Journal List > Cardiovasc Prev Pharmacother > v.3(4) > 1516079373

Cho, Rhee, and Lee: Body Weight Change and Cardiovascular Disease: Effect of Weight Gain, Weight Loss, and Weight Cycling

Abstract

Obesity is an independent risk factor for the development and progression of cardiovascular disease (CVD). Various cardiovascular outcomes are related to the association between body weight change and CVD. Metabolically healthy obese individuals could have a better prognosis in terms of cardiovascular morbidity and mortality than metabolically unhealthy obese individuals. Smoking cessation causes significant weight gain and consequent deterioration of the metabolic profile despite not impairing the cardiovascular benefits. Intentional weight loss has a consistent cardiovascular protective effect, but unintentional weight loss due to progressive catabolism and loss of muscle mass could be associated with poor cardiovascular outcomes. Obese individuals who are successful in losing weight with subsequent regain (weight cycling) could have an unfavorable cardiometabolic profile and the risk of CVD. Further studies are needed to evaluate the impact of weight changes on CVD by identifying unknown pathophysiology and to decide appropriate management and interventions for various phenotypes of weight change.

INTRODUCTION

Obesity is defined as abnormal accumulation of excess fat following the intake of energy nutrients, which exceeds the amount of used energy. The prevalence of obesity is continuously increasing, leading to a global pandemic and this prevalence has also been accelerating in Asia.1) Obesity is an independent risk factor for the development and progression of cardiovascular disease (CVD) including myocardial infarction, heart failure, stroke, thromboembolic disease, and peripheral arterial disease.2) Obesity is related to conventional risk factors of CVD such as hypertension, hyperlipidemia, and diabetes. Moreover, it increases insulin resistance and induces pro-coagulation, hypofibrinolysis, and oxidative stress through the action of inflammatory cytokines including adipokines that cause endothelial dysfunction and contribute to CVD.3)
Various cardiovascular outcomes are related to the association between body weight change and CVD. Metabolically healthy obese (MHO) individuals exhibit different body fat distribution and cardiovascular outcomes when compared with metabolically unhealthy obese (MUO) individuals.4) In addition, weight gain and consequent metabolic changes after smoking cessation (SC) are different from those associated with simple obesity.5) Unintentional loss of weight that is not due to lifestyle modifications is common among older adults and could be associated with poor cardiovascular outcomes.6) Failure to maintain a healthy weight and fluctuations in weight (commonly referred to as weight cycling) put a strain on the cardiometabolic system.7) Therefore, we aimed to review the pathophysiological mechanisms and clinical significance of weight change and its relationship with cardiovascular outcomes.

WEIGHT GAIN

Metabolically healthy vs. unhealthy obesity

Fat accumulation is heterogeneous. Subcutaneous and visceral adipose tissues differ in terms of blood flow and innervation, cell composition, and metabolic and endocrine functions.8) Unlike peripheral subcutaneous fat, visceral fat is mainly associated with the exacerbation of metabolic profiles.9)10) Regardless of the body mass index (BMI) or absolute fat volumes, a high visceral/subcutaneous adipose tissue ratio significantly worsens cardiometabolic risk and increases the possibility of subsequent CVD events.11)12) Moreover, fatty liver is associated with coronary artery calcification independent of the BMI and visceral fat.13) Thus, the risk of metabolic diseases and CVD could differ according to the phenotype of obesity, even with similar amount of weight gain. Although there is no established definition, absence of insulin resistance and metabolic disease in obese individuals is referred to as the MHO phenotype.4) In a prospective epidemiological study involving adult Caucasians, MHO individuals exhibited better fitness and better prognosis in terms of CVD mortality and morbidity than MUO individuals.14) In a meta-analysis by Kramer et al.,15) the risk of CVD was relatively lower in MHO subjects than in MUO subjects, but the risk significantly increased when compared with metabolically healthy normal-weight individuals even in the absence of metabolic abnormalities. The conversion from MHO to MUO phenotype over time has been commonly identified and is associated with an increase in the CVD risk in several studies.16)17) Therefore, MHO phenotype should not be considered a harmless condition. Further research should define MHO and evaluate its effects on CVD.

Weight gain after SC

Smoking is a modifiable risk factor for CVD and there is strong evidence suggesting the immediate benefits of SC.18) However, SC causes significant weight gain. In a meta-analysis combining 62 studies, a weight gain of approximately 4–5 kg was observed after 1 year of SC.19) Nicotine deficiency and subsequent changes in appetite and energy metabolism induced by SC lead to weight gain.5) Studies have demonstrated an increase in visceral fat and deterioration of metabolic profile characterized by elevated blood pressure and cholesterol, elevated fasting blood glucose, and insulin resistance after SC.20-22) Nevertheless, recent studies have demonstrated that weight gain and consequent worsening of metabolic profile after SC do not impair the protective benefit of SC regarding the development and prognosis of CVD.23-26)
The fear of weight gain could be associated with failure to start SC, not receiving treatment, and even relapse after SC.27)28) Some researchers have suggested that vigorous exercise combined with cognitive-behavioral therapy or medications could resolve this condition.29)30) However, there is a lack of sufficient evidence to recommend specific clinical methods for preventing weight gain after SC.31) Therefore, SC should be encouraged to lower the risk of CVD and future studies should focus on finding an appropriate intervention for weight gain and subsequent metabolic and cosmetic problems caused by SC.

WEIGHT LOSS

Intentional vs. unintentional weight loss (IWL vs. UWL)

Achieving weight loss through lifestyle modifications, bariatric surgery, or the use of drugs such as glucagon-like peptide-1 agonists in obese individuals can improve cardiometabolic conditions.32-34) IWL not only improves the metabolic profile but also improves the structure and function of the left ventricle directly or indirectly, contributing to the prevention of CVD.2) The importance of intensive lifestyle intervention through caloric restriction and exercise was strongly recognized in the Diabetes Prevention Program trial.35) Studies regarding the effectiveness of IWL in preventing CVD have demonstrated consistent cardiovascular benefits.36)37) However, some studies wherein the intention of weight loss was not identified have suggested that weight loss could be a warning sign of cardiovascular events.38)39) UWL caused by organic diseases such as malignancies, psychocognitive disorders, or unknown causes could be associated with morbidity and mortality.6) The pathophysiology of UWL is currently unknown, but it could be assumed that weight maintenance is impaired by alterations in the balance of energy intake, absorption, utilization, and loss.40) Compared to IWL, UWL was associated with older age, poorer health status, smoking, and lower BMI.41) Even after adjusting for these confounding factors, UWL was independently and significantly associated with the incidence of CVD and associated mortality.42)43) However, a meta-analysis involving 178,644 participants revealed that UWL did not show a protective effect against major adverse cardiovascular events even in overweight or obese participants.44)

Obesity paradox and sarcopenia

The concept of “obesity paradox” and CVD outcome, first introduced by Gruberg et al.,45) could be explained by the negative effect of UWL on the risk of CVD. The outcome of various CVDs including chronic heart failure showed a better “U-shaped” or “J-shaped” relationship in overweight to mildly obese individuals when compared with lean ones.46) In addition to the differences in regional fat distribution,8) the differences in molecular phenotyping of adipose tissue in this “low-risk” obesity, which is metabolically benign and protects against the risk of CVD, are in terms of following factors: secretomic profile, cell turnover and expansion, extracellular matrix fibrosis, angiogenesis, inflammation, and adipocyte browning.47) In addition, fitness is more important than “fatness” and it notably alters the relationship between obesity and CVD outcomes.48) Substantial evidence suggests that fitness is a critical component of obesity paradox and it significantly affects the major cardiovascular outcomes.14)49)50)
Sarcopenia is defined as involuntary weight loss with key characteristics of loss of muscle mass and weakening of muscle strength, resulting in poor physical performance.51) In a study involving elderly Korean individuals aged over 65 years, sarcopenia was confirmed via the loss of skeletal muscle mass on dual-energy X-ray absorptiometry in approximately 30% of the subjects and it was associated with the presence of CVD.52) Frailty (UWL with low levels of physical activity or illness) in the elderly individuals independently increases the risk of CVD and worsens the prognosis.53)54) The common factor between the obesity paradox and sarcopenia is a phenomenon that can be interpreted as a progressive catabolic state, loss of lean mass, and subsequent lack of fitness. With a progress in future research to clearly understand the pathophysiology of UWL, we should identify the intentionality and manage the causes of weight loss, bearing in mind that the risk of CVD could increase in people with loss of muscle mass and fitness, especially in elderly individuals.

Weight cycling

It is necessary to maintain a healthy weight in overweight or obese individuals who have achieved a healthy weight goal through intensive lifestyle intervention. However, weight regain is an important issue for those who were successful in losing weight. Weight cycling, the concept of failure to maintain a healthy weight, has a negative influence on the cardiometabolic system through increased cardiac load, glomerular damage, vascular injuries, and worsening insulin resistance (Figure 1).7) Weight cycling was related to increasing T-cell accumulation in the adipose tissue and impaired systemic glucose tolerance in an in vivo study.55) In the Look AHEAD study to understand the effect of weight regain, partial or full weight recovery was identified in the majority of the overweight and obese participants who achieved IWL of ≥3% of their initial weight.56) Furthermore, in a subsequent study by Berger et al.,57) cardiometabolic parameters that improved with weight loss deteriorated with weight regain among the participants of the Look AHEAD trial. Similar association with the deterioration of metabolic profile was consistently observed in other studies.58)59) The phenomenon of accelerated fat recovery after weight loss (catch-up fat) could explain the associations with abdominal obesity and metabolic diseases.60) The beneficial effects of cardiac structure and function achieved by weight loss are partially lost after weight is regained.61) Studies that confirmed the association of weight cycling with CVD outcomes mainly demonstrated its independent association with unfavorable CVD prevalence and prognosis.62-64) However, some researchers have argued that there was sparse evidence regarding the adverse effects of weight cycling on cardiometabolic risk and mortality.65)66)

CONCLUSION

Advancing from the past concept that emphasized only the increasing CVD risk of simple obesity and the protective effect of weight loss, a wide variety of CVD outcomes could be derived according to weight cycling as well as according to the various phenotypes of weight gain and weight loss. We suggest that it is important to evaluate not only the CVD risk with simple weight gain or BMI gain but also the causes of weight change and complementary health factors such as lean body mass and fitness. The definition of each phenotype of weight change and its categories have not been established definitively. Moreover, the pathophysiological aspects that cannot be explained by the current hypothesis remain a topic of further research. Therefore, future studies should focus on evaluating the impact of weight change on CVD by identifying unknown pathophysiology and formulating appropriate management and intervention strategies for the various phenotypes of weight change.

Notes

Conflict of Interest

The authors have no financial conflicts of interest.

Author Contributions

Supervision: Lee WY; Writing - original draft: Cho JH; Writing - review & editing: Rhee EJ, Lee WY.

REFERENCES

1. NCD Risk Factor Collaboration (NCD-RisC). Worldwide trends in body-mass index, underweight, overweight, and obesity from 1975 to 2016: a pooled analysis of 2416 population-based measurement studies in 128·9 million children, adolescents, and adults. Lancet. 2017; 390:2627–42.
2. Poirier P, Giles TD, Bray GA, Hong Y, Stern JS, Pi-Sunyer FX, Eckel RH; American Heart Association; Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. 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 Activity, and Metabolism. Circulation. 2006; 113:898–918.
crossref
3. Van Gaal LF, Mertens IL, De Block CE. Mechanisms linking obesity with cardiovascular disease. Nature. 2006; 444:875–80.
crossref
4. Stefan N, Häring HU, Hu FB, Schulze MB. Metabolically healthy obesity: epidemiology, mechanisms, and clinical implications. Lancet Diabetes Endocrinol. 2013; 1:152–62.
crossref
5. Harris KK, Zopey M, Friedman TC. Metabolic effects of smoking cessation. Nat Rev Endocrinol. 2016; 12:299–308.
crossref
6. McMinn J, Steel C, Bowman A. Investigation and management of unintentional weight loss in older adults. BMJ. 2011; 342:d1732.
crossref
7. Lee SH, Kim MK, Rhee EJ. Effects of cardiovascular risk factor variability on health outcomes. Endocrinol Metab. 2020; 35:217–26.
crossref
8. Tchkonia T, Thomou T, Zhu Y, Karagiannides I, Pothoulakis C, Jensen MD, Kirkland JL. Mechanisms and metabolic implications of regional differences among fat depots. Cell Metab. 2013; 17:644–56.
crossref
9. Wajchenberg BL. Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome. Endocr Rev. 2000; 21:697–738.
crossref
10. Lee JJ, Pedley A, Hoffmann U, Massaro JM, Levy D, Long MT. Visceral and intrahepatic fat are associated with cardiometabolic risk factors above other ectopic fat depots: The Framingham Heart Study. Am J Med. 2018; 131:684–692. e12.
crossref
11. Kaess BM, Pedley A, Massaro JM, Murabito J, Hoffmann U, Fox CS. The ratio of visceral to subcutaneous fat, a metric of body fat distribution, is a unique correlate of cardiometabolic risk. Diabetologia. 2012; 55:2622–30.
crossref
12. Figueroa AL, Takx RA, MacNabb MH, Abdelbaky A, Lavender ZR, Kaplan RS, Truong QA, Lo J, Ghoshhajra BB, Grinspoon SK, Hoffmann U, Tawakol A. Relationship between measures of adiposity, arterial inflammation, and subsequent cardiovascular events. Circ Cardiovasc Imaging. 2016; 9:e004043.
crossref
13. Liu J, Musani SK, Bidulescu A, Carr JJ, Wilson JG, Taylor HA, Fox CS. Fatty liver, abdominal adipose tissue and atherosclerotic calcification in African Americans: the Jackson Heart Study. Atherosclerosis. 2012; 224:521–5.
crossref
14. Ortega FB, Lee DC, Katzmarzyk PT, Ruiz JR, Sui X, Church TS, Blair SN. The intriguing metabolically healthy but obese phenotype: cardiovascular prognosis and role of fitness. Eur Heart J. 2013; 34:389–97.
crossref
15. Kramer CK, Zinman B, Retnakaran R. Are metabolically healthy overweight and obesity benign conditions?: a systematic review and meta-analysis. Ann Intern Med. 2013; 159:758–69.
crossref
16. Mongraw-Chaffin M, Foster MC, Anderson CA, Burke GL, Haq N, Kalyani RR, Ouyang P, Sibley CT, Tracy R, Woodward M, Vaidya D. Metabolically healthy obesity, transition to metabolic syndrome, and cardiovascular risk. J Am Coll Cardiol. 2018; 71:1857–65.
crossref
17. Eckel N, Li Y, Kuxhaus O, Stefan N, Hu FB, Schulze MB. Transition from metabolic healthy to unhealthy phenotypes and association with cardiovascular disease risk across BMI categories in 90 257 women (the Nurses' Health Study): 30 year follow-up from a prospective cohort study. Lancet Diabetes Endocrinol. 2018; 6:714–24.
18. Ockene IS, Miller NH. Cigarette smoking, cardiovascular disease, and stroke: a statement for healthcare professionals from the American Heart Association. Circulation. 1997; 96:3243–7.
crossref
19. Aubin HJ, Farley A, Lycett D, Lahmek P, Aveyard P. Weight gain in smokers after quitting cigarettes: metaanalysis. BMJ. 2012; 345:e4439.
crossref
20. Matsushita Y, Nakagawa T, Yamamoto S, Takahashi Y, Noda M, Mizoue T. Associations of smoking cessation with visceral fat area and prevalence of metabolic syndrome in men: the Hitachi health study. Obesity (Silver Spring). 2011; 19:647–51.
crossref
21. Kim BJ, Kim BS, Sung KC, Kang JH, Lee MH, Park JR. Association of smoking status, weight change, and incident metabolic syndrome in men: a 3-year follow-up study. Diabetes Care. 2009; 32:1314–6.
crossref
22. Stadler M, Tomann L, Storka A, Wolzt M, Peric S, Bieglmayer C, Pacini G, Dickson SL, Brath H, Bech P, Prager R, Korbonits M. Effects of smoking cessation on β-cell function, insulin sensitivity, body weight, and appetite. Eur J Endocrinol. 2014; 170:219–7.
crossref
23. Clair C, Rigotti NA, Porneala B, Fox CS, D'Agostino RB, Pencina MJ, Meigs JB. Association of smoking cessation and weight change with cardiovascular disease among adults with and without diabetes. JAMA. 2013; 309:1014–21.
crossref
24. Kim K, Park SM, Lee K. Weight gain after smoking cessation does not modify its protective effect on myocardial infarction and stroke: evidence from a cohort study of men. Eur Heart J. 2018; 39:1523–31.
crossref
25. Hu Y, Zong G, Liu G, Wang M, Rosner B, Pan A, Willett WC, Manson JE, Hu FB, Sun Q. Smoking cessation, weight change, type 2 diabetes, and mortality. N Engl J Med. 2018; 379:623–32.
crossref
26. Cho JH, Kwon HM, Park SE, Jung JH, Han KD, Park YG, Kim YH, Rhee EJ, Lee WY. Protective effect of smoking cessation on subsequent myocardial infarction and ischemic stroke independent of weight gain: a nationwide cohort study. PLoS One. 2020; 15:e0235276.
crossref
27. Meyers AW, Klesges RC, Winders SE, Ward KD, Peterson BA, Eck LH. Are weight concerns predictive of smoking cessation? A prospective analysis. J Consult Clin Psychol. 1997; 65:448–52.
crossref
28. Pomerleau CS, Zucker AN, Stewart AJ. Characterizing concerns about post-cessation weight gain: results from a national survey of women smokers. Nicotine Tob Res. 2001; 3:51–60.
crossref
29. Marcus BH, Albrecht AE, King TK, Parisi AF, Pinto BM, Roberts M, Niaura RS, Abrams DB. The efficacy of exercise as an aid for smoking cessation in women: a randomized controlled trial. Arch Intern Med. 1999; 159:1229–34.
crossref
30. King AC, Cao D, O'Malley SS, Kranzler HR, Cai X, deWit H, Matthews AK, Stachoviak RJ. Effects of naltrexone on smoking cessation outcomes and weight gain in nicotine-dependent men and women. J Clin Psychopharmacol. 2012; 32:630–6.
crossref
31. Farley AC, Hajek P, Lycett D, Aveyard P. Interventions for preventing weight gain after smoking cessation. Cochrane Database Syst Rev. 2012; 1:CD006219.
crossref
32. Buchwald H, Avidor Y, Braunwald E, Jensen MD, Pories W, Fahrbach K, Schoelles K. Bariatric surgery: a systematic review and meta-analysis. JAMA. 2004; 292:1724–37.
crossref
33. Yamaoka K, Tango T. Effects of lifestyle modification on metabolic syndrome: a systematic review and meta-analysis. BMC Med. 2012; 10:138.
crossref
34. Wilding JP, Batterham RL, Calanna S, Davies M, Van Gaal LF, Lingvay I, McGowan BM, Rosenstock J, Tran MT, Wadden TA, Wharton S, Yokote K, Zeuthen N, Kushner RF; STEP 1 Study Group. Once-weekly semaglutide in adults with overweight or obesity. N Engl J Med. 2021; 384:989–1002.
crossref
35. Diabetes Prevention Program (DPP) Research Group. The Diabetes Prevention Program (DPP): description of lifestyle intervention. Diabetes Care. 2002; 25:2165–71.
36. Zomer E, Gurusamy K, Leach R, Trimmer C, Lobstein T, Morris S, James WP, Finer N. Interventions that cause weight loss and the impact on cardiovascular risk factors: a systematic review and meta-analysis. Obes Rev. 2016; 17:1001–11.
crossref
37. Gong Q, Zhang P, Wang J, Ma J, An Y, Chen Y, Zhang B, Feng X, Li H, Chen X, Cheng YJ, Gregg EW, Hu Y, Bennett PH, Li G; Da Qing Diabetes Prevention Study Group. Morbidity and mortality after lifestyle intervention for people with impaired glucose tolerance: 30-year results of the Da Qing Diabetes Prevention Outcome Study. Lancet Diabetes Endocrinol. 2019; 7:452–61.
crossref
38. Galanis DJ, Harris T, Sharp DS, Petrovitch H. Relative weight, weight change, and risk of coronary heart disease in the Honolulu Heart Program. Am J Epidemiol. 1998; 147:379–86.
crossref
39. Stevens J, Erber E, Truesdale KP, Wang CH, Cai J. Long- and short-term weight change and incident coronary heart disease and ischemic stroke: the Atherosclerosis Risk in Communities Study. Am J Epidemiol. 2013; 178:239–48.
crossref
40. Bouras EP, Lange SM, Scolapio JS. Rational approach to patients with unintentional weight loss. Mayo Clin Proc. 2001; 76:923–9.
crossref
41. Meltzer AA, Everhart JE. Unintentional weight loss in the United States. Am J Epidemiol. 1995; 142:1039–46.
crossref
42. Wannamethee SG, Shaper AG, Lennon L. Reasons for intentional weight loss, unintentional weight loss, and mortality in older men. Arch Intern Med. 2005; 165:1035–40.
crossref
43. Lee AK, Woodward M, Wang D, Ohkuma T, Warren B, Sharrett AR, Williams B, Marre M, Hamet P, Harrap S, Mcevoy JW, Chalmers J, Selvin E. The risks of cardiovascular disease and mortality following weight change in adults with diabetes: results from ADVANCE. J Clin Endocrinol Metab. 2020; 105:152–62.
crossref
44. De Stefani FD, Pietraroia PS, Fernandes-Silva MM, Faria-Neto J, Baena CP. Observational evidence for unintentional weight loss in all-cause mortality and major cardiovascular events: a systematic review and meta-analysis. Sci Rep. 2018; 8:15447.
crossref
45. Gruberg L, Weissman NJ, Waksman R, Fuchs S, Deible R, Pinnow EE, Ahmed LM, Kent KM, Pichard AD, Suddath WO, Satler LF, Lindsay J Jr. The impact of obesity on the short-term and long-term outcomes after percutaneous coronary intervention: the obesity paradox? J Am Coll Cardiol. 2002; 39:578–84.
46. Hainer V, Aldhoon-Hainerová I. Obesity paradox does exist. Diabetes Care. 2013; 36 Suppl 2:S276–81.
crossref
47. Antonopoulos AS, Tousoulis D. The molecular mechanisms of obesity paradox. Cardiovasc Res. 2017; 113:1074–86.
crossref
48. Lavie CJ, De Schutter A, Milani RV. Healthy obese versus unhealthy lean: the obesity paradox. Nat Rev Endocrinol. 2015; 11:55–62.
crossref
49. McAuley PA, Beavers KM. Contribution of cardiorespiratory fitness to the obesity paradox. Prog Cardiovasc Dis. 2014; 56:434–40.
crossref
50. Moholdt T, Lavie CJ, Nauman J. Sustained physical activity, not weight loss, associated with improved survival in coronary heart disease. J Am Coll Cardiol. 2018; 71:1094–101.
51. Cruz-Jentoft AJ, Bahat G, Bauer J, Boirie Y, Bruyère O, Cederholm T, Cooper C, Landi F, Rolland Y, Sayer AA, Schneider SM, Sieber CC, Topinkova E, Vandewoude M, Visser M, Zamboni M; Writing Group for the European Working Group on Sarcopenia in Older People 2 (EWGSOP2), and the Extended Group for EWGSOP2. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. 2019; 48:16–31.
crossref
52. Chin SO, Rhee SY, Chon S, Hwang YC, Jeong IK, Oh S, Ahn KJ, Chung HY, Woo JT, Kim SW, Kim JW, Kim YS, Ahn HY. Sarcopenia is independently associated with cardiovascular disease in older Korean adults: the Korea National Health and Nutrition Examination Survey (KNHANES) from 2009. PLoS One. 2013; 8:e60119.
crossref
53. Matsuzawa Y, Konishi M, Akiyama E, Suzuki H, Nakayama N, Kiyokuni M, Sumita S, Ebina T, Kosuge M, Hibi K, Tsukahara K, Iwahashi N, Endo M, Maejima N, Saka K, Hashiba K, Okada K, Taguri M, Morita S, Sugiyama S, Ogawa H, Sashika H, Umemura S, Kimura K. Association between gait speed as a measure of frailty and risk of cardiovascular events after myocardial infarction. J Am Coll Cardiol. 2013; 61:1964–72.
crossref
54. Sergi G, Veronese N, Fontana L, De Rui M, Bolzetta F, Zambon S, Corti MC, Baggio G, Toffanello ED, Crepaldi G, Perissinotto E, Manzato E. Pre-frailty and risk of cardiovascular disease in elderly men and women: the Pro.V.A. study. J Am Coll Cardiol. 2015; 65:976–83.
55. Anderson EK, Gutierrez DA, Kennedy A, Hasty AH. Weight cycling increases T-cell accumulation in adipose tissue and impairs systemic glucose tolerance. Diabetes. 2013; 62:3180–8.
crossref
56. Wing RR, Espeland MA, Clark JM, Hazuda HP, Knowler WC, Pownall HJ, Unick J, Wadden T, Wagenknecht L; Action for Health in Diabetes (Look AHEAD) Study Group. Association of weight loss maintenance and weight regain on 4-year changes in CVD risk factors: the Action for Health in Diabetes (Look AHEAD) Clinical Trial. Diabetes Care. 2016; 39:1345–55.
crossref
57. Berger SE, Huggins GS, McCaffery JM, Jacques PF, Lichtenstein AH. Change in cardiometabolic risk factors associated with magnitude of weight regain 3 years after a 1-year intensive lifestyle intervention in type 2 diabetes mellitus: The Look AHEAD Trial. J Am Heart Assoc. 2019; 8:e010951.
crossref
58. Olson MB, Kelsey SF, Bittner V, Reis SE, Reichek N, Handberg EM, Merz CN. Weight cycling and high-density lipoprotein cholesterol in women: evidence of an adverse effect: a report from the NHLBIsponsored WISE study. J Am Coll Cardiol. 2000; 36:1565–71.
59. Vergnaud AC, Bertrais S, Oppert JM, Maillard-Teyssier L, Galan P, Hercberg S, Czernichow S. Weight fluctuations and risk for metabolic syndrome in an adult cohort. Int J Obes. 2008; 32:315–21.
crossref
60. Dulloo AG, Jacquet J, Montani JP. Pathways from weight fluctuations to metabolic diseases: focus on maladaptive thermogenesis during catch-up fat. Int J Obes Relat Metab Disord. 2002; 26 Suppl 2:S46–57.
crossref
61. de las Fuentes L, Waggoner AD, Mohammed BS, Stein RI, Miller BV 3rd, Foster GD, Wyatt HR, Klein S, Davila-Roman VG. Effect of moderate diet-induced weight loss and weight regain on cardiovascular structure and function. J Am Coll Cardiol. 2009; 54:2376–81.
crossref
62. Lissner L, Odell PM, D'Agostino RB, Stokes J 3rd, Kreger BE, Belanger AJ, Brownell KD. Variability of body weight and health outcomes in the Framingham population. N Engl J Med. 1991; 324:1839–44.
crossref
63. French SA, Folsom AR, Jeffery RW, Zheng W, Mink PJ, Baxter JE. Weight variability and incident disease in older women: the Iowa Women's Health Study. Int J Obes Relat Metab Disord. 1997; 21:217–23.
crossref
64. Bangalore S, Fayyad R, Laskey R, DeMicco DA, Messerli FH, Waters DD. Body-weight fluctuations and outcomes in coronary disease. N Engl J Med. 2017; 376:1332–40.
crossref
65. Lee JS, Kawakubo K, Kobayashi Y, Mori K, Kasihara H, Tamura M. Effects of ten year body weight variability on cardiovascular risk factors in Japanese middle-aged men and women. Int J Obes Relat Metab Disord. 2001; 25:1063–7.
crossref
66. Mehta T, Smith DL Jr, Muhammad J, Casazza K. Impact of weight cycling on risk of morbidity and mortality. Obes Rev. 2014; 15:870–81.
crossref

Figure 1.
Mechanisms of weight cycling effects on cardiometabolic health outcomes.7)
GFR = glomerular filtration rate.
cpp-2021-3-e12f1.tif
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