Skip to main content
NCBI home page
Wiley Open Access Collection logoLink to Wiley Open Access Collection
. 2014 Nov 19;16(1):77–87. doi: 10.1111/obr.12232

Consequences of obesity and weight loss: a devil's advocate position

R E Brown 1, J L Kuk 1
PMCID: PMC4312481  PMID: 25410935

Abstract

Obesity is associated with multiple negative health consequences and current weight management guidelines recommend all obese persons to lose weight. However, recent evidence suggests that not all obese persons are negatively affected by their weight and that weight loss does not necessarily always improve health. The purpose of this review is not to trivialize the significant health risks associated with obesity, but to discuss subpopulations of obese people who are not adversely affected, or may even benefit from higher adiposity, and in who weight loss per se may not always be the most appropriate recommendation. More specifically, this review will take a devil's advocate position when discussing the consequences of obesity and weight loss for adults with established cardiovascular disease and type 2 diabetes, weight cyclers, metabolically healthy obese adults, youth, older adults and obese individuals who are highly fit.

Keywords: Exercise, metabolically healthy obese, obesity paradox, older adults

Introduction

Obesity is a major global health challenge. Between 1980 and 2013, the prevalence of worldwide obesity has substantially increased from 28.8% to 36.9% in adult males and from 29.8% to 38.0% in adult females 1. The association between obesity and increased risk for chronic health conditions, such as cardiovascular disease (CVD) and type 2 diabetes (T2D), is well established 2 and obesity is now the fifth leading cause of death worldwide 3. According to national weight management guidelines, all obese adults should be advised to lose weight 4 and a modest weight loss of 5%–10% of body weight has been shown to significantly improve cardiometabolic risk factors 5. However, increasing evidence suggests that there may be subpopulations of obese individuals who are not adversely affected by their increased adiposity, or in whom weight loss may not always result in improved health outcomes, such as adults with established CVD or T2D, weight cyclers, metabolically healthy obese adults, youth, older adults or ‘fit and fat’ individuals. The purpose of this review is not to convince the reader that obesity is a benign condition or that weight loss cannot be beneficial for health. Rather, this review will attempt to bring light to the fact that obesity is a complex condition that is not always associated with deleterious health outcomes and that weight loss per se may not always be the most appropriate recommendation for all obese individuals. A summary of our findings is provided in Table 1.

Table 1.

Summary of evidence regarding effect of obesity and/or weight loss in subgroups of obese populations

Obesity subgroup Summary of evidence
CVD

  • Obesity is a significant risk factor for CVD.

  • ‘Obesity paradox’ – obese patients with established CVD or heart failure often have a better prognosis than leaner patients, although this may be modified by fitness.

  • Intentional weight loss via cardiac rehabilitation programmes can result in weight loss and improvements in CVD risk factors.

  • Effects of intentional weight loss in patients with heart failure are not known.

T2D

  • Obesity is a significant risk factor for T2D.

  • Evidence of an ‘obesity paradox’ in that obesity at time of diagnosis may be associated with lower mortality risk compared with normal weight.

  • Intentional weight loss associated with improved glycaemia and cardiometabolic risk factors, but the effect on cardiovascular outcomes and mortality in obese patients with T2D is less clear.

Weight cyclers

  • May be associated with adverse body composition, negative cardiometabolic health outcomes and increased mortality risk.

MHO phenotype

  • Inconsistent evidence as to whether MHO adults have similar health and mortality risk as metabolically healthy normal-weight adults.

  • Evidence regarding health outcomes following weight loss in MHO adults is equivocal.

  • A standardized definition of MHO is needed.

Youth

  • Obesity in youth is generally associated with negative cardiometabolic health outcomes that track into adulthood.

  • MHO children are more likely to retain MHO status as an adult.

  • Weight loss in obese youth is associated with positive health outcomes but there are currently no clear standardized guidelines for weight loss treatment for obese youth.

Older adults

  • Effects of obesity on morbidity and mortality are less clear in older adults than in younger adults.

  • Intentional weight loss can improve cardiometabolic health and physical function.

  • An exercise component is critical for weight management in the elderly to preserve or increase muscle mass and strength and to improve physical function.

‘Fat and fit’ individuals

  • Evidence that high cardiorespiratory fitness may be associated with positive metabolic health outcomes and lower mortality risk independent of obesity.

  • Exercise without weight loss is associated with improved body composition and improved cardiometabolic health.

Open in a new tab

CVD, cardiovascular disease; T2D, type 2 diabetes; MHO, metabolically healthy obese.

Individuals with cardiovascular disease and type 2 diabetes

Obesity is clearly an established risk factor for CVD 6 and T2D 7,8 and is associated with increased risk of hypertension, myocardial infarction, coronary artery disease, stroke and heart failure 9. Despite the established association between obesity and risk of CVD, there is a great deal of evidence that an ‘obesity paradox’ exists in obese individuals with CVD in that they tend to have better prognosis than normal-weight individuals. The obesity paradox has been recognized in patients with heart failure, hypertension,coronary artery disease and in those who have undergone cardiac revascularization 10–15. Several studies have demonstrated that obese adults with heart failure may have a similar or even lower mortality risk compared with normal-weight individuals 16–20. There is also evidence that obese persons who undergo coronary revascularization have a lower in-hospital mortality risk or risk of adverse cardiac events 21–24 and a significantly lower mortality risk compared with normal-weight patients 25. Recently, it has been suggested that an obesity paradox may also be present for adults with T2D 26, in that adults who have normal weight when diagnosed with T2D have a higher mortality risk than adults who are obese at the time of diagnosis 27 regardless if they have a history of CVD or not 28. As well, obese adults with both CVD and T2D have also been reported to have a lower mortality risk compared with normal-weight adults 29. Thus, although obesity is a significant risk factor for these conditions, once the disease is present obesity may in fact improve survival. However, some studies suggest that this obesity paradox may only exist in individuals with low cardiorespiratory fitness as there is no difference in mortality rates by obesity in individuals with high cardiorespiratory fitness 30,31.

Although the underlying mechanisms of the obesity paradox are unknown, there are several hypotheses. Because heart failure is considered a catabolic state, obese individuals with heart failure may have more metabolic reserve 32. Obesity is a common primary contributor to the development of heart failure in obese individuals and therefore normal-weight or lean persons who develop CVD or heart failure may have a greater genetic predisposition for CVD or be resistant to medical interventions 33. Further, adults with obesity may experience less unintentional weight loss and cachexia, may take more protective CVD medications and may have increased muscle mass than lean adults 11. In adults with T2D, it has been suggested that having normal weight at the time of diagnosis may imply a different pathophysiology of T2D than in those who are obese 34 and that it may actually be a sign of latent autoimmune diabetes in adults 27. As well, differences in lean mass 35 or in types of diabetes medications that are typically prescribed to lean versus obese individuals have also been suggested to play a role 36. Clearly, the mechanisms that are associated with better survival in obese patients with CVD or T2D requires further investigation.

The effects of weight loss in patients with CVD or T2D are also not clear. Several studies have demonstrated that intentional weight loss that is achieved through a cardiac rehabilitation programme 10,37,38 is associated with improved cardiovascular risk factors in obese patients with CVD. Conversely, weight loss in CVD patients that is achieved through other modalities, such as liquid protein diets or very-low-calorie diets, have been associated with arrhythmias, ventricular tachycardia and in some cases death 39. There is also evidence that body mass index (BMI) alone is not a good indicator of mortality risk following a cardiovascular event and that total weight loss may be associated with increased mortality risk, whereas fat loss is associated with lower mortality risk 40. However, this is in contrast to evidence that a higher body fat percentage is the strongest predictor of event-free survival in patients with heart failure 41. Further, there is little evidence for the effects of intentional weight loss on long-term prognosis in patients with heart failure, and thus more research in this area is needed 11,12. Thus, the relationship between adiposity and weight loss with mortality risk in CVD patients requires further investigation.

In obese adults with T2D, there is considerable evidence to suggest that intentional weight loss markedly improves glycaemia and other cardiometabolic risk factors 42–45. Some observational studies suggest that intentional weight loss is associated with decreased mortality risk in adults with T2D 46–48, although this is not a consistent finding 49. Recently, the Look AHEAD trial, the only trial to randomize overweight and obese adults with T2D to an intensive lifestyle intervention or usual care, was stopped prematurely because of a lack of evidence that the lifestyle treatment group experienced less CVD deaths or events than the control group, despite losing more weight and improving on most CVD risk factors 50. Furthermore, one study reported that among adults with CVD and T2D, weight loss but not weight gain was predictive of a higher risk of hospitalization, myocardial infarction, stroke and death 29.

Therefore, although obesity is an established risk factor for CVD and T2D, there is considerable evidence that an obesity paradox exists in obese individuals with CVD, and recently, there have been reports that this phenomenon may also exist in patients with T2D. However, the biological mechanisms for this paradox are unclear. Evidence regarding the effect of purposeful weight loss on obese individuals with either disease is not clear cut and more research in this area is warranted.

Weight cyclers

The prevalence of US adults who are obese and attempting weight loss is estimated to be 56% in men and 64% in women 51. Even when attempts at weight loss are successful, only about 20% of obese adults are able to maintain weight loss after 1 year 52. This can lead to a pattern of repeated episodes of weight loss followed by weight gain, referred to as weight cycling. Studies that have investigated the prevalence or the health effects of weight cycling show inconsistent results, possibly because of the different definitions used to describe weight cycling. Weight cycling has been defined as losing ≥20 pounds at least three times 53, gaining and losing ≥5% of body weight 54, losing and regaining ≥5 kg one or more times 55 and losing and regaining ≥5 kg five or more times 56.

While not all studies have shown detrimental effects of weight cycling 57–61, many have reported that weight cycling may be associated with a higher BMI, body fat percentage, waist circumference, greater fat mass distribution to the upper body, lower resting metabolic rate, increased risk of hypertension, decreased glucose tolerance and higher prevalence of low high-density lipoprotein cholesterol (HDL) compared with non-weight cyclers 62–67. It has also been reported that weight cycling is associated with lower self-esteem, a higher prevalence of binge eating, more frequent visits to the doctor and poorer perceived self-health 55,62,68–70. During a weight loss intervention, weight cyclers lose less fat and more lean mass than non-weight cyclers 71 and when weight is regained, a greater proportion of fat is regained than lean mass 72. Further, there are many studies that have demonstrated a higher mortality risk in individuals with a history of weight cycling, although this is not always observed 53,73–80. However, one study reported that only when weight was gained during young or middle age, but not old age, was weight cycling associated with increased mortality risk 54. In summary, there is some evidence that weight cycling is associated with multiple negative health outcomes, including increased mortality risk. However, whether or not losing weight and regaining it is safer or more dangerous than remaining obese and not attempting weight loss remains to be elucidated.

Metabolically healthy obese phenotype

Metabolically healthy obese (MHO) persons are a subset of obese individuals typically defined as having excess body fat, but are insulin sensitive, normotensive, have a favourable lipid profile and have less visceral fat than the typical individual with obesity-related comorbidities 81–84. Currently, there is no standardized definition of MHO and the underlying mechanisms of this phenotype are not clear. It has been suggested that a preserved insulin sensitivity 85, as well as high levels of physical activity and physical fitness 86–88 may differentiate metabolically healthy from unhealthy obese adults, although this is not always a consistent finding.

There is evidence that MHO adults are not at an elevated risk for CVD 89,90, myocardial infarction 91 and do not have excess mortality risk 92–94 compared with metabolically healthy normal weight adults. This is in contrast to others who have reported that MHO individuals are still at a higher risk for premature mortality 83,95, as well as T2D 89,96,97, heart failure 91 and subclinical atherosclerosis 98. However, it is important to note that the majority of the aforementioned studies defined MHO as the presence of ≤1 or ≤2 metabolic risk factors. Therefore, the majority of individuals defined as MHO in these studies were likely not truly metabolically healthy, which may explain the inconsistent findings regarding MHO and health risk. This may be due to the fact that a true MHO phenotype, defined as no clinical or subclinical metabolic risk factors, is quite rare and may only represent 3–6% of adults with obesity 83,99.

Whether or not weight loss improves cardiometabolic risk factors in MHO individuals is of interest. Several studies have reported that following weight loss, MHO individuals significantly improved body composition and cardiometabolic risk factors 100–102, as well as physical fitness 102. However, other studies have failed to show improvements in metabolic risk factors in MHO adults despite significant loss of body weight 103–105. Interestingly, weight loss in MHO adults may even have a detrimental effect on health, as after 6 months of caloric restriction, insulin sensitivity improved in at-risk obese women, but actually decreased by 13% in MHO women 106. Furthermore, some studies report that when obese adults who do not have comorbidities intentionally lose weight, they have a higher mortality risk compared with those who remain weight stable 46,47,107.

Given the existence of the MHO phenotype, the question becomes if all obese individuals should be advised to lose weight as the guidelines suggest and how obese people with no morbidities should be medically counselled. The Edmonton Obesity Staging System (EOSS) is a clinical staging system that was recently developed to evaluate the metabolic, psychological and physical health of obese patients and recommend treatment according to severity of health risk 108. The stages range from 0 to 4, indicating no obesity-related risk factors to severe end-stage disease. Individuals in stage 0 or 1 have no established obesity-related chronic diseases and it is recommended that they engage in lifestyle modification to prevent further weight gain, but not to necessarily lose weight. Conversely, only persons in stages 2–4 have established obesity-related disease and are counselled to lose weight. Because EOSS is a relatively new model, the clinical utility of EOSS is not yet established. However, given the inconclusive evidence that MHO individuals benefit from weight loss, EOSS may prove to be a valuable clinical tool in terms of better assessment and treatment of obese persons.

In summary, although there is evidence of an MHO phenotype, it may represent a rare subgroup of obese individuals. More research is needed to elucidate the mechanisms underlying the MHO phenotype and the effect of weight loss on cardiometabolic health and mortality in this population.

Youth

Obesity in children and adolescents is a growing public health concern as there has been a concomitant increase in obesity-related health conditions that is typically observed in adults, such as hyperlipidaemia 109, metabolic syndrome 110, non-alcoholic fatty liver disease 111 and T2D 112. The increased prevalence of childhood obesity is concerning because obese youth are more likely to remain obese as adults 113–121 and cardiometabolic risk factor clustering has been reported to track well from childhood into adulthood 122. Because obese youth will likely live a longer portion of their life as obese and with chronic health conditions, some have predicted that the youth of today will live unhealthier lives and perhaps have a shorter life expectancy than their parents 123.

Despite evidence that obese youth are at a greater risk for cardiometabolic health conditions as adults 120,124,125, several studies have reported that adult BMI is a better predictor of adult CVD and T2D risk factors than childhood BMI 126. Nonetheless, the pattern of obesity may also be important to consider, as individuals who were obese as both children and adults are more likely to develop T2D, hypertension, dyslipidaemia and CVD compared with individuals who remained normal weight as a child and adult 127–129. However, up to 31% of obese youth have been reported to be MHO 130 and there is evidence that MHO youth are more likely to retain their MHO status as an adult and have similar carotid intima-media thickness in adulthood as non-obese children 131. As well, a longer duration of obesity may be associated with greater insulin sensitivity 132. Moreover, although weight loss in obese youth is typically associated with improved metabolic outcomes 133, weight management goals for this age group are more ambiguous than in adults (i.e. 5–10% of body weight). Although some suggest that weight should be maintained or lost until BMI reaches less than the 85th percentile 134, there are currently no clear standardized guidelines for weight loss treatment for obese children and adolescents.

Older adults

Over the past several decades, the proportion of obese older adults in the United States has more than doubled to 35% 135,136. Given that both age and obesity are associated with increased risk for health conditions, a higher prevalence of obese older adults may pose a large threat to the healthcare system. However, the association between obesity and health risk is not as well understood in the elderly as it is in younger adults, and whether or not obese older adults should lose weight is controversial 137,138.

Some have suggested that increased adiposity may be beneficial for elderly individuals. Obesity in older adults has been associated with higher bone mineral density and decreased risk of osteoporosis 139–141, lower probability of serious injury from a fall 142 and lower risk of osteoporotic fracture 143. Although obesity is a risk factor for CVD and T2D at any age, the association appears to be stronger for younger adults than older adults 144,145. Furthermore, BMI may not be the most useful indicator of obesity-related health risk in the elderly because of the age-related changes in body composition that can occur without a change in BMI, such as increased visceral adiposity, and decreased lean mass 146. Indeed, high waist circumference has been associated with increased morbidity and mortality risk in older adults independent of BMI 147–149. Conversely, others have reported that obese older adults have a similar 150–152 or lower 153–155 mortality risk compared with normal-weight older adults, regardless if obesity is defined as high BMI, waist circumference, waist-to-hip ratio or body fat percentage 156,157.

Increasing evidence suggests that the length of time that an individual is obese is important to consider, as individuals who are obese throughout adulthood are at a higher risk for hip and knee osteoarthritis 158, low cognition scores 159 and disability 160 during old age compared with those who remain normal weight. Conversely, one study reported that longer duration of obesity was associated with greater insulin sensitivity in obese non-diabetic adults 132. Furthermore, the pattern of weight gain may also be important to consider as individuals who gain weight during young and middle adulthood have been reported to have a higher mortality risk compared with persons who only gain weight during old age 54,161.

Whether or not obese older adults should attempt weight loss is also a controversial issue 162. Some intervention studies suggest that weight loss in older adults results in improvements in osteoarthritis, physical functioning, T2D and coronary heart disease 163. However, weight loss in the elderly is often associated with loss of lean mass 164–167, loss of bone mass 166,168,169 and may be associated with risk of fractures 170. A recent systematic review concluded that adding an exercise component to energy restriction during weight loss interventions in obese elderly is critical for improvements in cardiovascular fitness, muscle strength, increasing fat mass and preserving lean mass 171. When exercise is added to a hypocaloric diet in obese older adults, there is evidence that they lose similar amounts of body weight as the diet-only group, but generally lose less lean mass, bone mineral density and bone mass, experience greater increases in muscle strength and insulin sensitivity and have a greater reduction in cardiometabolic risk factors compared with diet-only groups 164–166,169,172–174. Even exercise without weight loss can have beneficial effects in the obese elderly and has been associated with stable or increased bone mineral density 175,176, increases in lean mass and significant decreases in markers of inflammation 177. However, whether or not weight loss is more beneficial than exercise without weight loss is unclear. Thus, it is suggested that treatment goals for obese older adults should not necessarily focus on weight loss per se, but on lifestyle changes that improve physical function status and quality of life and that maintain or increase lean mass and muscular strength 138.

Therefore, the association between obesity and health risk in the elderly is still not fully understood. In older adults, obesity may impose less of a risk for morbidity and mortality compared with younger adults. Obese elderly adults who are prescribed to lose weight should be carefully monitored because of the loss of lean mass and bone mass that often accompanies weight loss, although adding an exercise component may partially ameliorate these effects.

‘Fit and fat’ individuals

There is a growing body of literature that has shown that physical fitness is a predictor of morbidity and mortality risk independently of BMI 86,178–180 and that adults who are obese and fit may have a comparable mortality risk as normal-weight and fit adults 179,181. This may be in part due to lower overall and visceral adiposity in fit individuals for a given BMI. Further, it is demonstrated that men with high cardiorespiratory fitness have been reported to have higher HDL levels, as well as lower triglyceride levels, prevalence of metabolic syndrome, risk of developing CVD risk factors and mortality risk, independent of adiposity 182–184. However, not all studies find that fitness completely ameliorates the negative health effects of obesity, as some have reported that obese and fit individuals are still at a higher mortality risk compared with normal-weight and fit persons 185,186. This is in contrast to a recent meta-analysis that showed that obese and fit individuals had a similar mortality risk as normal-weight and fit adults 187. Further, another study reported that although obese and fit individuals had a lower all-cause and cardiovascular mortality risk compared with normal-weight and unfit individuals, they still had a higher risk of incident T2D and prevalence of cardiovascular and T2D risk factors 188.

Several studies have shown the beneficial effects of exercise on cardiometabolic risk factors even in the absence of weight loss. This is because even one acute bout of exercise can significantly reduce insulin sensitivity, cholesterol, blood pressure, blood glucose and triglycerides transiently post-exercise, with the effects usually being greatest in high risk or diseased populations 189. Further, exercise without weight loss in obese adults is associated with significant increases in skeletal muscle 190, reduced visceral fat 190–194, reduced hepatic fat 195 and improved fitness.

Thus, evidence shows that it is possible to be physically fit despite a high level of adiposity. Although exercise alone is not typically associated with significant weight loss, it can lead to improved cardiometabolic risk factors and positive changes in body composition 31. Whether obese and fit individuals can attain similar morbidity and mortality risk as normal-weight and fit individuals is still controversial. In obese individuals who struggle to lose or maintain weight, health professionals should consider acknowledging exercise as a plausible method of reducing obesity-related comorbidities and premature mortality risk, regardless of weight loss achieved 31.

In addition to physical activity and having high cardiorespiratory fitness, several factors may influence health independent of obesity and weight loss. For example, diet quality can influence health independent of changes in body weight. A low glycaemic index diet for even a 24-h period is reported to improve glucose and insulin levels by 30% in adults with T2D 196. Furthermore, a short-term high fat diet has been observed to significantly increase liver fat, intramyocellular lipid content and fasting insulin levels and impair insulin sensitivity without a change in body weight in humans 197,198. Bariatric surgery is also reported to have health benefits that go beyond what is expected through weight loss alone that may be related to decreased systemic inflammation, modifications of the gut microbiota, exclusion of nutrients from the duodenum, increased incretin secretion and increases in bile acids 199,200. Thus, there are several situations in which weight loss may not be required to influence health.

Conclusion

In conclusion, obesity is a rapidly growing problem in both children and adults that is associated with numerous negative health outcomes, many of which can be prevented or ameliorated with modest weight loss. Current weight management guidelines recommend weight loss for all obese adults. However, it is evident that not all obese individuals, such as those who are elderly, metabolically healthy or highly fit, are at an increased risk for health problems. Further, whether weight loss is beneficial for all obese individuals is questionable. In fact, weight loss in obese populations with established CVD or T2D has been reported to be detrimental for longevity. As well, due to the low success rate for obese adults attempting weight loss 52, it is questionable whether the benefits of weight loss outweigh the potential negative effects of weight cycling. Therefore, an emphasis on maintaining a healthy lifestyle that includes a high level of physical activity and physical fitness may be a more appropriate recommendation for some obese populations than just focusing on the goal of weight loss alone. Future research should attempt to elucidate the mechanisms underlying the obesity paradox and the MHO phenotype, as well as continue to investigate the potentially differing effects of weight loss on various populations of obese people.

Conflict of interest statement

No conflict of interest was declared.

References

  1. Ng M, Fleming T, Robinson M, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2014;384:766–781. doi: 10.1016/S0140-6736(14)60460-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Must A, Spadano J, Coakley EH, Field AE, Colditz G, Dietz WH. The disease burden associated with overweight and obesity. JAMA. 1999;282:1523–1529. doi: 10.1001/jama.282.16.1523. [DOI] [PubMed] [Google Scholar]
  3. World Health Organization. Global Health Risks: Mortality and Burden of Disease Attributable to Selected Major Risks. Geneva, Switzerland: World Health Organization; 2009. [Google Scholar]
  4. Jensen MD, Ryan DH, Donato KA, et al. Executive summary: guidelines (2013) for the management of overweight and obesity in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and The Obesity Society published by The Obesity Society and American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Based on a systemic review from the The Obesity Expert Panel, 2013. Obesity. 2014;22(Suppl. 2):S5–S39. doi: 10.1002/oby.20821. [DOI] [PubMed] [Google Scholar]
  5. Lau DCW, Douketis JD, Morrison KM, Hramiak IM, Sharma AM, Ur E. 2006 Canadian clinical practice guidelines on the management and prevention of obesity in adults and children (summary) Can Med Assoc J. 2007;176:S1–S13. doi: 10.1503/cmaj.061409. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Lavie CJ, Milani RV, Ventura HO. Obesity and cardiovascular disease: risk factor, paradox, and impact of weight loss. J Am Coll Cardiol. 2009;53:1925–1932. doi: 10.1016/j.jacc.2008.12.068. [DOI] [PubMed] [Google Scholar]
  7. Chan JM, Rimm EB, Colditz GA, Stampfer MJ, Willett WC. Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men. Diabetes Care. 1994;17:961–969. doi: 10.2337/diacare.17.9.961. [DOI] [PubMed] [Google Scholar]
  8. Koh-Banerjee P, Wang Y, Hu FB, Spiegelman D, Willett WC, Rimm EB. Changes in body weight and body fat distribution as risk factors for clinical diabetes in US men. Am J Epidemiol. 2004;159:1150–1159. doi: 10.1093/aje/kwh167. [DOI] [PubMed] [Google Scholar]
  9. Douketis J, Sharma A. Obesity and cardiovascular disease: pathogenic mechanisms and potential benefits of weight reduction. Semin Vasc Med. 2005;5:25–33. doi: 10.1055/s-2005-871739. [DOI] [PubMed] [Google Scholar]
  10. Lavie CJ, Milani RV, Artham SM, Patel DA, Ventura HO. The obesity paradox, weight loss, and coronary disease. Am J Med. 2009;122:1106–1114. doi: 10.1016/j.amjmed.2009.06.006. [DOI] [PubMed] [Google Scholar]
  11. Lavie CJ, Alpert MA, Arena R, Mehra MR, Milani RV, Ventura HO. Impact of obesity and the obesity paradox on prevalence and prognosis in heart failure. JACC Heart Fail. 2013;1:93–102. doi: 10.1016/j.jchf.2013.01.006. [DOI] [PubMed] [Google Scholar]
  12. Clark AL, Fonarow GC, Horwich TB. Obesity and the obesity paradox in heart failure. Prog Cardiovasc Dis. 2014;56:409–414. doi: 10.1016/j.pcad.2013.10.004. [DOI] [PubMed] [Google Scholar]
  13. Lavie CJ, De Schutter A, Patel D, Artham SM, Milani RV. Body composition and coronary heart disease mortality – an obesity or a lean paradox? Mayo Clin Proc. 2011;86:857–864. doi: 10.4065/mcp.2011.0092. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Lavie CJ, De Schutter A, Patel DA, Romero-Corral A, Artham SM, Milani RV. Body composition and survival in stable coronary heart disease: impact of lean mass index and body fat in the ‘obesity paradox. J Am Coll Cardiol. 2012;60:1374–1380. doi: 10.1016/j.jacc.2012.05.037. [DOI] [PubMed] [Google Scholar]
  15. De Schutter A, Lavie CJ, Milani RV. The impact of obesity on risk factors and prevalence and prognosis of coronary heart disease-the obesity paradox. Prog Cardiovasc Dis. 2014;56:401–408. doi: 10.1016/j.pcad.2013.08.003. [DOI] [PubMed] [Google Scholar]
  16. Kunju S, Badarudeen S, Schwarz E. Impact of obesity in patients with congestive heart failure. Rev Cardiovasc Med. 2009;10:142–151. doi: 10.3909/ricm0463. [DOI] [PubMed] [Google Scholar]
  17. Horwich TB, Fonarow GC, Hamilton MA, MacLellan WR, Woo MA, Tillisch JH. The relationship between obesity and mortality in patients with heart failure. J Am Coll Cardiol. 2001;38:789–795. doi: 10.1016/s0735-1097(01)01448-6. [DOI] [PubMed] [Google Scholar]
  18. Uretsky S, Messerli FH, Bangalore S, et al. Obesity paradox in patients with hypertension and coronary artery disease. Am J Med. 2007;120:863–870. doi: 10.1016/j.amjmed.2007.05.011. [DOI] [PubMed] [Google Scholar]
  19. Oreopoulos A, Padwal R, Kalantar-Zadeh K, Fonarow GC, Norris CM, McAlister FA. Body mass index and mortality in heart failure: a meta-analysis. Am Heart J. 2008;156:13–22. doi: 10.1016/j.ahj.2008.02.014. [DOI] [PubMed] [Google Scholar]
  20. Fonarow GC, Srikanthan P, Costanzo MR, Cintron GB, Lopatin M ADHERE Scientific Advisory Committee and Investigators. An obesity paradox in acute heart failure: analysis of body mass index and inhospital mortality for 108,927 patients in the Acute Decompensated Heart Failure National Registry. Am Heart J. 2007;153:74–81. doi: 10.1016/j.ahj.2006.09.007. [DOI] [PubMed] [Google Scholar]
  21. Reeves BC, Ascione R, Chamberlain MH, Angelini GD. Effect of body mass index on early outcomes in patients undergoing coronary artery bypass surgery. J Am Coll Cardiol. 2003;42:668–676. doi: 10.1016/s0735-1097(03)00777-0. [DOI] [PubMed] [Google Scholar]
  22. Gruberg L, Weissman NJ, Waksman R, et al. The impact of obesity on the short-term and long-term outcomes after percutaneous coronary intervention: the obesity paradox? J Am Coll Cardiol. 2002;39:578–584. doi: 10.1016/s0735-1097(01)01802-2. [DOI] [PubMed] [Google Scholar]
  23. Gurm HS, Whitlow PL, Kip KE BARI Investigators. The impact of body mass index on short- and long-term outcomes in patients undergoing coronary revascularization insights from the Bypass Angioplasty Revascularization Investigation (BARI) J Am Coll Cardiol. 2002;39:834–840. doi: 10.1016/s0735-1097(02)01687-x. for the. [DOI] [PubMed] [Google Scholar]
  24. Minutello RM, Chou ET, Hong MK, et al. Impact of body mass index on in-hospital outcomes following percutaneous coronary intervention (report from the New York State Angioplasty Registry) Am J Cardiol. 2004;93:1229–1232. doi: 10.1016/j.amjcard.2004.01.065. [DOI] [PubMed] [Google Scholar]
  25. Galal W, van Gestel Y, Hoeks S, et al. The obesity paradox in patients with peripheral arterial disease. Chest. 2008;134:925–930. doi: 10.1378/chest.08-0418. [DOI] [PubMed] [Google Scholar]
  26. Tseng C-H. Obesity paradox: differential effects on cancer and noncancer mortality in patients with type 2 diabetes mellitus. Atherosclerosis. 2013;226:186–192. doi: 10.1016/j.atherosclerosis.2012.09.004. [DOI] [PubMed] [Google Scholar]
  27. Carnethon M, de Chavez P, Biggs M, et al. Association of weight status with mortality in adults with incident diabetes. JAMA. 2012;308:581–590. doi: 10.1001/jama.2012.9282. [DOI] [PMC free article] [PubMed] [Google Scholar]
  28. Thomas G, Khunti K, Curcin V, et al. Obesity paradox in people newly diagnosed with type 2 diabetes with and without prior cardiovascular disease. Diab Obes Metab. 2014;16:317–325. doi: 10.1111/dom.12217. [DOI] [PubMed] [Google Scholar]
  29. Doehner W, Erdmann E, Cairns R, et al. Inverse relation of body weight and weight change with mortality and morbidity in patients with type 2 diabetes and cardiovascular co-morbidity: an analysis of the PROactive study population. Int J Cardiol. 2012;162:20–26. doi: 10.1016/j.ijcard.2011.09.039. [DOI] [PubMed] [Google Scholar]
  30. Lavie CJ, McAuley PA, Church TS, Milani RV, Blair SN. Obesity and cardiovascular diseases: implications regarding fitness, fatness, and severity in the obesity paradox. J Am Coll Cardiol. 2014;63:1345–1354. doi: 10.1016/j.jacc.2014.01.022. [DOI] [PubMed] [Google Scholar]
  31. Swift DL, Johannsen NM, Lavie CJ, Earnest CP, Church TS. The role of exercise and physical activity in weight loss and maintenance. Prog Cardiovasc Dis. 2014;56:441–447. doi: 10.1016/j.pcad.2013.09.012. [DOI] [PMC free article] [PubMed] [Google Scholar]
  32. Lavie CJ, Mehra MR, Milani RV. Obesity and heart failure prognosis: paradox or reverse epidemiology? Eur Heart J. 2005;26:5–7. doi: 10.1093/eurheartj/ehi055. [DOI] [PubMed] [Google Scholar]
  33. Lavie CJ, Milani RV, Ventura HO, Romero-Corral A. Body composition and heart failure prevalence and prognosis: getting to the fat of the matter in the ‘obesity paradox. Mayo Clin Proc. 2010;85:605–608. doi: 10.4065/mcp.2010.0333. [DOI] [PMC free article] [PubMed] [Google Scholar]
  34. Zeng Q, Dong S. Weight and mortality in adults with diabetes. JAMA. 2012;308:2079. doi: 10.1001/jama.2012.14567. [DOI] [PubMed] [Google Scholar]
  35. Yano Y, Ishikawa S, Kario K. Weight and mortality in adults with diabetes. JAMA. 2012;308:2079–2080. doi: 10.1001/jama.2012.14564. [DOI] [PubMed] [Google Scholar]
  36. Jornayvaz F. Weight and mortality in adults with diabetes. JAMA. 2012;308:2080. doi: 10.1001/jama.2012.14561. [DOI] [PubMed] [Google Scholar]
  37. Ades PA, Savage PD, Lischke S, et al. The effect of weight loss and exercise training on flow-mediated dilatation in coronary heart disease: a randomized trial. Chest. 2011;140:1420–1427. doi: 10.1378/chest.10-3289. [DOI] [PMC free article] [PubMed] [Google Scholar]
  38. Sierra-Johnson J, Romero-Corral A, Somers VK, et al. Prognostic importance of weight loss in patients with coronary heart disease regardless of initial body mass index. Eur J Cardiovasc Prev Rehabil. 2008;15:336–340. doi: 10.1097/HJR.0b013e3282f48348. [DOI] [PubMed] [Google Scholar]
  39. Poirier P, Giles TD, Bray GA, et al. Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical. Circulation. 2006;113:898–918. doi: 10.1161/CIRCULATIONAHA.106.171016. [DOI] [PubMed] [Google Scholar]
  40. Allison DB, Zannolli R, Faith MS, et al. Weight loss increases and fat loss decreases all- cause mortality rate: results from two independent cohort studies. Int J Obes. 1999;23:603–611. doi: 10.1038/sj.ijo.0800875. [DOI] [PubMed] [Google Scholar]
  41. Lavie CJ, Osman AF, Milani RV, Mehra MR. Body composition and prognosis in chronic systolic heart failure: the obesity paradox. Am J Cardiol. 2003;91:891–894. doi: 10.1016/s0002-9149(03)00031-6. [DOI] [PubMed] [Google Scholar]
  42. Wilding JPH. The importance of weight management in type 2 diabetes mellitus. Int J Clin Pr. 2014;68:682–691. doi: 10.1111/ijcp.12384. [DOI] [PMC free article] [PubMed] [Google Scholar]
  43. Shantha GPS, Kumar AA, Kahan S, Cheskin LJ. Association between glycosylated hemoglobin and intentional weight loss in overweight and obese patients with type 2 diabetes mellitus: a retrospective cohort study. Diabetes Educ. 2012;38:417–426. doi: 10.1177/0145721712443293. [DOI] [PubMed] [Google Scholar]
  44. Aucott LS. Influences of weight loss on long-term diabetes outcomes. Proc Nutr Soc. 2008;67:54–59. doi: 10.1017/S0029665108006022. [DOI] [PubMed] [Google Scholar]
  45. Wing R, Lang W, Wadden T, et al. Benefits of modest weight loss in improving cardiovascular risk factors in overweight and obese individuals with type 2 diabetes. Diabetes Care. 2011;34:1481–1486. doi: 10.2337/dc10-2415. [DOI] [PMC free article] [PubMed] [Google Scholar]
  46. Williamson DF, Pamuk E, Thun M, Flanders D, Byers T, Heath C. Prospective study of intentional weight loss and mortality in never-smoking overweight US white women aged 40–64 years. Am J Epidemiol. 1995;141:1128–1141. doi: 10.1093/oxfordjournals.aje.a117386. [DOI] [PubMed] [Google Scholar]
  47. Williamson D, Pamuk E, Thun M, Flanders D, Byers T, Heath C. Prospective study of intentional weight loss and mortality in overweight white men aged 40 to 64 years. Am J Epidemiol. 1999;149:491–503. doi: 10.1093/oxfordjournals.aje.a009843. [DOI] [PubMed] [Google Scholar]
  48. Williamson DF, Thompson TJ, Thun M, Flanders D, Pamuk E, Byers T. Intentional weight loss and mortality among overweight individuals with diabetes. Diabetes Care. 2000;23:1499–1504. doi: 10.2337/diacare.23.10.1499. [DOI] [PubMed] [Google Scholar]
  49. Wedick NM, Barrett-connor E, Knoke JD, Wingard DL. The relationship between weight loss and all-cause mortality in older men and women with and without diabetes mellitus: the Rancho Bernardo Study. J Am Geriatr Soc. 2002;50:1810–1815. doi: 10.1046/j.1532-5415.2002.50509.x. [DOI] [PubMed] [Google Scholar]
  50. Wing RR, Bolin P, Brancati FL, et al. Cardiovascular effects of intensive lifestyle intervention in type 2 diabetes. N Engl J Med. 2013;369:145–154. doi: 10.1056/NEJMoa1212914. [DOI] [PMC free article] [PubMed] [Google Scholar]
  51. Weiss EC, Galuska DA, Khan LK, Serdula MK. Weight-control practices among U.S. adults, 2001–2002. Am J Prev Med. 2006;31:18–24. doi: 10.1016/j.amepre.2006.03.016. [DOI] [PubMed] [Google Scholar]
  52. McGuire MT, Wing RR, Hill JO. The prevalence of weight loss maintenance among American adults. Int J Obes. 1999;23:1314–1319. doi: 10.1038/sj.ijo.0801075. [DOI] [PubMed] [Google Scholar]
  53. Field A, Malspeis S, Willett W. Weight cycling and mortality among middle-aged and older women. Arch Intern Med. 2009;169:881–886. doi: 10.1001/archinternmed.2009.67. [DOI] [PMC free article] [PubMed] [Google Scholar]
  54. Taing KY, Ardern CI, Kuk JL. Effect of the timing of weight cycling during adulthood on mortality risk in overweight and obese postmenopausal women. Obesity. 2012;20:407–413. doi: 10.1038/oby.2011.207. [DOI] [PubMed] [Google Scholar]
  55. Lahti-Koski M, Männistö S, Pietinen P, Vartiainen E. Prevalence of weight cycling and its relation to health indicators in Finland. Obes Res. 2005;13:333–341. doi: 10.1038/oby.2005.45. [DOI] [PubMed] [Google Scholar]
  56. Cereda E, Malavazos AE, Caccialanza R, Rondanelli M, Fatati G, Barichella M. Weight cycling is associated with body weight excess and abdominal fat accumulation: a cross-sectional study. Clin Nutr. 2011;30:718–723. doi: 10.1016/j.clnu.2011.06.009. [DOI] [PubMed] [Google Scholar]
  57. Graci S, Izzo G, Savino S, et al. Weight cycling and cardiovascular risk factors in obesity. Int J Obes Relat Metab Disord. 2004;28:65–71. doi: 10.1038/sj.ijo.0802537. [DOI] [PubMed] [Google Scholar]
  58. Frederick IO, Rudra CB, Miller RS, Foster JC, Williams MA. Adult weight change, weight cycling, and prepregnancy obesity in relation to risk of preeclampsia. Epidemiology. 2006;17:428–434. doi: 10.1097/01.ede.0000221028.33245.0b. [DOI] [PubMed] [Google Scholar]
  59. Gallagher KI, Jakicic JM, Kiel DP, Page ML, Ferguson ES, Marcus BH. Impact of weight-cycling history on bone density in obese women. Obes Res. 2002;10:896–902. doi: 10.1038/oby.2002.123. [DOI] [PubMed] [Google Scholar]
  60. Simkin-Silverman LR, Wing RR, Plantinga P, Matthews KA, Kuller LH. Lifetime weight cycling and psychological health in normal-weight and overweight women. Int J Eat Disord. 1998;24:175–183. doi: 10.1002/(sici)1098-108x(199809)24:2<175::aid-eat7>3.0.co;2-b. [DOI] [PubMed] [Google Scholar]
  61. Schultz MG, Hordern MD, Leano R, Coombes JS, Marwick TH, Sharman JE. Lifestyle change diminishes a hypertensive response to exercise in type 2 diabetes. Med Sci Sports Exerc. 2011;43:764–769. doi: 10.1249/MSS.0b013e3181fcf034. [DOI] [PubMed] [Google Scholar]
  62. Strychar I, Lavoie M-E, Messier L, et al. Anthropometric, metabolic, psychosocial, and dietary characteristics of overweight/obese postmenopausal women with a history of weight cycling: a MONET (Montreal Ottawa New Emerging Team) study. J Am Diet Assoc. 2009;109:718–724. doi: 10.1016/j.jada.2008.12.026. [DOI] [PubMed] [Google Scholar]
  63. Guagnano M, Ballone E, Pace-Palitti V, et al. Risk factors for hypertension in obese women. The role of weight cycling. Eur J Clin Nutr. 2000;54:356–360. doi: 10.1038/sj.ejcn.1600963. [DOI] [PubMed] [Google Scholar]
  64. Olson MB, Kelsey SF, Bittner V, et al. Weight cycling and high-density lipoprotein cholesterol in women: evidence of an adverse effect: a report from the NHLBI-sponsored WISE Study. J Am Coll Cardiol. 2000;36:1565–1571. doi: 10.1016/s0735-1097(00)00901-3. [DOI] [PubMed] [Google Scholar]
  65. Lissner L, Andres R, Muller D, Shimokata H. Body weight variability in men: metabolic rate, health and longevity. Int J Obes. 1990;14:373–383. [PubMed] [Google Scholar]
  66. Rodin J, Radke-Sharpe N, Rebuffé-Scrive M, Greenwood M. Weight cycling and fat distribution. Int J Obes. 1990;14:303–310. [PubMed] [Google Scholar]
  67. Wallner SJ, Luschnigg N, Schnedl WJ, et al. Body fat distribution of overweight females with a history of weight cycling. Int J Obes Relat Metab Disord. 2004;28:1143–1148. doi: 10.1038/sj.ijo.0802736. [DOI] [PubMed] [Google Scholar]
  68. Field AE, Manson JE, Taylor CB, Willett WC, Colditz GA. Association of weight change, weight control practices, and weight cycling among women in the Nurses' Health Study II. Int J Obes Relat Metab Disord. 2004;28:1134–1142. doi: 10.1038/sj.ijo.0802728. [DOI] [PubMed] [Google Scholar]
  69. Nagle CM, Marquart L, Bain CJ, et al. Impact of weight change and weight cycling on risk of different subtypes of endometrial cancer. Eur J Cancer. 2013;49:2717–2726. doi: 10.1016/j.ejca.2013.03.015. [DOI] [PubMed] [Google Scholar]
  70. Luo J, Margolis KL, Adami H-O, Lopez AM, Lessin L, Ye W. Body size, weight cycling, and risk of renal cell carcinoma among postmenopausal women: the Women's Health Initiative (United States) Am J Epidemiol. 2007;166:752–759. doi: 10.1093/aje/kwm137. [DOI] [PubMed] [Google Scholar]
  71. Yoo H-J, Kim B-T, Park Y-W, Park K-H, Kim C-W, Joo N-S. Difference of body compositional changes according to the presence of weight cycling in a community-based weight control program. J Korean Med Sci. 2010;25:49–53. doi: 10.3346/jkms.2010.25.1.49. [DOI] [PMC free article] [PubMed] [Google Scholar]
  72. Beavers KM, Lyles MF, Davis CC, Wang X, Beavers DP, Nicklas BJ. Is lost lean mass from intentional weight loss recovered during weight regain in postmenopausal women? Am J Clin Nutr. 2011;94:767–774. doi: 10.3945/ajcn.110.004895. [DOI] [PMC free article] [PubMed] [Google Scholar]
  73. Hamm P, Shekelle RB, Stamler J. Large fluctuations in body weight during young adulthood and twenty-five-year risk of coronary death in men. Am J Epidemiol. 1989;129:312–318. doi: 10.1093/oxfordjournals.aje.a115135. [DOI] [PubMed] [Google Scholar]
  74. Blair S, Shaten J, Brownell K, Collins G, Lissner L. Body weight change, all-cause mortality, and cause-specific mortality in the Multiple Risk Factor Intervention Trial. Ann Intern Med. 1993;119(Pt 2):749–757. doi: 10.7326/0003-4819-119-7_part_2-199310011-00024. [DOI] [PubMed] [Google Scholar]
  75. Lissner L, Odell P, D'Agostino R, et al. Variability of body weight and health outcomes in the Framingham population. N Engl J Med. 1991;324:1839–1844. doi: 10.1056/NEJM199106273242602. [DOI] [PubMed] [Google Scholar]
  76. Arnold AM, Newman AB, Cushman M, Ding J, Kritchevsky S. Body weight dynamics and their association with physical function and mortality in older adults: the Cardiovascular Health Study. J Gerontol A Biol Sci Med Sci. 2010;65:63–70. doi: 10.1093/gerona/glp050. [DOI] [PMC free article] [PubMed] [Google Scholar]
  77. Reynolds M, Fredman L, Langenberg P, Magaziner J. Weight, weight change, mortality in a random sample of older community-dwelling women. J Am Geriatr Soc. 1999;47:1409–1414. doi: 10.1111/j.1532-5415.1999.tb01558.x. [DOI] [PubMed] [Google Scholar]
  78. Diaz VA, Mainous AG, Everett CJ. The association between weight fluctuation and mortality: results from a population-based cohort study. J Community Health. 2005;30:153–165. doi: 10.1007/s10900-004-1955-1. [DOI] [PubMed] [Google Scholar]
  79. Rzehak P, Meisinger C, Woelke G, Brasche S, Strube G, Heinrich J. Weight change, weight cycling and mortality in the ERFORT Male Cohort Study. Eur J Epidemiol. 2007;22:665–673. doi: 10.1007/s10654-007-9167-5. [DOI] [PubMed] [Google Scholar]
  80. Stevens VL, Jacobs EJ, Sun J, et al. Weight cycling and mortality in a large prospective US study. Am J Epidemiol. 2012;175:785–792. doi: 10.1093/aje/kwr378. [DOI] [PubMed] [Google Scholar]
  81. Karelis AD. Metabolically healthy but obese individuals. Lancet. 2008;372:1281–1283. doi: 10.1016/S0140-6736(08)61531-7. [DOI] [PubMed] [Google Scholar]
  82. Wildman RP, Muntner P, Reynolds K, et al. The obese without cardiometabolic risk factor clustering and the normal weight with cardiometabolic risk factor clustering. Arch Intern Med. 2008;168:1617–1624. doi: 10.1001/archinte.168.15.1617. [DOI] [PubMed] [Google Scholar]
  83. Kuk J, Ardern C. Are metabolically normal but obese individuals at lower risk for all-cause mortality? Diabetes Care. 2009;32:2297–2299. doi: 10.2337/dc09-0574. [DOI] [PMC free article] [PubMed] [Google Scholar]
  84. Camhi SM, Katzmarzyk PT. Differences in body composition between metabolically healthy obese and metabolically abnormal obese adults. Int J Obes. 2014;38:1142–1145. doi: 10.1038/ijo.2013.208. [DOI] [PMC free article] [PubMed] [Google Scholar]
  85. Vukovic R, Mitrovic K, Milenkovic T, et al. Insulin-sensitive obese children display a favorable metabolic profile. Eur J Pediatr. 2013;172:201–206. doi: 10.1007/s00431-012-1867-5. [DOI] [PubMed] [Google Scholar]
  86. Hayes L, Pearce MS, Firbank MJ, Walker M, Taylor R, Unwin NC. Do obese but metabolically normal women differ in intra-abdominal fat and physical activity levels from those with the expected metabolic abnormalities? A cross-sectional study. BMC Public Health. 2010;10:723. doi: 10.1186/1471-2458-10-723. [DOI] [PMC free article] [PubMed] [Google Scholar]
  87. Ortega FB, Lee D-C, Katzmarzyk PT, et al. The intriguing metabolically healthy but obese phenotype: cardiovascular prognosis and role of fitness. Eur Heart J. 2013;34:389–397. doi: 10.1093/eurheartj/ehs174. [DOI] [PMC free article] [PubMed] [Google Scholar]
  88. Poelkens F, Eijsvogels T, Brussee P, Verheggen R, Tack C, Hopman M. Physical fitness can partly explain the metabolically healthy obese phenotype in women. Exp Clin Endocrinol Diabetes. 2014;122:87–91. doi: 10.1055/s-0033-1363686. [DOI] [PubMed] [Google Scholar]
  89. Meigs JB, Wilson PWF, Fox CS, et al. Body mass index, metabolic syndrome, and risk of type 2 diabetes or cardiovascular disease. J Clin Endocrinol Metab. 2006;91:2906–2912. doi: 10.1210/jc.2006-0594. [DOI] [PubMed] [Google Scholar]
  90. Ogorodnikova A, Kim M, McGinn A, Muntner P, Khan U, Wildman R. Incident cardiovascular disease events in metabolically benign obese individuals. Obes (Silver Spring) 2012;20:651–659. doi: 10.1038/oby.2011.243. [DOI] [PMC free article] [PubMed] [Google Scholar]
  91. Mørkedal B, Vatten LJ, Romundstad PR, Laugsand LE, Janszky I. Risk of myocardial infarction and heart failure among metabolically healthy but obese individuals: HUNT (Nord-Trøndelag Health Study), Norway. J Am Coll Cardiol. 2014;63:1071–1078. doi: 10.1016/j.jacc.2013.11.035. [DOI] [PubMed] [Google Scholar]
  92. Calori G, Lattuada G, Piemonti L, et al. Prevalence, metabolic features, and prognosis of metabolically healthy obese Italian individuals. Diabetes Care. 2011;34:210–215. doi: 10.2337/dc10-0665. [DOI] [PMC free article] [PubMed] [Google Scholar]
  93. Hamer M, Stamatakis E. Metabolically healthy obesity and risk of all-cause and cardiovascular disease mortality. J Clin Endocrinol Metab. 2012;97:2482–2488. doi: 10.1210/jc.2011-3475. [DOI] [PMC free article] [PubMed] [Google Scholar]
  94. Kuk J, Ardern C, Church T, et al. Edmonton obesity staging system: association with weight history and mortality risk. Appl Physiol Nutr Metab. 2011;36:570–576. doi: 10.1139/h11-058. [DOI] [PubMed] [Google Scholar]
  95. Kramer C, Zinman B, Retnakaran R. Are metabolically healthy overweight and obesity benign conditions? Ann Intern Med. 2013;159:758–769. doi: 10.7326/0003-4819-159-11-201312030-00008. [DOI] [PubMed] [Google Scholar]
  96. Bell JA, Kivimaki M, Hamer M. Metabolically healthy obesity and risk of incident type 2 diabetes: a meta-analysis of prospective cohort studies. Obes Rev. 2014;15:504–515. doi: 10.1111/obr.12157. [DOI] [PMC free article] [PubMed] [Google Scholar]
  97. Hinnouho G-M, Czernichow S, Dugravot A, et al. Metabolically healthy obesity and the risk of cardiovascular disease and type 2 diabetes: the Whitehall II cohort study. Eur Hear J. 2014 doi: 10.1093/eurheartj/ehu123. doi: 10.1093/eurheartj/ehu123. [DOI] [PMC free article] [PubMed] [Google Scholar]
  98. Chang Y, Kim B-K, Yun KE, et al. Metabolically healthy obesity and coronary artery calcification. J Am Coll Cardiol. 2014;63:2679–2686. doi: 10.1016/j.jacc.2014.03.042. [DOI] [PubMed] [Google Scholar]
  99. Liu RH, Wharton S, Sharma AM, Ardern CI, Kuk JL. Influence of a clinical lifestyle-based weight loss program on the metabolic risk profile of metabolically normal and abnormal obese adults. Obesity. 2013;21:1533–1539. doi: 10.1002/oby.20219. [DOI] [PubMed] [Google Scholar]
  100. Janiszewski P, Ross R. Effects of weight loss among metabolically healthy obese men. Diabetes Care. 2010;33:1957–1959. doi: 10.2337/dc10-0547. [DOI] [PMC free article] [PubMed] [Google Scholar]
  101. Sesti G, Folli F, Perego L, Hribal ML, Pontiroli AE. Effects of weight loss in metabolically healthy obese subjects after laparoscopic adjustable gastric banding and hypocaloric diet. PLoS ONE. 2011;6:e17737. doi: 10.1371/journal.pone.0017737. [DOI] [PMC free article] [PubMed] [Google Scholar]
  102. Dalzill C, Nigam A, Juneau M, et al. Intensive lifestyle intervention improves cardiometabolic and exercise parameters in metabolically healthy obese and metabolically unhealthy obese individuals. Can J Cardiol. 2014;30:434–440. doi: 10.1016/j.cjca.2013.11.033. [DOI] [PubMed] [Google Scholar]
  103. Shin M-J, Hyun YJ, Kim OY, Kim JY, Jang Y, Lee JH. Weight loss effect on inflammation and LDL oxidation in metabolically healthy but obese (MHO) individuals: low inflammation and LDL oxidation in MHO women. Int J Obes (Lond) 2006;30:1529–1534. doi: 10.1038/sj.ijo.0803304. [DOI] [PubMed] [Google Scholar]
  104. Kantartzis K, Machann J, Schick F, et al. Effects of a lifestyle intervention in metabolically benign and malign obesity. Diabetologia. 2011;54:864–868. doi: 10.1007/s00125-010-2006-3. [DOI] [PubMed] [Google Scholar]
  105. Arsenault BJ, Côté M, Cartier A, et al. Effect of exercise training on cardiometabolic risk markers among sedentary, but metabolically healthy overweight or obese postmenopausal women with elevated blood pressure. Atherosclerosis. 2009;207:530–533. doi: 10.1016/j.atherosclerosis.2009.05.009. [DOI] [PMC free article] [PubMed] [Google Scholar]
  106. Karelis AD, Messier V, Brochu M, Rabasa-Lhoret R. Metabolically healthy but obese women: effect of an energy-restricted diet. Diabetologia. 2008;51:1752–1754. doi: 10.1007/s00125-008-1038-4. [DOI] [PubMed] [Google Scholar]
  107. Sørensen TIA, Rissanen A, Korkeila M, Kaprio J. Intention to lose weight, weight changes, and 18-y mortality in overweight individuals without co-morbidities. PLoS Med. 2005;2:e171. doi: 10.1371/journal.pmed.0020171. [DOI] [PMC free article] [PubMed] [Google Scholar]
  108. Sharma AM, Kushner RF. A proposed clinical staging system for obesity. Int J Obes (Lond) 2009;33:289–295. doi: 10.1038/ijo.2009.2. [DOI] [PubMed] [Google Scholar]
  109. Lamb MM, Ogden CL, Carroll MD, Lacher DA, Flegal KM. Association of body fat percentage with lipid concentrations in children and adolescents: United States, 1999–2004. Am J Clin Nutr. 2011;94:877–883. doi: 10.3945/ajcn.111.015776. [DOI] [PubMed] [Google Scholar]
  110. Weiss R, Dziura J, Burgert TS, et al. Obesity and the metabolic syndrome in children and adolescents. N Engl J Med. 2004;350:2362–2374. doi: 10.1056/NEJMoa031049. [DOI] [PubMed] [Google Scholar]
  111. Schwimmer JB, McGreal N, Deutsch R, Finegold MJ, Lavine JE. Influence of gender, race, and ethnicity on suspected fatty liver in obese adolescents. Pediatrics. 2005;115:e561–e565. doi: 10.1542/peds.2004-1832. [DOI] [PubMed] [Google Scholar]
  112. Reinehr T. Type 2 diabetes mellitus in children and adolescents. World J Diabetes. 2013;4:270–281. doi: 10.4239/wjd.v4.i6.270. [DOI] [PMC free article] [PubMed] [Google Scholar]
  113. Deshmukh-Taskar P, Nicklas TA, Morales M, Yang SJ, Zakeri I, Berenson GS. Tracking of overweight status from childhood to young adulthood: the Bogalusa Heart Study. Eur J Clin Nutr. 2006;60:48–57. doi: 10.1038/sj.ejcn.1602266. [DOI] [PubMed] [Google Scholar]
  114. Freitas D, Beunen G, Maia J, et al. Tracking of fatness during childhood, adolescence and young adulthood: a 7-year follow-up study in Madeira Island, Portugal. Ann Hum Biol. 2012;39:59–67. doi: 10.3109/03014460.2011.638322. [DOI] [PubMed] [Google Scholar]
  115. Herman KM, Craig CL, Gauvin L, Katzmarzyk PT. Tracking of obesity and physical activity from childhood to adulthood: the Physical Activity Longitudinal Study. Int J Ped Obes. 2009;4:281–288. doi: 10.3109/17477160802596171. [DOI] [PubMed] [Google Scholar]
  116. Singh AS, Mulder C, Twisk JWR, van Mechelen W, Chinapaw MJM. Tracking of childhood overweight into adulthood: a systematic review of the literature. Obes Rev. 2008;9:474–488. doi: 10.1111/j.1467-789X.2008.00475.x. [DOI] [PubMed] [Google Scholar]
  117. Starc G, Strel J. Tracking excess weight and obesity from childhood to young adulthood: a 12-year prospective cohort study in Slovenia. Public Heal Nutr. 2011;14:49–55. doi: 10.1017/S1368980010000741. [DOI] [PubMed] [Google Scholar]
  118. Freedman DS, Khan LK, Dietz WH, Srinivasan SR, Berenson GS. Relationship of childhood obesity to coronary heart disease risk factors in adulthood: the Bogalusa Heart Study. Pediatrics. 2001;108:712–718. doi: 10.1542/peds.108.3.712. [DOI] [PubMed] [Google Scholar]
  119. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med. 1997;337:869–873. doi: 10.1056/NEJM199709253371301. [DOI] [PubMed] [Google Scholar]
  120. Steinberger J, Moran A, Hong CP, Jacobs DR, Sinaiko AR. Adiposity in childhood predicts obesity and insulin resistance in young adulthood. J Pediatr. 2001;138:469–473. doi: 10.1067/mpd.2001.112658. [DOI] [PubMed] [Google Scholar]
  121. Gordon-larsen P, The NS, Adair LS. Longitudinal trends in obesity in the US from adolescence to the third decade of life. Obesity. 2011;18:1801–1804. doi: 10.1038/oby.2009.451. [DOI] [PMC free article] [PubMed] [Google Scholar]
  122. Camhi SM, Katzmarzyk PT. Tracking of cardiometabolic risk factor clustering from childhood to adulthood. Int J Pediatr Obes. 2010;5:122–129. doi: 10.3109/17477160903111763. [DOI] [PubMed] [Google Scholar]
  123. Olshansky SJ, Passaro DJ, Hershow RC, et al. A potential decline in life expectancy in the United States in the 21st century. N Engl J Med. 2005;352:1138–1145. doi: 10.1056/NEJMsr043743. [DOI] [PubMed] [Google Scholar]
  124. Baker JL, Olsen LW, Sørensen TIA. Childhood body-mass index and the risk of coronary heart disease in adulthood. N Engl J Med. 2007;357:2329–2337. doi: 10.1056/NEJMoa072515. [DOI] [PMC free article] [PubMed] [Google Scholar]
  125. Morrison JA, Friedman LA, Gray-McGuire C. Metabolic syndrome in childhood predicts adult cardiovascular disease 25 years later: the Princeton Lipid Research Clinics Follow-up Study. Pediatrics. 2007;120:340–345. doi: 10.1542/peds.2006-1699. [DOI] [PubMed] [Google Scholar]
  126. Lloyd L, Langley-Evans S, McMullen S. Childhood obesity and adult cardiovascular disease risk: a systematic review. Int J Obes. 2010;34:18–28. doi: 10.1038/ijo.2009.61. [DOI] [PubMed] [Google Scholar]
  127. Park MH, Sovio U, Viner RM, Hardy RJ, Kinra S. Overweight in childhood, adolescence and adulthood and cardiovascular risk inlater life: pooled analysis of three british birth cohorts. PLoS ONE. 2013;8:e70684. doi: 10.1371/journal.pone.0070684. [DOI] [PMC free article] [PubMed] [Google Scholar]
  128. Juonala M, Magnussen CG, Berenson GS, et al. Childhood adiposity, adult adiposity, and cardiovascular risk factors. N Engl J Med. 2011;365:1876–1885. doi: 10.1056/NEJMoa1010112. [DOI] [PubMed] [Google Scholar]
  129. Freedman D, Patel D, Srinivasan S, et al. The contribution of childhood obesity to adult carotid intima-media thickness: the Bogalusa Heart Study. Int J Obes. 2008;32:749–756. doi: 10.1038/sj.ijo.0803798. [DOI] [PubMed] [Google Scholar]
  130. Prince RL, Kuk JL, Ambler KA, Dhaliwal J, Ball GDC. Predictors of metabolically healthy obesity in children. Diabetes Care. 2014;37:1462–1468. doi: 10.2337/dc13-1697. [DOI] [PubMed] [Google Scholar]
  131. Li S, Chen W, Srinivasan SR, Xu J, Berenson GS. Relation of childhood obesity/cardiometabolic phenotypes to adult cardiometabolic profile: the Bogalusa Heart Study. Am J Epidemiol. 2012;176(Suppl. 7):S142–S149. doi: 10.1093/aje/kws236. [DOI] [PMC free article] [PubMed] [Google Scholar]
  132. Muscelli E, Camastra S, Gastaldelli A, et al. Influence of duration of obesity on the insulin resistance of obese non-diabetic patients. Int J Obes. 1998;22:262–267. doi: 10.1038/sj.ijo.0800580. [DOI] [PubMed] [Google Scholar]
  133. Reinehr T. Effectiveness of lifestyle intervention in overweight children. Proc Nutr Soc. 2011;70:494–505. doi: 10.1017/S0029665111000577. [DOI] [PubMed] [Google Scholar]
  134. Spear BA, Barlow SE, Ervin C, et al. Recommendations for treatment of child and adolescent overweight and obesity. Pediatrics. 2007;120(Suppl. 4):S254–S288. doi: 10.1542/peds.2007-2329F. [DOI] [PubMed] [Google Scholar]
  135. Flegal KM, Carroll MD, Kuczmarski RJ, Johnson CL. Overweight and obesity in the United States: prevalence and trends, 1960–1994. Int J Obes Relat Metab Disord. 1998;22:39–47. doi: 10.1038/sj.ijo.0800541. [DOI] [PubMed] [Google Scholar]
  136. Fakhouri THI, Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity among older adults in the United States, 2007–2010. NCHS Data Brief. 2012;106:1–8. [PubMed] [Google Scholar]
  137. Brown RE, Kuk JL. Age-related differences in the consequences of obesity on cardiovascular disease, type 2 diabetes, osteoarthritis, cancer, physical function, osteoporosis, cognitive function, and mortality risk in the elderly. Heal Aging Clin Care Elder. 2014;6:25–32. [Google Scholar]
  138. Jahangir E, De Schutter A, Lavie CJ. Low weight and overweightness in older adults: risk and clinical management. Prog Cardiovasc Dis. 2014;57:127–133. doi: 10.1016/j.pcad.2014.01.001. [DOI] [PubMed] [Google Scholar]
  139. Villareal DT, Apovian CM, Kushner RF, Klein S. Obesity in older adults: technical review and position statement of the American Society for Nutrition and NAASO, The Obesity Society. Obes Res. 2005;13:1849–1863. doi: 10.1038/oby.2005.228. [DOI] [PubMed] [Google Scholar]
  140. Albala C, Yáñez M, Devoto E, Sostin C, Zeballos L, Santos JL. Obesity as a protective factor for postmenopausal osteoporosis. Int J Obes Relat Metab Disord. 1996;20:1027–1032. [PubMed] [Google Scholar]
  141. Dytfeld J, Ignaszak-Szczepaniak M, Gowin E, Michalak M, Horst-Sikorska W. Influence of lean and fat mass on bone mineral density (BMD) in postmenopausal women with osteoporosis. Arch Gerontol Geriatr. 2011;53:e237–e242. doi: 10.1016/j.archger.2011.01.002. [DOI] [PubMed] [Google Scholar]
  142. Himes CL, Reynolds SL. Effect of obesity on falls, injury, and disability. J Am Geriatr Soc. 2012;60:124–129. doi: 10.1111/j.1532-5415.2011.03767.x. [DOI] [PubMed] [Google Scholar]
  143. De Laet C, Kanis JA, Odén A, et al. Body mass index as a predictor of fracture risk: a meta-analysis. Osteoporos Int. 2005;16:1330–1338. doi: 10.1007/s00198-005-1863-y. [DOI] [PubMed] [Google Scholar]
  144. Narayan K, Boyle J, Thompson T, Gregg E, Williamson D. Effect of BMI on lifetime risk for diabetes in the U.S. Diabetes Care. 2007;30:1562–1566. doi: 10.2337/dc06-2544. [DOI] [PubMed] [Google Scholar]
  145. Canning KL, Brown RE, Jamnik VK, Kuk JL. Relationship between obesity and obesity-related morbidities weakens with aging. J Gerontol A Biol Sci Med Sci. 2014;69:87–92. doi: 10.1093/gerona/glt026. [DOI] [PubMed] [Google Scholar]
  146. Kuk JL, Saunders TJ, Davidson LE, Ross R. Age-related changes in total and regional fat distribution. Ageing Res Rev. 2009;8:339–348. doi: 10.1016/j.arr.2009.06.001. [DOI] [PubMed] [Google Scholar]
  147. Chang S-H, Beason T, Hunleth J, Colditz G. A systematic review of body fat distribution and mortality in older people. Maturitas. 2012;72:175–191. doi: 10.1016/j.maturitas.2012.04.004. [DOI] [PMC free article] [PubMed] [Google Scholar]
  148. Janssen I, Katzmarzyk PT, Ross R. Waist circumference and not body mass index explains obesity-related health risk. Am J Clin Nutr. 2004;79:379–384. doi: 10.1093/ajcn/79.3.379. [DOI] [PubMed] [Google Scholar]
  149. Nicklas BJ, Cesari M, Penninx BWJH, et al. Abdominal obesity is an independent risk factor for chronic heart failure in older people. J Am Geriatr Soc. 2006;54:413–420. doi: 10.1111/j.1532-5415.2005.00624.x. [DOI] [PubMed] [Google Scholar]
  150. Kuk JL, Ardern CI. Influence of age on the association between various measures of obesity and all-cause mortality. J Am Geriatr Soc. 2009;57:2077–2084. doi: 10.1111/j.1532-5415.2009.02486.x. [DOI] [PubMed] [Google Scholar]
  151. Landi F, Zuccalà G, Gambassi G, et al. Body mass index and mortality among older people living in the community. J Am Geriatr Soc. 1999;47:1072–1076. doi: 10.1111/j.1532-5415.1999.tb05229.x. [DOI] [PubMed] [Google Scholar]
  152. Corrada M, Kawas C, Mozaffar F, Paganini-Hill A. Association of body mass index and weight change with all-cause mortality in the elderly. Am J Epidemiol. 2006;163:938–949. doi: 10.1093/aje/kwj114. [DOI] [PMC free article] [PubMed] [Google Scholar]
  153. Grabowski DC, Ellis JE. High body mass index does not predict mortality in older people: analysis of the Longitudinal Study of Aging. J Am Geriatr Soc. 2001;49:968–979. doi: 10.1046/j.1532-5415.2001.49189.x. [DOI] [PubMed] [Google Scholar]
  154. Kaiser R, Winning K, Uter W, et al. Functionality and mortality in obese nursing home residents: an example of ‘risk factor paradox'? J Am Med Dir Assoc. 2010;11:428–435. doi: 10.1016/j.jamda.2009.10.004. [DOI] [PubMed] [Google Scholar]
  155. Janssen I. Morbidity and mortality risk associated with an overweight BMI in older men and women. Obes (Silver Spring) 2007;15:1827–1840. doi: 10.1038/oby.2007.217. [DOI] [PubMed] [Google Scholar]
  156. Batsis J, Singh S, Lopez-Jimenez F. Anthropometric measurements and survival in older Americans: results from the third National Health and Nutrition Examination Survey. J Nutr Heal Aging. 2014;18:123–130. doi: 10.1007/s12603-013-0366-3. [DOI] [PubMed] [Google Scholar]
  157. Kuk JL, Ardern CI. Influence of age on the association between various measures of obesity and all-cause mortality. J Am Geriatr Soc. 2009;57:2077–2084. doi: 10.1111/j.1532-5415.2009.02486.x. [DOI] [PubMed] [Google Scholar]
  158. Holliday KL, McWilliams DF, Maciewicz RA, Muir KR, Zhang W, Doherty M. Lifetime body mass index, other anthropometric measures of obesity and risk of knee or hip osteoarthritis in the GOAL case-control study. Osteoarthr Cartil. 2011;19:37–43. doi: 10.1016/j.joca.2010.10.014. [DOI] [PubMed] [Google Scholar]
  159. Sabia S, Kivimaki M, Shipley MJ, Marmot MG, Singh-manoux A. Body mass index over the adult life course and cognition in late midlife: the Whitehall II Cohort Study. Am J Clin Nutr. 2009;89:601–607. doi: 10.3945/ajcn.2008.26482. [DOI] [PMC free article] [PubMed] [Google Scholar]
  160. Strandberg TE, Stenholm S, Strandberg AY, Salomaa VV, Pitkälä KH, Tilvis RS. The ‘obesity paradox,’ frailty, disability, and mortality in older men: a prospective, longitudinal cohort study. Am J Epidemiol. 2013;178:1452–1460. doi: 10.1093/aje/kwt157. [DOI] [PubMed] [Google Scholar]
  161. Adams KF, Leitzmann MF, Ballard-Barbash R, et al. Body mass and weight change in adults in relation to mortality risk. Am J Epidemiol. 2014;179:135–144. doi: 10.1093/aje/kwt254. [DOI] [PMC free article] [PubMed] [Google Scholar]
  162. Waters DL, Ward AL, Villareal DT. Weight loss in obese adults 65years and older: a review of the controversy. Exp Gerontol. 2013;48:1054–1061. doi: 10.1016/j.exger.2013.02.005. [DOI] [PMC free article] [PubMed] [Google Scholar]
  163. Bales CW, Buhr G. Is obesity bad for older persons? A systematic review of the pros and cons of weight reduction in later life. J Am Med Dir Assoc. 2008;9:302–312. doi: 10.1016/j.jamda.2008.01.006. [DOI] [PubMed] [Google Scholar]
  164. Frimel T, Sinacore D, Villareal D. Exercise attenuates the weight-loss reduction in muscle mass in frail obese older adults. Medicine (Baltimore) 2008;40:1213–1219. doi: 10.1249/MSS.0b013e31816a85ce. [DOI] [PMC free article] [PubMed] [Google Scholar]
  165. Armamento-Villareal R, Sadler C, Napoli N, et al. Weight loss in obese older adults increases serum sclerostin and impairs hip geometry but both are prevented by exercise training. J Bone Miner Res. 2012;27:1215–1221. doi: 10.1002/jbmr.1560. [DOI] [PMC free article] [PubMed] [Google Scholar]
  166. Shah K, Armamento-Villareal R, Parimi N, et al. Exercise training in obese older adults prevents increase in bone turnover and attenuates decrease in hip bone mineral density induced by weight loss despite decline in bone-active hormones. J Bone Miner Res. 2011;26:2851–2859. doi: 10.1002/jbmr.475. [DOI] [PMC free article] [PubMed] [Google Scholar]
  167. Kelly KR, Haus JM, Solomon TPJ, et al. A low-glycemic index diet and exercise intervention reduces TNF(alpha) in isolated mononuclear cells of older, obese adults. J Nutr. 2011;141:1089–1094. doi: 10.3945/jn.111.139964. [DOI] [PMC free article] [PubMed] [Google Scholar]
  168. Ensrud KE, Fullman RL, Barrett-Connor E, et al. Voluntary weight reduction in older men increases hip bone loss: the osteoporotic fractures in men study. J Clin Endocrinol Metab. 2005;90:1998–2004. doi: 10.1210/jc.2004-1805. [DOI] [PubMed] [Google Scholar]
  169. Villareal D, Chode S, Parimi N, et al. Weight loss, exercise, or both and physical function in obese older adults. N Engl J Med. 2011;364:1218–1229. doi: 10.1056/NEJMoa1008234. [DOI] [PMC free article] [PubMed] [Google Scholar]
  170. Ensrud K, Cauley J, Lipschutz R, Cummings S. Weight change and fractures in older women. Study of Osteoporotic Fractures Research Group. Arch Intern Med. 1997;157:857–863. [PubMed] [Google Scholar]
  171. Miller CT, Fraser SF, Levinger I, et al. The effects of exercise training in addition to energy restriction on functional capacities and body composition in obese adults during weight loss: a systematic review. PLoS ONE. 2013;8:e81692. doi: 10.1371/journal.pone.0081692. [DOI] [PMC free article] [PubMed] [Google Scholar]
  172. Villareal DT, Banks M, Sinacore DR, Siener C, Klein S. Effect of weight loss and exercise on frailty in obese older adults. Arch Intern Med. 2006;166:860–866. doi: 10.1001/archinte.166.8.860. [DOI] [PubMed] [Google Scholar]
  173. Shah K, Stufflebam A, Hilton TN, Sinacore DR, Klein S, Villareal DT. Diet and exercise interventions reduce intrahepatic fat content and improve insulin sensitivity in obese older adults. Obesity (Silver Spring) 2009;17:2162–2168. doi: 10.1038/oby.2009.126. [DOI] [PMC free article] [PubMed] [Google Scholar]
  174. Bouchonville M, Armamento-Villareal R, Shah K, et al. Weight loss, exercise or both and cardiometabolic risk factors in obese older adults: results of a randomized controlled trial. Int J Obes. 2014;38:423–431. doi: 10.1038/ijo.2013.122. [DOI] [PMC free article] [PubMed] [Google Scholar]
  175. Shah K, Armamento-Villareal R, Parimi N, et al. Exercise training in obese older adults prevents increase in bone turnover and attenuates decrease in hip bone mineral density induced by weight loss despite decline in bone-active hormones. J Bone Miner Res. 2011;26:2851–2859. doi: 10.1002/jbmr.475. [DOI] [PMC free article] [PubMed] [Google Scholar]
  176. Beavers DP, Beavers KM, Loeser RF, et al. The independent and combined effects of intensive weight loss and exercise training on bone mineral density in overweight and obese older adults with osteoarthritis. Osteoarthr Cartil. 2014;22:726–733. doi: 10.1016/j.joca.2014.04.002. [DOI] [PMC free article] [PubMed] [Google Scholar]
  177. Lambert C, Wright N, Finck B, Villareal D. Exercise but not diet-induced weight loss decreases skeletal muscle inflammatory gene expression in frail obese elderly persons. J Appl Physiol. 2008;105:473–478. doi: 10.1152/japplphysiol.00006.2008. [DOI] [PMC free article] [PubMed] [Google Scholar]
  178. Wei M, Kampert JB, Barlow CE, et al. Relationship between low cardiorespiratory fitness and mortality in normal-weight, overweight, and obese men. JAMA. 1999;282:1547–1553. doi: 10.1001/jama.282.16.1547. [DOI] [PubMed] [Google Scholar]
  179. Lee CD, Blair SN, Jackson AS. Cardiorespiratory fitness, body composition, and all-cause and cardiovascular disease mortality in men. Am J Clin Nutr. 1999;69:373–380. doi: 10.1093/ajcn/69.3.373. [DOI] [PubMed] [Google Scholar]
  180. Hayes L, Pearce MS, Unwin NC. Lifecourse predictors of normal metabolic parameters in overweight and obese adults. Int J Obes. 2006;30:970–976. doi: 10.1038/sj.ijo.0803213. [DOI] [PubMed] [Google Scholar]
  181. McAuley PA, Sui X, Church TS, Hardin JW, Myers JN, Blair SN. The joint effects of cardiorespiratory fitness and adiposity on mortality risk in men with hypertension. Am J Hypertens. 2009;22:1062–1069. doi: 10.1038/ajh.2009.122. [DOI] [PubMed] [Google Scholar]
  182. Lee S, Kuk J, Katzmarzyk P, Blair S, Church T, Ross R. Cardiorespiratory fitness attenuates metabolic risk independent of abdominal subcutaneous and visceral fat in men. Diabetes Care. 2005;28:895–901. doi: 10.2337/diacare.28.4.895. [DOI] [PubMed] [Google Scholar]
  183. Lee D, Sui X, Artero EG, et al. Long-term effects of changes in cardiorespiratory fitness and body mass index on all-cause and cardiovascular disease mortality in men: the Aerobics Center Longitudinal Study. Circulation. 2011;124:2483–2490. doi: 10.1161/CIRCULATIONAHA.111.038422. [DOI] [PMC free article] [PubMed] [Google Scholar]
  184. Lee D-C, Sui X, Church TS, Lavie CJ, Jackson AS, Blair SN. Changes in fitness and fatness on the development of cardiovascular disease risk factors hypertension, metabolic syndrome, and hypercholesterolemia. J Am Coll Cardiol. 2012;59:665–672. doi: 10.1016/j.jacc.2011.11.013. [DOI] [PMC free article] [PubMed] [Google Scholar]
  185. Stevens J, Cai J, Evenson K, Thomas R. Fitness and fatness as predictors of mortality from all causes and from cardiovascular disease in men and women in the Lipid Research Clinics Study. Am J Epidemiol. 2002;156:832–841. doi: 10.1093/aje/kwf114. [DOI] [PubMed] [Google Scholar]
  186. Hu FB, Willett WC, Li T, Stampfer MJ, Colditz GA, Manson JE. Adiposity as compared with physical activity in predicting mortality among women. N Engl J Med. 2004;351:2694–2703. doi: 10.1056/NEJMoa042135. [DOI] [PubMed] [Google Scholar]
  187. Barry VW, Baruth M, Beets MW, Durstine JL, Liu J, Blair SN. Fitness vs. fatness on all-cause mortality: a meta-analysis. Prog Cardiovasc Dis. 2014;56:382–390. doi: 10.1016/j.pcad.2013.09.002. [DOI] [PubMed] [Google Scholar]
  188. Fogelholm M. Physical activity, fitness and fatness: relations to mortality, morbidity and disease risk factors. A systematic review. Obes Rev. 2010;11:202–221. doi: 10.1111/j.1467-789X.2009.00653.x. [DOI] [PubMed] [Google Scholar]
  189. Thompson PD, Crouse SF, Goodpaster B, Kelley D, Moyna N, Pescatello L. The acute versus the chronic response to exercise. Med Sci Sports Exerc. 2001;33(6 Suppl):S438–S445. doi: 10.1097/00005768-200106001-00012. discussion S452–3. [DOI] [PubMed] [Google Scholar]
  190. Lee S, Kuk JL, Davidson LE, et al. Exercise without weight loss is an effective strategy for obesity reduction in obese individuals with and without Type 2 diabetes. J Appl Physiol. 2005;99:1220–1225. doi: 10.1152/japplphysiol.00053.2005. [DOI] [PubMed] [Google Scholar]
  191. Ross R, Dagnone D, Jones P, et al. Reduction in obesity and related comorbid conditions after diet-induced weight loss or exercise-induced weight loss in men: randomized, controlled trial. Ann Intern Med. 2000;133:92–103. doi: 10.7326/0003-4819-133-2-200007180-00008. [DOI] [PubMed] [Google Scholar]
  192. Ross R, Janssen I, Dawson J, et al. Exercise-induced reduction in obesity and insulin resistance in women: a randomized controlled trial. Obes Res. 2004;12:789–798. doi: 10.1038/oby.2004.95. [DOI] [PubMed] [Google Scholar]
  193. Giannopoulou I, Ploutz-Snyder LL, Carhart R, et al. Exercise is required for visceral fat loss in postmenopausal women with type 2 diabetes. J Clin Endocrinol Metab. 2005;90:1511–1518. doi: 10.1210/jc.2004-1782. [DOI] [PubMed] [Google Scholar]
  194. Gan SK, Kriketos AD, Ellis BA, Thompson CH, Kraegen EW, Chisholm DJ. Changes in aerobic capacity and visceral fat but not myocyte lipid levels predict increased insulin action after exercise in overweight and obese men. Diabetes Care. 2003;26:1706–1713. doi: 10.2337/diacare.26.6.1706. [DOI] [PubMed] [Google Scholar]
  195. Johnson NA, Sachinwalla T, Walton DW, et al. Aerobic exercise training reduces hepatic and visceral lipids in obese individuals without weight loss. Hepatology. 2009;50:1105–1112. doi: 10.1002/hep.23129. [DOI] [PubMed] [Google Scholar]
  196. Järvi AE, Karlström BE, Granfeldt YE, Björck IE, Asp NG, Vessby BO. Improved glycemic control and lipid profile and normalized fibrinolytic activity on a low-glycemic index diet in type 2 diabetic patients. Diabetes Care. 1999;22:10–18. doi: 10.2337/diacare.22.1.10. [DOI] [PubMed] [Google Scholar]
  197. Westerbacka J, Lammi K, Häkkinen A-M, et al. Dietary fat content modifies liver fat in overweight nondiabetic subjects. J Clin Endocrinol Metab. 2005;90:2804–2809. doi: 10.1210/jc.2004-1983. [DOI] [PubMed] [Google Scholar]
  198. Bachmann OP, Dahl DB, Brechtel K, et al. Effects of intravenous and dietary lipid challenge on intramyocellular lipid content and the relation with insulin sensitivity in humans. Diabetes. 2001;50:2579–2584. doi: 10.2337/diabetes.50.11.2579. [DOI] [PubMed] [Google Scholar]
  199. Aron-Wisnewsky J, Clement K. The effects of gastrointestinal surgery on gut microbiota: potential contribution to improved insulin sensitivity. Curr Atheroscler Rep. 2014;16:454. doi: 10.1007/s11883-014-0454-9. [DOI] [PubMed] [Google Scholar]
  200. Laferrère B, Teixeira J, McGinty J, et al. Effect of weight loss by gastric bypass surgery versus hypocaloric diet on glucose and incretin levels in patients with type 2 diabetes. J Clin Endocrinol Metab. 2008;93:2479–2485. doi: 10.1210/jc.2007-2851. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Obesity Reviews are provided here courtesy of Wiley

RESOURCES