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Objective To systematically review associations between intake of saturated fat and trans unsaturated fat and all cause mortality, cardiovascular disease (CVD) and associated mortality, coronary heart disease (CHD) and associated mortality, ischemic stroke, and type 2 diabetes.Design Systematic review and meta-analysis.Data sources Medline, Embase, Cochrane Central Registry of Controlled Trials, Evidence-Based Medicine Reviews, and CINAHL from inception to 1 May 2015, supplemented by bibliographies of retrieved articles and previous reviews.Eligibility criteria for selecting studies Observational studies reporting associations of saturated fat and/or trans unsaturated fat (total, industrially manufactured, or from ruminant animals) with all cause mortality, CHD/CVD mortality, total CHD, ischemic stroke, or type 2 diabetes.Data extraction and synthesis Two reviewers independently extracted data and assessed study risks of bias. Multivariable relative risks were pooled. Heterogeneity was assessed and quantified. Potential publication bias was assessed and subgroup analyses were undertaken. The GRADE approach was used to evaluate quality of evidence and certainty of conclusions.Results For saturated fat, three to 12 prospective cohort studies for each association were pooled (five to 17 comparisons with 90 501-339 090 participants). Saturated fat intake was not associated with all cause mortality (relative risk 0.99, 95% confidence interval 0.91 to 1.09), CVD mortality (0.97, 0.84 to 1.12), total CHD (1.06, 0.95 to 1.17), ischemic stroke (1.02, 0.90 to 1.15), or type 2 diabetes (0.95, 0.88 to 1.03). There was no convincing lack of association between saturated fat and CHD mortality (1.15, 0.97 to 1.36; P=0.10). For trans fats, one to six prospective cohort studies for each association were pooled (two to seven comparisons with 12 942-230 135 participants). Total trans fat intake was associated with all cause mortality (1.34, 1.16 to 1.56), CHD mortality (1.28, 1.09 to 1.50), and total CHD (1.21, 1.10 to 1.33) but not ischemic stroke (1.07, 0.88 to 1.28) or type 2 diabetes (1.10, 0.95 to 1.27). Industrial, but not ruminant, trans fats were associated with CHD mortality (1.18 (1.04 to 1.33) v 1.01 (0.71 to 1.43)) and CHD (1.42 (1.05 to 1.92) v 0.93 (0.73 to 1.18)). Ruminant trans-palmitoleic acid was inversely associated with type 2 diabetes (0.58, 0.46 to 0.74). The certainty of associations between saturated fat and all outcomes was “very low.” The certainty of associations of trans fat with CHD outcomes was “moderate” and “very low” to “low” for other associations.Conclusions Saturated fats are not associated with all cause mortality, CVD, CHD, ischemic stroke, or type 2 diabetes, but the evidence is heterogeneous with methodological limitations. Trans fats are associated with all cause mortality, total CHD, and CHD mortality, probably because of higher levels of intake of industrial trans fats than ruminant trans fats. Dietary guidelines must carefully consider the health effects of recommendations for alternative macronutrients to replace trans fats and saturated fats.

Understanding the reasons for the contrasting changes in obesity, blood pressure, and total cholesterol will provide useful insights that could help to mitigate the adverse eff ects of the epidemic of obesity more rapidly than the necessary societal and structural changes needed to reverse the prevalence of obesity itself.\\n In the long term, the most eff ective means of stemming the tsunami of cardiovascular disease globally is through population-level risk-factor control, whereby the population average of a given risk factor is reduced.6 In high-income countries, the reductions in key cardiovascular disease risk factors at the population level are attributable to changes in the food supply (ie, reduction in animal products and sodium consumption), and through increased physical activity.15 However, given that macroeconomic and macrosocial factors influence the pattern of food consumption, sedentariness, and decrease in utilitarian activity secondary to changes in the types of occupation, transportation, and automation at work and home, the solutions for population-level risk-factor control in all countries, especially in middle-income and low-income countries, will be complex and will take time. Developing solutions will require novel and as yet unavailable data to shed light on the complex interactions between agricultural and food policies (which aff ect the costs and promotion of diff erent types of foods), industrialisation (the nature of jobs), transportation, urban design, community architecture (which aff ects the expenditure of energy during utilitarian activity), economic changes, and social and cultural values, all of which influence health behaviours and which ultimately aff ect cardiovascular risk factors and cardiovascular disease (and several other related chronic diseases).

Some studies, mainly from high-income countries (HICs), report that women receive less care (investigations and treatments) for cardiovascular disease than do men and might have a higher risk of death. However, very few studies systematically report risk factors, use of primary or secondary prevention medications, incidence of cardiovascular disease, or death in populations drawn from the community. Given that most cardiovascular disease occurs in low-income and middle-income countries (LMICs), there is a need for comprehensive information comparing treatments and outcomes between women and men in HICs, middle-income countries, and low-income countries from community-based population studies. In the Prospective Urban Rural Epidemiological study (PURE), individuals aged 35–70 years from urban and rural communities in 27 countries were considered for inclusion. We recorded information on participants' sociodemographic characteristics, risk factors, medication use, cardiac investigations, and interventions. 168 490 participants who enrolled in the first two of the three phases of PURE were followed up prospectively for incident cardiovascular disease and death. From Jan 6, 2005 to May 6, 2019, 202 072 individuals were recruited to the study. The mean age of women included in the study was 50·8 (SD 9·9) years compared with 51·7 (10) years for men. Participants were followed up for a median of 9·5 (IQR 8·5–10·9) years. Women had a lower cardiovascular disease risk factor burden using two different risk scores (INTERHEART and Framingham). Primary prevention strategies, such as adoption of several healthy lifestyle behaviours and use of proven medicines, were more frequent in women than men. Incidence of cardiovascular disease (4·1 [95% CI 4·0–4·2] for women vs 6·4 [6·2–6·6] for men per 1000 person-years; adjusted hazard ratio [aHR] 0·75 [95% CI 0·72–0·79]) and all-cause death (4·5 [95% CI 4·4–4·7] for women vs 7·4 [7·2–7·7] for men per 1000 person-years; aHR 0·62 [95% CI 0·60–0·65]) were also lower in women. By contrast, secondary prevention treatments, cardiac investigations, and coronary revascularisation were less frequent in women than men with coronary artery disease in all groups of countries. Despite this, women had lower risk of recurrent cardiovascular disease events (20·0 [95% CI 18·2–21·7] versus 27·7 [95% CI 25·6–29·8] per 1000 person-years in men, adjusted hazard ratio 0·73 [95% CI 0·64-0·83]) and women had lower 30-day mortality after a new cardiovascular disease event compared with men (22% in women versus 28% in men; p<0·0001). Differences between women and men in treatments and outcomes were more marked in LMICs with little differences in HICs in those with or without previous cardiovascular disease. Treatments for cardiovascular disease are more common in women than men in primary prevention, but the reverse is seen in secondary prevention. However, consistently better outcomes are observed in women than in men, both in those with and without previous cardiovascular disease. Improving cardiovascular disease prevention and treatment, especially in LMICs, should be vigorously pursued in both women and men. Full funding sources are listed at the end of the paper (see Acknowledgments).

Dietary patterns containing nuts are associated with a lower risk of CVD mortality, and increased nut consumption has been shown to have beneficial effects on CVD risk factors including serum lipid levels. Recent studies have reported on the relationship between nut intake and CVD outcomes and mortality. Our objective was to systematically review the literature and quantify associations between nut consumption and CVD outcomes and all-cause mortality. Five electronic databases (through July 2015), previous reviews and bibliographies of qualifying articles were searched. In the twenty included prospective cohort studies (n 467 389), nut consumption was significantly associated with a lower risk of all-cause mortality (ten studies; risk ratio (RR) 0·81; 95 % CI 0·77, 0·85 for highest v. lowest quantile of intake, P het=0·04, I 2=43 %), CVD mortality (five studies; RR 0·73; 95 % CI 0·68, 0·78; P het=0·31, I 2=16 %), all CHD (three studies; RR 0·66; 95 % CI 0·48, 0·91; P het=0·0002, I 2=88 %) and CHD mortality (seven studies; RR 0·70; 95 % CI 0·64, 0·76; P het=0·65, I 2=0 %), as well as a statistically non-significant reduction in the risk of non-fatal CHD (three studies; RR 0·71; 95 % CI 0·49, 1·03; P het=0·03, I 2=72 %) and stroke mortality (three studies; RR 0·83; 95 % CI 0·69, 1·00; P het=0·54, I 2=0 %). No evidence of association was found for total stroke (two studies; RR 1·05; 95 % CI 0·69, 1·61; P het=0·04, I 2=77 %). Data on total CVD and sudden cardiac death were available from one cohort study, and they were significantly inversely associated with nut consumption. In conclusion, we found that higher nut consumption is associated with a lower risk of all-cause mortality, total CVD, CVD mortality, total CHD, CHD mortality and sudden cardiac death.

A standardized data workflow is described for large-scale serum metabolomic studies using multisegment injection-capillary electrophoresis-mass spectrometry. Multiplexed separations increase throughput (<4 min/sample) for quantitative determination of 66 polar/ionic metabolites in serum filtrates consistently detected (coefficient of variance (CV) <30%) with high frequency (>75%) from a multi-ethnic cohort of pregnant women ( n = 1,004). We outline a validated protocol implemented in four batches over a 7-month period that includes details on preventive maintenance, sample workup, data preprocessing and metabolite authentication. We achieve stringent quality control (QC) and robust batch correction of long-term signal drift with good mutual agreement for a wide range of metabolites, including serum glucose as compared to a clinical chemistry analyzer (mean bias = 11%, n = 668). Control charts for a recovery standard (mean CV = 12%, n = 2,412) and serum metabolites in QC samples (median CV = 13%, n = 202) demonstrate acceptable intermediate precision with a median intraclass coefficient of 0.87. We also report reference intervals for 53 serum metabolites from a diverse population of women in their second trimester of pregnancy. A standardized protocol and data workflow for high-throughput analysis of the maternal serum metabolome is outlined. It uses multisegment injection–capillary electrophoresis–mass spectrometry and is applied to a multi-ethnic cohort of pregnant women.

•We meta-analyzed diet trends of energy, macronutrients, and foods in 47 countries.•We found a greater increase in country income is related to larger carbohydrate intake decreases.•Saturated fat intake decreased in Northern Europe and Eastern Europe and was stable in other regions.•East Asia and Southeast Asia had increased meat, fish, dairy, egg, fruit, and vegetable intakes.•Fruit, nut, root vegetable, and legume consumption was below recommendations in most regions. We aimed to systematically examine trends in dietary energy, macronutrient, and food consumption in different geographic regions. We searched Medline, Embase, CINAHL, and organizations for studies and reports using individual-level dietary assessments from 1950 to 2019 (PROSPERO CRD42022302843) and quantified changes using multivariable linear mixed-effects models. We identified 109 articles and reports from 47 countries, including Europe and Australasia (47% of studies), Asia (30%), Latin America (13%), the Middle East (6%), and North America (4%). In Southeast and East Asia, carbohydrate intake decreased, whereas fat consumption increased; the opposite pattern occurred in North America; and fat decreased while carbohydrate intake remained stable in Europe and Australasia. Consumption of carbohydrate and fat were stable in South Asia, Latin America, and the Middle East, but data were limited in these regions. A greater increase in national gross domestic product over time was associated with decreased carbohydrate and increased fat and protein intake. Dietary saturated fatty acid intake decreased in Northern and Eastern Europe and was stable in other regions. Changes in food varied by region; East and Southeast Asia increased meat, fish, dairy, egg, fruit, and vegetable consumption and decreased intake of grains, roots and tubers, legumes, whereas North America decreased dairy and red meat but increased eggs, nuts, poultry, and vegetable oil intake. Intakes of fruits, nuts, legumes, and roots and tubers were below recommendations in most regions. Our findings indicate regional variations in dietary trends and identify countries that would benefit from nutritional policies aimed at decreasing lower-quality carbohydrate foods and increasing consumption of fruits, vegetables, nuts, legumes, and dairy.

We sought to determine if differences in the distribution and characteristics of adipose tissue between South Asians and white Caucasians account for differences in risk factors for cardiovascular disease. We recruited 108 healthy South Asians (36.8 years) and white Caucasians (34.2 years) within three BMI strata. Body composition, adipocyte size, abdominal fat area, and hepatic adiposity were assessed and related to fasting glucose, insulin, lipids and adiponectin. After adjustment for age, sex, and BMI, South Asians compared to white Caucasians had higher ln fasting insulin (mean difference (MD): 0.44; 95% CI: 0.20-0.69), lower HDL cholesterol (md: -0.13; 95% CI:-0.26 to -0.01), and lower adiponectin (md: -2.38; 95% CI: -3.59 to -1.17). South Asians also had more body fat (md: 2.69; 95% CI: 0.70 to 4.69), lower lean muscle mass (md: -3.25; 95%CI: -5.35 to -1.14), increased waist to hip ratio (md: 0.03; 95% CI: 0.01-0.05), less superficial subcutaneous abdominal adipose tissue (md: -2.94; 95% CI: -5.56 to-0.32), more deep/visceral to superficial adipose tissue ratio (md 0.34; 95% CI: 0.02 to 0.65), and more liver fat (md: 7.43%; 95% CI: 2.30 to 12.55%). Adipocyte area was increased in South Asians compared to white Caucasians (md: 64.26; 95% CI: 24.3 to 104.1) units(2). Adjustment for adipocyte area attenuated the ethnic differences in insulin (md: 0.22; 95% CI: -0.07 to 0.51), HDL (md: -0.01; 95% CI: -0.16 to 0.13) and adiponectin (md: -1.11; 95% CI: -2.61 to 0.39). Adjustment for differences in adipocyte area and fat distribution attenuated the ethnic difference in liver fat (md: 5.19; 95% CI: 0.31 to 10.06). South Asians have an increased adipocyte area compared to white Caucasians. This difference accounts for the ethnic differences in insulin, HDL cholesterol, adiponectin, and ectopic fat deposition in the liver.

Gestational diabetes Mellitus (GDM) affects 1 in 7 births and is associated with numerous adverse health outcomes for both mother and child. GDM is suspected to share a large common genetic background with type 2 diabetes (T2D). The aim of our study was to characterize different GDM polygenic risk scores (PRSs) and test their association with GDM using data from the South Asian Birth Cohort (START). PRSs were derived for 832 South Asian women from START using the pruning and thresholding (P + T), LDpred, and GraBLD methods. Weights were derived from a multi-ethnic and a white Caucasian study of the DIAGRAM consortium. GDM status was defined using South Asian-specific glucose values in response to an oral glucose tolerance test. Association with GDM was tested using logistic regression. Results were replicated in South Asian women from the UK Biobank (UKB) study. The top ranking P + T, LDpred and GraBLD PRSs were all based on DIAGRAM’s multi-ethnic study. The best PRS was highly associated with GDM in START (AUC = 0.62, OR = 1.60 [95% CI = 1.44–1.69]), and in South Asian women from UKB (AUC = 0.65, OR = 1.69 [95% CI = 1.28–2.24]). Our results highlight the importance of combining genome-wide genotypes and summary statistics from large multi-ethnic studies to optimize PRSs in South Asians.

BackgroundThe cardiovascular disease (CVD) burden among South Asians is high. Lifestyle interventions have been effective in the primary prevention of CVD, but this has not been replicated, through a synthesis of randomised trials, in South Asians.MethodsFour electronic databases (MEDLINE, Embase, CENTRAL and CINAHL), two clinical trial registries and references of included articles were searched through June 2022 (featuring ≥90% South Asian participants). Random-effects pairwise meta-analyses were performed, and heterogeneity was quantified with the I2 statistic. The Grades of Recommendation, Assessment, Development, and Evaluation (GRADE) framework was used to report on the quality of evidence (International Prospective Register of Systematic Reviews registration (PROSPERO).ResultsThirty-five studies were included. Twelve tested diet and physical activity interventions; 18 tested diet alone; and 5 tested physical activity alone. All reported effects of the intervention(s) on at least one established risk factor for CVD, including blood pressure (systolic blood pressure (SBP), diastolic blood pressure (DBP) and blood lipids (high-density lipoprotein cholesterol (HDLc), low-density lipoprotein cholesterol (LDLc) or triglycerides). No trials reported clinical CVD. There is moderate-quality evidence that diet and physical activity interventions improve SBP (mean difference (MD) −2.72 mm Hg, 95% CI −4.11 to –1.33) and DBP (MD −1.53 mm Hg, 95% CI −2.57 to –0.48); high-quality to moderate-quality evidence that diet-only interventions improve DBP (MD −2.05 mm Hg, 95% CI −2.93 to −1.16) and blood lipids (triglycerides (MD −0.10 mmol/L, 95% CI −0.14 to −0.06) and LDLc (MD −0.19 mmol/L, 95% CI −0.32 to −0.06)); and moderate-quality evidence that physical activity-only interventions improve SBP (MD −9.7 mm Hg, 95% CI −11.05 to −8.35), DBP (MD −7.29 mm Hg, 95% CI −8.42 to −6.16) and HDLc (MD 0.08 mmol/L, 95% CI 0.04 to 0.11) compared with usual care.ConclusionsLifestyle interventions improve blood pressure and blood lipid profiles in adult South Asians at risk of CVD. Tailored interventions should be used to modify cardiovascular risk factors in this at-risk group.PROSPERO registration numberCRD42018090419.

Moderately elevated blood levels of homocysteine are weakly correlated with coronary heart disease (CHD) risk, but causality remains uncertain. When folate levels are low, the TT genotype of the common C677T polymorphism (rs1801133) of the methylene tetrahydrofolate reductase gene (MTHFR) appreciably increases homocysteine levels, so \"Mendelian randomization\" studies using this variant as an instrumental variable could help test causality. Nineteen unpublished datasets were obtained (total 48,175 CHD cases and 67,961 controls) in which multiple genetic variants had been measured, including MTHFR C677T. These datasets did not include measurements of blood homocysteine, but homocysteine levels would be expected to be about 20% higher with TT than with CC genotype in the populations studied. In meta-analyses of these unpublished datasets, the case-control CHD odds ratio (OR) and 95% CI comparing TT versus CC homozygotes was 1.02 (0.98-1.07; p = 0.28) overall, and 1.01 (0.95-1.07) in unsupplemented low-folate populations. By contrast, in a slightly updated meta-analysis of the 86 published studies (28,617 CHD cases and 41,857 controls), the OR was 1.15 (1.09-1.21), significantly discrepant (p = 0.001) with the OR in the unpublished datasets. Within the meta-analysis of published studies, the OR was 1.12 (1.04-1.21) in the 14 larger studies (those with variance of log OR<0.05; total 13,119 cases) and 1.18 (1.09-1.28) in the 72 smaller ones (total 15,498 cases). The CI for the overall result from large unpublished datasets shows lifelong moderate homocysteine elevation has little or no effect on CHD. The discrepant overall result from previously published studies reflects publication bias or methodological problems.