Summary Background Elevated blood pressure and glucose, serum cholesterol, and body mass index (BMI) are risk factors for cardiovascular diseases (CVDs); some of these factors also increase the risk of chronic kidney disease (CKD) and diabetes. We estimated CVD, CKD, and diabetes mortality attributable to these four cardio-metabolic risk factors for all countries and regions between 1980 and 2010. Methods We used data on risk factor exposure by country, age group, and sex from pooled analysis of population-based health surveys. Relative risks for cause-specific mortality were obtained from pooling of large prospective studies. We calculated the population attributable fractions (PAF) for each risk factor alone, and for the combination of all risk factors, accounting for multi-causality and for mediation of the effects of BMI by the other three risks. We calculated attributable deaths by multiplying the cause-specific PAFs by the number of disease-specific deaths from the Global Burden of Diseases, Injuries, and Risk Factors 2010 Study. We propagated the uncertainties of all inputs to the final estimates. Findings In 2010, high blood pressure was the leading risk factor for dying from CVDs, CKD, and diabetes in every region, causing over 40% of worldwide deaths from these diseases; high BMI and glucose were each responsible for about 15% of deaths; and cholesterol for 10%. After accounting for multi-causality, 63% (10.8 million deaths; 95% confidence interval 10.1–11.5) of deaths from these diseases were attributable to the combined effect of these four metabolic risk factors, compared with 67% (7.1 million deaths; 6.6–7.6) in 1980. The mortality burden of high BMI and glucose nearly doubled between 1980 and 2010. At the country level, age-standardised death rates attributable to these four risk factors surpassed 925 deaths per 100,000 among men in Belarus, Mongolia, and Kazakhstan, but were below 130 deaths per 100,000 for women and below 200 for men in some high-income countries like Japan, Singapore, South Korea, France, Spain, The Netherlands, Australia, and Canada. Interpretations The salient features of the cardio-metabolic epidemic at the beginning of the twenty-first century are the large role of high blood pressure and an increasing impact of obesity and diabetes. There has been a shift in the mortality burden from high-income to low- and middle-income countries.

The renin-angiotensin system (RAS) plays a crucial role and angiotensinogen levels, this relationship persisted in the regulation of fluid volume, thereby influencing for ACE in multivariate analyses controlling for BP, blood pressure (BP). Obesity is an important risk factor hypertension status, age, and gender. The for hypertension, however the physiologic basis for this insertion/deletion polymorphism of the ACE gene was relationship has not been clarified. In a population surassociated with variation in the levels of ACE, but inconvey we examined the potential relationship between the sistently with body mass index. Variants of the angio-RAS and obesity. Based on community sampling, 449 tensinogen gene leading to amino acid substitutions at individuals were recruited from metropolitan Kingston, positions 174 and 235 did not influence levels either of Jamaica. Serum angiotensin-converting enzyme (ACE) angiotensinogen or obesity. These data suggest that and circulating angiotensinogen levels were measured obesity may alter the levels of ACE and angiotensinand the associated genes were typed for previously ogen, and provide a potential pathway through which described polymorphisms. Obese individuals (body obesity leads to elevation of BP. mass index Ͼ31) had significantly higher serum ACE

Aims/HypothesesWe hypothesized that there is decreased synthesis of glutathione (GSH) in type 2 diabetes (T2DM) especially in the presence of microvascular complications, and this is dependent on the degree of hyperglycemia.MethodsIn this case-control study, we recruited 16 patients with T2DM (7 without and 9 with microvascular complications), and 8 age- and sex-matched non-diabetic controls. We measured GSH synthesis rate using an infusion of [2H2]-glycine as isotopic tracer and collection of blood samples for liquid chromatography mass spectrometric analysis.ResultsCompared to the controls, T2DM patients had lower erythrocyte GSH concentrations (0.90 ± 0.42 vs. 0.35 ± 0.30 mmol/L; P = 0.001) and absolute synthesis rates (1.03 ± 0.55 vs. 0.50 ± 0.69 mmol/L/day; P = 0.01), but not fractional synthesis rates (114 ± 45 vs. 143 ± 82%/day; P = 0.07). The magnitudes of changes in patients with complications were greater for both GSH concentrations and absolute synthesis rates (P-values ≤ 0.01) compared to controls. There were no differences in GSH concentrations and synthesis rates between T2DM patients with and without complications (P-values > 0.1). Fasting glucose and HbA1c did not correlate with GSH concentration or synthesis rates (P-values > 0.17).ConclusionsCompared to non-diabetic controls, patients with T2DM have glutathione deficiency, especially if they have microvascular complications. This is probably due to reduced synthesis and increased irreversible utilization by non-glycemic mechanisms.

With mortality risk now higher from non-communicable than communicable diseases in sub-Saharan Africa and elsewhere, systematic measurement, detection and genuine control of hypertension once treated can go hand-in-hand with other adult health programmes in primary care. Cost implications are not great. The data from this collaborative study suggest that such efforts should be well rewarded.

Objectives: To examine maternal nutritional status and its relationship to infant weight and body proportions. Design: Retrospective study of births from January±December 1990. Setting: University Hospital of the West Indies, Jamaica. Subjects: Records for 2394 live, singleton births, between 200±305 d gestation. Main outcome measures: Birth weight, crown heel length, head circumference, ponderal index, head circumference:length ratio, placental weight, placental:birth weight ratio. Results: Mothers who were lighter had babies who had lower birth weight, were shorter, had smaller heads and had a higher HC:L ratio. Shorter and thinner women had babies who had lower birth weights, were shorter, had smaller heads and lighter placentas. Thinner women also had babies with a lower placental:birth weight ratio, and their BMI's were not linearly related to ponderal index and HC:L ratio. Women whose ®rst trimester Hb levels were`9.5 g/dl had babies with the lowest birth weight, crown heel length, placental weight and ponderal index. These measurements increased as the Hb levels rose to 12.5 g/dl but then fell at Hb levels b 12.5 g/dl. In the second and third trimester Hb levels were negatively associated with birth weight, crown heel length, head circumference, placenta weight and ponderal index. Conclusions: The data support the hypothesis that poor maternal nutrition is associated with foetal growth restraint. Poor maternal nutrition as indicated by low weight, height, and BMI are associated with smaller, shorter babies with smaller heads. Haemoglobin levels b 12.5 g/dl in pregnancy are associated with lighter, shorter, thinner babies, with smaller heads.