Background: Cardiovascular diseases (CVDs) are the greatest cause of death globally, and their reduction is a key public-health target. High blood pressure (BP) affects 1 in 3 people in the United Kingdom, and previous studies have shown that milk consumption is associated with lower BP.Objective: We investigated whether intact milk proteins lower 24-h ambulatory blood pressure (AMBP) and other risk markers of CVD.Design: The trial was a double-blinded, randomized, 3-way–crossover, controlled intervention study. Forty-two participants were randomly assigned to consume 2 × 28 g whey protein/d, 2 × 28 g Ca caseinate/d, or 2 × 27 g maltodextrin (control)/d for 8 wk separated by a 4-wk washout. The effects of these interventions were examined with the use of a linear mixed-model ANOVA.Results: Thirty-eight participants completed the study. Significant reductions in 24-h BP [for systolic blood pressure (SBP): −3.9 mm Hg; for diastolic blood pressure (DBP): −2.5 mm Hg; P = 0.050 for both)] were observed after whey-protein consumption compared with control intake. After whey-protein supplementation compared with control intake, peripheral and central systolic pressures [−5.7 mm Hg (P = 0.007) and −5.4 mm Hg (P = 0.012), respectively] and mean pressures [−3.7 mm Hg (P = 0.025) and −4.0 mm Hg (P = 0.019), respectively] were also lowered. Flow-mediated dilation (FMD) increased significantly after both whey-protein and calcium-caseinate intakes compared with control intake [1.31% (P < 0.001) and 0.83% (P = 0.003), respectively]. Although both whey protein and calcium caseinate significantly lowered total cholesterol [−0.26 mmol/L (P = 0.013) and −0.20 mmol/L (P = 0.042), respectively], only whey protein decreased triacylglycerol (−0.23 mmol/L; P = 0.025) compared with the effect of the control. Soluble intercellular adhesion molecule 1 and soluble vascular cell adhesion molecule 1 were reduced after whey protein consumption (P = 0.011) and after calcium-caseinate consumption (P = 0.039), respectively, compared with after control intake.Conclusions: The consumption of unhydrolyzed milk proteins (56 g/d) for 8 wk improved vascular reactivity, biomarkers of endothelial function, and lipid risk factors. Whey-protein supplementation also lowered 24-h ambulatory SBP and DBP. These results may have important implications for public health. This trial was registered at clinicaltrials.gov as NCT02090842.

Epidemiological studies show an inverse association between dairy consumption and blood pressure (BP) but there are few data on the postprandial effects of milk proteins. This study examined their effects, compared to maltodextrin, on postprandial BP and other CVD risk markers in volunteers with mild and pre-hypertension over an 8 h period. In this double-blinded, randomised, cross-over, controlled study 27 adults ingested a high-fat, isoenergetic breakfast and lunch with 28 g whey protein, 28 g Ca-caseinate or 27 g maltodextrin. Whey protein reduced systolic BP compared with Ca-caseinate (−15.2 ± 13.6 mmHg) and maltodextrin (−23.4 ± 10.5 mmHg) up to 5 h post-ingestion. There was an improvement in arterial stiffness after whey protein compared with maltodextrin (incremental Area Under the Curve- iAUC0–8h: +14.4 ± 6.2%). Despite similar glucose levels after both whey protein and Ca-caseinate, whey protein induced a higher insulin response than Ca-caseinate (iAUC0–8h: +219.5 ± 54.6 pmol/L). Ca-caseinate induced less suppression of non-esterified fatty acids than whey protein (iAUC0–5h: −58.9 ± 135.5 μmol/L) and maltodextrin (iAUC0–5h: −106.9 ± 89.4 μmol/L) and induced a smaller postprandial triacylglycerol response than whey protein (iAUC0–8h: −1.68 ± 0.6 mmol/L). Milk proteins co-ingestion with high-fat meals may have the potential to maintain or improve CVD risk factors.

No abstract

Cardiovascular diseases are the major cause of death in the world and their reduction is a key public health target (1) . Epidemiological studies have shown that milk consumption has beneficial impacts on the cardiovascular system (2) . The aim of this study was to investigate if intact dairy proteins can improve vascular function in mildly hypertensive adults. This was an 8-wk double-blinded, randomised, cross-over, controlled intervention study. Forty-two participants were randomised to consume 2 × 28 g of whey protein, Ca-caseinate and 2 × 27 g maltodextrin (control) daily. A linear mixed-model ANOVA was used to assess the impacts of the interventions. Thirty-eight participants completed the study. We found significant reductions in peripheral and central systolic pressure (−5·7 mmHg, p = 0·007; −5·4 mmHg, p = 0·012, respectively) and mean pressure (-3·7 mmHg, p = 0·025; -4·0 mmHg, p = 0·019, respectively) assessed by pulse wave analysis after whey protein supplementation compared with control. Flow-mediated dilation increased significantly after both whey protein and Ca-caseinate compared with control (1·31 %, p < 0·001, and 0·83 %, p = 0·003, respectively). Both whey protein and Ca-caseinate significantly reduced total cholesterol (-0·26 mmol/L, p = 0·013; -0·20 mmol/L, p = 0·042, respectively), however only whey protein decreased triacylglycerol (-0·23 mmol/L, p = 0·025) too, compared with control. Adhesion molecules were also lowered: sICAM-1 and sVCAM-1 were reduced after whey protein (p = 0·011) and Ca-caseinate consumption (p = 0·039) compared with control, respectively. The 8-week consumption of intact milk proteins resulted in improvements in vascular reactivity, biomarkers of endothelial function and lipid risk factors with greater benefit after whey protein supplementation. This may have important implications for public health. This trial was registered at clinicaltrials.gov as NCT02090842.

No abstract

No abstract

Evidence suggests that whey protein can enhance glycaemic control (1) and that this effect is primarily due the insulinotropic effect of the amino acid L-leucine (2) . The Whey2Glo study aimed to compare the effects of whey protein isolate (WPI) with partially hydrolysed wheat protein (PHWP) and determine whether the L-leucine content of the PHWP treatment had an impact on postprandial glycaemia and gut hormones in participants with normal to moderately elevated fasting glucose concentrations. An acute, doubleblind, controlled, cross-over study was conducted in 9 adults (mean±SD age: 61 ± 6 y, BMI: 24.4 ± 2.0 kg/m 2 and fasting glucose: 5.43 ± 0.94 mmol/L). After an overnight fast, they were randomised to consume iso-energetic sequential high-fat test meals at breakfast (0 min; 4.2 MJ, 52 g fat, 96 g carbohydrate and 37 g protein) and lunch (330 min; 2.6 MJ, 32 g fat, 47 g carbohydrate and 37 g protein), containing 25 g of either WPI, PHWP, or PHWP plus leucine (1.3 g) on separate occasions at least 3 weeks apart. Blood samples were collected before (fasting) and at 30, 60, 90, 120, 180, 240, 300, 330, 360, 390, 420 and 480 min after breakfast to measure serum insulin (primary outcome), glucose and gut hormones. Postprandial time course profiles were analysed using a 2-way repeated measures ANOVA and the summary measures area (AUC) and incremental area under the curve (iAUC) were calculated and analysed using 1-way repeated measures ANOVA.There was a significant effect of protein treatment on the postprandial insulin response (P = 0.009), with a higher AUC and iAUC observed after the meals containing PHWP plus leucine compared to PHWP alone (P ≤ 0.011). The WPI containing meals also induced a higher insulin AUC than PHWP alone (P = 0.046) whereas the iAUC for the C-peptide response was significantly lower compared with PHWP plus leucine (P = 0.049). PHWP alone significantly increased the iAUC for the glucose-dependent insulinotropic polypeptide response compared to WPI (P = 0.045). Although fasting glucose concentrations were significantly different prior to the intake of the WPI compared with the PHWP (P = 0.022) containing meals, the iAUC for the postprandial glucose responses were found to be similar between protein treatments. No significant differences were observed for the ghrelin and glucagon like peptide-1 responses after the three protein interventions. Our data supports the hypothesis that L-leucine has a postprandial insulinotropic effect and may be one of the bioactive amino acids in WPI. However, despite the higher postprandial insulin concentrations, there was no effect on the postprandial glucose response which may represent a power issue for this secondary outcome measure. These findings need confirmation in larger, sufficiently powered postprandial studies in those with normal and hyper-glycaemia.