Metabolically healthy obesity: different prevalences using different criteria

Velho, S.; Paccaud, Fred; Waeber, Gérard; Vollenweider, Péter; Marques‐Vidal, Pedro

doi:10.1038/ejcn.2010.114

Cited by 218 publications

(221 citation statements)

References 36 publications

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“…The lack of consensus criteria to define MHO does not allow the accurate estimation of the prevalence of the MHO and MAO phenotypes, making the comparison between different studies difficult (4,7). In this sense, the reported prevalence of MHO varies widely, ranging from 3 to 57% of obese patients, depending on the method used to define this condition (5,(8)(9)(10).…”

Section: Resultsmentioning

confidence: 99%

Increased Cardiometabolic Risk Factors and Inflammation in Adipose Tissue in Obese Subjects Classified as Metabolically Healthy

et al. 2014

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OBJECTIVEIt has been suggested that individuals with the condition known as metabolically healthy obesity (MHO) may not have the same increased risk for the development of metabolic abnormalities as their non-metabolically healthy counterparts. However, the validity of this concept has recently been challenged, since it may not translate into lower morbidity and mortality. The aim of the current study was to compare the cardiometabolic/inflammatory profile and the prevalence of impaired glucose tolerance (IGT) and type 2 diabetes (T2D) in patients categorized as having MHO or metabolically abnormal obesity (MAO). RESEARCH DESIGN AND METHODSWe performed a cross-sectional analysis to compare the cardiometabolic/inflammatory profile of 222 MHO and 222 MAO patients (62% women) matched by age, including 255 lean subjects as reference (cohort 1). In a second cohort, we analyzed the adipokine profile and the expression of genes involved in inflammation and extracellular matrix remodeling in visceral adipose tissue (VAT; n = 82) and liver (n = 55). RESULTSThe cardiometabolic and inflammatory profiles (CRP, fibrinogen, uric acid, leukocyte count, and hepatic enzymes) were similarly increased in MHO and MAO in both cohorts. Moreover, above 30% of patients classified as MHO according to fasting plasma glucose exhibited IGT or T2D. The profile of classic (leptin, adiponectin, resistin) as well as novel (serum amyloid A and matrix metallopeptidase 9) adipokines was almost identical in MHO and MAO groups in cohort 2. Expression of genes involved in inflammation and tissue remodeling in VAT and liver showed a similar alteration pattern in MHO and MAO individuals. CONCLUSIONSThe current study provides evidence for the existence of a comparable adverse cardiometabolic profile in MHO and MAO patients; thus the MHO concept should be applied with caution. A better identification of the obesity phenotypes and a more precise diagnosis are needed for improving the management of obese individuals.

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Section: Resultsmentioning

confidence: 99%

Increased Cardiometabolic Risk Factors and Inflammation in Adipose Tissue in Obese Subjects Classified as Metabolically Healthy

et al. 2014

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“…For instance, we have previously demonstrated that only 5% of all obese subjects were considered as MHO by all six definitions used (Velho et al, 2010). As no consensus exists regarding the definition of MHO, it is thus understandable that the conclusions of the statistical analyses are also not unequivocal.…”

Section: Discussionmentioning

confidence: 96%

“…Determination of the prevalence of metabolically healthy obese individuals The diagnosis of MHO was obtained based on a BMIX30 kg/m 2 and six different sets of cardiometabolic abnormalities (Karelis et al, 2004;Meigs et al, 2006;AguilarSalinas et al, 2008;Wildman et al, 2008;Lynch et al, 2009), as described in a previous paper (Velho et al, 2010). As one definition of MHO includes CRP levels (Wildman et al, 2008), analysis of CRP levels was not performed for this definition.…”

Section: Biological Datamentioning

confidence: 99%

“…Several authors have suggested that metabolically healthy obesity (MHO) subjects present with lower inflammation levels (Karelis et al, 2005;Shin et al, 2006;Koster et al, 2010) and that this lower level contributes to their favourable metabolic profile. Still, there is currently no standard definition of MHO, and we have previously shown that the use of different diagnostic criteria for MHO leads to a considerable difference in prevalence levels (Velho et al, 2010). Further, some MHO definition criteria consider inflammatory markers (Wildman et al, 2008), thereby biasing the relationship between MHO and inflammation.…”

Section: Introductionmentioning

confidence: 99%

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The association between inflammatory biomarkers and metabolically healthy obesity depends of the definition used

et al. 2011

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Background/Objectives: To assess the distribution of interleukin (IL)-1b, IL-6, tumour necrosis factor (TNF)-a and C-reactive protein (CRP) according to the different definitions of metabolically healthy obesity (MHO). Subjects/Methods: A total of 881 obese (body mass index (BMI) X30 kg/m 2 ) subjects derived from the population-based CoLaus Study participated in this study. MHO was defined using six sets of criteria including different combinations of waist, blood pressure, total high-density lipoprotein cholesterol or low-density lipoprotein -cholesterol, triglycerides, fasting glucose, homeostasis model, high-sensitivity CRP, and personal history of cardiovascular, respiratory or metabolic diseases. IL-1b, IL-6 and TNF-a were assessed by multiplexed flow cytometric assay. CRP was assessed by immunoassay. Results: On bivariate analysis some, but not all, definitions of MHO led to significantly lower levels of IL-6, TNF-a and CRP compared with non-MH obese subjects. Most of these differences became nonsignificant after multivariate analysis. An posteriori analysis showed a statistical power between 9 and 79%, depending on the inflammatory biomarker and MHO definition considered. Further increasing sample size to overweight þ obese individuals (BMIX25 kg/m 2 , n ¼ 2917) showed metabolically healthy status to be significantly associated with lower levels of CRP, while no association was found for IL-1b. Significantly lower IL-6 and TNF-a levels were also found with some but not all MHO definitions, the differences in IL-6 becoming nonsignificant after adjusting for abdominal obesity or percent body fat. Conclusions: MHO individuals present with decreased levels of CRP and, depending on MHO definition, also with decreased levels in IL-6 and TNF-a. Conversely, no association with IL-1b levels was found.

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“…For example, Pima Indians, who have the highest prevalence of reported obesity in the world, have a low prevalence of hypertension [47]. To summarise, the genetic pleiotropic associations may in part explain why some obese individuals remain metabolically healthy despite having excessive accumulation of body fat [48][49][50][51][52][53]. This phenomenon is described in the current literature as 'healthy obesity' and, to date, little is known about the factors that protect obese individuals from metabolic disturbances [54].…”

Section: Discussionmentioning

confidence: 99%

Pleiotropic effects of obesity-susceptibility loci on metabolic traits: a meta-analysis of up to 37,874 individuals

et al. 2013

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Aims/hypothesis Genetic pleiotropy may contribute to the clustering of obesity and metabolic conditions. We assessed whether genetic variants that are robustly associated with BMI and waist-to-hip ratio (WHR) also influence metabolic and cardiovascular traits, independently of obesity-related traits, in meta-analyses of up to 37,874 individuals from six European population-based studies. Methods We examined associations of 32 BMI and 14 WHR loci, individually and combined in two genetic predisposition scores (GPSs), with glycaemic traits, blood lipids and BP, with and without adjusting for BMI and/or WHR. Results We observed significant associations of BMIincreasing alleles at five BMI loci with lower levels of 2 h glucose (RBJ [also known as DNAJC27], QPTCL: effect sizes −0.068 and −0.107 SD, respectively), HDL-cholesterol (SLC39A8: −0.065 SD, MTCH2: −0.039 SD), and diastolic BP (SLC39A8: −0.069 SD), and higher and lower levels of LDL-and total cholesterol (QPTCL: 0.041 and 0.042 SDs, respectively, FLJ35779 [also known as POC5]: −0.042 and −0.041 SDs, respectively) (all p<2.4×10 −4 ), independent of BMI. The WHR-increasing alleles at two WHR loci were significantly associated with higher proinsulin (GRB14: 0.069 SD) and lower fasting glucose levels (CPEB4: −0.049 SD), independent of BMI and WHR. A higher GPS-BMI was associated with lower systolic BP (−0.005 SD), diastolic BP (−0.006 SD) and 2 h glucose (−0.013 SD), while a higher GPS-WHR was associated with lower HDL-cholesterol Electronic supplementary material The online version of this article (doi:10.1007/s00125-013-2985-y) contains peer-reviewed but unedited supplementary material, which is available to authorised users. J. V. van Vliet-Ostaptchouk : M. M. van der Klauw :

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Metabolically healthy obesity: different prevalences using different criteria

Cited by 218 publications

References 36 publications

Increased Cardiometabolic Risk Factors and Inflammation in Adipose Tissue in Obese Subjects Classified as Metabolically Healthy

Increased Cardiometabolic Risk Factors and Inflammation in Adipose Tissue in Obese Subjects Classified as Metabolically Healthy

The association between inflammatory biomarkers and metabolically healthy obesity depends of the definition used

Pleiotropic effects of obesity-susceptibility loci on metabolic traits: a meta-analysis of up to 37,874 individuals

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