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Background: Inverse associations between dietary protein and hypertension have been reported, which may be attributed to specific amino acids. Objective: We examined whether the intake of glutamic acid, arginine, cysteine, lysine, or tyrosine was associated with blood pressure (BP) levels (n = 3086) and incident hypertension (n = 1810) in the Rotterdam Study. Design: We calculated BP levels in quartiles of amino acid intake as a percentage of total protein intake (% of protein) with adjust

Background: Mild metabolic acidosis, which can be caused by diet, may result in elevated blood pressure (BP). Objective: The objective was to examine whether dietary acid load was associated with incident hypertension in a cohort of older Dutch adults from the Rotterdam Study. Design: The analyses included 2241 participants aged ≥55 y who were free of hypertension at baseline (1990-1993) and who had complete dietary and BP data. Dietary data were obtained from a 170-item food-frequency questionnaire. We used 2 measures to characterize dietary acid load: 1) potential renal acid load (PRAL) by using an algorithm including protein, phosphorus, potassium, calcium, and magnesium, and 2) estimated net endogenous acid production (NEAP) based on protein and potassium. HRs for 6-y incidence of hypertension were obtained in tertiles of PRAL and NEAP with adjustment for age, sex, BMI, smoking, education, and intakes of alcohol, fiber, and total energy. Results: We identified 1113 incident cases of hypertension during 8707 person-years of follow-up. The median dietary acid load ranged from -14.6 to 19.9 mEq/d across categories of PRAL. Hypertension risk was not significantly associated with dietary acid load. The multivariate HRs (95% CIs) in consecutive tertiles of PRAL were 1.00 (reference), 1.01 (0.87, 1.17), and 1.02 (0.88, 1.18) (P trend = 0.83). The median dietary acid loads were 30.4, 36.7, and 43.7 mEq/d, respectively, in consecutive tertiles of NEAP. Corresponding HRs for NEAP were 1.00 (reference), 0.92 (0.80, 1.07), and 0.94 (0.81, 1.10) (P-trend = 0.46). Conclusion: The findings from this prospective cohort study provided no evidence of an association between dietary acid load and risk of hypertension in older adults.

Background: Mild metabolic acidosis, which can be caused by diet, may result in elevated blood pressure (BP). Design: The analyses included 2241 participants aged =55 y who were free of hypertension at baseline (1990–1993) and who had complete dietary and BP data. Dietary data were obtained from a 170-item food-frequency questionnaire. We used 2 measures to characterize dietary acid load: 1) potential renal acid load (PRAL) by using an algorithm including protein, phosphorus, potassium, calcium, and magnesium, and 2) estimated net endogenous acid production (NEAP) based on protein and potassium. HRs for 6-y incidence of hypertension were obtained in tertiles of PRAL and NEAP with adjustment for age, sex, BMI, smoking, education, and intakes of alcohol, fiber, and total energy. Results: We identified 1113 incident cases of hypertension during 8707 person-years of follow-up. The median dietary acid load ranged from -14.6 to 19.9 mEq/d across categories of PRAL. Hypertension risk was not significantly associated with dietary acid load. The multivariate HRs (95% CIs) in consecutive tertiles of PRAL were 1.00 (reference), 1.01 (0.87, 1.17), and 1.02 (0.88, 1.18) (P trend = 0.83). The median dietary acid loads were 30.4, 36.7, and 43.7 mEq/d, respectively, in consecutive tertiles of NEAP. Corresponding HRs for NEAP were 1.00 (reference), 0.92 (0.80, 1.07), and 0.94 (0.81, 1.10) (P-trend = 0.46). Conclusion: The findings from this prospective cohort study provided no evidence of an association between dietary acid load and risk of hypertension in older adults

Background - Little is known about the relation of different dietary protein types with blood pressure (BP). We examined whether intake of total, plant, animal, dairy, meat, and grain protein was related to BP in a cross sectional cohort of 20,820 Dutch adults, aged 20–65 y and not using antihypertensive medication. Design - Mean BP levels were calculated in quintiles of energy-adjusted protein with adjustment for age, sex, BMI, education, smoking, and intake of energy, alcohol, and other nutrients including protein from other sources. In addition, mean BP difference after substitution of 3 en% carbohydrates or MUFA with protein was calculated. Results - Total protein and animal protein were not associated with BP (ptrend = 0.62 and 0.71 respectively), both at the expense of carbohydrates and MUFA. Systolic BP was 1.8 mmHg lower (ptrend36 g/d) than in the lowest (

Evidence suggests a small beneficial effect of dietary protein on blood pressure (BP), especially for plant protein. We examined the relationship between several types of dietary protein (total, plant, animal, dairy, meat and grain) and the risk of hypertension in a general population of 3588 Dutch adults, aged 26–65 years, who were free of hypertension at baseline. Measurements were done at baseline and after 5 and 10 years of follow-up. Hazard ratios (HR), with 95 % CI, for incident hypertension were obtained in tertiles of energy-adjusted protein, using time-dependent Cox regression models. Models were adjusted for age, sex, BMI, education, smoking, baseline systolic BP, dietary confounders and protein from other sources (if applicable). Mean BP was 118/76 mmHg at baseline. Protein intake was 85 (sd 22) g/d (approximately 15 % of energy) with 62 % originating from animal sources. The main sources of protein were dairy products (28 %), meat (24 %) and grain (19 %). During the follow-up, 1568 new cases of hypertension were identified (44 % of the participants). Energy-adjusted intake of total protein, plant protein and animal protein was not significantly associated with hypertension risk (all HR approximately 1·00, P>0·60). Protein from grain showed a significant inverse association with incident hypertension, with a HR of 0·85 (95 % CI 0·73, 1·00, Ptrend = 0·04) for the upper tertile ( = 18 g/d) v. the lower tertile ( <14 g/d), whereas dairy protein and meat protein were not associated with incident hypertension. In conclusion, higher intake of grain protein may contribute to the prevention of hypertension, which warrants confirmation in other population-based studies and randomised controlled trials.

Background: The consumption of dairy products may influence the risk of cardiovascular disease (CVD) and total mortality, but conflicting findings have been reported. Objective: The objective was to examine the associations of milk, total dairy products, and high- and low-fat dairy intakes with the risk of CVD [including coronary heart disease (CHD) and stroke] and total mortality. Design: PubMed, EMBASE, and SCOPUS were searched for articles published up to February 2010. Of >5000 titles evaluated, 17 met the inclusion criteria, all of which were original prospective cohort studies. Random-effects meta-analyses were performed with summarized dose-response data. Milk as the main dairy product was pooled in these analyses. Results: In 17 prospective studies, there were 2283 CVD, 4391 CHD, 15,554 stroke, and 23,949 mortality cases. A modest inverse association was found between milk intake and risk of overall CVD [4 studies; relative risk (RR): 0.94 per 200 mL/d; 95% CI: 0.89, 0.99]. Milk intake was not associated with risk of CHD (6 studies; RR: 1.00; 95% CI: 0.96, 1.04), stroke (6 studies; RR: 0.87; 95% CI: 0.72, 1.05), or total mortality (8 studies; RR per 200 mL/d: 0.99; 95% CI: 0.95, 1.03). Limited studies of the association of total dairy products and of total high-fat and total low-fat dairy products (per 200 g/d) with CHD showed no significant associations. Conclusion: This dose-response meta-analysis of prospective studies indicates that milk intake is not associated with total mortality but may be inversely associated with overall CVD risk; however, these findings are based on limited numbers.

01 augustus 2010, Contains fulltext : 88397.pdf (publisher's version ) (Closed access), BACKGROUND: The C282Y mutation of the hemochromatosis (HFE)-gene increases body iron status. Among Caucasians, the carrier frequency of this mutation is 8-9%. C282Y carriers may be more susceptible to iron-induced atherosclerosis due to higher iron levels. It has also been postulated that the C282Y mutation could alter aspects of iron metabolism. We examined the relationship between the C282Y mutation, iron status, and carotid intima-media thickness (IMT) as a marker of atherosclerosis. METHODS AND RESULTS: The present study comprised 764 Dutch men and post-menopausal women aged 50-70 years. Mean and maximum carotid IMT were assessed by B-mode ultrasonography. Blood was sampled for assessment of the C282Y mutation and body iron status. Parameters of iron status (e.g. ferritin and non-transferrin bound iron) were significantly higher in C282Y carriers (n=80; 10%) compared to non-carriers (P-values <0.001), however, there was no difference in the carotid IMT measures. Among non-smokers (n=222), carotid IMT was 0.051 mm (95% CI: 0.005; 0.096) lower in carriers compared to non-carriers (P=0.03), which remained after adjustment for iron parameters. Within the subgroup of carriers, higher carotid IMT values were observed across sex-specific quartiles of ferritin (mean IMT: 0.789, 0.787, 0.814, and 0.865 mm; P-trend=0.08), whereas this association was absent in non-carriers. CONCLUSION: Overall, we found no association of HFE genotype with carotid IMT, despite higher iron status. Interestingly, C282Y carriers may be hyper responsive to vascular damage which needs to be confirmed in prospective cohort studies.

Background - Elevated blood pressure (BP), which is a major risk factor for cardiovascular disease, is highly prevalent worldwide. Recently, interest has grown in the role of dietary protein in human BP. We performed a systematic review of all published scientific literature on dietary protein, including protein from various sources, in relation to human BP. Methodology/Principal Findings - We performed a MEDLINE search and a manual search to identify English language studies on the association between protein and blood pressure, published before June 2010. A total of 46 papers met the inclusion criteria. Most observational studies showed no association or an inverse association between total dietary protein and BP or incident hypertension. Results of biomarker studies and randomized controlled trials indicated a beneficial effect of protein on BP. This beneficial effect may be mainly driven by plant protein, according to results in observational studies. Data on protein from specific sources (e.g. from fish, dairy, grain, soy, and nut) were scarce. There was some evidence that BP in people with elevated BP and/or older age could be more sensitive to dietary protein. Conclusions/Significance - In conclusion, evidence suggests a small beneficial effect of protein on BP, especially for plant protein. A blood pressure lowering effect of protein may have important public health implications. However, this warrants further investigation in randomized controlled trials. Furthermore, more data are needed on protein from specific sources in relation to BP, and on the protein-BP relation in population subgroups

Diet and lifestyle play an important role in maintaining a healthy blood pressure. Whether intake of dairy products could reduce population blood pressure remains to be established. We examined the association of (specific types of) dairy food intake with blood pressure and risk of hypertension using data from two Dutch population-based cohort studies; i.e. the MORGEN study and the Rotterdam study. Blood pressure level was not consistently associated with overall dairy intake or intake of specific dairy foods in 21,553 Dutch adults from the MORGEN study. However, both in the MORGEN study and in the Rotterdam study, the risk of hypertension was reduced by ~20% in subjects who consumed more than 150 mL of low-fat dairy per day. Other dairy foods, i.e. fermented dairy, high-fat dairy, milk and milk products, and cheese, were not consistently associated with risk of hypertension. In addition, we assessed the effect of two dairy components on human blood pressure, i.e. lactotripeptides and cis-9, trans-11 conjugated linoleic acid, in controlled intervention studies. These dairy components did not affect blood pressure.

Diet and lifestyle are important for maintaining a healthy blood pressure (BP). The role of dairy in the prevention of hypertension, however, is not yet clear. We studied the relation of dairy intake with BP in 21,553 Dutch participants aged 20¿65 y who did not use antihypertensive medication. In addition, the risk of hypertension was examined in 3454 of these participants with a 5-y follow-up. Dairy consumption was assessed at baseline (1993¿1997) using a semiquantitative FFQ that included 178 foods and beverages. Baseline BP and odds ratios (OR) (95% CI) for incident hypertension were calculated in categories of energy-adjusted dairy intake with adjustment for age, sex, socioeconomic status, BMI, smoking, alcohol use, and dietary intakes. Participants had a median intake of 344 g/d (2.3 servings) for total dairy and 174 g/d (1.2 servings) for low-fat dairy. Mean BP was 120/76 mm Hg. Intake of total dairy, specific dairy groups (i.e. low-fat, high-fat, fermented) and dairy products (i.e. cheese, yogurt) were not consistently related to BP. Of 3454 participants who were followed, 713 developed hypertension. The risk of hypertension tended to be inversely related to low-fat dairy intake, with multivariate OR (95% CI) of 1.00, 0.78 (0.61, 1.00), 0.81 (0.63, 1.03), and 0.82 (0.64, 1.06; P-trend: 0.24) in consecutive quartiles. We conclude that variations in BP in a general middle-aged Dutch population cannot be explained by overall dairy intake. A beneficial effect of low-fat dairy on risk of hypertension, however, cannot be excluded, which warrants further investigation in prospective population-based studies

Background: Little is known about the effect of different types of dairy food products on the development of hypertension. Objective: The objective was to determine whether the incidence of hypertension in older Dutch subjects is associated with intake of dairy products. Design: We examined the relation between dairy intake and incident hypertension in 2245 participants of the Rotterdam Study aged 55 y with complete dietary and blood pressure data, who were free of hypertension at baseline (1990–1993). Blood pressure was reexamined in 1993–1995 and in 1997–1999. Hazard ratios (HRs) with 95% CIs for 2- and 6-y incidence of hypertension were obtained in quartiles of energy-adjusted dairy intake, with adjustment for age, sex, BMI, smoking, educational level, dietary factors, and intake of alcohol and total energy. Results: Risk of hypertension after 2 y of follow-up (664 incident cases) was inversely associated with dairy product intake. After adjustment for confounders, HRs (95% CIs) were 1.00, 0.82 (0.67, 1.02), 0.67 (0.54, 0.84), and 0.76 (0.61, 0.95) in consecutive quartiles of total dairy product intake (P for trend = 0.008). Corresponding HRs for low-fat dairy products were 1.00, 0.75 (0.60, 0.92), 0.77 (0.63, 0.96), and 0.69 (0.56, 0.86) (P for trend = 0.003). Analysis of specific types of dairy products showed an inverse association with milk and milk products (P for trend = 0.07) and no association with high-fat dairy or cheese (P > 0.6). After 6 y of follow-up (984 incident cases), the associations with hypertension were attenuated to risk reductions of 20% for both total and low-fat dairy products between the extreme quartiles of intake (P for trend = 0.07 and 0.09, respectively

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Milk-derived peptides with ACE-inhibiting properties may have antihypertensive effects in humans. We conducted a randomized double-blind placebo-controlled trial to examine the blood pressure lowering potential of 2 ACE-inhibiting lactotripeptides, ie, Isoleucine-Proline-Proline and Valine-Proline-Proline. We included 135 Dutch subjects with elevated systolic blood pressure who were otherwise healthy and who received no current antihypertensive treatment. After a 2-week run-in period on placebo, subjects randomly received a daily dose of 200 mL dairy drink with 14 mg lactotripeptides obtained by concentrating fermented milk, enzymatic hydrolysis, or chemical synthesis, or placebo for 8 weeks, followed by a 2-week wash-out. The primary outcome was 8-week change in office systolic blood pressure. Secondary outcomes were change in diastolic blood pressure, home blood pressure, 24-hour ambulatory blood pressure, plasma ACE-activity, and plasma angiotensin II. Blood pressure at baseline was on average 142/84 mm Hg. Lactotripeptides did not significantly change systolic blood pressure (P=0.46) or diastolic blood pressure (P=0.31) compared with placebo. The mean difference (95%-CI) in systolic blood pressure response between treatment and placebo was 2.8 mm Hg (-2.6;8.2) for concentrated fermented milk lactotripeptides, -0.5 mm Hg (-6.0;5.0) for enzymatic lactotripeptides, and 1.6 mm Hg (-3.9;6.9) for synthetic lactotripeptides. Treatment neither had a significant effect on secondary outcome measures. In conclusion, the present study does not support the hypothesis of a blood pressure lowering effect of the lactotripeptides Isoleucine-Proline-Proline and Valine-Proline-Proline.

Background: Humans and animals show a certain consistency in the response of their serum lipids to fat-modified diets. This may indicate a genetic basis underlying this response. Coffee oil might be used as a model substance to investigate which genes determine differences in the serum lipid response. Before carrying out such studies our objective was to investigate to what extent the effect of coffee oil on serum lipid concentrations is reproducible within subjects. Methods: The serum lipid response of 32 healthy volunteers was measured twice in separate five-week periods in which coffee oil was administered (69 mg cafestol / day). Results: Total cholesterol levels increased by 24% in period 1 (range: 0; 52%) and 18% in period 2 (1; 48%), LDL cholesterol by 29 % (-9;71%) and 20% (-12;57%), triglycerides by 66% (16;175%) and 58% (-13;202%), and HDL cholesterol did not change significantly: The range of the HDL response was -19;25% in period 1 and -20;33% in period 2. The correlation between the two responses was 0.20 (95%CI -0.16, 0.51) for total cholesterol, 0.16 (95%CI -0.20, 0.48) for LDL, 0.67 (95%CI 0.42, 0.83) for HDL, and 0.77 (95%CI 0.56, 0.88) for triglycerides. Conclusions: The responses of total and LDL cholesterol to coffee oil were poorly reproducible within subjects. The responses of HDL and triglycerides, however, appeared to be highly reproducible. Therefore, investigating the genetic sources of the variation in the serum-lipid response to coffee oil is more promising for HDL and triglycerides.