Bisphenol A (BPA) exposure has been associated with diabetes and related metabolic disorders, such as obesity, but studies of the association of urinary BPA concentrations with central obesity risk are limited. The aim of this study was to prospectively investigate the association between urinary BPA and incident central obesity in a Chinese population aged ≥40 years.The study followed 888 participants from Shanghai, China, who did not have central obesity at baseline (in 2009) for 4 years. Concentrations of BPA were measured in baseline morning spot urine samples. Central obesity was defined as waist circumference ≥90 cm in men and ≥80 cm in women.During a mean follow-up of 4 years, 124 (14.0%) participants developed central obesity. Each 1-unit increase in log [BPA] was positively associated with a 2.30-fold risk of incident central obesity (95% confidence interval [CI] 1.39-3.78; P < 0.001) after adjustment for confounders. Compared with the lowest tertile of urinary BPA concentration, Tertiles 2 and 3 were associated with a higher risk of incident central obesity (odds ratios 1.73 [95% CI 1.04-2.88] and 1.81 [95% CI 1.08-3.05], respectively). Stratified analysis showed significant associations of BPA with incident central obesity in women and individuals <60 years of age, with normal weight, non-smokers, non-drinkers, or non-hypertensives.The results indicate that higher urinary BPA concentrations may be associated with a greater risk of incident central obesity in Chinese adults. The study emphasizes the effects of BPA exposure on metabolic risk from a public health perspective.
Background Previous studies indicated that apolipoprotein measurements predicted cardiovascular disease (CVD) risk; however, associations between apolipoproteins and carotid intima-media thickness (CIMT) were less explored. Methodology and Principal Findings The cross-sectional study included 6069 participants aged 40 years or older with NGT from Shanghai, China. Serum fasting traditional lipids (total cholesterol [TC], low-density lipoprotein cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C] and triglycerides [TG]), apoA-I and apoB were assessed. A high-resolution B-mode ultrasonography was performed to measure CIMT. We found CIMT increased progressively across the quartiles of serum apoB (p for trend <0.0001). In logistic regression, concentrations of apoB (odds ratio [OR] 1.27, 95% confidence interval [CI] 1.18–1.36), TC (OR 1.23, 95% CI 1.14–1.32), LDL-C (OR 1.25, 95% CI 1.16–1.34) and TG (OR 1.11, 95% CI 1.04–1.20) were significantly related to elevated CIMT after adjusted for age and sex. Meanwhile, the apoB/apoA-I ratio (OR 1.25, 95% CI 1.17–1.34) related to elevated CIMT. ApoB (OR 1.23, 95% CI 1.00–1.51) and the apoB/apoA-I ratio (OR 1.19, 95% CI 1.04–1.36) remained significantly associated with elevated CIMT, after adjusted for the traditional CVD risk factors including traditional lipids. Conclusions and Significance There were significant associations between serum apoB, the apoB/apoA-I ratio and elevated CIMT. Serum apoB and the apoB/apoA-I ratio might be independent predictors of early atherosclerosis in NGT.
<b>Objective</b> We aimed to determine the individual and combined associations of lifestyle and metabolic factors with new-onset diabetes and major cardiovascular events among Chinese population aged 40 years or older. <p><b>Research design and methods </b>Baseline lifestyle information, waist circumference, blood pressure, lipid profiles and glycemic status were obtained in a nationwide, multicenter, prospective study of 170 240 participants. During the up to 5 years of follow-up, we detected 7 847 diabetes according to the American Diabetes Association 2010 criteria and 3 520 cardiovascular events including cardiovascular death, myocardial infarction, stroke, and hospitalized or treated heart failure.</p> <p><b>Results: </b>Based on 36.13% (population-attributable fraction, PAF) risk attributed to metabolic risk components collectively, physical inactivity (8.59%), sedentary behavior (6.35%), and unhealthy diet (4.47%) moderately contributed to incident diabetes. Physical inactivity (13.34%), unhealthy diet (8.70%), and current smoking (3.38%) significantly contributed to the risk of major cardiovascular events, on the basis of 37.42% PAF attributed to a cluster of metabolic risk factors. Significant associations of lifestyle health status with diabetes and cardiovascular events were found across all metabolic health categories. Risks of new-onset diabetes and major cardiovascular events increased simultaneously according to the worsening of lifestyle and metabolic health status.</p> <p><b>Conclusions: </b>We showed robust effects of lifestyle status on new-onset diabetes and major cardiovascular events regardless of metabolic status and a graded increment of risk according to the combination of lifestyle and metabolic health, highlighting the importance of lifestyle modification regardless of the present metabolic status.</p>
Abstract Aims/hypothesis Metformin use has been associated with reduced incident dementia in diabetic patients in observational studies. However, the causality between the two in the general population is unclear. This study uses Mendelian randomization (MR) to investigate the causal effect of metformin targets on Alzheimer’s disease (AD) and potential causal mechanisms in the brain linking the two. Methods Genetic proxies for the effects of metformin drug targets were identified as variants in the gene for the corresponding target that associated with HbA 1c level (N=344,182) and expression level of the corresponding gene (N≤31,684). The cognitive outcomes were derived from genome-wide association studies comprising of 527,138 middle-aged Europeans, including 71,880 AD or AD-by-proxy patients. MR estimates representing lifelong metformin use on AD and cognitive function in the general population were generated. Effect of expression level of 22 metformin-related genes in brain cortex (N=6,601 donors) on AD was further estimated. Results Genetically proxied metformin use equivalent to a 6.75 mmol/mol (1.09%) reduction of HbA 1c was associated with 4% lower odds of AD (odds ratio [OR]=0.964, 95%CI=0.982∼0.946, P=1.06×10 −4 ) in non-diabetic individuals. One metformin target, mitochondrial complex 1 (MCI), showed a robust effect on AD (OR=0.88, P=4.73×10 −4 ) that was independent of AMPK. MR of expression in brain cortex tissue showed that decreased MCI-related gene, NDUFA2 , expression was associated with reduced AD risk (OR=0.95, P=4.64×10 −4 ) and less cognitive decline. Conclusion/interpretation Metformin use is likely to cause reduced AD risk in the general population. Mitochondrial function and the NDUFA2 gene are likely mechanisms of action in dementia protection. Research in context What is already known about this subject Metformin is an anti-diabetic drug with repurposing potential for dementia prevention. In a search of PubMed, Embase and clinicaltrials.gov , a few observational studies suggested the association of metformin use with reduced dementia incidence in diabetic patients What is the key question? What is the effect of genetically proxied metformin use on Alzheimer’s disease (AD) and cognitive function in the general population, especially for those without diabetes? Is the causal role between the two at least partly influenced by mechanisms in the brain? What are the new findings? In a Mendelian randomization analysis of over 527,138 individuals (71,880 AD or AD-by-proxy cases), genetically proxied metformin use equivalent to a 6.75 mmol/mol (1.09%) reduction of HbA 1c was associated with 14% lower odds of AD (odds ratio=0.86), where mitochondrial complex I is a key effect modifier. Expression level of a mitochondrial complex I related gene, NDUFA2 , showed an effect on reducing AD risk and less cognitive decline in brain. How might this impact on clinical practice in the foreseeable future? Our study predicts the efficacy of metformin on reducing AD risk and reducing cognitive decline in the general population, especially for those without diabetes. Mitochondrial function and a mitochondrial related gene, NDUFA2 , could be considered as a novel drug target for dementia prevention. Graphical abstract Tweet Effect of metformin targets reduced 4% of Alzheimer’s disease risk in non-diabetic individuals. @oldz84 @tomgaunt @mendel_random @mrc_ieu
Hypertension is the leading global risk factor for cardiovascular disease and premature death. Recommendations from current guidelines of blood pressure (BP) management differ in many ways; therefore, we did an overview and comparative analysis of major clinical guidelines of BP management in people with and without diabetes, including the definition and classification of hypertension, initiation of antihypertensive drug therapy, BP control targets, and antihypertensive treatment strategies. BP management in patients with diabetes was discussed in great detail using both hypertension and diabetes guidelines. We conclude that high-level evidence from high-quality clinical studies is urgently needed to settle uncertainties on BP management recommendations.高血压是全球心血管疾病和过早死亡的主要危险因素。当前的血压管理指南推荐意见在许多方面存在差异，因此我们对糖尿病与非糖尿病人群主要血压管理临床指南进行了概述及比较分析，包括高血压的定义和分类，降压药物干预启动阈值，血压控制目标以及降压治疗策略。对于高血压合并糖尿病患者，我们纳入高血压及糖尿病相关指南进行详细讨论。我们得出结论:急需高质量临床研究提供高水平证据来解决血压管理指南推荐意见的不确定性。.
Context Limited population-based study focused on relationship between eosinophil and type 2 diabetes (T2D). Objectives We aimed to evaluate the relationship between peripheral eosinophil percentage and glucose metabolism and insulin resistance in a large sample size of Chinese population aged 40 and older. Design and Methods A cross-sectional study was performed among 9,111 Chinese adults including 3,561 men and 5,550 women. The glucose metabolism status was confirmed by 75-g oral glucose tolerance test. Homeostasis model assessment of insulin resistance index and serum insulin levels were used to evaluate insulin resistance. Homeostasis model assessment-B was used to evaluate β cell function. Results The average age of participants was 58.5 years. The prevalence of T2D decreased across the tertiles of eosinophil percentage (21.3%, 18.2% and 16.9%, P<0.0001). Each one tertile increase of eosinophil percentage inversely associated with risk of T2D when referred not only to normal glucose tolerance (NGT) (odds ratio (OR) 0.81, 95% CI 0.76–0.87, P< 0.0001), but also to impaired glucose regulation (OR 0.89, 95% CI 0.83–0.97, P = 0.006), respectively, after adjustment for the confounding factors. Compared with the first tertile, the third tertile of eosinophil percentage associated with a 23% decrease of insulin resistance in NGT participants after full adjustments (P = 0.005). Each 1-standard deviation of increment of eosinophil percentage associated with a 37% decrease of insulin resistance (P = 0.005). Conclusions Higher peripheral eosinophil percentage was associated with decreased risk of T2D. The inverse relation to insulin resistance was detected in NGT participants.
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