Body mass index, diabetes, and mortality in French women: explaining away a "paradox".
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ABSTRACT:
SUBMITTER: Lajous M
PROVIDER: S-EPMC4122290 | biostudies-literature | 2014 Jan
REPOSITORIES: biostudies-literature
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Project description:Unlike the general population, among hemodialysis patients body mass index (BMI) is related to blood pressure (BP) and mortality inversely. To explore the reasons for this risk-factor paradox, the cross-sectional association of obesity with the following factors was examined: the prevalence of hypertension, its control, and echocardiographic left ventricular mass index (LVMI). Longitudinal follow-up explored the relationship of BMI with all-cause mortality. Furthermore, it explored whether poorer survival in leaner individuals was related to either high BP or greater LVMI. Among 368 hemodialysis patients, both the prevalence of hypertension and its poor control were inversely related to BMI. BMI was also inversely associated with evidence of excess extracellular fluid volume, but adjustment for this variable did not completely remove the inverse relationship between BP and BMI. Over 1122 patient-years of cumulative follow-up (median: 2.7 years), 119 patients (32%) died. In the first 2 years of follow-up, the mortality hazard for the lowest BMI group was increased; thereafter, the survival curves were similar. Adjusting for several risk factors including BP and LVMI did not remove the inverse relationship of BMI with mortality. In conclusion, leaner patients on dialysis have a higher prevalence of hypertension, poorer control of hypertension, more LVMI, and greater evidence of extracellular fluid volume excess. However, volume explains the greater prevalence or poorer control of hypertension only partially. Leaner patients have an accelerated mortality rate in the first 2 years; this is not completely explained by BP, LVMI, or other cardiovascular or dialysis-specific risk factors.
| S-EPMC3241970 | biostudies-literature
Project description:ObjectiveWe conducted a systematic review and meta-analysis of studies to quantify the association between body mass index (BMI) and the risks of all-cause and cardiovascular mortality in patients with type 2 diabetes.MethodsWe included studies assessing the impact of BMI on all-cause and cardiovascular mortality in patients with type 2 diabetes. Data were combined using a random-effects dose-response model.ResultsSixteen cohort studies on all-cause mortality (n = 445,125) and two studies on cardiovascular mortality (n = 92,841) were evaluated in the meta-analysis. A non-linear association was observed between BMI and all-cause mortality among patients with type 2 diabetes. With a BMI nadir of 28-30 kg/m2, the risk of all-cause mortality displayed a U-shaped increase. With a BMI nadir of 29-31 kg/m2, the risk of cardiovascular mortality exhibited a gradual non-linear increase for BMI > 31 kg/m2. Subgroup analyses suggested that study location, diabetes duration, and smoking history may have contributed to heterogeneity among the studies.ConclusionsAn obesity paradox exists for patients with type 2 diabetes with respect to all-cause and cardiovascular mortality. Study location, diabetes duration, and smoking history might contribute to heterogeneity among obesity paradox studies of patients with type 2 diabetes.
| S-EPMC5207428 | biostudies-literature
Project description:BackgroundThe relation between body weight and mortality among persons with type 2 diabetes remains unresolved, with some studies suggesting decreased mortality among overweight or obese persons as compared with normal-weight persons (an "obesity paradox").MethodsWe studied participants with incident diabetes from the Nurses' Health Study (8970 participants) and Health Professionals Follow-up Study (2457 participants) who were free of cardiovascular disease and cancer at the time of a diagnosis of diabetes. Body weight shortly before diagnosis and height were used to calculate the body-mass index (BMI, the weight in kilograms divided by the square of the height in meters). Multivariable Cox models were used to estimate the hazard ratios and 95% confidence intervals for mortality across BMI categories.ResultsThere were 3083 deaths during a mean period of 15.8 years of follow-up. A J-shaped association was observed across BMI categories (18.5 to 22.4, 22.5 to 24.9 [reference], 25.0 to 27.4, 27.5 to 29.9, 30.0 to 34.9, and ≥35.0) for all-cause mortality (hazard ratio, 1.29 [95% confidence interval {CI}, 1.05 to 1.59]; 1.00; 1.12 [95% CI, 0.98 to 1.29]; 1.09 [95% CI, 0.94 to 1.26]; 1.24 [95% CI, 1.08 to 1.42]; and 1.33 [95% CI, 1.14 to 1.55], respectively). This relationship was linear among participants who had never smoked (hazard ratios across BMI categories: 1.12, 1.00, 1.16, 1.21, 1.36, and 1.56, respectively) but was nonlinear among participants who had ever smoked (hazard ratios across BMI categories: 1.32, 1.00, 1.09, 1.04, 1.14, and 1.21) (P=0.04 for interaction). A direct linear trend was observed among participants younger than 65 years of age at the time of a diabetes diagnosis but not among those 65 years of age or older at the time of diagnosis (P<0.001 for interaction).ConclusionsWe observed a J-shaped association between BMI and mortality among all participants and among those who had ever smoked and a direct linear relationship among those who had never smoked. We found no evidence of lower mortality among patients with diabetes who were overweight or obese at diagnosis, as compared with their normal-weight counterparts, or of an obesity paradox. (Funded by the National Institutes of Health and the American Diabetes Association.).
| S-EPMC3966911 | biostudies-literature
Project description:Emerging literature suggests that obesity may be "protective" against mortality and cardiovascular outcomes, while dysglycemia may worsen outcomes regardless of obesity. The authors measured the association of weight, smoking, and glycemia with mortality in the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). Among 5423 ALLHAT participants without established diabetes or cardiovascular disease, 3980 (73%) had normal fasting glucose and 1443 (27%) had impaired fasting glucose (IFG) levels at study entry. After a median of 4.9 years follow-up, 554 (10%) had died (37% cardiovascular). IFG was associated with higher all-cause mortality (adjusted hazard ratio [HR], 1.23; 95% confidence interval [CI], 1.02-1.50), while obesity was associated with lower all-cause mortality (adjusted HR, 0.76; 95% CI, 0.60-0.96). However, after excluding underweight individuals (body mass index [BMI] <22 kg/m(2) ) and smokers, neither obesity nor IFG was associated with all-cause mortality [corrected]. Although obesity appeared protective against mortality, this association was not significant in never-smokers or after exclusion of BMI <22 kg/m(2) . The obesity paradox may result from confounding by a sicker, underweight referent population and smoking.
| S-EPMC4091725 | biostudies-literature
Project description:BackgroundPrevious studies found normal weight compared to overweight/obese adults with type 2 diabetes had a higher mortality risk, and body-mass index (BMI)-mortality studies do not typically account for baseline diabetes status.ObjectiveTo determine if diabetes influences the BMI-mortality relationship.DesignUsing a prospective study design, we analyzed data from a nationally representative sample of US adults participating in the National Health Interview Survey from 1997 to 2002, and followed for mortality through 2006.ParticipantsExcluding those with heart disease or cancer, our final analytic sample included 74,710 (34,805 never smoker) adults.Main measuresBMI was calculated from self-reported height and weight. Diabetes status was based on self-reported diagnosis from a health professional. We used direct age standardization to calculate all-cause mortality rates and adjusted Cox models for all-cause mortality hazard ratios by BMI quintile; this was done separately for adults with diabetes and without diabetes.Key resultsAmong never smokers, mean age was 50.1 years and 43 % were men. Mean BMI was 27.4 kg/m(2), 26 % were obese, and 2,035 (5 %) reported diagnosed diabetes. After 9 years, there were 4,355 deaths (754 of 4,740 with diabetes; 3,601 of 69,970 without) among 74,710 participants, and 1,238 (247 of 2,035 with diabetes; 991 of 32,770 without) among 34,805 never smokers. We observed a qualitative interaction with diabetes on the BMI-mortality relationship (p = 0.002). Death rates were substantially higher among participants with diabetes compared to those without diabetes across all BMI quintiles. However, death rates in participants with diabetes fell with increasing BMI quintile, while rates followed a J-shaped curve among those without diabetes. In adjusted Cox models, BMI was positively associated with mortality in adults without diabetes, but inversely associated with mortality among participants with diabetes.ConclusionsMortality increased with increasing BMI in adults without diabetes, but decreased with increasing BMI among their counterparts with diabetes. Future studies need to be better designed to answer the question of whether normal weight adults with diabetes have a higher risk of mortality, by minimizing the possibility of reverse causation. Future studies should also account for prevalent diabetes in all investigations of the BMI-mortality relationship.
| S-EPMC3889975 | biostudies-literature
Project description:BackgroundObesity, typically quantified in terms of Body Mass Index (BMI) exceeding threshold values, is considered a leading cause of premature death worldwide. For given body size (BMI), it is recognized that risk is also affected by body shape, particularly as a marker of abdominal fat deposits. Waist circumference (WC) is used as a risk indicator supplementary to BMI, but the high correlation of WC with BMI makes it hard to isolate the added value of WC.Methods and findingsWe considered a USA population sample of 14,105 non-pregnant adults (age ≥ 18) from the National Health and Nutrition Examination Survey (NHANES) 1999-2004 with follow-up for mortality averaging 5 yr (828 deaths). We developed A Body Shape Index (ABSI) based on WC adjusted for height and weight: ABSI ≡ WC/(BMI(2/3)height(1/2)). ABSI had little correlation with height, weight, or BMI. Death rates increased approximately exponentially with above average baseline ABSI (overall regression coefficient of +33% per standard deviation of ABSI [95% confidence interval: +20%-+48%), whereas elevated death rates were found for both high and low values of BMI and WC. 22% (8%-41%) of the population mortality hazard was attributable to high ABSI, compared to 15% (3%-30%) for BMI and 15% (4%-29%) for WC. The association of death rate with ABSI held even when adjusted for other known risk factors including smoking, diabetes, blood pressure, and serum cholesterol. ABSI correlation with mortality hazard held across the range of age, sex, and BMI, and for both white and black ethnicities (but not for Mexican ethnicity), and was not weakened by excluding deaths from the first 3 yr of follow-up.ConclusionsBody shape, as measured by ABSI, appears to be a substantial risk factor for premature mortality in the general population derivable from basic clinical measurements. ABSI expresses the excess risk from high WC in a convenient form that is complementary to BMI and to other known risk factors.
| S-EPMC3399847 | biostudies-literature
Project description:Depression and obesity are complex global health problems. Recent studies suggest that a genetic predisposition to obesity might be accentuated in people with depression, but these analyses are prone to bias. Here, we tested the hypothesis that depression accentuates genetic susceptibility to obesity and applied negative control experiments to test whether any observed interactions were real or driven by confounding and statistical biases. We used data from up to 378 000 Europeans in UK Biobank, a 73 variant body mass index (BMI) genetic risk score, two depression measures [depression symptoms (DS), major depression (MD)] and an antidepressant usage variable available. We tested whether (i) depression and (ii) antidepressant treatment accentuated genetic susceptibility to obesity. Finally, we performed negative control experiments by sampling individuals at random so that they had BMI distributions identical to depression cases and controls. Depression was associated with an accentuation of an individual's genetic risk of obesity with evidence of interactions for both DS and MD (Pinteraction = 7 × 10-4 and 7 × 10-5 respectively). Antidepressant usage within DS cases accentuated genetic obesity risk (Pinteraction = 9 × 10-4), but not for MD (Pinteraction = 0.13). Negative control experiments suggested that the observed interactions for MD (empirical-P = 0.067) may be driven by statistical biases or confounding factors but were not possible with the larger DS groups. Antidepressant usage interaction also appears to be driven by statistical artefacts (empirical-P = 0.510 using MD and 0.162 using DS). We have highlighted the importance of running negative experiments to confirm putative interactions in gene-environment studies. We provide some tentative evidence that depression accentuates an individual's genetic susceptibility to higher BMI but demonstrated that the BMI distributions within cases and controls might drive these interactions.
| S-EPMC9557895 | biostudies-literature
Project description:This study examined the association of sport participation with health outcomes and whether this relation differs between body mass index (BMI)-level subpopulations. Research outcomes for sport participation were compared with other types of leisure-time physical activity (PA). We used the Cox proportional hazards regression models to assess the associations of sport participation, and four other PA types (cycling, gardening, doing odd jobs, and walking), with the risk of prediabetes, type 2 diabetes mellitus (T2DM), and all-cause mortality in 97,212 individuals (58.4% women; mean age: 46.5 years) in the Dutch LifeLines cohort. Outcomes were stratified by three BMI levels: healthy weight (BMI: 18.5-24.9 kg/m2 ), overweight (BMI: 25.0-29.9 kg/m2 ), and obesity (BMI: 30.0 kg/m2 or above). Sport participation was associated with lower health risks, but only significantly so for prediabetes (HR = 0.86, 95% CI: 0.81-0.92). For healthy weight persons, sport participation was associated with the largest risk reductions, with significantly lower risks of prediabetes (HR = 0.78, 95% CI: 0.68-0.90) and all-cause mortality (HR = 0.79, 95% CI 0.65-0.96). Other PA types were not associated with significantly lower health risks, with the exception of cycling, for which significantly lower health risks for persons with overweight were found. Our findings show that sport participation is associated with lower health risks, especially prediabetes, but the effect varies between BMI levels, with the strongest link for persons with a healthy weight. Sport participation, together with cycling, is likely to be more effective in reducing health risks than other types of PA.
| S-EPMC8251809 | biostudies-literature
Project description:BackgroundCardiovascular disease accounts for about one-third of all premature deaths (ie, age < 70) in Cuba. Yet, the relevance of major risk factors, including systolic blood pressure (SBP), diabetes, and body-mass index (BMI), to cardiovascular mortality in this population remains unclear.MethodsIn 1996-2002, 146,556 adults were recruited from the general population in five areas of Cuba. Participants were interviewed, measured (height, weight and blood pressure) and followed up by electronic linkage to national death registries until Jan 1, 2017; in 2006-08, 24,345 participants were resurveyed. After excluding all with missing data, cardiovascular disease at recruitment, and those who died in the first 5 years, Cox regression (adjusted for age, sex, education, smoking, alcohol and, where appropriate, BMI) was used to relate cardiovascular mortality rate ratios (RRs) at ages 35-79 years to SBP, diabetes and BMI; RR were corrected for regression dilution to give associations with long-term average (ie, 'usual') levels of SBP and BMI.ResultsAfter exclusions, there were 125,939 participants (mean age 53 [SD12]; 55% women). Mean SBP was 124 mmHg (SD15), 5% had diabetes, and mean BMI was 24.2 kg/m2 (SD3.6); mean SBP and diabetes prevalence at recruitment were both strongly related to BMI. During follow-up, there were 4112 cardiovascular deaths (2032 ischaemic heart disease, 832 stroke, and 1248 other). Cardiovascular mortality was positively associated with SBP (>=120 mmHg), diabetes, and BMI (>=22.5 kg/m2): 20 mmHg higher usual SBP about doubled cardiovascular mortality (RR 2.02, 95%CI 1.88-2.18]), as did diabetes (2.15, 1.95-2.37), and 10 kg/m2 higher usual BMI (1.92, 1.64-2.25). RR were similar in men and in women. The association with BMI and cardiovascular mortality was almost completely attenuated following adjustment for the mediating effect of SBP. Elevated SBP (>=120 mmHg), diabetes and raised BMI (>=22.5 kg/m2) accounted for 27%, 14%, and 16% of cardiovascular deaths, respectively.ConclusionsThis large prospective study provides direct evidence for the effects of these major risk factors on cardiovascular mortality in Cuba. Despite comparatively low levels of these risk factors by international standards, the strength of their association with cardiovascular death means they nevertheless exert a substantial impact on premature mortality in Cuba.
| S-EPMC8157418 | biostudies-literature
Project description:ObjectiveTo explore the effect of maternal body mass index (BMI) on steroid hormone profiles in women with gestational diabetes mellitus (GDM) and those with normal glucose tolerance (NGT).MethodsWe enrolled 79 women with NGT and 80 women with GDM who had a gestational age of 24-28 weeks. The participants were grouped according to their BMI. We quantified 11 steroid hormones profiles by liquid chromatography-tandem mass spectrometry and calculated the product-to-precursor ratios in the steroidogenic pathway.ResultsWomen with GDM and BMI<25kg/m2 showed higher concentrations of dehydroepiandrosterone (DHEA) (p<0.001), testosterone (T) (p=0.020), estrone (E1) (p=0.010) and estradiol (E2) (p=0.040) and lower Matsuda index and HOMA-β than women with NGT and BMI<25kg/m2. In women with GDM, concentrations of E1 (p=0.006) and E2 (p=0.009) declined, accompanied by reduced E2/T (p=0.008) and E1/androstenedione (A4) (p=0.010) in the BMI>25 kg/m2 group, when compared to that in the BMI<25 kg/m2 group. The values of E2/T and E1/A4 were used to evaluate the cytochrome P450 aromatase enzyme activity in the steroidogenic pathway. Both aromatase activities negatively correlated with the maternal BMI and positively correlated with the Matsuda index in women with GDM.ConclusionsNGT women and GDM women with normal weight presented with different steroid hormone profiles. Steroidogenic pathway profiling of sex hormones synthesis showed a significant increase in the production of DHEA, T, E1, and E2 in GDM women with normal weight. Additionally, the alteration of steroid hormone metabolism was related to maternal BMI in women with GDM, and GDM women with overweight showed reduced estrogen production and decreased insulin sensitivity compared with GDM women with normal weight.
| S-EPMC9681895 | biostudies-literature