What Amino Acid Will Clean Plack From Your Arteries.

J Nutr. 2022 Sep; 145(9): 2130–2138.

Amino Acid Intakes Are Inversely Associated with Arterial Stiffness and Primal Blood Pressure level in Women^{1, 2}

Amy Jennings

ⁱⁱⁱSection of Nutrition, Norwich Medical School, University of East Anglia, Norwich, United Kingdom; and

Alex MacGregor

³Department of Nutrition, Norwich Medical School, University of Eastward Anglia, Norwich, United Kingdom; and

Ailsa Welch

ⁱⁱⁱDepartment of Nutrition, Norwich Medical School, University of E Anglia, Norwich, Great britain; and

Phil Chowienczyk

^fourSection of Twin Enquiry and Genetic Epidemiology, King's College London, London, Uk

Tim Spector

^fourDepartment of Twin Research and Genetic Epidemiology, King's Higher London, London, United Kingdom

Aedín Cassidy

³Department of Nutrition, Norwich Medical School, University of East Anglia, Norwich, United Kingdom; and

Received 2022 Mar 31; Revised 2022 May 11; Accepted 2022 Jul 2.

Abstruse

Background: Although data suggest that intakes of total protein and specific amino acids (AAs) reduce blood pressure, data on other cardiovascular disease run a risk factors are limited.

Objective: We examined associations between intakes of AAs with known mechanistic links to cardiovascular health and direct measures of arterial stiffness, central blood pressure, and atherosclerosis.

Methods: In a cantankerous-sectional study of 1898 female twins aged xviii–75 y from the TwinsUK registry, intakes of vii cardioprotective AAs (arginine, cysteine, glutamic acrid, glycine, histidine, leucine, and tyrosine) were calculated from nutrient-frequency questionnaires. Direct measures of arterial stiffness and atherosclerosis included cardinal systolic blood pressure (cSBP), mean arterial pressure (MAP), augmentation index (AI), pulse wave velocity (PWV), and intima–media thickness (IMT). ANCOVA was used to assess the associations between endpoints of arterial stiffness and intake (per quintile), adjusting for potential confounders.

Results: In multivariable analyses, higher intakes of total protein and seven potentially cardioprotective AAs were associated with lower cSBP, MAP, and PWV. Higher intakes of glutamic acid, leucine, and tyrosine were most strongly associated with PWV, with corresponding differences of −0.4 ± 0.2 g/south (P-trend = 0.02), −0.4 ± 0.2 k/s (P-trend = 0.03), and −0.4 ± 0.2 m/south (P-trend = 0.03), comparing farthermost quintiles. There was a significant interaction between AA intakes and protein source, and higher intakes of AAs from vegetable sources were associated with lower central blood pressure and AI. Higher intakes of glutamic acrid, leucine, and tyrosine from brute sources were associated with lower PWV.

Conclusions: These data provide evidence to suggest that intakes of several AAs are associated with cardiovascular benefits across blood pressure reduction in good for you women. The magnitude of the observed associations was like to those previously reported for other lifestyle factors. Increasing intakes of these AAs could exist an important and readily achievable mode to reduce cardiovascular disease risk.

Keywords: protein, amino acids, claret pressure, arterial stiffness, cardiovascular

Introduction

Dietary protein intake has received increased attention for its part in preventing cardiovascular illness, particularly in relation to claret pressure–lowering effects. A higher total protein intake has been inversely associated with both systolic and diastolic claret pressure in a number of observational studies (1). Furthermore, a meta-analysis of xl randomized, controlled trials reported pregnant decreases in blood force per unit area with increased intakes of total (systolic −1.viii mm Hg and diastolic −i.2 mm Hg), creature (systolic −2.5 mm Hg and diastolic −ane.0 mm Hg), and vegetable (systolic −two.3 mm Hg and diastolic −ane.3 mm Hg) protein (2). Other studies, however, have establish that information technology is poly peptide from vegetable sources that is inversely related to blood pressure, with no significant effects for brute protein (iii, iv). Furthermore, plant protein has been shown to exist a strong marker of dietary quality, whereas the findings for brute protein are currently equivocal (5).

The mechanisms explaining the vasoactive properties of dietary poly peptide are likely to exist dependent on the amino acid composition and the source of the poly peptide. A number of amino acids, including glutamic acrid, arginine, glycine, cysteine, and histidine, have been shown to modulate concentrations of nitric oxide, a potent vasodilator (6–9). In addition, leucine has been shown to modulate insulin/phosphoinositide 3-kinase signaling in animal models (10), and cysteine has been shown to increase glucose uptake and concentrations of glucose transporter iii and glucose transporter four in vitro; in rat models, dietary cysteine has been shown to reduce insulin resistance and glucose intolerance (xi, 12). Tyrosine is thought to reduce claret force per unit area by stimulating catecholamine synthesis in the encephalon (13), whereas histidine has been shown to inhibit vascular expression of the angiotensin converting enzyme mRNA in hypertensive rats (ix). To our noesis, only 1 previous cross-sectional written report has examined associations between intakes of amino acids with established vasoprotective properties and blood force per unit area and showed that a higher intake of tyrosine was related to a two.iv mm Hg lower systolic blood pressure level (14). Other cross-sectional and longitudinal studies, which take examined associations between blood pressure and all amino acids, reported inverse associations between higher intakes of glutamic acid, histidine, and tyrosine and systolic blood pressure (xv–17). Higher intakes of glutamic acid and cysteine has also been associated with a decreased risk of stroke mortality and incidence in women (eighteen, 19).

There is evidence to suggest that measures of fundamental arterial role are better predictors of cardiovascular events than brachial claret pressure (twenty). Arterial stiffness provides assessment of both the structure and function of the artery, and pulse wave velocity (PWV)^five is considered to be the gold standard measurement and near consistently predictive of cardiovascular disease risk (20). The measurement of key claret pressure with the utilize of the augmentation index (AI) is considered to be a stiff predictor of atherosclerosis (20), and intima–media thickness (IMT) predicts future incidence of coronary heart disease (21).

To our knowledge, no previous cross-exclusive studies accept examined associations betwixt the intakes of these seven potentially cardioprotective amino acids and in vivo measures of arterial stiffness and atherosclerosis. Therefore, we examined associations betwixt these 7 amino acids, which have known mechanistic links to blood pressure, and endpoints of arterial stiffness (PWV and AI), atherosclerosis (IMT), and central and peripheral blood pressure in a accomplice of good for you women aged xviii–75y. On the basis of previous research, it was hypothesized that participants with college intakes of arginine, cysteine, glutamic acid, glycine, histidine, leucine, and tyrosine would have improved arterial stiffness and central claret pressure level.

Methods

Report population.

The current study used data nerveless from female twin pairs in the TwinsUK registry, a nationwide registry that consists of developed twin volunteers recruited from the general population through national media campaigns in the United Kingdom (22). All participants were unaware of the specific hypotheses being tested, and were non selected on the basis of the variables being studied. Zygosity was derived past questionnaire and confirmed by multiplex Deoxyribonucleic acid fingerprinting (PE Practical Biosystems). Informed consent was obtained from all participants and ethical blessing for the study was gained from St. Thomas's Infirmary Research Ethics committee. The participants included in this assay were female twin pairs anile 18–75 y, and were a sample of the full population grouping (n = 5725) who had completed both FFQs and had a clinical assessment of arterial stiffness and atherosclerosis progression between 1996 and 2000. Of the 5119 twins who completed an FFQ, 36% (due north = 1857) were excluded for having an incomplete FFQ (>10 food items were left bare) or implausible energy intake [the ratio of the FFQ-derived gauge of total energy intake to estimated basal metabolic rate brutal 2 SDs outside the hateful ratio (<0.52 or >2.58) for this accomplice] (23). A further 27% of participants (northward = 1364) did not attend a clinical session for vascular cess, which left 1898 participants (949 twin pairs) for the current analysis. PWV and IMT were measured in a subset of 900 participants of the total population who were part of a planned longitudinal study on the heritability of arterial stiffness, of which 728 (81%) completed a valid FFQ and were included in these analyses. A ability calculation related to a clinically significant association with a PWV of 0.4 m/s at an α level of 0.05 revealed 98% power to see an association with 728 participants. This population has previously been shown to be representative of the general population in terms of blood pressure and dietary intake (22, 23).

Assessment of arterial stiffness, central blood pressure and IMT.

Measurements were performed during a unmarried visit to a quiet, temperature-controlled (22–24°C) clinical laboratory. Peripheral systolic blood pressure (pSBP) and peripheral diastolic blood pressure (pDBP) were measured by a trained nurse who used an automated cuff sphygmomanometer (OMRON HEM713C) with the participant in the seated position for at least 3 min before taking 3 measurements. Measures of primal claret pressure and AI were obtained with the subject in a supine position with the use of the SphygmoCor system (Atcor Medical), as described previously for this cohort (24). Intraoperator and interoperator reproducibility, expressed every bit intraclass correlations, were 0.82 and 0.84, respectively (25). In a subset of the population (northward = 728) who were part of a written report on the heritability of arterial stiffness, PWV was calculated from sequential recordings of electrocardiogram-referenced carotid and femoral pressure waveforms obtained by tonometry with the employ of the aforementioned device and transducer, as previous described (26).

Cess of amino acid intake.

Participants completed a 131-item validated FFQ (27, 28). Intakes of amino acids were derived predominantly with the use of UK nutrient composition data simply with additional data from the USDA (29, 30). The intake of glutamic acid in these datasets relates to glutamic acid plus glutamine. Values for eighteen private amino acids were assigned to each of the foods listed in the FFQ, and for recipes, values for each ingredient in the dishes were assigned with the use of the data sources described above. When values for total protein from the amino acid database and the latest United kingdom nutrient composition tables differed, the amino acid composition of the food items was modified to friction match the about up-to-date data (29). Intake of private amino acids was calculated as the frequency of consumption of each food multiplied by the amino acrid content of the food for the advisable portion size (31). All foods were classified as of either animal or vegetable origin and for mixed dishes the proportions contributed by fauna and vegetable sources were calculated past breaking downwardly the ingredients into foods that were attributable to a single source. Amino acid data are presented as a percentage of total energy intake in club to best represent the relative proportion to total dietary intake.

Assessment of covariates.

Intakes of energy and nutrients associated with arterial stiffness was determined from the FFQ as previously described. Height was measured to the nearest 0.5 cm with the use of a wall-mounted stadiometer, weight (low-cal clothing only) was measured to the nearest 0.1 kg with digital scales, and BMI was calculated (kilograms per meter squared). Information on family medical history, medication use, lifestyle, and demographic variables were obtained past standardized nurse-administered questionnaire. Concrete activity was classified as inactive, moderate, and active during piece of work, abode, and leisure fourth dimension with the use of a questionnaire strongly correlated in this cohort with more in-depth assessment recording how much time subjects spent in moderate and vigorous nonweight-bearing and weight-bearing action on average per calendar week. The mean time spent in physical activity per calendar week for each physical activeness level was as follows: inactive, 16 min; light activity, 36 min; moderate activity, 102 min; and heavy action, 199 min (32). Under-reporting of energy intake was based on a comparison of total predicted energy expenditure with reported energy intake and establishing quantitative limits to define under-reporters based on CIs calculated by taking into account within-subject variation in energy intake and expenditure (33, 34). Considering excluding participants who nether-report can introduce considerable bias, nether-reporting was considered to be a covariate in all multivariable models (35).

Statistical analysis.

Statistical analyses were performed with Stata statistical software, version 11.2. The assay focused on associations in twins every bit individuals, with SEs adjusted through robust regression with the use of the cluster selection in Stata to take into account dependency within twin pairs. Quintiles of intake were calculated for total protein and the amino acids with known mechanistic links to outcomes associated with cardiovascular illness (arginine, cysteine, glutamic acid, glycine, histidine, leucine, and tyrosine). There was a pregnant interaction betwixt amino acid intake and protein source for PWV, so all analyses were stratified by source (all, vegetable, and animate being). ANCOVA was used to calculate adjusted means and evaluate statistical trends beyond these quintiles of intake. All models were adjusted for age (years); current smoking (yes or no); physical activeness (inactive, moderately agile, or active); BMI (kilograms per meter squared); use of hormone replacement therapy (yes or no); utilize of blood force per unit area or statin medication (yes or no); use of vitamin supplements (yes or no); employ of oral contraceptives (yep or no); menopausal status (pre- or postmenopausal); family history of heart illness or hypertension (yeah or no); under-reporting of dietary intake (yeah or no); and intake of carbohydrates (percentage of energy); SFAs, MUFAs, and PUFAs (percentage of energy); booze (grams); and sodium, potassium, and magnesium (milligrams). In addition, models including private amino acids were adapted for intakes of the other vi amino acids and PWV was adjusted for mean arterial force per unit area (MAP). Unadjusted values in the text are means ± SDs (IQRs) and adjusted values are means ± SEs. A P value < 0.05 was considered to be statistically significant.

Results

The baseline characteristics of the population of 1898 female participants are presented in Table i . A total of 83.3% (n = 1581) of participants classified as normotensive (pSBP <140 mm Hg and pDBP <90 mm Hg; data not shown). At that place were no differences in BMI, free energy intake, or protein intake between the report participants and those excluded from the analyses; however, the participants were younger than those excluded (46.iv ± 12.4 y vs. 50.6 ± 12.9 y, P < 0.01; information not shown).

TABLE ane

Characteristics, vascular function, and dietary intake of the study population¹

	Value
Characteristics
Historic period, y	46.three ± 12.4 (37.0, 56.0)
BMI, kg/mtwo	25.3 ± 4.v (22.two, 27.4)
Female	100
Dizygotic	70.9
Current smoker	18.half dozen
Physically agile	22.vii
Uses hormone replacement therapy	sixteen.3
Uses blood pressure level or statin medication	10.8
Uses vitamin supplements	54.7
Uses oral contraceptives	2.2
Postmenopausal	40.8
Has family unit history of hypertension or heart illness	38.2
Vascular function
Peripheral systolic pressure, mm Hg	119 ± xvi (108, 129)
Peripheral diastolic pressure, mm Hg	76.2 ± 11.3 (68.0, 83.0)
Key systolic pressure, mm Hg	111 ± 17 (99, 121)
Central diastolic pressure, mm Hg	77.4 ± eleven.5 (70.0, 84.8)
Central pulse pressure level, mm Hg	33.5 ± 9.3 (27.0, 38.0)
Mean arterial pressure, mm Hg	92.3 ± 13.3 (76.4, 96.iii)
Augmentation index, %	138 ± 26 (122, 156)
Pulse moving ridge velocity,2 m/s	9.1 ± 1.eight (8.0, 10.1)
Intima–media thickness,ii mm	0.seven ± 0.2 (0.half dozen, 0.8)
Dietary intake
Free energy, kcal/d	2007 ± 534 (1632, 2348)
Poly peptide, g/d	lxxx.2 ± 21.6 (65.3, 93.9)
Poly peptide every bit a proportion of body weight, thousand/kg	1.ii ± 0.4 (1.0, one.5)
Arginine, % protein/d	5.four ± 0.4 (5.two, five.7)
Cysteine, % poly peptide/d	1.iv ± 0.1 (i.four, 1.5)
Glutamic acid, % protein/d	19.eight ± 1.1 (19.1, 20.four)
Glycine, % protein/d	4.0 ± 0.3 (3.8, 4.ii)
Histidine, % protein/d	2.8 ± 0.i (2.7, two.9)
Leucine, % protein/d	7.9 ± 0.2 (seven.8, 8.0)
Tyrosine, % protein/d	3.5 ± 0.1 (3.4, three.five)
Carbohydrates, % free energy/d	48.ii ± six.3 (44.iv, 52.2)
Saturated fat, % energy/d	xi.6 ± ii.9 (9.65, 13.four)
Monounsaturated fat, % energy/d	ten.4 ± 2.2 (9.0, 11.8)
Polyunsaturated fatty, % energy/d	6.nine ± 1.7 (5.8, 8.0)
Alcohol, yard/d	9.ix ± 13.vi (1.two, thirteen.4)
Sodium, mg/d	2300 ± 785 (1760, 2750)
Potassium, mg/d	4200 ± 1110 (3430, 4850)
Magnesium, mg/d	364 ± 100 (295, 422)

Full poly peptide intake was 85.1 ± 23.4 g/d and protein contributed sixteen.2% to total energy intake. Of the vii amino acids investigated, glutamic acid (3.2% energy intake) and leucine (1.3% energy intake) made the greatest contribution to total free energy intake. Animal and vegetable sources contributed a similar corporeality to intakes of arginine (52% brute), glutamic acid (51% creature), and glycine (55% beast), whereas intakes of histidine (60% animal), tyrosine (62% animal), and leucine (61% animal) was predominantly from brute sources ( Effigy 1 ). Conversely, vegetable sources contributed more to cysteine intake (42% animal). Generally, correlations between the amino acids investigated ranged from 0.03 (glutamic acid and leucine) to 0.61 (leucine and tyrosine), although stronger correlations were observed between glycine and leucine (0.70) and arginine and glycine (0.77).

The percentage contribution of animal and vegetable foods to amino acrid intake and fundamental dietary sources in 1898 women anile 18–75 y.

In multivariable analyses, college intakes of full protein and the 7 private amino acids examined were significantly associated with lower peripheral and fundamental claret pressure ( Table 2 ), with the exception of full poly peptide for key pulse pressure (cPP) (P-tendency 0.06) and glycine for pDBP (P-trend 0.11) and central diastolic blood force per unit area (P-trend = 0.08). The magnitude of association was greatest for tyrosine intake, with differences between quintile 5 and quintile 1 of −v.vi ± 1.3 mm Hg for pSBP (P-trend < 0.01), −five.5 ± 1.three mm Hg for primal systolic blood force per unit area (cSBP) (P-trend < 0.01), −2.three ± 0.seven mm Hg for cPP (P-tendency < 0.01), and −iv.0 ± 1.1 mm Hg for MAP (P-trend < 0.01) (Tabular array 2). A higher leucine intake was too associated with significantly lower systolic claret pressure (peripheral and central), cPP, and MAP, with differences between extreme quintiles of intake of −5.iv ± one.iii mm Hg (P-trend < 0.01), −v.v ± 1.3 mm Hg (P-trend < 0.01), −two.6 ± 0.7 mm Hg (P-trend < 0.01), and −3.viii ± ane.1 mm Hg (P-tendency < 0.01), respectively. For arterial stiffness, glutamic acrid, leucine, and tyrosine intakes were significantly inversely associated with PWV (afterward adjustment for MAP) with corresponding differences of −0.four ± 0.2 m/s (P-trend = 0.01), −0.4 ± 0.2 g/s (P-trend = 0.04) and −0.four ± 0.ii m/due south (P-trend = 0.02), comparing extremes of intake. Sensitivity analysis showed that the magnitude of associations with PWV were non markedly inverse when protein was residually adjusted for energy intake (Q5–Q1, –0.2 ± 0.two k/southward, P-trend = 0.ten), when amino acids were expressed equally a pct of protein (leucine Q5–Q1, –0.5 ± 0.2 g/southward, P-tendency 0.03; tyrosine Q5–Q1, –0.four ± 0.ii thou/s, P-trend = 0.04; glutamic acid Q5–Q1, –0.4 ± 0.ii thou/southward, P-trend = 0.19), or when potential under-reporters of energy intake were excluded from the analyses (leucine Q5–Q1, –0.vi ± 0.3 m/s, P-trend = 0.05; tyrosine Q5–Q1, –0.5 ± 0.3 m/due south, P-tendency = 0.06; glutamic acid Q5–Q1, –0.two ± 0.iii m/southward, P-trend = 0.08).

TABLE 2

Measures of fundamental blood pressure and arterial stiffness by quintile of total poly peptide and individual amino acids in women anile 18–75 y¹

	Protein	Arginine	Cysteine	Glutamic acid	Glycine	Histidine	Leucine	Tyrosine
Intake, % energy
Q1	12.viii ± 1.1	0.7 ± 0.07	0.1 ± 0.01	2.6 ± 0.1	0.v ± 0.05	0.three ± 0.03	one.0 ± 0.ane	0.iv ± 0.04
Q2	xiv.8 ± 0.4	0.8 ± 0.02	0.two ± 0.01	3.0 ± 0.ane	0.half-dozen ± 0.02	0.iv ± 0.01	1.2 ± 0.04	0.5 ± 0.02
Q3	sixteen.one ± 0.3	0.ix ± 0.02	0.2 ± 0.00	three.two ± 0.1	0.6 ± 0.02	0.4 ± 0.01	1.3 ± 0.03	0.6 ± 0.01
Q4	17.four ± 0.4	1.0 ± 0.03	0.ii ± 0.01	3.4 ± 0.ane	0.7 ± 0.02	0.5 ± 0.01	1.4 ± 0.03	0.6 ± 0.02
Q5	19.nine ± i.5	i.1 ± 0.1	0.3 ± 0.02	3.8 ± 0.3	0.8 ± 0.ane	0.half-dozen ± 0.05	one.6 ± 0.one	0.7 ± 0.1
pSBP, mm Hg
Q1	120 ± 0.viii	121 ± 0.9	120 ± 0.9	121 ± 0.9	121 ± 0.9	121 ± 0.nine	122 ± 0.9	122 ± 0.9
Q2	121 ± 0.8	121 ± 0.8	122 ± 0.9	120 ± 0.viii	120 ± 0.eight	120 ± 0.viii	121 ± 0.eight	121 ± 0.eight
Q3	119 ± 08	120 ± 0.8	120 ± 0.8	120 ± 0.viii	121 ± 0.8	120 ± 0.8	120 ± 0.7	119 ± 0.eight
Q4	119 ± 0.eight	119 ± 0.8	118 ± 0.7	117 ± 0.8	118 ± 0.seven	118 ± 0.8	118 ± 0.8	118 ± 0.8
Q5	118 ± 0.8	116 ± 0.nine	118 ± 0.9	118 ± 0.ix	117 ± 0.ix	117 ± 0.9	116 ± 0.nine	116 ± 0.9
P-trend	<0.01	<0.01	<0.01	<0.01	<0.01	<0.01	<0.01	<0.01
pDBP, mm Hg
Q1	76.8 ± 0.5	76.8 ± 0.6	76.7 ± 0.6	77.4 ± 0.six	76.6 ± 0.6	77.0 ± 0.6	77.5 ± 0.6	77.seven ± 0.vi
Q2	77.half dozen ± 0.v	76.9 ± 0.6	77.viii ± 0.6	77.1 ± 0.5	76.five ± 0.6	76.9 ± 0.half dozen	77.three ± 0.5	77.3 ± 05
Q3	75.viii ± 0.vi	76.6 ± 0.5	75.9 ± 0.6	76.0 ± 0.six	77.0 ± 0.6	76.vii ± 0.6	76.iv ± 0.v	76.three ± 0.five
Q4	75.7 ± 0.v	75.vi ± 0.six	75.ane ± 0.5	74.viii ± 0.six	75.four ± 0.5	75.iii ± 0.5	75.1 ± 0.5	75.1 ± 0.6
Q5	74.ix ± 0.six	74.8 ± 0.6	75.3 ± 0.6	75.5 ± 0.six	75.three ± 0.7	74.nine ± 0.7	74.5 ± 0.6	74.5 ± 0.6
P-trend	<0.01	0.02	0.01	0.01	0.11	0.02	<0.01	<0.01
cSBP, mm Hg
Q1	112 ± 0.8	112 ± 0.ix	112 ± 0.eight	113 ± 0.8	112 ± 0.9	113 ± 0.nine	113 ± 0.8	113 ± 0.8
Q2	112 ± 0.8	112 ± 0.viii	113 ± 0.8	112 ± 0.8	112 ± 0.8	112 ± 0.8	113 ± 0.8	112 ± 0.8
Q3	111 ± 0.8	112 ± 0.eight	111 ± 0.8	111 ± 0.8	113 ± 0.8	112 ± 0.eight	111 ± 0.vii	111 ± 0.8
Q4	111 ± 0.8	110 ± 0.8	109 ± 0.seven	109 ± 0.7	110 ± 0.seven	110 ± 0.7	110 ± 0.8	110 ± 0.8
Q5	109 ± 0.8	108 ± 0.8	109 ± 0.viii	109 ± 0.nine	109 ± 0.nine	109 ± 0.9	108 ± 0.8	108 ± 0.8
P-trend	<0.01	<0.01	<0.01	<0.01	0.01	<0.01	<0.01	<0.01
cDBP, mm Hg
Q1	78.0 ± 0.half-dozen	78.1 ± 0.six	78.0 ± 0.6	78.seven ± 0.6	77.9 ± 0.half-dozen	78.3 ± 0.6	78.vii ± 0.6	78.9 ± 0.6
Q2	78.8 ± 0.6	78.one ± 0.half dozen	79.i ± 0.6	78.three ± 0.6	77.7 ± 0.6	78.1 ± 0.6	78.five ± 0.6	78.v ± 0.6
Q3	77.1 ± 0.6	78.0 ± 0.5	77.3 ± 0.6	77.2 ± 0.6	78.3 ± 0.6	77.9 ± 0.six	77.seven ± 0.half-dozen	77.4 ± 0.half dozen
Q4	77.0 ± 0.six	76.ix ± 0.half dozen	76.3 ± 0.5	76.1 ± 0.six	76.7 ± 0.6	76.7 ± 0.v	76.4 ± 0.six	76.5 ± 0.half-dozen
Q5	76.2 ± 0.vi	75.9 ± 0.6	76.5 ± 0.vii	76.eight ± 0.6	76.4 ± 0.7	76.1 ± 0.vii	75.8 ± 0.6	75.7 v 0.6
P-tendency	0.01	0.02	0.01	0.01	0.08	0.02	<0.01	<0.01
cPP, mm Hg
Q1	34.1 ± 0.4	34.4 ± 0.5	33.9 ± 0.5	34.2 ± 0.v	34.0 ± 0.v	34.6 ± 0.5	34.5 ± 0.5	34.iv ± 0.5
Q2	33.4 ± 0.4	34.ane ± 0.iv	34.1 ± 0.v	33.viii ± 0.4	33.eight ± 0.4	33.half dozen ± 0.4	34.0 ± 0.4	33.9 ± 0.4
Q3	33.7 ± 0.4	33.7 ± 0.4	34.0 ± 0.4	33.9 ± 0.v	34.three ± 0.iv	34.0 ± 0.four	33.4 ± 0.four	33.seven ± 0.4
Q4	33.seven ± 0.iv	33.v ± 0.four	32.9 ± 0.4	32.viii ± 0.four	32.9 ± 0.4	32.ix ± 0.4	33.6 ± 0.4	33.3 ± 0.four
Q5	32.6 ± 0.4	31.8 ± 0.5	32.vi ± 0.5	32.7 ± 0.5	32.five ± 0.5	32.5 ± 0.5	31.9 ± 0.5	32.ane ± 0.5
P-trend	0.06	<0.01	0.02	0.02	0.02	0.01	<0.01	<0.01
MAP, mm Hg
Q1	93.1 ± 0.half-dozen	93.1 ± 0.7	92.viii ± 0.seven	93.7 ± 0.vii	92.9 ± 0.vii	93.4 ± 0.7	94.0 ± 0.7	94.i ± 0.7
Q2	93.7 ± 0.6	93.5 ± 0.7	94.four ± 0.7	93.4 ± 0.6	92.8 ± 0.7	93.iii ± 0.vii	93.6 ± 0.half-dozen	93.8 ± 0.6
Q3	92.3 ± 0.six	93.0 ± 0.six	92.7 ± 0.7	92.3 ± 0.vii	93.eight ± 0.half-dozen	93.two ± 0.6	92.seven ± 0.6	92.four ± 0.vi
Q4	91.viii ± 0.six	92.0 ± 0.6	90.7 ± 0.six	90.7 ± 0.vi	91.5 ± 0.half-dozen	91.4 ± 0.6	91.3 ± 0.vi	91.3 ± 0.7
Q5	90.7 ± 0.vii	90.0 ± 0.7	91.two ± 0.7	91.7 ± 0.vii	xc.viii ± 0.8	90.5 ± 0.8	ninety.2 ± 0.7	90.1 ± 0.7
P-tendency	<0.01	<0.01	<0.01	0.01	0.03	<0.01	<0.01	<0.01
PWV,2 grand/s
Q1	9.three ± 0.1	nine.1 ± 0.2	9.4 ± 0.ii	ix.3 ± 0.2	9.2 ± 0.two	ix.ii ± 0.one	9.4 ± 0.2	9.iv ± 0.2
Q2	9.three ± 0.1	ix.2 ± 0.ane	9.two ± 0.one	9.v ± 0.1	ix.two ± 0.i	9.4 ± 0.1	9.iii ± 0.ane	9.3 ± 0.1
Q3	9.one ± 0.1	9.2 ± 0.one	9.1 ± 0.1	9.0 ± 0.1	9.ii ± 0.1	nine.1 ± 0.1	9.2 ± 0.1	ix.ii ± 0.1
Q4	9.0 ± 0.i	9.one ± 0.i	ix.0 ± 0.1	9.0 ± 0.1	9.1 ± 0.1	ix.0 ± 0.1	9.0 ± 0.ane	8.9 ± 0.one
Q5	9.one ± 0.ane	9.1 ± 0.1	9.0 ± 0.ane	8.9 ± 0.ane	nine.1 ± 0.1	nine.0 ± 0.i	8.9 ± 0.1	9.0 ± 0.1
P-trend	0.06	0.79	0.05	0.01	0.69	0.15	0.02	0.02

No meaning associations were observed betwixt intake of total protein or the private amino acids assessed and either AI or IMT (information not shown). The results were not altered after exclusion of the low proportion (11%) of participants who reported taking blood pressure or statin medication (data not shown).

Higher intakes of amino acids from vegetable sources were inversely associated with cSBP and AI. Intakes of arginine, glycine, histidine, leucine and tyrosine were significantly associated with −2.0 to −2.4 mm Hg lower cSBP values and intake of cysteine, glutamic acrid, lysine, and tyrosine with −3.five% to −v.7% lower AI, comparison extreme quintiles of intake (all P-tendency < 0.05) ( Table 3 ). Higher intakes of arginine and glycine from vegetable sources were also significantly associated with lower pSBP (arginine Q5–Q1, −2.iii ± 1.four mm Hg, P-trend = 0.02; and glycine Q5–Q1, −ii.half-dozen ± ane.5 mm Hg, P-trend = 0.04) (Table 3). Furthermore, intake of arginine from vegetable sources was associated with lower cPP (Q5–Q1, −1.two ± 0.8 mm Hg, P-tendency = 0.04) and MAP (Q5–Q1, −i.2 ± one.ane mm Hg, P-trend = 0.03). In relation to intakes of amino acids from animate being sources, significant changed associations were observed betwixt glutamic acid, leucine, and tyrosine intakes and PWV, with respective differences of −0.three ± 0.2 yard/s (P-trend = 0.03), −0.3 ± 0.2 m/due south (P-trend = 0.02), and −0.4 ± 0.2 thou/south (P-trend = 0.02) between extreme quintiles of intake. Total vegetable protein intake and total animal protein intake were not associated with whatever of the outcomes assessed (P-trend all > 0.05), and there were no pregnant associations for IMT (data not shown).

TABLE 3

Measures of central claret pressure and arterial stiffness between extreme quintiles of full protein and individual amino acids from vegetable and animal sources in women aged 18–75 y¹

	Protein	Arginine	Cysteine	Glutamic acid	Glycine	Histidine	Lysine	Tyrosine
Vegetable sources
Intake, % energy
Q1	4.6 ± 0.4	0.3 ± 0.03	0.1 ± 0.01	1.0 ± 0.1	0.2 ± 0.02	0.one ± 0.01	0.iii ± 0.04	0.1 ± 0.02
Q2	5.four ± 0.two	0.iii ± 0.01	0.1 ± 0.00	1.2 ± 0.05	0.2 ± 0.01	0.i ± 0.00	0.iv ± 0.03	0.ii ± 0.01
Q3	half-dozen.0 ± 0.2	0.3 ± 0.01	0.one ± 0.00	1.3 ± 0.04	0.three ± 0.01	0.ii ± 0.00	0.4 ± 0.03	0.2 ± 0.02
Q4	6.6 ± 0.ii	0.4 ± 0.01	0.ane ± 0.00	1.5 ± 0.06	0.iii ± 0.01	0.2 ± 0.01	0.5 ± 0.03	0.2 ± 0.02
Q5	eight.0 ± 0.ix	0.five ± 0.one	0.2 ± 0.02	1.8 ± 0.ii	0.3 ± 0.04	0.2 ± 0.03	0.6 ± 0.ane	0.2 ± 0.04
pSBP, mm Hg
Q5–Q1	−two.6 ± 1.five	−two.three ± 1.4	0.three ± i.vii	−0.2 ± 1.7	−2.6 ± i.5	−2.i ± 1.iv	−2.0 ± one.4	−2.0 ± 1.iv
P-trend	0.12	0.02	0.96	0.78	0.04	0.05	0.05	0.05
pDBP, mm Hg
Q5–Q1	−1.9 ± i.0	−0.9 ± 0.9	−i.0 ± 1.1	−1.0 ± one.1	−i.i ± 1.0	−1.6 ± 1.0	−ane.half dozen ± 0.9	−1.vi ± 0.9
P-tendency	0.07	0.08	0.29	0.27	0.15	0.05	0.03	0.04
cSBP, mm Hg
Q5–Q1	−two.8 ± i.5	−2.i ± i.three	−0.two ± i.6	−0.7 ± 1.half dozen	−2.4 ± 1.iv	−2.1 ± 1.4	−2.0 ± 1.iii	−ii.0 ± 1.3
P-trend	0.08	0.02	0.71	0.63	0.03	0.04	0.03	0.04
cDBP, mm Hg
Q5–Q1	−i.7 ± one.0	−i.0 ± 1.0	−0.8 ± one.ane	−0.7 ± one.1	−1.0 ± 1.0	−1.five ± 1.0	−ane.3 ± 1.0	−1.3 ± 1.0
P-tendency	0.xi	0.09	0.39	0.41	0.17	0.07	0.07	0.07
cPP, mm Hg
Q5–Q1	−i.ii ± 0.9	−1.ii ± 0.8	0.5 ± 0.9	−0.1 ± 0.9	−ane.4 ± 0.8	−0.6 ± 0.viii	−0.seven ± 0.seven	−0.7 ± 0.7
P-trend	0.29	0.04	0.66	0.88	0.04	0.23	0.15	0.15
MAP, %
Q5–Q1	−one.8 ± one.2	−1.ii ± 1.ane	−0.half dozen ± 1.3	−0.two ± 1.3	−ane.7 ± 1.2	−1.8 ± 1.1	−ane.5 ± 1.1	−i.5 ± 1.one
P-tendency	0.13	0.03	0.51	0.71	0.05	0.05	0.06	0.06
AI, mm Hg
Q5–Q1	−3.8 ± 2.iii	−1.vi ± 2.2	−iv.three ± 2.3	−5.7 ± 2.4	−1.7 ± two.2	−1.half dozen ± ii.3	−3.five ± 2.i	−three.vi ± 2.1
P-tendency	0.07	0.eighteen	0.03	0.03	0.06	0.19	0.03	0.03
PWV,2 mm Hg
Q5–Q1	−0.2 ± 0.two	0.ane ± 0.2	−0.2 ± 0.2	−0.3 ± 0.2	−0.0 ± 0.iii	−0.1 ± 0.2	−0.2 ± 0.2	−0.2 ± 0.2
P-trend	0.32	0.74	0.15	0.21	0.99	0.65	0.26	0.46
Animal sources
Intake, % free energy
Q1	6.3 ± 1.2	0.3 ± 0.1	0.1 ± 0.01	one.ii ± 0.2	0.2 ± 0.05	0.2 ± 0.04	0.v ± 0.one	0.2 ± 0.04
Q2	viii.6 ± 0.4	0.iv ± 0.02	0.1 ± 0.05	1.six ± 0.one	0.3 ± 0.02	0.iii ± 0.01	0.vii ± 0.04	0.3 ± 0.02
Q3	9.9 ± 0.four	0.5 ± 0.02	0.1 ± 0.02	1.8 ± 0.1	0.4 ± 0.02	0.3 ± 0.01	0.8 ± 0.04	0.4 ± 0.02
Q4	eleven.4 ± 0.5	0.6 ± 0.03	0.1 ± 0.01	2.1 ± 0.1	0.4 ± 0.02	0.iii ± 0.02	0.9 ± 0.05	0.iv ± 0.02
Q5	14.1 ± 1.6	0.viii ± 0.one	0.2 ± 0.02	2.5 ± 0.three	0.6 ± 0.1	0.iv ± 0.05	1.two ± 0.1	0.v ± 0.one
pSBP, mm Hg
Q5–Q1	−ane.ix ± 1.four	−2.2 ± 1.iii	−1.iii ± one.3	−two.2 ± ane.3	−1.8 ± 1.3	−2.1 ± 1.4	−2.1 ± i.iii	−2.1 ± 1.3
P-tendency	0.17	0.07	0.30	0.21	0.12	0.17	0.11	0.1
pDBP, mm Hg
Q5–Q1	−1.6 ± 1.0	−1.seven ± 0.9	−i.4 ± one.0	−2.0 ± i.0	−1.four ± 1.0	−1.4 ± 1.0	−1.9 ± i.0	−1.nine ± 1.0
P-trend	0.11	0.ten	0.nineteen	0.07	0.14	0.12	0.05	0.05
cSBP, mm Hg
Q5–Q1	−2.1 ± i.3	−ii.2 ± 1.3	−i.5 ± 1.three	−two.five ± 1.3	−1.7 ± i.3	−two.ii ± one.4	−two.3 ± 1.3	−2.four ± i.3
P-trend	0.15	0.10	0.30	0.17	0.16	0.sixteen	0.x	0.08
cDBP, mm Hg
Q5–Q1	−1.five ± ane.0	−one.seven ± 0.9	−ane.5 ± 1.0	−1.9 ± 1.0	−1.4 ± i.0	−1.3 ± 1.0	−i.7 ± 1.0	−1.viii ± 1.0
P-trend	0.18	0.13	0.22	0.11	0.15	0.xviii	0.09	0.08
cPP, mm Hg
Q5–Q1	−0.half dozen ± 0.seven	−0.5 ± 0.7	−0.0 ± 0.7	−0.6 ± 0.7	−0.three ± 0.7	−0.ix ± 0.7	−0.half-dozen ± 0.7	−0.vi ± 0.vii
P-trend	0.43	0.35	0.84	0.73	0.54	0.44	0.50	0.47
MAP, %
Q5–Q1	−1.4 ± one.1	−ane.7 ± i.1	−1.iii ± ane.1	−one.vii ± ane.1	−1.5 ± 1.ane	−1.5 ± ane.1	−i.6 ± 1.1	−one.7 ± one.1
P-trend	0.29	0.16	0.36	0.25	0.19	0.23	0.17	0.xiv
AI, mm Hg
Q5–Q1	−ane.four ± 2.2	−0.1 ± 2.one	−1.three ± 2.1	−1.5 ± 2.2	−0.nine ± 2.2	−0.nine ± two.2	−2.one ± two.2	−2.5 ± two.ane
P-tendency	0.85	0.71	0.79	0.75	0.85	0.95	0.73	0.58
PWV,2 mm Hg
Q5–Q1	−0.i ± 0.2	−0.1 ± 0.2	−0.2 ± 0.2	−0.three ± 0.2	−0.0 ± 0.2	−0.one ± 0.ii	−0.iii ± 0.ii	−0.4 ± 0.two
P-trend	0.11	0.44	0.25	0.03	0.69	0.22	0.02	0.02

Word

To our noesis, this is the outset cross-sectional study to examine associations between amino acids that accept known mechanistic links to cardiovascular illness and a range of in vivo measures of arterial stiffness and central claret pressure associated with cardiovascular affliction hazard. We showed that higher intakes of all 7 of the amino acids examined (arginine, cysteine, glutamic acrid, glycine, histidine, leucine, and tyrosine) were significantly associated with improved measures of peripheral and central blood pressure. Higher intakes of glutamic acid, leucine, and tyrosine were also associated with lower PWV. These associations were pregnant after aligning for a number of important covariates known to exist associated with vascular health, including lifestyle factors, medication utilize, and other nutrients. The magnitude of the changed associations ranged from −ii.eight to −5.5 mm Hg for systolic claret force per unit area, −1.5 to −iii.two mm Hg for central diastolic blood force per unit area, and −0.40 to −0.45 g/s for PWV.

It was previously estimated that a small reduction in systolic claret force per unit area of 5 mm Hg would potentially atomic number 82 to an overall reduction in mortality from stroke, coronary heart affliction, or all-cause mortality (36). Intakes of the amino acids investigated in the current study were associated with a mean departure in pSBP of −4.1 mm Hg (range: −ii.6 to −5.6 mm Hg). The magnitude of these associations is similar to those previously reported for established lifestyle risk factors for hypertension, including sodium intake, physical activity, and alcohol consumption (37). For PWV, the calibration of the association was 0.4 thousand/s, which is similar to the magnitude of change previously associated with non smoking supplementation with northward–iii FAs and, to the differences observed between individuals with or without metabolic syndrome, hypertension, or hypercholesterolemia (38, 39).

Our results provide further insights into the vascular effects of these amino acids and a potential caption to support the reduction in blood force per unit area observed with higher protein intake in a contempo meta-analysis (ii). Our findings are consistent with randomized, controlled trials reporting decreases in pSBP of 2 mm Hg with 40 g of milk or soy poly peptide and 1.4 mm Hg with a nutrition substituting 10% of energy from carbohydrate with that from poly peptide (40, 41). Furthermore, cross-exclusive studies of amino acid intake and blood pressure have reported intakes of tyrosine and glutamic acid to be associated with, on boilerplate, a 2 mm Hg reduction in pSBP (14, 15), and intake of histidine with a 4% reduced run a risk of an increase in pSBP of 16 mm Hg (16).

These current results, however, do not support the findings of the INTERMAP (INTERnational report of MAcro- and micronutrients and claret Pressure), which showed that higher glycine intake was associated with an increment in claret pressure, and those of the Rotterdam report, which found no significant associations between intakes of glutamic acid, arginine, and cysteine and claret pressure level or take a chance of hypertension (14, 17). A number of factors, including study design, could account for these divergent findings; interestingly, there were differences in habitual dietary patterns between studies and consequently in the major sources of amino acids. For case, in the INTERMAP, meat contributed to 33–47% of dietary glycine intake and fish to 6–thirteen%, compared with 25% and 18%, respectively, in our participants. Food sources of poly peptide vary greatly in their nonprotein constituents and accept previously been shown to have differing associations with cardiovascular disease risk in women, with ruby-red meat associated with a thirteen% increased chance and fish intake with a xix% reduced hazard (42).

Considering of the stiff interrelations previously reported between claret pressure and poly peptide source, and considering we observed a significant interaction in the current analyses, nosotros further examined the relation between amino acid intake and arterial stiffness according to poly peptide source. Poly peptide from vegetable sources, just not animal sources, has previously been shown to be associated with a −1.one mm Hg reduction in pSBP and 15% reduction in take chances of hypertension (3, 4). Nosotros found that college intakes of amino acids from vegetable sources, only not animal sources, were associated with lower systolic blood force per unit area, MAP, and AI. Intakes of glutamic acid, leucine, and tyrosine from animal sources were associated with lower a PWV of 0.3–0.4 chiliad/s between extreme quintiles of intake. These information provide support for a previous study from Japan reporting an changed relation between higher brute protein intake and blood pressure (43), but do not support those studies in Western populations in which animal poly peptide was found to be unrelated to claret pressure level (3). Fish in the current report contributed >3 times more to glutamic acrid intake than previously reported in a Great britain cohort, which may offer some explanation for this finding (15). Studies in hypertensive rats provide evidence to suggest that protein from fish is more effective at lowering blood pressure than casein over a two mo period (44), and a meta-analysis of adult man trials revealed that north–3 FAs were effective at improving PWV by 0.33 thou/s (39). Fish intake has likewise been associated with overall diet quality (5). The underlying mechanism of interaction between amino acrid intake and PWV observed in the electric current report is unclear, and information technology must be considered that in our study brute sources contributed more than to leucine and tyrosine than vegetable sources; these analyses may exist reflecting our findings for intake from all sources, which were inherently adjusted for poly peptide source. The reasons why we observed associations with total protein and non animal protein when the correlation between total and brute poly peptide intakes was and then high (r = 0.89, P < 0.01) remains unclear.

The findings of the current study reflect intakes of amino acids that are readily achievable in the habitual diet. The difference in PWV of 0.4 m/southward shown betwixt extreme quintiles of intakes of glutamic acrid, leucine, and tyrosine equates to a 3.53 chiliad, 1.64 thousand, and 0.76 g deviation in intake, respectively. This intake tin be incorporated into the nutrition past consuming approximately one-half of a medium steak (74 g), a medium salmon fillet (100 k), or a 500 mL drinking glass of skimmed milk.

Strengths of the electric current study include the big sample of well-characterized participants and the rigorous assessment of a range of in vivo measures of arterial stiffness and cardinal blood pressure. Information technology is well established that aortic stiffness, every bit assessed by PWV, is able to predict future cardiovascular events and all-cause mortality (45). The publication of reference values for PWV and the improver of PWV to traditional gamble biomarkers in recent guidelines for hypertension management demonstrate prognostic ability (46, 47). It was notable that the associations observed in the current analysis were shown in a population in which over 80% were classified as normotensive, and it is plausible that whatsoever associations would be more pronounced in a hypertensive group. These participants previously have been shown to exist representative of the general population in terms of blood pressure and diet (23, 24), and these data have been used in previous studies of dietary exposure (48). The FFQ used in the electric current study was used to rank participants according to their amino acid intake. Although the FFQ has not been shown to accurately quantify amino acid intake, it has previously been validated against 24 h recalls and shown to classify over 85% of participants into the same or adjacent quintile of protein intake, demonstrating its ability to rank participants co-ordinate to their habitual protein intake (49).

The limitations of the current report include the cross-sectional pattern that meant we were unable to infer causality Numerous hypothesis-driven comparisons were fabricated in our analysis that we felt were justified, given the novel and exploratory nature of the analyses. The inclusion of twin pairs within the same sample may introduce bias, but this was reduced by bookkeeping for the clustering within twin pairs in all statistical analyses and with the employ of a sample shown to be representative of the general population in terms of outcome variables and dietary intake. Validated biomarkers, such as 24 h urine nitrogen, are bachelor for total protein intake, but they were not measured in the current study and may have reduced potential measurement mistake (l). Furthermore, rest confounding may accept occurred despite the multivariable modeling adjusted for a range of dietary and lifestyle confounder variables (such as age, smoking, concrete activity, BMI, medication use, and intakes of other nutrients associated with vascular health).

In decision, these novel data suggest that intakes of selected amino acids is associated with arterial stiffness and cardinal claret force per unit area, with significant associations observed for PWV and cSBP similar in magnitude to established lifestyle take a chance factors for hypertension, such as physical activeness, not smoking, and reduced intakes of sodium and alcohol (37, 38). The intakes of amino acids associated with lower arterial stiffness and central blood pressure are easily doable in the habitual diet, making these findings very relevant for public wellness strategies to reduce cardiovascular disease risk. Our findings highlight the need for more intervention trials examining dietary achievable intakes of amino acids and cardiovascular outcomes.

Acknowledgments

AJ, AW, and AC conducted the dietary analyses and adult the amino acid database; AM and TS set up and coordinated the collection of all data; PC conducted the vascular function assessments; AJ performed the statistical analysis; AJ and AC wrote the paper; and AC had primary responsibility for the final content. All authors read and approved the last manuscript.

Footnotes

^fiveAbbreviations used: AI, augmentation index; cPP, central pulse pressure; cSBP, primal systolic blood force per unit area; IMT, intima–media thickness; INTERMAP, INTERnational study of MAcro- and micronutrients and blood Pressure; MAP, mean arterial pressure level; pDBP, peripheral diastolic blood pressure; pSBP, peripheral systolic blood pressure; PWV, pulse moving ridge velocity.

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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548168/

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