced body weight, this change in efficiency accounts for a significant portion of the changes in nonresting energy expenditure.99Table 1. Potential Adaptations to the Weight-Reduced StateDecreased energy expenditure ↓ Resting energy expenditure ↓ Nonexercise and planned activity, changes in efficiency ↓ Thermogenesis (digestion)Changes in substrate metabolism ↓ Fat oxidationIncreased energy intake Homeostatic signals: changes in appetite-related hormones Nonhomeostatic signals: motivation, reward, attention, behaviorBecause total energy expenditure naturally decreases after weight reduction, increases in physical activity with exercise might be more than compensatory and contribute to the maintenance of a higher level of overall energy expenditure. Particularly with the addition of resistance training, exercise might also increase lean body mass and basal/resting metabolic rate.102 With the use of the historic studies in West Bengalese men by Rosenbaum et al,103 an alternative explanation could relate to the improved matching of energy intake with energy expenditure when levels of energy expenditure are high. Furthermore, successful maintenance of weight loss is associated with sustained, high levels of physical activity.104–108Changes in Substrate OxidationGenerally, individuals who are weight reduced are positioned to store rather than burn fat (Table 1), especially in the absence of increases in physical activity. This is reflected by an increase in the respiratory quotient (RQ), a measure of relative carbohydrate versus fat oxidation.109–112 Moreover, a significant correlation has been found between RQ after weight reduction and the spontaneous rate of body weight gain after cessation of the period of low energy intake.113,114 Thus, if carbohydrate is preferentially oxidized and fat stored, the metabolic response to sustained weight reduction appears to compensate for the diminished energy storage to return body composition to the previous energy-replete state.Increases in insulin sensitivity are expected after weight reduction and in part explain the increase in RQ. This increase in insulin sensitivity, however, is variably predictive of weight regain.115,116 Of added interest, in studies of reduced obese subjects, not only did insulin sensitivity improve but so did the ability of insulin to suppress fat oxidation; however, fasting leg RQ or skeletal muscle macronutrient oxidation did not change.117 Moreover, changes in the tissue-specific regulation of lipoprotein lipase, the lipid-partitioning triglyceride-rich lipoprotein hydrolytic enzyme, are also seen after weight loss. In reduced obese subjects, increases in upregulation of lipoprotein lipase by meals and insulin are seen in adipose tissue,118 with opposite effects in skeletal muscle.115Overall, these findings suggest that increases in lipid partitioning and the reduced capacity for fat oxidation contribute to the increase in RQ in the reduced obese state and the weight gain that so often follows. Importantly, changes in insulin sensitivity, substrate partitioning, and/or oxidative metabolism do not change the energetic value of the calorie. To regain the lost weight, energy intake must still exceed energy expenditure.Changes in Energy IntakeNot only is the weight-reduced state associated with reduced energy expenditure, but it is also associated with an increased drive to eat and resultant increased energy intake. In fact, all aspects of the regulation of energy intake are affected by weight loss (Table 1). It is clear that appetite is enhanced with calorie-restricted weight loss,119–121 the mechanisms of which are likely due to a complex interaction between physiological or homeostatic signals and reward/motivation/behavior-related signals. Adiposity-related signals, such as leptin and insulin, are reduced with weight loss, resulting in enhanced hunger and reduced satiety signaling in the brain as well as reduced energy expenditure.122,123 Of note, changes in leptin with weight loss have been shown to be predictive of weight regain.124 Short-term gut-related peptides such as ghrelin, PYY, and GLP-1, which play important roles in the meal-to-meal signaling of appetite, are altered by weight loss, favoring increased food intake.125–128 Recently, neuroimaging studies have shown that the weight-reduced state is associated with enhanced signaling in the motivation, reward, attention, and behavioral centers of the brain129–131 and that these brain responses respond to physiological signals such as leptin.132In summary, although caloric restriction results in short-term weight loss, it is extremely difficult for individuals to maintain this weight loss over the long term. Significant advances over the last couple of decades have been made toward understanding the complex mechanisms responsible for the regulation of energy balance. The weight-reduced state is clearly associated with a dysregulation of these mechanisms, resulting in a milieu promoting weight regain and thus being one of the major obstacles of “treating” obesity and reducing its comorbidities.Prevention of Overweight/ObesityBiological mechanisms that favor weight regain in the weight-reduced state, limited success with interventions to maintain weight loss, adverse effects of overweight that are amplified when overweight occurs during critical developmental periods, and adverse effects that increase with duration of overweight all argue for identifying strategies to achieve and maintain a healthy body weight beginning in utero and early childhood and continuing throughout the life course.How Much Behavior Change Is Needed to Achieve Healthier Weights?Permanent voluntary changes in body weight require permanent changes in behavior. The types of behavior change needed are similar regardless of whether the goal is to maintain weight loss or prevent excessive weight gain. However, the magnitude of behavior changes needed is greater if the goal is to achieve and maintain a significant weight loss versus to prevent the gradual weight gain experienced by many people today. The reasons for this have been explained in detail but relate to the manner in which energy balance is regulated.133,134 The overweight or obese state appears to be defended by both biological and behavioral compensatory mechanisms, so that negative energy balance and weight loss are opposed by a lowering of energy expenditure and an increased desire to eat. The greater the negative energy balance and weight loss, the greater is the compensation. Thus, maintaining the reduced obese state requires substantial and permanent behavior changes from the overweight or obese state. Lesser weight losses would require lesser behavior change to maintain.