Article

Urinary and plasma magnesium and risk of ischemic heart disease

Top Institute Food and Nutrition, Wageningen, Netherlands and Cardiology, University of Groningen, University Medical Center Groningen, Groningen, Netherlands.
American Journal of Clinical Nutrition (Impact Factor: 6.92). 03/2013; 97(6):1299. DOI: 10.3945/ajcn.112.054114
Source: PubMed

ABSTRACT BACKGROUND: Previous studies on dietary magnesium and risk of ischemic heart disease (IHD) have yielded inconsistent results, in part because of a lack of direct measures of actual magnesium uptake. Urinary excretion of magnesium, an indicator of dietary magnesium uptake, might provide more consistent results. OBJECTIVE: The objective was to investigate whether urinary magnesium excretion and plasma magnesium are associated with IHD risk. DESIGN: We examined 7664 adult participants free of known cardiovascular disease in the Prevention of Renal and Vascular End-Stage Disease (PREVEND) study-a prospective population-based cohort study. Urinary magnesium excretion was measured in 2 baseline 24-h urine collections. RESULTS: Mean ± SD urinary magnesium excretion was 4.24 ± 1.65 mmol/24 h for men and 3.54 ± 1.40 mmol/24 h for women. During a median follow-up of 10.5 y (IQR: 9.9-10.8 y), 462 fatal and nonfatal IHD events occurred. After multivariable adjustment, urinary magnesium excretion had a nonlinear relation with IHD risk (P-curvature = 0.01). The lowest sex-specific quintile (men: <2.93 mmol/24 h; women: <2.45 mmol/24 h) had an increased risk of fatal and nonfatal IHD (multivariable HR: 1.60; 95% CI: 1.28, 2.00) compared with the upper 4 quintiles of urinary magnesium excretion. A similar increase in risk of the lowest quintile was observed for mortality related to IHD (HR: 1.70; 95% CI: 1.10, 2.61). No associations were observed between circulating magnesium and risk of IHD. CONCLUSIONS: Low urinary magnesium excretion was independently associated with a higher risk of IHD incidence. An increased dietary intake of magnesium, particularly in those with the lowest urinary magnesium, could reduce the risk of IHD.

1 Follower
 · 
150 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Nutritional factors such as magnesium, folic acid, vitamin B12, vitamin B6, L-arginine, and polyunsaturated fatty acids (PUFAs) appear to be of significant benefit for patients with coronary heart disease, and in the prevention and arresting the progression of heart failure and cardiac arrhythmias. In addition, ingestion of adequate amount of protein and maintaining normal concentrations of plasma albumin seem to be essential for these patients. These nutrients closely interact with the metabolism of L-arginine-nitric oxide system, essential fatty acids and eicosanoids such that beneficial products such as nitric oxide, prostaglandin E1, prostacyclin, prostaglandin I3, lipoxins, resolvins and protectins are generated and synthesis of pro-inflammatory cytokines is suppressed that results in platelet anti-aggregation, vasodilatation, angiogenesis and prevention of coronary heart disease, cardiac arrhythmias and stabilization of heart failure. This implies that subjects at high risk of coronary heart disease, cardiac arrhythmias and heart failure and those who have these diseases need to be screened for plasma levels of magnesium, folic acid, vitamin B12, vitamin B6, L-arginine, nitric oxide, various PUFAs, lipoxin A4, resolvins, protectins, asymmetrical dimethylarginine (ADMA-an endogenous inhibitor of nitric oxide), albumin, and various eicosanoids and cytokines and correct their abnormalities to restore normal physiology.
    Nutrition 09/2014; 31(2). DOI:10.1016/j.nut.2014.08.011 · 3.05 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Assessing magnesium by 24-h urinary excretion Dear Editor: We read with great interest the article by Veronese et al. (1). In their carefully performed parallel-group randomized controlled trial, they found that 12 wk of magnesium supplementation improved physical performance variables in healthy elderly women (mean 6 SD age: 72 6 5 y). This was particularly so among women who did not meet the Recommended Dietary Allowance for magnesium intake. These findings underscore the importance of sufficient magnesium intake for adequate muscle function. We laud the authors for using 24-h urinary excretion of magnesium as a marker of magnesium uptake. Timed 24-h urine collections can be used to accurately determine magnesium absorption (2), and clinical trials have consistently shown that dietary manipulation of magne-sium is reflected in 24-h urinary magnesium excretion (3). We re-cently showed that 24-h urinary excretion of magnesium, as an estimate of gastrointestinal uptake of dietary magnesium, is prospec-tively associated with risk of hypertension (4) and heart disease (5). Importantly, the validity of findings on the basis of 24-h urinary excretions heavily relies on complete and accurately collected 24-h urine specimens. Veronese et al. (1) found an increase in 24-h urinary magnesium excretion of 1.36 mmol/24 h after supplementation of 900 mg magnesium oxide/d. Because 1.36 mmol is equivalent to ;33 mg of magnesium and 900 mg magnesium oxide/d corresponds to 300 mg of bioavailable magnesium, the reported increment appears to be rather low. Several factors may contribute to this discrepancy. First, compliance to the treatment might have been lower than re-ported. This is, however, not very likely because of the high reported percentage of prescribed magnesium supplements ingested. Second, the low increment in magnesium excretion after supplementation may be due to a lower rate of gastrointestinal absorption than the 30% which is usually taken as an estimate for magnesium (2, 4). Indeed, the fractional absorption of magnesium oxide has been shown to be lower than that of other forms of magnesium (6, 7). Third, there may have been potential undercollection of 24-h urine due to missed voids or urinary incontinence. Together, these 3 factors may have contributed to the absence of correlations between changes in 24-h urinary magnesium excretion and changes in physical performance variables (1). It would be of interest if the authors could give an indication of which of the aforementioned factors may be most likely. For in-stance, the authors could perform a check on completeness of the 24-h urinary collections by examining the differences between actually measured and expected 24-h urinary creatinine excretions (8, 9). Large differences between observed and expected values are indicative of inaccurate or incomplete collections. If little or no undercollection was present in the 24-h urine samples, does this mean that future clinical trials should use higher supplementation doses of magnesium oxide or use a magnesium preparation with a higher bioavailability? Perhaps the authors have alternative ex-planations for the relatively low increase in 24-h urinary excretion of magnesium after magnesium oxide supplementation of 900 mg/d for 12 wk. Nevertheless, the results by Veronese et al. undeniably highlight the importance of sufficient magnesium intake for delaying the age-related decline in physical performance. Furthermore, their findings add to the necessity of preventing magnesium deficiency and to the awareness of the favorable health effects of magnesium in general. None of the authors declared a conflict of interest.
    American Journal of Clinical Nutrition 01/2015; 101(1):240-241. DOI:10.3945/ajcn.114.098186 · 6.92 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Purpose of review Restriction of dietary sodium is recommended at a population level as well as for groups at high cardiovascular risk, and chronic kidney disease (CKD). This review addresses recent evidence for the protective effect of dietary sodium restriction in CKD patients specifically. Recent findings Sodium intake in CKD populations is generally high, and often above population average. Recent data demonstrated that moderately lower sodium intake in CKD patients is associated with substantially better long-term outcome of renin-angiotensin-aldosterone system (RAAS)-blockade, in diabetic and nondiabetic CKD, related to better effects of RAAS-blockade on proteinuria, independent of blood pressure. This is in line with better short-term efficacy of RAAS-blockade during moderate sodium restriction in diabetic and nondiabetic CKD. This effect of sodium restriction is likely mediated by its effects on volume status. Sustainable sodium restriction can be achieved by approaches on the basis of behavioral sciences. Summary Moderate restriction of dietary sodium can substantially improve the protective effects of RAAS-blockade in CKD, by specific renal effects apparent from proteinuria reduction. The latter precludes straightforward extrapolation of data from nonrenal populations to CKD. Concerns regarding the adverse effects of a very low sodium intake should not distract from the protective effects of moderate sodium restriction. Prospective studies should assess the efficacy and sustainability of different strategies to target high sodium intake in CKD, along with measures at population level.
    Current Opinion in Nephrology and Hypertension 09/2014; 23(6). DOI:10.1097/MNH.0000000000000073 · 4.24 Impact Factor

Full-text

Download
163 Downloads
Available from
May 26, 2014