Mag-K-Taurine

AOR04246

Magnesium, potassium & taurine

  • Supports healthy blood pressure and regulates heart rhythm
  • Maintains the activity of nerves and muscles
  • Protects the heart from cellular damage
  • Provides a correct balance of magnesium, potassium, and taurine
Gluten Free
Non-GMO
Vegan

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Magnesium and potassium are electrolyte minerals that have many important functions, including maintaining the activity of nerves and muscles, regulating water retention and supporting a healthy acid-base balance. Studies suggest that 50-90% of the population is deficient in magnesium, and deficiencies in potassium often occur along with magnesium deficiencies since the minerals are closely related in function. Taurine is the most abundant free amino acid within the heart muscle and shares many of the same functions as magnesium, making it an ideal complement to the mineral.

Magnesium, potassium and taurine are essential for healthy cardiovascular function. The heart health benefits of magnesium and potassium are mostly due to their electrolyte effects on cells and nerves, supporting the ability of nerves to transmit signals and the ability of muscles to contract, both of which are important to regulate heart rhythm. A deficiency in either magnesium or potassium can result in high blood pressure, and many studies have found supplementation with either mineral to be effective for lowering blood pressure. Even mild deficiencies in potassium may result in nervous disorders, insomnia, and irregular heartbeat. Nutritional research has also proven taurine’s ability to lower blood pressure, stabilize membranes and regulate the heartbeat. In repeated studies, taurine has been shown effective for regulating heartbeat, as well as for minimizing the damage caused by a lack of oxygen to the heart tissues.

Mag-K-Taurine is ideal for those looking for a synergistic, highly absorbable mineral supplement to correct a magnesium or electrolyte deficiency. Mag-K-Taurine is especially effective in maintaining healthy blood pressure and to counterbalance an irregular heartbeat.

AOR Advantage

AOR’s Mag-K-Taurine is an electrolyte formula free of sugars that fill most electrolyte supplements. It provides an important balance of magnesium and potassium for good nerve and muscle contractility along with taurine for maintained heart function.

NPN

80059998

Discussion

Taurine helps support cardiovascular function. Magnesium and potassium are minerals that are factors in the maintenance of good health and help maintain proper muscle function.

Guarantees

AOR™ guarantees that all ingredients have been declared on the label. Contains no wheat, gluten, corn, nuts, peanuts, sesame seeds, sulphites, mustard, soy, dairy, eggs, fish, shellfish or any animal by product.

Adult Dosage

Take one capsule four times daily with/without food, or as directed by a qualified health care practitioner.

Cautions

Consult a health care practitioner prior to use if you are pregnant or breastfeeding.

Main Applications
  • Cardiovascular health
  • Brain function
Disclaimer

The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide or replace medical advice to individuals from a qualified health care professional. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes.

Serving Size: One Capsule
Magnesium (as magnesium citrate)
70 mg
Potassium ( as potassium chloride)
25 mg
Taurine
375 mg

Non-medicinal Ingredients: silicon dioxide and sodium stearyl fumarate. Capsule: hypromellose.

Hypertension: Magnesium (M)
Study 1:
In a 2016 meta-analysis, the antihypertensive effect of oral Mg supplementation on blood pressure (BP) was performed. It synthesized available evidence from randomized, double-blind, placebo-controlled trials. In total, 34 trials involving 2028 normotensive and hypertensive participants were reviewed. Weighted mean differences of changes in BP and serum Mg were calculated by random-effects meta-analysis. Mg supplementation at a median dose of 368 mg/d for a median duration of 3 months significantly reduced systolic BP by 2.00 mm Hg (95% confidence interval, 0.43–3.58) and diastolic BP by 1.78 mm Hg (95% confidence interval, 0.73–2.82); these reductions were accompanied by 0.05 mmol/L (95% confidence interval, 0.03, 0.07) elevation of serum Mg compared with placebo. The researchers found that Mg supplementation with a dose of 300 mg/d or duration of 1 month is sufficient to elevate serum Mg and reduce BP. The findings indicate a causal effect of Mg supplementation on lowering BPs in adults.
Xi Zhang, Yufeng Li, Liana C. et al. Effects of Magnesium Supplementation on Blood Pressure. Hypertension. 2016;68:324–333 doi.org/10.1161/HYPERTENSIONAHA.116.07664

Study 2:
Mg intake of 500 mg/d to 1000 mg/d may reduce blood pressure (BP) as much as 5.6/2.8 mm Hg. The combination of increased intake of Mg and K coupled with reduced sodium intake is more effective in reducing BP than single mineral intake and is often as effective as one antihypertensive drug in treating hypertension. Mg also increases the effectiveness of all antihypertensive drug classes. Preliminary evidence suggests that insulin sensitivity, hyperglycemia, diabetes mellitus, left ventricular hypertrophy, and dyslipidemia may be improved with increased Mg intake. Various genetic defects in magnesium transport are associated with hypertension and possibly with cardiovascular disease. Oral Mg acts as a natural calcium channel blocker, increases nitric oxide, improves endothelial dysfunction, and induces direct and indirect vasodilation. https://pubmed.ncbi.nlm.nih.gov/22051430/

Study 3:
Mg status has a direct effect upon the relaxation capability of vascular smooth muscle cells and the regulation of the cellular placement of other cations important to blood pressure – cellular sodium:potassium (Na:K) ratio and intracellular calcium (iCa(2+)). As a result, nutritional Mg has both direct and indirect impacts on the regulation of blood pressure and therefore on the occurrence of hypertension. Hypertension occurs when cellular Na:K ratios become too high, a consequence of a high Na, low K diet or, indirectly, through a Mg deficient state which causes a pseudo K deficit. Mg supplementation above 15 mmol per day are required to normalize HBP in unmedicated hypertensive patients while 15 mmol per day will lower HBP in patients treated with antihypertensive medications. In most humans, healthy blood pressure depends upon a balance of both Na:K and Mg:Ca ratios at both cellular and whole body levels which, in turn, require adequate, long-term intakes of nutritional magnesium. https://pubmed.ncbi.nlm.nih.gov/15692166/

Hypertension: Potassium (K)
Study 1:
Several systematic reviews and meta-analyses reported a consistent association between increased potassium (K) intake and blood pressure (BP) reduction. The most rigorous review is a 2013 meta-analysis of 22 randomized controlled trials by Aburto et al.. The review reported that increased K intake reduced systolic blood pressure (SBP) by 3.49 mm Hg (95% CI, 1.82-5.15 mm Hg) and diastolic blood pressure (DBP) by 1.96 mm Hg (95% CI, 0.86-3.06 mm Hg). Notably, BP reduction was only seen in those with hypertension. There was no significant dose response according to the amount of potassium consumed. Although the magnitude of BP reduction is largest when the sodium intake is high, there still appears to be evidence of additive benefit when dietary interventions combine potassium increases with sodium reduction strategies. https://www.bmj.com/content/346/bmj.f1378

Study 2:
The combination of increased intake of Mg and K coupled with reduced sodium intake is more effective in reducing BP than single mineral intake and is often as effective as one antihypertensive drug in treating hypertension. https://pubmed.ncbi.nlm.nih.gov/22051430/

Hypertension: Taurine (T)
Study 1:
Supplementation with T prevents the development of hypertension in several animal models. In those models, taurine-mediated reductions in blood pressure appear to be mediated by a combination of diminished [Ca2+]i, oxidative stress, sympathetic activity and inflammatory activity, as well as an improvement in renal function. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5933890/

Study 2:
Advances in extensive studies on experimental models indicate that T is preventive against hypertension. https://jbiomedsci.biomedcentral.com/articles/10.1186/1423-0127-17-S1-S6

Stroke, and Cardiovascular Disease (CVD): Magnesium (M)
Study 1:
A 2018 Editorial of OpenHeart states that Mg plays an important role in cardiovascular health. It is instrumental for the proper maintenance of cellular membrane potential, functioning of the mitochondria and plays a key role in the body’s antioxidative pathways. As a result, Mg deficiency can lead to serious morbidity and mortality and has been implicated in multiple CVD such as hypertension, cardiomyopathy, cardiac arrhythmia, atherosclerosis, dyslipidaemia and diabetes. Studies have suggested that prompt diagnosis and timely supplementation of Mg may be beneficial in patients with certain cardiac conditions. https://openheart.bmj.com/content/5/2/e000775

Study 2:
In a 2016 study published in the Journal of the American Heart Association (JAHA) involving 9 824 participants (mean age 65.1 years, 56.8% female) with a median follow‐up of 8.7 years, using a multivariable Cox proportional hazard models, the researchers found that a 0.1 mmol/L increase in serum Mg level was associated with a lower risk for coronary heart disease (CHD) mortality (hazard ratio: 0.82, 95% CI 0.70–0.96). Furthermore, they divided serum magnesium in quartiles, with the second and third quartile combined as reference group (0.81–0.88 mmol/L). Low serum Mg (≤0.80 mmol/L) was associated with an increased risk of CHD mortality (N=431, hazard ratio: 1.36, 95% CI 1.09–1.69) and sudden cardiac death (SCD) (N=217, hazard ratio: 1.54, 95% CI 1.12–2.11). Low serum magnesium was associated with accelerated subclinical atherosclerosis (expressed as increased carotid intima‐media thickness: +0.013 mm, 95% CI 0.005–0.020) and increased QT‐interval, mainly through an effect on heart rate (RR‐interval: −7.1 ms, 95% CI −13.5 to −0.8). Additional adjustments for carotid intima‐media thickness and heart rate did not change the associations with CHD mortality and SCD. Conclusion: Low serum Mg is associated with an increased risk of CHD mortality and SCD. https://www.ahajournals.org/doi/10.1161/JAHA.115.002707

Study 3:
A 2013 prospective study examined the association between dietary and plasma magnesium and risk of coronary heart disease (CHD) among women in the Nurses’ Health Study. Mg is associated with lower risk of sudden cardiac death, possibly through antiarrhythmic mechanisms. It influences endothelial function, inflammation, blood pressure, and diabetes, but a direct relation with risk of CHD had not been established. Methods and Results: The association for Mg intake was examined among 86 323 women free of disease in 1980. Information on Mg intake and lifestyle factors was ascertained every 2 to 4 years through questionnaires. Through 2008, 3614 cases of CHD (2511 nonfatal/1103 fatal) were documented. For plasma Mg, the researchers conducted a nested case–control analysis, with 458 cases of incident CHD (400 nonfatal/58 fatal) matched to controls (1:1) on age, smoking, fasting status, and date of blood sampling. Higher Mg intake was not associated with lower risk of total CHD (P‐linear trend=0.12) or nonfatal CHD (P‐linear trend=0.88) in multivariable models. However, magnesium intake was inversely associated with risk of fatal CHD. The RR comparing quintile 5 to quintile 1 of Mg intake was 0.61 (95% CI, 0.45 to 0.84; P‐linear trend=0.003). The association between Mg intake and risk of fatal CHD appeared to be mediated partially by hypertension. Plasma Mg levels above 2.0 mg/dL were associated with lower risk of CHD, although not independent of other cardiovascular biomarkers (RR, 0.67; 95% CI, 0.44 to 1.04). Conclusions: Dietary and plasma Mg were not associated with total CHD incidence in this population of women. However, Mg intake was inversely associated with fatal CHD, which may be mediated in part by hypertension. https://www.ahajournals.org/doi/10.1161/JAHA.113.000114

Stroke, and Cardiovascular Disease (CVD): Potassium (K)
Study 1:
A dose-response relationship between dietary K and risk of stroke has been reported. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1121081/

Study 2:
A 1987, twelve-year prospective study showed that for every 10-mmol increase in K intake per day, there was a 40% reduction in stroke-associated mortality. https://pubmed.ncbi.nlm.nih.gov/3796701/

Study 3:
A 2011 meta-analysis of 11 prospective studies of K intake, stroke, and CVD involving ∼250,000 individuals showed the strongest association with reduction of risk of stroke by 21% for every 1.64-g/d (423-mmol/d) increase in K intake and a trend toward a lower risk of CVD. https://pubmed.ncbi.nlm.nih.gov/21371638/

Stroke, and Cardiovascular Disease (CVD): Taurine (T)
Study 1:
The health effects of T have been confirmed epidemiologically by the WHO-coordinated Cardiovascular Diseases and Alimentary Comparison (CARDIAC) Study covering 61 populations in the world. Accumulating evidence from this study indicate that common T intakes reduce CVD risks and contribute to the longevity of the Japanese, which have the lowest coronary heart disease (CHD) mortality in developed countries. https://pubmed.ncbi.nlm.nih.gov/19239132/

Study 2:
Taurine has been approved for the treatment of congestive heart failure (CHF) in Japan and shows promise in the treatment of several other diseases. Like other heart failure medications, T not only diminishes the common symptoms of CHF (breathlessness on exertion and edema) but also eliminates or decreases the need for administering other heart failure medication. Although it exerts a mild positive inotropic effect on the hypodynamic heart and promotes natriuresis and diuresis, the major therapeutic effect of long-term T administration appears to involve a reduction in the actions of norepinephrine and angiotensin II, which are known to decrease myocardial performance through elevations in afterload pressure, ventricular remodeling and fluid remodeling. Recent studies have shown that T therapy improves the exercise capacity of patients with heart failure. T supplementation might prolong the lifespan of heart failure patients because it elevates high energy phosphate content of the heart, which is an important determinant of mortality among patients suffering from CFT. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5933890/