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Magnesium, Uric acid, Green tea, and Cocoa

July 2017


Magnesium, inflammation, and obesity in chronic disease.

About 60% of adults in the United States do not consume the estimated average requirement for magnesium, but widespread pathological conditions attributed to magnesium deficiency have not been reported. Nevertheless, low magnesium status has been associated with numerous pathological conditions characterized as having a chronic inflammatory stress component. In humans, deficient magnesium intakes are mostly marginal to moderate (approximately 50% to <100% of the recommended dietary allowance). Animal experiments indicate that signs of marginal-to-moderate magnesium deficiency can be compensated or exacerbated by other factors influencing inflammatory and oxidative stress; recent studies suggest a similar happening in humans. This suggestion may have significance in obesity, which is characterized as having a chronic low-grade inflammation component and an increased incidence of a low magnesium status. Marginal-to-moderate magnesium deficiency through exacerbating chronic inflammatory stress may be contributing significantly to the occurrence of chronic diseases such as atherosclerosis, hypertension, osteoporosis, diabetes mellitus, and cancer.

Nutr Rev. 2010 Jun;68(6):333-40

Magnesium metabolism and its disorders.

Magnesium is the fourth most abundant cation in the body and plays an important physiological role in many of its functions. Magnesium balance is maintained by renal regulation of magnesium reabsorption. The exact mechanism of the renal regulation is not fully understood. Magnesium deficiency is a common problem in hospital patients, with a prevalence of about 10%. There are no readily available and easy methods to assess magnesium status. Serum magnesium and the magnesium tolerance test are the most widely used. Measurement of ionised magnesium may become more widely available with the availability of ion selective electrodes. Magnesium deficiency and hypomagnesaemia can result from a variety of causes including gastrointestinal and renal losses. Magnesium deficiency can cause a wide variety of features including hypocalcaemia, hypokalaemia and cardiac and neurological manifestations. Chronic low magnesium state has been associated with a number of chronic diseases including diabetes, hypertension, coronary heart disease, and osteoporosis. The use of magnesium as a therapeutic agent in asthma, myocardial infarction, and pre-eclampsia is also discussed. Hypermagnesaemia is less frequent than hypomagnesaemia and results from failure of excretion or increased intake. Hypermagnesaemia can lead to hypotension and other cardiovascular effects as well as neuromuscular manifestations. Causes and management of hypermagnesaemia are discussed.

Clin Biochem Rev. 2003 May;24(2):47-66

Effects of magnesium depletion on inflammation in chronic disease.

PURPOSE OF REVIEW: To update findings supporting the opinion that commonly occurring subclinical magnesium deficiency induced by a low dietary intake is a predisposing factor for chronic inflammatory stress that contributes to the incidence of chronic diseases such as cardiovascular disease and diabetes. RECENT FINDINGS: Both deficient magnesium intakes (<250 mg/day) and serum magnesium concentrations (≤ 0.75 mmol/l) have been associated with elevated serum C-reactive protein concentration, a widely used indicator of inflammation. Achieving magnesium intakes or serum magnesium concentrations that indicate an adequate magnesium status generally attenuates elevated serum C-reactive protein to concentrations that are not indicative of chronic low-grade inflammation. Individuals that are obese or have chronic diseases for which low-grade inflammation is a risk factor are commonly found to be magnesium-deficient. SUMMARY: Subclinical magnesium deficiency caused by low dietary intake often occurring in the population is a predisposing factor for chronic inflammatory stress that is conducive for chronic disease. Magnesium deficiency should be considered a nutrient of significant concern for health and well-being.

Curr Opin Clin Nutr Metab Care. 2014 Nov;17(6):525-30

Role of magnesium in the pathogenesis and treatment of migraine.

Magnesium is an important intracellular element that is involved in numerous cellular functions. Deficiencies in magnesium may play an important role in the pathogenesis of migraine headaches by promoting cortical spreading depression, alteration of neurotransmitter release and the hyperaggregation of platelets. Given this multifaceted role of magnesium in migraine, the use of magnesium in both acute and preventive headache treatment has been researched as a potentially simple, inexpensive, safe and well-tolerated option. Studies have shown that preventive treatment with oral magnesium and acute headache treatment with intravenous magnesium may be effective, particularly in certain subsets of patients. In this review, the pathogenesis of migraine will be discussed, with an emphasis on the role of magnesium. Studies on the use of intravenous and oral magnesium in migraine treatment will be discussed and recommendations will be made regarding the use of magnesium in treating migraine headaches.

Expert Rev Neurother. 2009 Mar;9(3):369-79

Why all migraine patients should be treated with magnesium.

Magnesium, the second most abundant intracellular cation, is essential in many intracellular processes and appears to play an important role in migraine pathogenesis. Routine blood tests do not reflect true body magnesium stores since <2% is in the measurable, extracellular space, 67% is in the bone and 31% is located intracellularly. Lack of magnesium may promote cortical spreading depression, hyperaggregation of platelets, affect serotonin receptor function, and influence synthesis and release of a variety of neurotransmitters. Migraine sufferers may develop magnesium deficiency due to genetic inability to absorb magnesium, inherited renal magnesium wasting, excretion of excessive amounts of magnesium due to stress, low nutritional intake, and several other reasons. There is strong evidence that magnesium deficiency is much more prevalent in migraine sufferers than in healthy controls. Double-blind, placebo-controlled trials have produced mixed results, most likely because both magnesium deficient and non-deficient patients were included in these trials. This is akin to giving cyanocobalamine in a blinded fashion to a group of people with peripheral neuropathy without regard to their cyanocobalamine levels. Both oral and intravenous magnesium are widely available, extremely safe, very inexpensive and for patients who are magnesium deficient can be highly effective. Considering these features of magnesium, the fact that magnesium deficiency may be present in up to half of migraine patients, and that routine blood tests are not indicative of magnesium status, empiric treatment with at least oral magnesium is warranted in all migraine sufferers.

J Neural Transm (Vienna). 2012 May;119(5):575-9

Relation between serum magnesium level and migraine attacks.

OBJECTIVE: The determination of serum magnesium levels in migraine. METHODS: In a case control study performed between January 2007 and December 2007 at Tabriz University of Medical Sciences, Tabriz, Iran, 140 migraine patients were enrolled and their level of serum magnesium was determined and the results were compared with 140 healthy people who did not have any headache, kidney, or gastrointestinal disorders, and no consumption of magnesium complements. RESULTS: Migraine patients (22 male, 118 female) with a mean age of 33.82+/-10.31 and 140 healthy people (26 male, 114 female) with a mean age of (34.19+/-9.95) were enrolled. Forty patients had aura and 100 patients did not have aura. The average serum magnesium level in the patient group (26.14+/-4.3) was significantly lower than the control (31.09+/-4.32) group (p=0.000). There was no significant difference between the mean level of serum magnesium in patients with migraine with aura and without aura, however, there was a significant linear relationship between the amount of serum magnesium and the frequency of headache. CONCLUSION: Serum magnesium in migraine patients was significantly lower than the normal population and related to the frequency of migraine attacks, supporting the use of magnesium in prevention and treatment of migraine.

Neurosciences (Riyadh). 2011 Oct;16(4):320-3

Magnesium and osteoporosis: current state of knowledge and future research directions.

A tight control of magnesium homeostasis seems to be crucial for bone health. On the basis of experimental and epidemiological studies, both low and high magnesium have harmful effects on the bones. Magnesium deficiency contributes to osteoporosis directly by acting on crystal formation and on bone cells and indirectly by impacting on the secretion and the activity of parathyroid hormone and by promoting low grade inflammation. Less is known about the mechanisms responsible for the mineralization defects observed when magnesium is elevated. Overall, controlling and maintaining magnesium homeostasis represents a helpful intervention to maintain bone integrity.

Nutrients. 2013 Jul 31;5(8):3022-33

Dietary magnesium intake and risk of stroke: a meta-analysis of prospective studies.

BACKGROUND: Prospective studies of dietary magnesium intake in relation to risk of stroke have yielded inconsistent results. OBJECTIVE: We conducted a dose-response meta-analysis to summarize the evidence regarding the association between magnesium intake and stroke risk. DESIGN: Relevant studies were identified by searching PubMed and EMBASE from January 1966 through September 2011 and reviewing reference lists of retrieved articles. We included prospective studies that reported RRs with 95% CIs of stroke for ≥3 categories of magnesium intake. Results from individual studies were combined by using a random-effects model. RESULTS: Seven prospective studies, with 6,477 cases of stroke and 241,378 participants, were eligible for inclusion in the meta-analysis. We observed a modest but statistically significant inverse association between magnesium intake and risk of stroke. An intake increment of 100 mg Mg/d was associated with an 8% reduction in risk of total stroke (combined RR: 0.92; 95% CI: 0.88, 0.97), without heterogeneity among studies (P = 0.66, I(2) = 0%). Magnesium intake was inversely associated with risk of ischemic stroke (RR: 0.91; 95% CI: 0.87, 0.96) but not intracerebral hemorrhage (RR: 0.96; 95% CI: 0.84, 1.10) or subarachnoid hemorrhage (RR: 1.01; 95% CI: 0.90, 1.14). CONCLUSION: Dietary magnesium intake is inversely associated with risk of stroke, specifically ischemic stroke.

Am J Clin Nutr. 2012 Feb;95(2):362-6

Serum magnesium in patients with acute ischemic stroke.

Magnesium (Mg) has important effects within the vascular system. Magnesium deficiency was shown to trigger vasoconstriction and enhance vascular endothelial injury, thus promoting the development and progression of atherosclerosis. However, it is still not completely understood whether low serum Mg also promotes the occurrence of stroke. We hereby intended to investigate Mg levels in serum in the early stage of ischemic stroke and to evaluate the relationship between serum Mg concentration and the development of neurological deficits. The study included forty patients with acute ischemic stroke (26 women and 14 men), mean age 56 +/- 4 years, without any other serious injuries. Twenty-one healthy subjects, sex- and age-matched were selected as controls. The serum Mg concentrations were measured colorimetrically on a Hitachi 917 autoanalyzer. Serum levels of Mg were checked on admission, and at 48 hours after the onset of ischemic stroke. Using NIHSS, the neurological deficit was assessed on the 1st day, and 48 hours later. Statistical analysis was performed using the Student t test. The results confirm that there is a relationship between a low Mg concentration in serum at 48 hours after onset of ischemic stroke and the intensity of the neurological deficit. Mean value was 1.39 +/- 0.213 mmol/L (on admission), 1.47 +/- 0.181 mmol/L (at 48 hours after the onset of stroke) versus 1.66 +/- 0.138 mmol/L (in controls). Severity of paresis degree was higher in the patients with low Mg levels (p < 0.05). The serum Mg concentration has been suggested to possibly affect the neurologic state. A decrease in the serum Mg concentration indicates the severity of the injury. A magnesium substitution therapy may be useful.

Rom J Intern Med. 2007;45(3):269-73

Circulating and dietary magnesium and risk of cardiovascular disease: a systematic review and meta-analysis of prospective studies.

BACKGROUND: Clinical hypomagnesemia and experimental restriction of dietary magnesium increase cardiac arrhythmias. However, whether or not circulating or dietary magnesium at usual concentrations or intakes influences the risk of cardiovascular disease (CVD), including fatal ischemic heart disease (IHD), is unclear. OBJECTIVE: We performed a systematic review and meta-analysis to investigate prospective associations of circulating and dietary magnesium with incidence of CVD, IHD, and fatal IHD. DESIGN: Multiple literature databases were systematically searched without language restriction through May 2012. Inclusion decisions and data extraction were performed in duplicate. Linear dose-response associations were assessed by using random-effects meta-regression. Potential nonlinear associations were evaluated by using restricted cubic splines. RESULTS: Of 2,303 articles, 16 studies met the eligibility criteria; these studies comprised 313,041 individuals and 11,995 CVD, 7,534 IHD, and 2,686 fatal IHD events. Circulating magnesium (per 0.2 mmol/L increment) was associated with a 30% lower risk of CVD (RR: 0.70; 95% CI: 0.56, 0.88 per 0.2 mmol/L) and trends toward lower risks of IHD (RR: 0.83; 95% CI: 0.75, 1.05) and fatal IHD (RR: 0.61; 95% CI: 0.37, 1.00). Dietary magnesium (per 200-mg/d increment) was not significantly associated with CVD (RR: 0.89; 95% CI: 0.75, 1.05) but was associated with a 22% lower risk of IHD (RR: 0.78; 95% CI: 0.67, 0.92). The association of dietary magnesium with fatal IHD was nonlinear (P < 0.001), with an inverse association observed up to a threshold of ~250 mg/d (RR: 0.73; 95% CI: 0.62, 0.86), compared with lower intakes. CONCLUSION: Circulating and dietary magnesium are inversely associated with CVD risk, which supports the need for clinical trials to evaluate the potential role of magnesium in the prevention of CVD and IHD.

Am J Clin Nutr. 2013 Jul;98(1):160-73