A recent study was published that helps to remind us of the importance of proper nutrition to maintain health. This study found that approximately 10% of hypertensive patients have a genetic defect which responds to a low dose of riboflavin (1.6mg) by providing a double digit lowering of both systolic and diastolic blood pressure (1). This genetic defect is very prevalent in some populations, such as in Mexico, where 32% of the population are thought to possess it. Other nutritional approaches to lowering blood pressure have demonstrated encouraging responses but require additional study to confirm their value. Considering the low cost, low risk and that 43% of the population has uncontrolled hypertension , even with pharmacological intervention (2), should make a nutritional approach to controlling hypertension appealing to the conservative practitioner.
Note: These mini-reviews are designed as updates and direct the reader to the full text of current research. The abstracts presented here are no substitute for reading and critically reviewing the full text of the original research. Where permitted we will direct the reader to that full text.
Riboflavin offers a targeted strategy for managing hypertension in patients with the MTHFR 677TT genotype: a 4-y follow-up.
] Am J Clin Nutr.
2012 Mar;95(3):766-72. Epub 2012 Jan 25.
Wilson CP, Ward M, McNulty H, Strain JJ, Trouton TG, Horigan G, Purvis J, Scott JM. BACKGROUND:
We recently reported that the elevated blood pressure (BP) observed in patients with cardiovascular disease who are homozygous for the 677C?T polymorphism (TT genotype) in the gene encoding methylenetetrahydrofolate reductase (MTHFR) was responsive to supplementation with riboflavin-the cofactor for MTHFR. OBJECTIVE:
The objective was to investigate the effect of riboflavin on BP targeted at patients with the TT genotype 4 y after initial investigation, during which time major changes in the clinical guidelines for antihypertensive therapy were introduced. DESIGN:
A total of 83 patients (representing all 3 genotypes) who participated in a placebo-controlled riboflavin intervention for 16 wk in 2004 agreed to take part. Nested within this follow-up, those with the TT genotype (n = 31) proceeded to intervention with riboflavin (1.6 mg/d for 16 wk) or placebo, conducted in a crossover style whereby the 2004 treatment groups were reversed. RESULTS:
At follow-up in 2008, as in 2004, patients with the TT genotype had higher systolic BP (P < 0.01), with a nonsignificant trend noted for higher diastolic BP (P = 0.051). Despite the marked changes in antihypertensive therapy that had occurred, BP remained unchanged in patients with the TT genotype at the time of follow-up. Riboflavin supplementation (administered in 2004 and 2008) produced an overall decrease in systolic (-9.2 ± 12.8 mm Hg; P = 0.001) and diastolic (-6.0 ± 9.9 mm Hg; P = 0.003) BP. CONCLUSIONS:
Optimizing riboflavin status offers a low-cost targeted strategy for managing elevated BP in this genetically at-risk group. These findings, if confirmed in the general population, could have important implications for the prevention of hypertension.
Melatonin reduces night blood pressure in patients with nocturnal hypertension.
] Am J Med.
Grossman E, Laudon M, Yalcin R, Zengil H, Peleg E, Sharabi Y, Kamari Y, Shen-Orr Z, Zisapel N. PURPOSE:
Nocturnal hypertension is associated with a high risk of morbidity and mortality. A blunted nocturnal surge in melatonin excretion has been described in nondipping hypertensive patients. We therefore studied the potency of melatonin to reduce nighttime blood pressure (BP) in treated hypertensive patients with nocturnal hypertension. PATIENTS AND METHODS:
Thirty-eight treated hypertensive patients (22 males, mean age 64+/-11 years) with confirmed nocturnal hypertension (mean nighttime systolic BP >125 mm Hg), according to repeated 24-hour ambulatory blood pressure monitoring (ABPM), were randomized in a double-blind fashion to receive either controlled release (CR)-melatonin 2 mg or placebo 2 hours before bedtime for 4 weeks. A 24-hour ABPM was then performed. RESULTS:
Melatonin treatment reduced nocturnal systolic BP significantly from 136+/-9 to 130+/-10 mm Hg (P=.011), and diastolic BP from 72+/-11 to 69+/-9 mm Hg (P=.002), whereas placebo had no effect on nocturnal BP. The reduction in nocturnal systolic BP was significantly greater with melatonin than with placebo (P=.01), and was most prominent between 2:00 AM and 5:00 AM (P=.002). CONCLUSIONS:
Evening CR-melatonin 2 mg treatment for 4 weeks significantly reduced nocturnal systolic BP in patients with nocturnal hypertension. Thus, an addition of melatonin 2 mg at night to stable antihypertensive treatment may improve nocturnal BP control in treated patients with nocturnal hypertension.
L-arginine and hypertension.
] J Nutr.
2004 Oct;134(10 Suppl):2807S-2811S; discussion 2818S-2819S.
Hypertension is a major healthcare problem afflicting nearly 50 million individuals in the United States. Despite its strong causal association with cardiovascular disease complications including myocardial infarction, heart failure, and stroke, the majority of patients with hypertension do not achieve optimal blood pressure control. The prevalence of hypertension is expected to increase with the aging population, growing obesity epidemic, and rising incidence
of metabolic syndrome. Endothelial dysfunction and reduced nitric oxide (NO) bioactivity represent prominent pathophysiological abnormalities associated with hypertensive cardiovascular disease. Individuals with hypertension exhibit blunted epicardial and resistance vascular dilation to endothelium-derived nitric oxide (EDNO) agonists in the peripheral and coronary circulation that likely contributes to mechanisms of altered vascular tone in hypertension. The amino acid L-arginine serves as the principal substrate for vascular NO production. Numerous studies, though not uniformly, demonstrate a beneficial effect of acute and chronic L-arginine supplementation on EDNO production and endothelial function, and L-arginine has been shown to reduce systemic blood pressure in some forms of experimental hypertension. This brief review discusses the potential role of L-arginine in hypertension, and reviews possible mechanisms of L-arginine action including modulation of EDNO production, alteration of asymmetrical dimethylarginine (ADMA):L-arginine balance, and possible improvement of insulin sensitivity. In view of the rising prevalence of hypertension, randomized human clinical studies investigating the potential therapeutic role of L-arginine may be warranted.
Oral arginine reduces systemic blood pressure in type 2 diabetes: its potential role in nitric oxide generation.
] J Am Coll Nutr.
Huynh NT, Tayek JA. OBJECTIVES:
Arginine is converted in the endothelial cells to nitric oxide (NO) and citrulline. NO is a potent vasodilator in humans, but diabetics may have a reduced generation of NO which results in endothelial dysfunction. The aim of this study was to evaluate the effects of oral arginine on nitric oxide production, counter-regulatory hormones and blood pressure in mildly hypertensive type 2 diabetic patients. METHODS:
A prospective, crossover clinical trial was performed over a three-day stay in the General Clinical Research Center. Six patients with type 2 diabetes mellitus and mild hypertension consented and were given orally three grams of arginine per hour for 10 hours on either day 2 or day 3. On both days 2 and 3, blood pressure was monitored between 5 AM and 4 PM and mean pressure determined. RESULTS:
Oral arginine increased plasma citrulline from 31.3 +/- 6.0 to 41.5 +/- 6.0 micro mol/L (mean +/- SEM; p < 0.05) which may reflect an increased conversion of arginine into NO and citrulline. Arginine reduced systolic BP from 135 +/- 7 to 123 +/- 8 mmHg; p < 0.05. Diastolic BP fell from 86.9 +/- 1.7 to 80.7 +/- 2.4 mmHg; p < 0.05). The reduction in BP was noted to occur two hours after starting oral arginine, and BP returned to normal within one hour of stopping the arginine. The oral arginine had no effect on C-peptide, insulin or other hormone concentrations. CONCLUSIONS:
These data suggest that oral arginine may increase endothelial nitric oxide synthase (NOS) to increase vascular NO and temporally reduce blood pressure in mildly hypertensive type 2 diabetic patients.
Fish oil supplementation improves large arterial elasticity in overweight hypertensive patients.
] Eur J Clin Nutr.
2008 Dec;62(12):1426-31. Epub 2007 Sep 5.
Wang S, Ma AQ, Song SW, Quan QH, Zhao XF, Zheng XH. OBJECTIVES:
To observe the effect of fish oil supplementation on arterial elasticity and blood pressure (BP) in overweight hypertensive patients. SUBJECTS AND METHODS:
This was a double-blind, randomized and placebo-controlled clinical study, in which 52 overweight hypertensive patients from a community were selected and randomly allocated to two groups (26 in the fish oil group (3 g day(-1), fish oil capsules) and 26 in the placebo group (only capsules). All the subjects were follow-up for 8 weeks. The arterial elasticity was determined by CVProfilor DO-2020 and expressed as elasticity indexes (C(1)-large artery and C(2)-small artery). During the follow-up, totally nine cases were dropped out (three cases from the fish oil group and six cases from the placebo group). RESULTS:
After 8 weeks follow-up, the large artery elasticity in the fish oil group, compared with its baseline, was significantly improved (C(1): 15.5+/-1.5 vs 12.8+/-3.7 ml mm Hg(-1) x 10), whereas no effects were found in the placebo group (C(1): 13.0+/-3.4 vs 13.4+/-3.8 ml mm Hg(-1) x 10), P=0.027, RM-ANOVA across the two groups. The small artery elasticity (C(2)), BP and pulse pressure were not found any changes, either in the fish oil group or in the placebo group. At same time, the serum soluble vascular cell adhesion molecule-1(sVCAM-1) and leptin levels, the lipid profile and insulin sensitivity
index (ISI) as well, did not show significant differences between two groups. CONCLUSIONS:
Fish oil supplementation certainly would improve large arterial elasticity but no effect on BP in overweight hypertensive patients. Further study is needed to confirm the benefits of fish oil supplementation on age-related increases in arterial stiffness.
Blood pressure lowering efficacy of coenzyme Q10 for primary hypertension.
] Cochrane Database Syst Rev.
2009 Oct 7;(4):CD007435.
Ho MJ, Bellusci A, Wright JM. BACKGROUND:
Studies have shown that coenzyme Q10 deficiency is associated with cardiovascular disease. Hypertension is a commonly measured surrogate marker for non-fatal and fatal cardiovascular endpoints such as heart attacks and strokes. Clinical trials have suggested that coenzyme Q10 supplementation can effectively lower blood pressure (BP). OBJECTIVES:
To determine the blood pressure lowering effect of coenzyme Q10 in primary hypertension. SEARCH STRATEGY: The Cochrane Central Register of Controlled Trials (2009 Issue 2), MEDLINE (1966 -May 2008), EMBASE (1982 - May 2008), and CINAHL (1970 - May 2008) as well as the reference lists of articles were searched for relevant clinical trials in any language. SELECTION CRITERIA:
Double-blind, randomized, placebo-controlled parallel or crossover trials evaluating the BP lowering efficacy of coenzyme Q10 for a duration of at least 3 weeks in patients with primary hypertension. DATA COLLECTION AND ANALYSIS:
The primary author independently assessed the risk of bias and extracted the data. The second author verified data extraction. MAIN RESULTS:
Three clinical trials with a total of 96 participants were evaluated for the effects of coenzyme Q10 on blood pressure compared to placebo. Treatment with coenzyme Q10 in subjects with systolic BP (SBP) > 140 mmHg or diastolic BP (DBP) > 90 mmHg resulted in mean decreases in SBP of 11 mmHg (95% CI 8, 14) and DBP of 7 mmHg (95% CI 5, 8). AUTHORS' CONCLUSIONS:
Due to the possible unreliability of some of the included studies, it is uncertain whether or not coenzyme Q10 reduces blood pressure in the long-term management of primary hypertension.
Potassium magnesium supplementation for four weeks improves small distal artery compliance and reduces blood pressure in patients with essential hypertension.
] Clin Exp Hypertens.
Wu G, Tian H, Han K, Xi Y, Yao Y, Ma A.
It has been postulated that the loss of arterial compliance may precede cardiovascular diseases, and that arterial compliance is an important parameter to consider when evaluating arterial diseases such as essential hypertension (EH) and the effects of antihypertensive treatment. In all, 133 EH patients and 147 healthy subjects were enrolled in this study. Large arterial compliance (C1) and small arterial compliance (C2) were measured by the CVProfilor DO-2020 CardioVascular Profiling System. Thirty-five patients randomly received magnesium potassium supplementation (magnesium, 70.8 mg/d; potassium, 217.2 mg/d) for four weeks, and 32 patients received lacidipin (4 mg/d) as a control. Before and after the four weeks, blood pressure, C1, and C2 were measured. It was found that arterial compliance was significantly lower in EH patients compared with healthy subjects (C1: 12.53 +/- 0.33 vs. 15.63 +/- 0.30 ml/mmHg x 10, p < 0.01;C2: 3.79 +/- 0.17 vs. 5.69 +/- 0.25 ml/mmHg x 100, p < 0.01). On lacidipine, systolic and diastolic BP decreased 13.27 +/- 1.76 mm Hg and 6.33 +/- 1.55 mm Hg, and C1 and C2 compliance values increased 25.05% +/- 4.49% and 34.50% +/- 7.40%, respectively. On K+ and Mg2+ supplementation, systolic and diastolic BP decreased 7.83 +/- 1.87 mm Hg and 3.67 +/- 1.03 mm Hg, and C1 and C2 compliance values increased 12.44% +/- 4.43% and 45.25% +/- 6.67%, respectively. Decreases in systemic vascular resistance (mean arterial pressure divided by cardiac output) by 11.9% and 16.6 % (p < 0.01) were seen between the drug-induced changes, respectively. Both large arterial compliance and small arterial compliance were decreased in essential hypertension patients. In essential hypertension patients, magnesium and potassium supplementation could improve small arterial compliance, while lacidipine improved large arterial compliance significantly.