Objective. This systematic review aimed to measure the association between neutrophil lymphocyte ratio (NLR) and cardiovascular disease (CVD) risk. Methods. Relevant studies were identified from ...Medline and Scopus databases. Observational studies with NLR as a study factor were eligible for review. The outcomes of interest were any type of CVD including acute coronary syndrome, coronary artery disease, stroke, or a composite of these cardiovascular events. Mean differences in NLR between CVD and non-CVD patients were pooled using unstandardized mean difference (USMD). Odds ratios of CVD between high and low NLR groups were pooled using a random effects model. Results. Thirty-eight studies (n=76,002) were included. High NLR was significantly associated with the risks of CAD, ACS, stroke, and composite cardiovascular events with pooled ORs of 1.62 (95% CI: 1.38-1.91), 1.64 (95% CI: 1.30, 2.05), 2.36 (95% CI: 1.44, 2.89), and 3.86 (95% CI: 1.73, 8.64), respectively. In addition, mean NLRs in CAD, ACS, and stroke patients were significantly higher than in control groups. Conclusion. High NLR was associated with CAD, ACS, stroke, and composite cardiovascular events. Therefore, NLR may be a useful CVD biomarker.
Background: Studies of single nutrients on depression have produced inconsistent results, and they have failed to consider the complex interactions between nutrients. An increasing number of studies ...in recent years are investigating the association of overall dietary patterns and depression.Objective: This study aimed to systematically review current literature and conduct meta-analyses of studies addressing the association between dietary patterns and depression.Design: Six electronic databases were searched for articles published up to August 2013 that examined the association of total diet and depression among adults. Only studies considered methodologically rigorous were included. Two independent reviewers completed study selection, quality rating, and data extraction. Effect sizes of eligible studies were pooled by using random-effects models. A summary of the findings was presented for studies that could not be meta-analyzed.Results: A total of 21 studies were identified. Results from 13 observational studies were pooled. Two dietary patterns were identified. The healthy diet pattern was significantly associated with a reduced odds of depression (OR: 0.84; 95% CI: 0.76, 0.92; P < 0.001). No statistically significant association was observed between the Western diet and depression (OR: 1.17; 95% CI: 0.97, 1.68; P = 0.094); however, the studies were too few for a precise estimate of this effect.Conclusions: The results suggest that high intakes of fruit, vegetables, fish, and whole grains may be associated with a reduced depression risk. However, more high-quality randomized controlled trials and cohort studies are needed to confirm this finding, specifically the temporal sequence of this association.
Depleted nitric oxide levels in the human body play a major role in cardiovascular disease pathogenesis. Inorganic nitrate/nitrite (rich dietary sources include beetroot and spinach) can act as a ...nitric oxide donor because nitrate/nitrite can be metabolized to produce nitric oxide.
This review and meta-analysis sought to investigate the role of inorganic nitrate/nitrite in preventing or treating cardiovascular disease risk factors in humans.
Electronic databases, including Medline, Embase, Cumulative Index to Nursing and Allied Health Literature, Cochrane, and Scopus, were searched.
Experimental trials examining the effect of oral inorganic nitrate/nitrite intake on cardiovascular disease risk factors were included for systematic analysis.
Thirty-four studies were included for qualitative synthesis, 23 of which were eligible for meta-analysis. Included studies measured the following outcomes: blood pressure, endothelial function, arterial stiffness, platelet aggregation, and/or blood lipids. Inorganic nitrate intake was found to significantly reduce resting blood pressure (systolic blood pressure: -4.80 mmHg, P < 0.0001; diastolic blood pressure: -1.74 mmHg, P = 0.001), improve endothelial function (flow-mediated dilatation: 0.59%, P < 0.0001), reduce arterial stiffness (pulse wave velocity: -0.23 m/s, P < 0.0001; augmentation index: -2.1%, P = 0.05), and reduce platelet aggregation by 18.9% (P < 0.0001).
Inorganic nitrate consumption represents a simple strategy for targeting cardiovascular disease risk factors. Future studies investigating the long-term effects of inorganic nitrate on cardiovascular disease outcomes are warranted.
Abstract Background Platelets with high hemostatic activity play an important role in the pathophysiology of coronary artery disease(CAD) and mean platelet volume(MPV) has been proposed as an ...indicator of platelet reactivity. Thus, MPV may emerge as a potential marker of CAD risk. The aim of this study was to conduct a systematic review and meta-analysis comparing mean difference in MPV between patients with CAD and controls and pooling the odds ratio of CAD in those with high versus low MPV. Methods Medline and Scopus databases were searched up to 12 March 2013. All observational studies that considered MPV as a study's factor and measured CAD as an outcome were included. Two reviewers independently selected the studies and extracted the data. Results Forty studies were included in this meta-analysis. The MPV was significantly larger in patients with CAD than controls with the unstandardized mean difference of 0.70 fL (95% CI: 0.55, 0.85). The unstandardized mean difference of MPV in patients with acute coronary event and in patients with chronic stable angina was 0.84 fL (95% CI: 0.63, 1.04) and 0.46 fL (95% CI: 0.11, 0.81) respectively. Patients with larger MPV (≥ 7.3 fL) also had a greater odds of having CAD than patients with smaller MPV with a pooled odds ratio of 2.28 (95% CI: 1.46, 3.58). Conclusion Larger MPV was associated with CAD. Thus, it might be helpful in risk stratification, or improvement of risk prediction if combining it with other risk factors in risk prediction models.
Vitamin D supplementation effects with or without calcium in pregnancy for reducing risk of preeclampsia and gestational or pregnancy induced hypertension are controversial. Literature was ...systematically searched in Medline, Scopus and Cochrane databases from inception to July 2017. Only randomized controlled trials (RCTs) in English were selected if they had any pair of interventions (calcium, vitamin D, both, or placebo). Systematic review with two-step network-meta-analysis was used to indirectly estimate supplementary effects. Twenty-seven RCTs with 28,000 women were eligible. A direct meta-analysis suggested that calcium, vitamin D, and calcium plus vitamin D could lower risk of preeclampsia when compared to placebo with the pooled risk ratios (RRs) of 0.54 (0.41, 0.70), 0.47 (0.24, 0.89) and 0.50 (0.32, 0.78), respectively. Results of network meta-analysis were similar with the corresponding RRs of 0.49 (0.35, 0.69), 0.43 (0.17, 1.11), and 0.57 (0.30, 1.10), respectively. None of the controls were significant. Efficacy of supplementation, which was ranked by surface under cumulative ranking probabilities, were: vitamin D (47.4%), calcium (31.6%) and calcium plus vitamin D (19.6%), respectively. Calcium supplementation may be used for prevention for preeclampsia. Vitamin D might also worked well but further large scale RCTs are warranted to confirm our findings.
Hypertension is a key risk factor for major adverse cardiovascular events but remains difficult to treat in many individuals. Dietary interventions are an effective approach to lower blood pressure ...(BP) but are not equally effective across all individuals. BP is heritable, and genetics may be a useful tool to overcome treatment response heterogeneity. We investigated whether the genetics of BP could be used to identify individuals with hypertension who may receive a particular benefit from lowering sodium intake and boosting potassium levels.
In this observational genetic study, we leveraged cross-sectional data from up to 296 475 genotyped individuals drawn from the UK Biobank cohort for whom BP and urinary electrolytes (sodium and potassium), biomarkers of sodium and potassium intake, were measured. Biologically directed genetic scores for BP were constructed specifically among pathways related to sodium and potassium biology (pharmagenic enrichment scores), as well as unannotated genome-wide scores (conventional polygenic scores). We then tested whether there was a gene-by-environment interaction between urinary electrolytes and these genetic scores on BP.
Genetic risk and urinary electrolytes both independently correlated with BP. However, urinary sodium was associated with a larger BP increase among individuals with higher genetic risk in sodium- and potassium-related pathways than in those with comparatively lower genetic risk. For example, each SD in urinary sodium was associated with a 1.47-mm Hg increase in systolic BP for those in the top 10% of the distribution of genetic risk in sodium and potassium transport pathways versus a 0.97-mm Hg systolic BP increase in the lowest 10% (
=1.95×10
). This interaction with urinary sodium remained when considering estimated glomerular filtration rate and indexing sodium to urinary creatinine. There was no strong evidence of an interaction between urinary sodium and a standard genome-wide polygenic score of BP.
The data suggest that genetic risk in sodium and potassium pathways could be used in a precision medicine model to direct interventions more specifically in the management of hypertension. Intervention studies are warranted.
The authors performed a meta-analysis to estimate the magnitude of polymorphism effects for the complement component C3 gene (C3) and their possible mode of action on age-related macular degeneration ...(AMD). The meta-analysis included 16 and 7 studies for rs2230199 and rs1047286, respectively. Data extraction and risk of bias assessments were performed in duplicate, and heterogeneity and publication bias were explored. There was moderate evidence for association between both polymorphisms and AMD in Caucasians. For rs2230199, patients with CG and GG genotypes were 1.44 (95% confidence interval (CI): 1.33, 1.56) and 1.88 (95% CI: 1.59, 2.23) times more likely to have AMD than patients with the CC genotype. For rs1047286, GA and AA genotypes had 1.27 (95% CI: 1.15, 1.41) and 1.70 (95% CI: 1.27, 2.11) times higher risk of AMD than did GG genotypes. These gene effects suggested an additive model. The population attributable risks for the GG/GC and AA/GA genotypes are approximately 5%-10%. Subgroup analysis by ethnicity indicates that these variants are very infrequent in Asians and that the observed gene effects are based largely on the high frequency within Caucasian populations. This meta-analysis supports the association between C3 and AMD and provides a robust estimate of the genetic risk.
We conducted a genome-wide association meta-analysis of 4,604 endometriosis cases and 9,393 controls of Japanese and European ancestry. We show that rs12700667 on chromosome 7p15.2, previously found ...to associate with disease in Europeans, replicates in Japanese (P = 3.6 × 10(-3)), and we confirm association of rs7521902 at 1p36.12 near WNT4. In addition, we establish an association of rs13394619 in GREB1 at 2p25.1 with endometriosis and identify a newly associated locus at 12q22 near VEZT (rs10859871). Excluding cases of European ancestry of minimal or unknown severity, we identified additional previously unknown loci at 2p14 (rs4141819), 6p22.3 (rs7739264) and 9p21.3 (rs1537377). All seven SNP effects were replicated in an independent cohort and associated at P <5 × 10(-8) in a combined analysis. Finally, we found a significant overlap in polygenic risk for endometriosis between the genome-wide association cohorts of European and Japanese descent (P = 8.8 × 10(-11)), indicating that many weakly associated SNPs represent true endometriosis risk loci and that risk prediction and future targeted disease therapy may be transferred across these populations.
The relationship between overweight or obesity and depressive symptoms in individuals with or without cardio-metabolic abnormalities is unclear. In a cross-sectional study we examined the odds of ...experiencing depressive symptoms in overweight or obese older adults with or without metabolic abnormalities.
The participants included 3318 older adults from the Hunter Community Study Cohort with a Body Mass Index (BMI) ≥ 18.5 kgm
, stratified by BMI and metabolic health risk. Obesity was defined as BMI ≥ 30 kgm
and metabolically healthy as the absence of metabolic risk factors, according to International Diabetic Federation criteria for metabolic syndromes. Moderate to severe depressive symptoms were defined as a Centre for Epidemiological Studies Depression Scale (CES-D) score ≥ 16.
Compared to the metabolically healthy normal weight (MHNW) group, the odds of experiencing moderate/severe depressive symptoms were higher in those classified as a metabolically unhealthy normal weight (MUNW) (odds ratio (OR) = 1.25, 95% Confidence Interval (CI): 0.76-2.06) or metabolically unhealthy obesity (MUO) (OR = 1.48, 95% CI: 1.00-2.19), but not in those classified as metabolically unhealthy overweight (MUOW) (OR = 0.96, 95% CI: 0.63-1.45), metabolically healthy overweight (MHOW) (OR = 0.80, 95% CI: 0.51-1.26), and metabolically healthy obesity (MHO) (OR = 1.03, 95% CI: 0.65-1.64). Compared with MHNW males, the odds of moderate/severe depressive symptoms were increased in all other BMI category-metabolic health groups for males and females.
Our relatively small sample size and cross-sectional design did not allow us to robustly establish causality.
The odds of experiencing moderate/severe depressive symptoms were increased in metabolically unhealthy older adults regardless of normal weight or obesity, with the odds of having moderate/severe depressive symptoms being higher in females than in males.
Insulinemia and type 2 diabetes (T2D) have been associated with endometrial cancer risk in numerous observational studies. However, the causality of these associations is uncertain. Here we use a ...Mendelian randomization (MR) approach to assess whether insulinemia and T2D are causally associated with endometrial cancer.
We used single nucleotide polymorphisms (SNPs) associated with T2D (49 variants), fasting glucose (36 variants), fasting insulin (18 variants), early insulin secretion (17 variants), and body mass index (BMI) (32 variants) as instrumental variables in MR analyses. We calculated MR estimates for each risk factor with endometrial cancer using an inverse-variance weighted method with SNP-endometrial cancer associations from 1287 case patients and 8273 control participants.
Genetically predicted higher fasting insulin levels were associated with greater risk of endometrial cancer (odds ratio OR per standard deviation = 2.34, 95% confidence internal CI = 1.06 to 5.14, P = .03). Consistently, genetically predicted higher 30-minute postchallenge insulin levels were also associated with endometrial cancer risk (OR = 1.40, 95% CI = 1.12 to 1.76, P = .003). We observed no associations between genetic risk of type 2 diabetes (OR = 0.91, 95% CI = 0.79 to 1.04, P = .16) or higher fasting glucose (OR = 1.00, 95% CI = 0.67 to 1.50, P = .99) and endometrial cancer. In contrast, endometrial cancer risk was higher in individuals with genetically predicted higher BMI (OR = 3.86, 95% CI = 2.24 to 6.64, P = 1.2x10(-6)).
This study provides evidence to support a causal association of higher insulin levels, independently of BMI, with endometrial cancer risk.
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