Obesity paradox in stroke - Myth or reality? A systematic review

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obesity 576 date (epub): 3/2017Publication date (collection): /2017AbstractBackground and purposeBoth stroke and obesity show an increasing incidence worldwide. While obesity is an established risk factor for stroke, its
obesity 630 /2017AbstractBackground and purposeBoth stroke and obesity show an increasing incidence worldwide. While obesity is an established risk factor for stroke, its influence on outcome in ischemic stroke is less clear.
obesity 814 ischemic stroke is less clear. Many studies suggest a better prognosis in obese patients after stroke (“ obesity paradox”). This review aims at assessing the clinical outcomes of obese patients after stroke by performing
obesity 1772 were observed in major part of studies (observational study design, inaccuracy of BMI in reflecting obesity , lacking body weight measurement, selection bias, survival bias).ConclusionMost observational data indicate
obesity 1989 survival benefit of obese patients after stroke, but a number of methodological concerns exist. No obesity paradox was observed in patients after IVT. There is a need for well-designed randomized controlled
obesity 3243 adults (31.3%) were overweight and more than 700 million (9.6%) were obese by 2015. Keeping in mind that obesity is an independent predictor of ischemic stroke and especially affects younger patients, obese patients
obesity 3707 participants to address the relationship between excess body weight and stroke incidence.[[1]] Overweight and obesity were significantly associated with progressively increasing risk of ischemic stroke.[[1]] It has been
obesity 5087 or advanced cancers.[[9]–[14]] The decreased mortality rate in obese patients is also termed as “ obesity paradox” in the literature.[[15]–[17]]While obesity is an established risk factor for stroke, its
obesity 5143 rate in obese patients is also termed as “obesity paradox” in the literature.[[15]–[17]]While obesity is an established risk factor for stroke, its influence on clinical outcome, mortality, and thrombolysis
obesity 5315 clinical outcome, mortality, and thrombolysis in acute ischemic stroke is still under debate. Since both obesity and stroke are major public health issues, it is important to fully understand the association between
obesity 5567 review aims at assessing the clinical outcome of obese patients after stroke. In addition, the impact of obesity on acute stroke treatment by thrombolysis will be discussed by using a thorough literature search.Search
obesity 5816 unlimited PubMed search (MEDLINE) was performed on December 6, 2015, using the MeSH terms: stroke AND obesity OR overweight AND outcome OR mortality, the last two mentioned in title or abstract. This search was
obesity 5998 abstract. This search was combined with two further searches: first using the MeSH term stroke AND obesity paradox, and second using the MeSH terms stroke AND obesity AND thrombolysis, the latter mentioned in
obesity 6058 searches: first using the MeSH term stroke AND obesity paradox, and second using the MeSH terms stroke AND obesity AND thrombolysis, the latter mentioned in title and abstract. In addition, we screened reference lists
obesity 6282 retrieved reports for further publications. Studies were included if they investigated the association of obesity with outcome and mortality after stroke in humans or outcome after intravenous thrombolysis (IVT) with
obesity 6521 Only papers written in English were considered. We excluded studies investigating the association of obesity with outcome and mortality in other diseases than stroke (i.e. cardiovascular diseases, diabetes or
obesity 7027 outcome measures were functional status expressed by modified Rankin Scale (mRS) and mortality. For obesity measures, we adopted the following BMI threshold categories from WHO: < 18.5 kg/m2 for underweight,
obesity 7231 underweight, 18.5 to 24.9 kg/m2 for normal weight, 25.0 to 29.9 kg/m2 for overweight, and ≥ 30.0 kg/m2 for obesity . In many studies investigating the Asian population, BMI thresholds were adapted according to WPRO (WHO
obesity 7538 underweight, 18.5 to 22.9 kg/m2 for normal weight, 23.0 to 24.9 kg/m2 for overweight, and ≥ 25.0 kg/m2 for obesity . We followed the PRISMA guidelines for this systematic review (S1 File).ResultsWe identified 183 unique
obesity 8654 rehabilitation and hospital discharge outcomes.[[28],[29],[31],[32],[34],[36]] One study used central obesity as measurement and investigated the prognostic performance of waist-to-height ratio on mortality after
obesity 10830 patients with ischemic stroke and reported an independent association between mortality and severe obesity at 3 months (OR 2.01, 95% CI 1.12–1.38).[[26]] In this study, overweight and obese patients had similar
obesity 12770 survivors to be more likely overweight or obese.[[19]] Furthermore, they found an age-dependent effect of obesity on post-stroke mortality: the association of higher BMI with mortality risk was strongest in younger
obesity 13145 authors concluded that younger stroke patients would especially benefit from vigorous efforts to prevent obesity .[[19]] Bell et al. reported similar results with lower poststroke mortality in overweight and obese
obesity 14054 in overweight or obese patients.[[23]]The research group of Olsen and colleagues, who first reported obesity paradox in stroke patients,[[18]] investigated in a subsequent study the relationship between BMI and
obesity 16099 the occurrence of hemorrhagic transformation with increasing BMI.[[31]] As compared to normal weight, obesity was independently associated with lower risk of hemorrhagic transformation after acute ischemic stroke
obesity 17584 lean, overweight and obese patients after adjusting for confounders.[[29]] However, overweight and obesity were significantly associated with lower risk of major vascular events (recurrent stroke, myocardial
obesity 20076 discharge destination, and mortality. We could not identify studies assessing the relationship between obesity and stroke outcome after intra-arterial thrombolysis or mechanical thrombectomy.Sarikaya et al. were
obesity 20674 intracranial hemorrhages were comparable in both groups.[[41]] Furthermore, multivariate analyses identified obesity as an independent predictor of unfavorable clinical outcome and mortality after IVT.[[41]] In a subsequent
obesity 23221 remained statistically significant after adjusting for confounding risk factors. These results hint to an obesity paradox in stroke in terms of higher survival rates and better functional outcome in stroke patients
obesity 23358 higher survival rates and better functional outcome in stroke patients with excess body weight. No obesity paradox was observed for acute stroke patients treated with IVT, whereas no data were available for
obesity 23545 data were available for intra-arterial thrombolysis or mechanical thrombectomy.The association between obesity and favorable outcome after stroke was strong and consistent in many studies. The findings are in analogy
obesity 24203 Furthermore, there is neither a biologically graded nor a linear relationship between the degree of obesity and risk of mortality. Thus, mortality was lowest rather in overweight patients and significantly higher
obesity 24609 Therefore, the results do not allow the conclusion “the fatter, the better”. Another explanation for “ obesity paradox” in stroke may be that time of follow-up in cited studies (range 1 week to 11.5 years, median
obesity 24779 studies (range 1 week to 11.5 years, median 30 months) was too short to detect detrimental effects of obesity . In comparison, harmful impact of obesity on cardiovascular outcomes in Framingham-Study was evident
obesity 24821 30 months) was too short to detect detrimental effects of obesity. In comparison, harmful impact of obesity on cardiovascular outcomes in Framingham-Study was evident after a follow-up period of 8 years in men
obesity 26919 prognostic factors for favorable outcome after stroke. Ryu et al. criticized that many studies reporting obesity paradox did not adjust for stroke severity.[[23]] They observed an inverse relationship between BMI
obesity 27289 assumed to be a mediator between levels of BMI and poststroke mortality, contradicting the existence of obesity paradox. [[23]] Similar findings were also reported by Kim and colleagues: the initially observed association
obesity 27792 presentation and allowing prevention measurements in an early stage. Treatment bias may be another cause of obesity paradox as it has been shown that physicians treat obese patients more aggressively than lean patients
obesity 28149 though comparable risk profile.[[50]]A further methodological limitation concerns the measurement of obesity . Although BMI was the most commonly used tool for this purpose, its diagnostic accuracy is highly questionable.[[51]]
obesity 28455 analysis, BMI ≥ 30 kg/m2 had a high specificity of 96%, but a poor sensitivity of 43% in assessment of obesity . Consequently, half of the obese participants were missed for identification. Moreover, body mass index
obesity 28873 alternative tools such as waist-to-hip ratio or waist circumference to be more precise in the measurement of obesity . Of note, obesity paradox was no more existent when BMI was replaced by waist-to-hip ratio.[[52]]The
obesity 28891 waist-to-hip ratio or waist circumference to be more precise in the measurement of obesity. Of note, obesity paradox was no more existent when BMI was replaced by waist-to-hip ratio.[[52]]The obesity paradox could
obesity 28982 Of note, obesity paradox was no more existent when BMI was replaced by waist-to-hip ratio.[[52]]The obesity paradox could also be a result of statistical distortion due to a survival bias. Olsen et al. first
obesity 29102 could also be a result of statistical distortion due to a survival bias. Olsen et al. first reported an obesity paradox in stroke patients, but questioned their observation in a second survey later on and discussed
obesity 30445 overweight, obese, and normal-weight patients.[[27]] Furthermore, publication bias may be another reason for obesity paradox. The majority of studies were retrospective and therefore differences in data quality may also
obesity 30635 data quality may also distort the results. This could partially explain the findings in IVT (lack of obesity paradox), where data are collected prospectively and data quality is suspected to be higher than in
obesity 30967 stroke were probably excluded due to lack of body weight measurement.From a biological point of view, obesity paradox could be explained by potentially protective effects of adipose tissue, which is now increasingly
obesity 31499 inflammatory cytokines.[[9]] Both mechanisms may impede the poststroke pro-inflammatory state.[[9]]Data on obesity and its impact on clinical outcome after IVT are rather limited and incongruent. Whereas some studies
obesity 32098 activator inhibitor-1 which seems to be overexpressed in adipose tissue.[[54],[55]] In general, no obesity paradox was observed for patients treated with IVT. Moreover, the risk for sICH and probability for
obesity 33726 (secondary prevention) with respect to longer life expectancy and detrimental cardiovascular effects of obesity over years. No obesity paradox was observed in patients after IVT, thus there is no need to change the
obesity 33749 respect to longer life expectancy and detrimental cardiovascular effects of obesity over years. No obesity paradox was observed in patients after IVT, thus there is no need to change the current dosage scheme
obesity 34272 prospective and account for methodological limitations of the former studies (inaccuracy of BMI in measuring obesity , false estimation of body weight, lacking adjustment for comorbidities).Supporting informationS1 FigStudy

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