Whether intake of alpha-linolenic acid (ALA), the plant-derived n-3 polyunsaturated fatty acid (PUFA), could prevent cardiovascular diseases is not yet clear. We examined the associations of ALA ...intake with 10-year incidence of coronary heart disease (CHD) and stroke in the Netherlands.
Data were collected from a general population of 20,069 generally healthy men and women, aged 20 to 65 years. Habitual diet was assessed at baseline (1993-1997) with a validated 178-item food frequency questionnaire. Incidences of CHD and stroke were assessed through linkage with mortality and morbidity registers. Hazard ratios (HR) were calculated with multivariable Cox proportional hazards models, adjusted for age, gender, lifestyle, and dietary factors.
During 8-13 years of follow-up, we observed 280 incident CHD events (19% fatal) and 221 strokes (4% fatal). Intakes of energy-adjusted ALA in quintiles ranged from less than 1.0 g/d in the bottom quintile (Q1) to more than 1.9 g/d in the top quintile (Q5). ALA intake was not associated with incident CHD, with HRs varying between 0.89 and 1.01 (all p>0.05) in Q2-Q5 compared with the bottom quintile of ALA intake. For incident stroke, however, participants in Q2-Q5 had a 35-50% lower risk compared with the reference group. HRs were 0.65 (0.43-0.97), 0.49 (0.31-0.76), 0.53 (0.34-0.83), and 0.65 (0.41-1.04) for Q2-Q5 respectively.
In this general Dutch population, ALA intake was not associated with incident CHD. The data suggested that a low intake of ALA may be a risk factor for incident stroke. These results warrant confirmation in other population-based studies and in trials.
This paper summarizes the current epidemiological evidence on coffee consumption in relation to blood pressure (BP) and risk of hypertension. Data from cross-sectional studies suggest an inverse ...linear or U-shaped association of habitual coffee use with BP in different populations. Prospective studies suggest a protective effect of high coffee intake (4 or more cups per day) against hypertension, mainly in women. Furthermore, the risk of hypertension may be lower in coffee abstainers. Randomized controlled trials, which are mostly of short duration (1-12 weeks), have shown that coffee intake around 5 cups per day causes a small elevation in BP (approximately 2/1 mmHg) when compared to abstinence or use of decaffeinated coffee. With regard to underlying biological mechanisms, most research has been devoted to BP-raising effects of caffeine. However, there are many other substances in coffee, such as polyphenols, soluble fibre and potassium, which could exert a beneficial effect in the cardiovascular system. Although the precise nature of the relation between coffee and BP is still unclear, most evidence suggests that regular intake of caffeinated coffee does not increase the risk of hypertension.
Vitamin D plays an essential role in bone mineralization and calcium homeostasis. More recently, there has been growing evidence for a role of vitamin D in extraskeletal health, including beneficial ...effects in the cardiovascular system. Daylight exposure and vitamin D intake in many western populations are insufficient for maintaining an adequate vitamin D status. It is at present unclear whether vitamin D supplementation could improve cardiovascular health. This paper summarizes the evidence from observational studies and randomized-controlled trials on the relation of vitamin D with blood pressure (BP) and risk of cardiovascular diseases (CVDs). Epidemiological data suggest that optimal vitamin D status is important for CVD prevention, but results from different studies are conflicting and confounding cannot be ruled out. Randomized-controlled trials of vitamin D supplementation and BP have yielded inconsistent results, and trials that addressed the effect of vitamin D on CVDs are lacking. It is therefore premature to recommend supplemental vitamin D intake specifically for the prevention of hypertension or CVDs. Data from large, well-controlled clinical trials in this field with vitamin D supplements of sufficiently high doses are awaited to settle this issue.
American Journal of Hypertensionadvance online publication 16 September 2010; doi:10.1038/ajh.2010.199
Abstract
Background: Consumption of coffee, one of the most popular beverages around the world, has been associated with a lower risk of cardiovascular and all-cause mortality in population-based ...studies. However, little is known about these associations in patient populations.
Objective: This prospective study aimed to examine the consumption of caffeinated and decaffeinated coffee in relation to cardiovascular disease (CVD) mortality, ischemic heart disease (IHD) mortality, and all-cause mortality in patients with a prior myocardial infarction (MI).
Design: We included 4365 Dutch patients from the Alpha Omega Cohort who were aged 60–80 y (21% female) and had experienced an MI <10 y before study enrollment. At baseline (2002–2006), dietary data including coffee consumption over the past month was collected with a 203-item validated food-frequency questionnaire. Causes of death were monitored until 1 January 2013. HRs for mortality in categories of coffee consumption were obtained from multivariable Cox proportional hazard models, adjusting for lifestyle and dietary factors.
Results: Most patients (96%) drank coffee, and the median total coffee intake was 375 mL/d (∼3 cups/d). During a median follow-up of 7.1 y, a total of 945 deaths occurred, including 396 CVD-related and 266 IHD-related deaths. Coffee consumption was inversely associated with CVD mortality, with HRs of 0.69 (95% CI: 0.54, 0.89) for >2–4 cups/d and 0.72 (0.55, 0.95) for >4 cups/d, compared with 0–2 cups/d. Corresponding HRs were 0.77 (95% CI: 0.57, 1.05) and 0.68 (95% CI: 0.48, 0.95) for IHD mortality and 0.84 (95% CI: 0.71, 1.00) and 0.82 (95% CI: 0.68, 0.98) for all-cause mortality, respectively. Similar associations were found for decaffeinated coffee and for coffee with additives.
Conclusion: Drinking coffee, either caffeinated or decaffeinated, may lower the risk of CVD and IHD mortality in patients with a prior MI. This study was registered at clinicaltrials.gov as NCT03192410.
Scope
Coffee is associated with a lower risk of cancer, cardiovascular disease, and type 2 diabetes at the population level. However, individual susceptibility to the effects of coffee consumption ...will cause heterogeneity in health responses between individuals. In this critical review determinants of inter‐individual variability in cancer and cardiometabolic health outcomes in response to coffee and caffeine consumption are systematically evaluated.
Methods and results
Embase and MEDLINE are searched for observational studies and clinical trials that examined variation in the response to coffee consumption. A total of 74 studies meet the inclusion criteria, which report variation in cancer (n = 24) and cardiometabolic health (n = 50) outcomes. The qualitative analysis shows that sex, BMI, smoking, alcohol intake, menopausal status, and genetic polymorphisms are probable or possible determinants of inter‐individual variability in cancer and cardiometabolic health outcomes in response to coffee and caffeine consumption, albeit the majority of studies have insufficient statistical power to detect significant interaction between these factors and coffee consumption.
Conclusion
Several genetic and non‐genetic determinants of inter‐individual variability in the responses to coffee and caffeine consumption are identified, indicating that some of the health benefits of coffee may only occur in a subgroup of subjects.
Coffee is associated with a reduced risk of cancer, cardiovascular disease, and type 2 diabetes. However, individual susceptibility to the effects of coffee consumption may cause heterogeneity in health responses between individuals. In this critical review, several genetic and non‐genetic determinants of inter‐individual variability in cancer and cardiometabolic health outcomes in response to coffee consumption are identified and evaluated.
Effective food policies in Europe require insight into the environmental impact of consumers’ diet to contribute to global nutrition security in an environmentally sustainable way. The present study ...therefore aimed to assess the environmental impact associated with dietary intake across four European countries, and to explain sources of variations in environmental impact by energy intake, demographics and diet composition. Individual-level dietary intake data were obtained from nationally-representative dietary surveys, by using two non-consecutive days of a 24-h recall or a diet record, from Denmark (DK, n = 1710), Czech Republic (CZ, n = 1666), Italy (IT, n = 2184), and France (FR, n = 2246). Dietary intake data were linked to a newly developed pan-European environmental sustainability indicator database that contains greenhouse gas emissions (GHGE) and land use (LU) values for ∼900 foods. To explain the variation in environmental impact of diets, multilevel regression models with random intercept and random slopes were fitted according to two levels: adults (level 1, n = 7806) and country (level 2, n = 4). In the models, diet-related GHGE or LU was the dependent variable, and the parameter of interest, i.e. either total energy intake or demographics or food groups, the exploratory variables. A 200-kcal higher total energy intake was associated with a 9% and a 10% higher daily GHGE and LU. Expressed per 2000 kcal, mean GHGE ranged from 4.4 (CZ) to 6.3 kgCO2eq/2000 kcal (FR), and LU ranged from 5.7 (CZ) to 8.0 m2*year/2000 kcal (FR). Dietary choices explained most of the variation between countries. A 5 energy percent (50 g/2000 kcal) higher meat intake was associated with a 10% and a 14% higher GHGE and LU density, with ruminant meat being the main contributor to environmental footprints. In conclusion, intake of energy, total meat and the proportion of ruminant meat explained most of the variation in GHGE and LU of European diets. Contributions of food groups to environmental footprints however varied between countries, suggesting that cultural preferences play an important role in environmental footprints of consumers. In particular, Findings from the present study will be relevant for national-specific food policy measures towards a more environmentally-friendly diet.
OBJECTIVE The antihypertensive effect of fish oil was estimated from randomized trials using metaregression analysis. Modification of the blood pressure (BP) effect by age, gender, blood pressure, ...and body mass index was examined.
METHODS A total of 90 randomized trials of fish oil and BP were identified through MEDLINE (1966–March 2001). Trials with co-interventions, patient populations, non-placebo controls, or duration of < 2 weeks were excluded. A total of 36 trials (50 strata) were included, 22 of which had a double-blind design. Original reports were retrieved for data collection on sample size, study design, duration, fish oil dose, BP changes and baseline characteristics of trial populations. Pooled BP estimates were obtained by metaregression analysis, weighted for trial sample sizes. Stratified analyses according to population characteristics were performed.
RESULTS Intake of fish oil was high in most trials (median dose3.7 g/day). Fish oil reduced systolic BP by 2.1 mmHg 95% confidence interval (CI)1.0, 3.2;P < 0.01 and diastolic BP by 1.6 mmHg (95% CI1.0. 2.2;P < 0.01). Restricting the analysis to double-blind trials yielded BP reductions of 1.7 mmHg (95% CI0.3, 3.1) and 1.5 mmHg (95% CI0.6, 2.3), respectively. BP effects tended to be larger in populations that were older (> 45 years) and in hypertensive populations (BP ≥ 140/90 mmHg).
CONCLUSIONS High intake of fish oil may lower BP, especially in older and hypertensive subjects. The antihypertensive effect of lower doses of fish oil (< 0.5 g/day) however, remains to be established.
BACKGROUND—Despite compelling evidence for sodium’s adverse effects on blood pressure, it remains uncertain whether excess sodium intake is a risk factor for coronary heart disease (CHD) in the ...overall population and in potentially more susceptible subgroups.
METHODS AND RESULTS—We prospectively followed 7543 adults aged 28 to 75 years and free of cardiovascular and kidney disease in 1997/1998 of the Prevention of Renal and Vascular End-stage Disease (PREVEND) study. Sodium excretion was measured in two 24-hour urine collections at baseline. Potential susceptibility factors were blood pressure and plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP). Median 24-hour sodium excretion was 137 mmol (Q1–Q3, 106–171 mmol). During a median follow-up of 10.5 (Q1–Q39.9–10.8) years, 452 CHD events occurred. In the entire cohort, there was no association between each 1-g/d (43 mmol/24 h) increment in sodium excretion and CHD risk (adjusted hazard ratio, 1.07; 95% confidence interval, 0.98–1.18; P=0.15). However, the association of sodium excretion with CHD risk tended to be modified by mean arterial pressure (Pinteraction=0.08) and was modified by NT-proBNP (Pinteraction=0.002). When stratified, each 1-g/d increment in sodium excretion was associated with an increased risk for CHD in subjects with hypertension (adjusted hazard ratio, 1.14; 95% confidence interval, 1.01–1.28; n=2363) and in subjects with NT-proBNP concentrations above the sex-specific median (adjusted hazard ratio, 1.16; 95% confidence interval, 1.03–1.30; n=3771).
CONCLUSIONS—Overall, there was no association between sodium excretion and risk of CHD. The association between sodium excretion and CHD risk was modified by NT-proBNP. Higher sodium excretion was associated with an increased CHD risk among subjects with increased NT-proBNP concentrations or with hypertension.
Scope
Cocoa, rich in flavan‐3‐ols, improves vascular function, but the contribution of specific flavan‐3‐ols is unknown. We compared the effects of pure epicatechin, a major cocoa flavan‐3‐ol, and ...chocolate.
Methods and results
In a randomized crossover study, twenty healthy men (40–80 years) were supplemented with: (1) 70g dark chocolate (150 mg epicatechin) with placebo capsules; (2) pure epicatechin capsules (2 × 50 mg epicatechin) with 75g white chocolate; and (3) placebo capsules with 75 g white chocolate (0 mg epicatechin). Vascular function (flow‐mediated dilation (FMD) and augmentation index (AIx)) were measured before and 2 hours after interventions. Epicatechin metabolites time‐profiles were measured in blood to calculate the bioavailability. Pure epicatechin did not significantly improve FMD (+0.75%; p = 0.10) or AIx (–2.2%; p = 0.23) compared to placebo. Dark chocolate significantly improved FMD (+0.96%; p = 0.04) and AIx (–4.6%; p = 0.02). Differences in improvements in FMD (+ 0.21%; p = 0.65) or Aix (–2.4%; p = 0.20) between pure epicatechin and dark chocolate were not significant. The bioavailability of epicatechin did not differ between pure epicatechin and dark chocolate (p = 0.14).
Conclusions
Despite differences in epicatechin dose, improvements in vascular function after pure epicatechin and chocolate were similar and the bioavailability did not differ, suggesting a role for epicatechin.
Acute vascular effects of pure epicatechin and dark chocolate are compared. The bioavailability of epicatechin does not differ between pure epicatechin and dark chocolate. Improvements in vascular function after pure epicatechin and chocolate are also not significantly different and the bioavailability is similar. These results suggest a role for epicatechin.
To study the associations of non-alcoholic fatty liver disease (NAFLD), chronic kidney disease (CKD), and serum uric acid (SUA) in patients with post-myocardial infarction (MI) patients, and the ...relationship of SUA with 12-year mortality risk.
We included 3,396 patients (60-80 years old, 78% men) of the Alpha Omega Cohort. Multivariable prevalence ratios (PRs) were obtained for the association of NAFLD fatty liver index (FLI), ≥77 (women) and ≥79 (men) with CKD estimated glomerular filtration rate (eGFR), <60 mL/min per 1.73 m
. We calculated sensitivity and specificity of SUA to detect the (combined) presence and absence of NAFLD and CKD. Cause-specific mortality was monitored from enrolment (2002-2006) through December 2018. Hazard ratios (HRs) for all-cause and cardiovascular disease (CVD) mortality in SUA categories were obtained from multivariable Cox models.
Median baseline FLI was 67 (men, 68; women, 64), and mean ± SD eGFR was 81 ± 20 mL/min per 1.73 m
(17% with CKD). Sex-specific FLI was associated with higher CKD prevalence (PR
, 1.94; 95% confidence interval: 1.57, 2.39). Baseline SUA was 0.36 ± 0.09 mmol/L. With increasing SUA concentrations, specificity for the presence of NAFLD, CKD, or both increased, and sensitivity decreased. During 12 (interquartile range, 9-14) years of follow-up, 1,592 patients died (713 from CVD). HRs ranged from 1.08 (0.88, 1.32) for SUA ≤0.25 mmol/L to 2.13 (1.75, 2.60) for SUA >0.50 mmol/L vs. SUA >0.30-0.35 mmol/L for all-cause mortality. For CVD mortality, HRs ranged from 1.05 (0.77, 1.44) to 2.43 (1.83, 3.25).
NAFLD and CKD were strongly associated, which was reflected by higher SUA concentrations. SUA was a strong predictor of 12-year mortality risk after MI.
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