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Do worse baseline risk factors explain the association of healthy obesity with increased mortality risk? Whitehall II Study.

ABSTRACT: OBJECTIVE:To describe 20-year risk factor trajectories according to initial weight/health status and investigate the extent to which baseline differences explain greater mortality among metabolically healthy obese (MHO) individuals than healthy non-obese individuals. METHODS:The sample comprised 6529 participants in the Whitehall II study who were measured serially between 1991-1994 and 2012-2013. Baseline weight (non-obese or obese; body mass index (BMI) ?30?kg/m2) and health status (healthy or unhealthy; two or more of hypertension, low high-density lipoprotein cholesterol (HDL-C), high triglycerides, high glucose, and high homeostatic model assessment of insulin resistance (HOMA-IR)) were defined. The relationships of baseline weight/health status with 20-year trajectories summarizing ~25,000 observations of systolic and diastolic blood pressures, HDL-C, triglycerides, glucose, and HOMA-IR were investigated using multilevel models. Relationships of baseline weight/health status with all-cause mortality up until July 2015 were investigated using Cox proportional hazards regression. RESULTS:Trajectories tended to be consistently worse for the MHO group compared to the healthy non-obese group (e.g., glucose by 0.21 (95% CI 0.09, 0.33; p?

SUBMITTER: Johnson W

PROVIDER: S-EPMC6268092 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Do worse baseline risk factors explain the association of healthy obesity with increased mortality risk? Whitehall II Study.

Johnson William W Bell Joshua A JA Robson Ellie E Norris Tom T Kivimäki Mika M Hamer Mark M

International journal of obesity (2005) 20180814 8

<h4>Objective</h4>To describe 20-year risk factor trajectories according to initial weight/health status and investigate the extent to which baseline differences explain greater mortality among metabolically healthy obese (MHO) individuals than healthy non-obese individuals.<h4>Methods</h4>The sample comprised 6529 participants in the Whitehall II study who were measured serially between 1991-1994 and 2012-2013. Baseline weight (non-obese or obese; body mass index (BMI) ≥30 kg/m<sup>2</sup>) and ...[more]

PMID: 30108269

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Project description:BackgroundMetabolically healthy obesity is hypothesized to be a benign condition but whether this is the case for dementia remains debated. We examined the role of age at assessment of metabolic-obesity phenotypes in associations with incident dementia.MethodsObesity (body mass index ≥ 30 kg/m2) and poor metabolic health (≥ 2 of elevated serum triglycerides, low HDL-C, elevated blood pressure, and elevated serum fasting glucose) were used to define four metabolic-obesity phenotypes (metabolically healthy (MHNO) and unhealthy non-obesity (MUNO), metabolically healthy (MHO) and unhealthy obesity (MUO)) at < 60, 60 to < 70, and ≥ 70 years using 6 waves of data from the Whitehall II study and their associations with incident dementia was examined using Cox regression.ResultsAnalyses with exposures measured < 60, 60 to < 70, and ≥ 70 years involved 410 (5.8%), 379 (5.6%), and 262 (7.4%) incident dementia cases over a median follow-up of 20.8, 10.3, and 4.2 years respectively. In analyses of individual components, obesity before 60 years (HR 1.41, 95% CI: [1.08, 1.85]) but not at older ages was associated with dementia; unhealthy metabolic status when present < 60 years (HR 1.33, 95% CI: [1.08, 1.62]) and 60 to < 70 years (HR 1.32, 95% CI: [1.07, 1.62]) was associated with dementia. Compared to the metabolically healthy non-obesity group, the risk of dementia was higher in those with metabolically healthy obesity before 60 years (1.69; 95% CI: [1.16, 2.45]); this was not the case when metabolic-obesity phenotype was present at 60 to < 70 years or ≥ 70 years. Analyses at older ages were on smaller numbers due to death and drop-out but inverse probability weighting to account for missing data yielded similar results.ConclusionsIndividuals with metabolically healthy obesity before age 60 had a higher risk of incident dementia over a 27-year follow-up; the excess risk dissipates when metabolic health and obesity are measured after 70 years.

Project description:Aims/hypothesisReversion from prediabetes to normoglycaemia is accompanied by an improvement in cardiovascular risk factors, but it is unclear whether this translates into a reduction in risk of cardiovascular disease (CVD) events or death. Hence, we studied the probability of reversion from prediabetes to normoglycaemia and the associated risk of future CVD and death using data from the Whitehall II observational cohort study.MethodsThree glycaemic criteria for prediabetes (fasting plasma glucose [FPG] 5.6-6.9 mmol/l, 2 h plasma glucose [2hPG] 7.8-11.0 mmol/l, and HbA1c 39-47 mmol/mol [5.7-6.4%]) were assessed in 2002-2004 and 2007-2009 for 5193 participants free of known diabetes at enrolment. Among participants with prediabetes in the first examination, we calculated the probability of reversion to normoglycaemia by re-examination according to each glycaemic criterion. Poisson regression analysis was used to estimate and compare incidence rates of a composite endpoint of a CVD event or death in participants with prediabetes who did vs did not revert to normoglycaemia. Analyses were adjusted for age, sex, ethnicity and previous CVD.ResultsBased on the FPG criterion, 820 participants had prediabetes and 365 (45%) of them had reverted to normoglycaemia in 5 years. The corresponding numbers were 324 and 120 (37%) for the 2hPG criterion and 1709 and 297 (17%) for the HbA1c criterion. During a median follow-up of 6.7 (interquartile range 6.3-7.2) years, 668 events of non-fatal CVD or death occurred among the 5193 participants. Reverting from 2hPG-defined prediabetes to normoglycaemia vs remaining prediabetic or progressing to diabetes was associated with a halving in event rate (12.7 vs 29.1 per 1000 person-years, p = 0.020). No association with event rate was observed for reverting from FPG-defined (18.6 vs 18.2 per 1000 person-years, p = 0.910) or HbA1c-defined prediabetes to normoglycaemia (24.5 vs 22.9 per 1000 person-years, p = 0.962).Conclusions/interpretationMost people with HbA1c-defined prediabetes remained prediabetic or progressed to diabetes during 5 years of follow-up. In contrast, reversion to normoglycaemia was frequent among people with FPG- or 2hPG-defined prediabetes. Only reversion from 2hPG-defined prediabetes to normoglycaemia was associated with a reduction in future risk of CVD and death.

Project description:Background Increased vagal modulation is a mechanism that may partially explain the protective effect of healthy lifestyles. However, it is unclear how healthy lifestyles relate to vagal regulation longitudinally. We prospectively examined associations between a comprehensive measure of 4 important lifestyle factors and vagal modulation, indexed by heart rate variability (HRV) over 10 years. Methods and Results The fifth (1997-1999), seventh (2002-2004), and ninth (2007-2009) phases of the UK Whitehall II cohort were analyzed. Analytical samples ranged from 2059 to 3333 (mean age: 55.7 years). A healthy lifestyle score was derived by giving participants 1 point for each healthy factor: physically active, not smoking, moderate alcohol consumption, and healthy body mass index. Two vagally mediated HRV measures were used: high-frequency HRV and root mean square of successive differences of normal-to-normal R-R intervals. Cross-sectionally, a positively graded association was observed between the healthy lifestyle score and HRV at baseline (Poverall?0.001). Differences in HRV according to the healthy lifestyle score remained relatively stable over time. Compared with participants who hardly ever adhered to healthy lifestyles, those with consistent healthy lifestyles displayed higher high-frequency HRV (?=0.23; 95% CI, 0.10-0.35; P=0.001) and higher root mean square of successive differences of normal-to-normal R-R intervals (?=0.15; 95% CI, 0.07-0.22; P?0.001) at follow-up after covariate adjustment. These differences in high-frequency HRV and root mean square of successive differences of normal-to-normal R-R intervals are equivalent to ?6 to 20 years differences in chronological age. Compared with participants who reduced their healthy lifestyle scores, those with stable scores displayed higher subsequent high-frequency HRV (?=0.24; 95% CI, 0.01-0.48; P=0.046) and higher root mean square of successive differences of normal-to-normal R-R intervals (?=0.15; 95% CI, 0.01-0.29; P=0.042). Conclusions Maintaining healthy lifestyles is positively associated with cardiac vagal functioning, and these beneficial adaptations may be lost if not sustained.

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Do worse baseline risk factors explain the association of healthy obesity with increased mortality risk? Whitehall II Study.

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Do worse baseline risk factors explain the association of healthy obesity with increased mortality risk? Whitehall II Study.

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