Magnesium For Prevention and Treatment of Coronary Artery Disease by Jeffrey Dach MD

Despite the best efforts of mainstream cardiology, a shocking number of Americans still suffer from angina and coronary artery disease. Even though millions of Americans take statin drugs, blood pressure pills, water pills, beta blockers, calcium channel blockers and other cardiac medications, national cardiac mortality data shows little progress. What if the answer lies in magnesium, a simple, inexpensive mineral that most doctors overlook? My office routinely checks the RBC Magnesium, and when found low, we give magnesium supplements. The result can be dramatic with improved energy, and improvement in blood pressure, prevention of arrythmias and resolution of cardiac symptoms. What is the mechanism of magnesium’s health benefits? Magnesium works through multiple mechanisms that address the root causes of atherosclerosis and coronary artery disease.

Header Image: Crystal structure of Mg2SiO4 (olivine, Pnma) projected onto the (a, b) plane. Green: magnesium atoms, yellow: silicon atoms, blue: oxygen atoms. Author Perditax, Public Domain, Wikimedia commons.

Our Soils Are Depleted of Magnesium

Magnesium deficiency is widespread because modern diets are low in magnesium because of processed foods and agricultural practices that deplete soil mineral content. Many common medications, especially proton pump inhibitor antacids prevent GI absorption, and thiazide diuretics (hydrochlorothiazide) increase urinary magnesium excretion. These drugs deplete our magnesium stores. (22) (34-36)

In 2025, Dr. Weiguo Zhang reviewed the global problem of magnesium deficiency writing:

Magnesium is an essential mineral required for energy metabolism, glucose regulation, cardiovascular function, bone integrity, and neural activity… dietary magnesium deficiency remains a widespread and underrecognized global public health concern. The recommended dietary allowance (RDA) is 420 mg/day …. Globally, an estimated 2.4 billion people, or roughly 31% of the global population, fail to meet the recommended magnesium intake levels. This deficiency reflects…soil nutrient depletion from intensive agriculture, food processing losses, aged populations…magnesium deficiency is associated with elevated risks of cardiovascular disease, metabolic disorders, bone loss, and neuropsychiatric conditions. (22)

Left Image: The average mineral content of calcium, magnesium, and iron in cabbage, lettuce, tomatoes, and spinach has dropped 80–90% between 1914 and 2018. Vertical axis: milligrams. Horizontal axis: year.  Figure 2. Courtesy of Workinger, Jayme L., Robert P. Doyle, and Jonathan Bortz. “Challenges in the Diagnosis of Magnesium Status.” Nutrients, (2018) p.1202. (32)

Magnesium Mechanisms Reviewed by Dr. DiNicolantonio in 2022

In 2022, Dr. James DiNicolantonio reviewed the many mechanisms of magnesium in preventing and treating cardiovascular disease, writing:

Magnesium is an essential mineral found in the body. It is naturally present in many foods and is also available as a dietary supplement. It serves as a cofactor in more than 300 enzymatic reactions, such as those responsible for regulating blood pressure, glycaemic control and lipid peroxidation. It is therefore also critical to the cardiovascular system. The adult body contains approximately 24 g of magnesium, with 50% to 60% present in bones with the rest being contained in soft tissues. Serum magnesium represents less than 1% of total body magnesium. In industrialized western countries, a low intake of magnesium often predisposes to a high prevalence of magnesium deficiency increasing the risk of cardiovascular events and cardiovascular death. This article aims to review of effect of magnesium deficiency on the cardiovascular system. (18)

What are the adverse health consequences of magnesium deficiency? And what are the mechanisms magnesium uses to heal the body? Here are a few of them:

Coronary Artery Disease is an Inflammatory Process and Magnesium Reduces Inflammatory Markers

In 2006, Dr. Stephan J Ott demonstrated that coronary artery plaque is fundamentally a polymicrobial biofilm demonstrated by multiple independent labs using 16s ribosome genetic sequencing of atherosclerotic plaque specimens. The plaque in your arteries is not just a passive buildup of cholesterol. It is an active infectious process driven by the microbes originating in the gut and pharynx causing immune reaction and calcification. Infection is one of the strongest triggers in the human body for an inflammatory reaction, thus causing soft tissue calcification in response to intense inflammation. (1)

Magnesium Reduces Inflammatory Markers

Magnesium deficiency activates inflammatory markers such as Nuclear Factor Kappa B (NF-κB) and the NLRP3 inflammasome, increasing cytokines like CRP, IL-6, and TNF-alpha. This promotes plaque formation, endothelial activation, and white cell (monocyte) migration into the plaque. Magnesium supplementation reduces inflammation and reliably lowers inflammatory markers. Multiple randomized controlled trials and meta-analyses confirm this benefit, especially in patients who are deficient.

In 2022, Dr. Nicola Veronese did a meta-analysis of 17 randomized trials and found magnesium reduces CRP (C-reactive protein), a non-specific inflammatory marker, and increased Nitric Oxide (NO) levels. Magnesium (Mg) reduces the inflammatory progression of the atherosclerotic plaque. In 2022, Dr Nicola Veronese writes:

In meta-analysis, Mg supplementation significantly decreased serum C reactive protein (CRP) and increased nitric oxide (NO) levels. In descriptive findings, Mg supplementation significantly reduced plasma fibrinogen, tartrate-resistant acid phosphatase type 5, tumor necrosis factor-ligand superfamily member 13B, ST2 protein, and IL-1. In conclusion, Mg supplementation may significantly reduce different human inflammatory markers, in particular serum CRP and NO levels. (2)

Magnesium Improves Mitochondrial Function

Magnesium is the single most important nutrient for our mitochondria, the power plants inside every cell. Magnesium is required for ATP synthesis, the Tricarboxylic Acid (TCA) cycle, and electron transport chain enzymes, all present inside the mitochondria. Without adequate magnesium, mitochondria cannot produce energy efficiently. Magnesium deficiency leads to increased oxidative stress, calcium overload, and impaired energy metabolism in heart muscle and vascular cells lining the blood vessels. Restoring magnesium improves ATP production and cardiac diastolic function, especially helpful in patients with heart failure.

In 2020, Drs. Man Liu and Samuel Dudley reviewed the mechanisms of magnesium’s benefits and stated that magnesium(Mg) supplementation improves mitochondrial function and cardiac diastolic performance in diabetics, The authors write:

Mg deficiency plays detrimental roles in cardiovascular diseases …and [supplementation benefits] heart failure, arrhythmias and other cardiovascular diseases…Mg supplementation has shown significant therapeutic effects in HF [heart failure] and CVD [cardio-vascular disease] …. It has also been shown to improve atrial fibrillation (AF) , ventricular arrhythmias (VA), and arrhythmias in acute myocardial infarction (MI). (3)

Magnesium Has Antioxidant Properties

Arterial bifurcations are the weak point. Arterial wall cracks and breaks in the intima lining are induced by sheer flow stress at arterial bifurcations, allowing entrance of poly-microbial infection and oxidized LDL particles inciting inflammation, soft tissue calcification and progression of atherosclerotic plaque. Microbial infection of the atherosclerotic plaque, inflammation, calcification and oxidative stress are the initiating events of atherosclerosis.

Magnesium deficiency increases reactive oxygen species (ROS) from mitochondria and depletes our antioxidant defense, namely glutathione, our major intracellular antioxidant, and superoxide dismutase. At the cellular level, magnesium stabilizes cell membranes, supports antioxidants, and reduces lipid peroxidation. Magnesium directly counters oxidative damage to cells. (3)

Magnesium Improves Nitric Oxide Synthesis and Endothelial Function

The weak link in our vascular tree is the endothelium, the inner lining of our arteries. Endothelial dysfunction means our arteries become stiff, narrowed, and subject to damaging effects inflammation. Enter Nitric Oxide, the protector of endothelial function. Magnesium increases Nitric Oxide (NO) at the endothelium by  increasing for endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) production. This extra Nitric Oxide dilates our blood vessels and keeps them healthy. Low magnesium RBC levels indicate magnesium deficiency, and a reduction in nitric oxide production (NO), vasoconstriction, increased adhesion molecules and increases risk for thrombosis (clot formation).

In 2000, Dr. Michael Shechter conducted a randomized trial of oral magnesium in 50 patients with stable coronary artery disease showing magnesium supplementation improves flow-mediated dilation and improves exercise tolerance. Flow-mediated dilatation is the standard clinical test for endothelial dysfunction,  (4)

Dr. Mark Houston: Take Magnesium with Your Blood Pressure Pills

Dr. Mark Houston is a cardiologist and director of the Hypertension Institute and recognized expert in in preventive cardiology and hypertension. In 2011, Dr. Houston states that magnesium increases effectiveness of all antihypertensive drug classes, writing:

Magnesium also increases the effectiveness of all antihypertensive drug classes. It also notes that magnesium intake of 500–1000 mg/day may reduce BP by as much as 5.6/2.8 mm Hg and that combining magnesium (with potassium and reduced sodium) is often as effective as one antihypertensive drug. (23)

In 2013, Dr. Andrea Rosanoff analyzed seven studies with 135 patients showed a strong blood pressure lowering effect when magnesium is added to existing antihypertensive medications, particularly in those with higher baseline systolioc blood pressure greater than 155 mm Hg. Magnesium supplementation reduced blood pressure around 18.7 mm Hg systolic and 10.9 mm Hg diastolic in this specific population of hypertensives already on blood pressure medication. (24)

Magnesium Reduces Atherosclerotic Plaque, Improves  Glycemic Control and Insulin Sensitivity:

In 2019, Dr. Hamid Reza Talari conducted a randomized, placebo-controlled trial for diabetics with kidney failure on hemodialysis who received a modest dose of only 150 mg of magnesium oxide, one of the cheapest and poorly absorbed forms of magnesium. For those who can afford it, magnesium glycinate is the preferred form of magnesium. Dr. Talari studied the effect of magnesium oxide supplementation using ultrasound imaging of the carotid arteries, showing significant reduction in mean carotid intima-media thickness (CIMT), meaning less atherosclerotic plaque buildup in the carotid arteries. Note: The carotid arteries are the two large arteries on either side of the neck supplying blood flow to the brain.

Dr. Talari’s study also showed magnesium improves diabetes with decrease in fasting insulin, reduction of Hemoglobin A1c (HbA1c), reduction in high-sensitivity CRP (hs-CRP), increase in  total antioxidant capacity (TAC) and lower cholesterol. Dr. Talari’s is particularly convincing because it was conducted in a very high-risk diabetics with advanced kidney disease on dialysis, producing improvements for both vascular and metabolic markers with the inexpensive magnesium oxide. Note: magnesium glycinate is the preferred form of magnesium (5)

Magnesium Supplementation Slows and Reverses Atherosclerotic Plaque Progression

There are many other human clinical trials showing magnesium supplementation can actually slow or even reverse the progression of atherosclerotic plaque in the arteries. In my experience, correcting magnesium deficiency is very beneficial for reducing risk for coronary artery disease. Here are six additional key human studies confirming the benefits of magnesium:

1. Magnesium Reduces Carotid Intima-Media Thickness in Hemodialysis Patients 

In this 2008 double-blind randomized controlled trial by Dr. Faruk Turgut, patients with chronic kidney disease on hemodialysis received oral magnesium supplementation. Ultrasound measurements of the carotid arteries showed a significant reduction in intima-media thickness, a direct marker of atherosclerotic plaque burden, compared with baseline. In contrast, the placebo group showed progression of plaque thickness during the same period. This study provides clear visual proof that magnesium can help shrink existing plaque in very high-risk dialysis patients. (6)

2. Magnesium Reduces Carotid Intima-Media Thickness in Hemodialysis Patients 

In this 2013 double-blind, randomized, placebo-controlled trial by Dr. Mohammad  Mortazavi involved 54 patients with kidney failure on hemodialysis. Those given oral magnesium oxide showed a significant decrease in carotid intima-media thickness (plaque marker), while the placebo group experienced an increase. The plaque-reducing effect remained statistically significant even after adjusting for other risk factors. (7)

3. Subclinical Atherosclerosis in Hypertensive Women 

In this 2017 randomized controlled trial by Dr. Ana Cunha, women with hypertension who were already taking thiazide diuretics (a “water pill” class of blood-pressure medication known to deplete magnesium) received oral magnesium supplementation. The magnesium group showed improved endothelial function and a clear slowing of subclinical atherosclerosis progression as measured by carotid intima-media thickness and related vascular imaging markers. Many of my hypertensive patients are on similar medications, making this study especially relevant. (8)

4. Coronary Artery Calcium Score (CT Imaging) 

In 2014, Dr. A Hruby found self reported magnesium intake was inversely associated with coronary artery calcification. (37)

In 2020, Dr. Ji-Xia Pen studied vascular calcification in a rat model finding magnesium sulfate reduced vascular calcification in a dose dependent manner. (38)

In 1989, Dr. Nagase found that myocardial disorders in diabetic KK mice where caused by magnesium deficiency and reversed by magnesium supplementation. (39)

In patients with chronic kidney disease (CKD), magnesium supplementation reduces vascular calcification, and calcium score is inversely associated with serum magnesium levels. (40-42)

Hemodialysis Patients 

In this 2009 study by Dr. David Spiegel, magnesium carbonate as a phosphate binder (providing supplemental magnesium) was given to hemodialysis patients with kidney failure. Serial CT scans measured coronary artery calcium (CAC) scores over 18 months. The magnesium group showed only about an 8% increase in calcium score, dramatically less than the typical 50% or greater progression of calcium score seen with standard calcium-based binders. This is one of the most striking demonstrations that magnesium can markedly slow dangerous coronary plaque calcification measured by calcium score. (9)

5. Coronary Artery Calcification (CT Imaging) in CKD Patients

In this 2019 randomized controlled trial by Dr. Yusuke Sakaguchi, patients with stage 3–4 chronic kidney disease received oral magnesium oxide. Serial CT calcium scoring showed that the magnesium group had significantly slower progression of coronary artery calcification, while the control group did not. This provides strong randomized evidence of the benefit of magnesium in a non-dialysis chronic kidney disease (CKD) population. (10)

6. Arterial Calcifications (Vascular Imaging) in Hemodialysis Patients 

In this 2014 study by Dr. Ioannis P. Tzanakis, hemodialysis patients with kidney failure were given magnesium supplementation showing a clear slowing of progression of arterial calcification. Standard vascular imaging techniques documented slower advancement of calcified plaque burden compared with controls. Once again, magnesium demonstrated a direct benefit with slowed progression of atherosclerotic plaque. (11)

Important Point: All of these clincial studies used real-world patients with advanced disease, on hemodialysis with kidney disease and hypertension, and relatively modest doses of magnesium, often inexpensive forms such as magnesium oxide or citrate. Yet the imaging showed measurable plaque improvement or slowed progression. This high quality evidence that should make every cardiologist, nephrologist and primary care jump out of their seats and take notice. (36-42)

Animal Studies Confirm Magnesium Reduces Atherosclerotic Plaque

Animal models provide clear mechanistic proof that magnesium supplementation directly reduces atherosclerotic plaque formation, carotid intima-media thickness (CIMT), and vascular calcification across multiple species and disease models. Here are six well-designed animal studies.

Rabbits: Dietary magnesium suppresses atherosclerotic lesions in the aorta.

In 1990 Dr. Ouchi studies male New Zealand white rabbits (n = 31) on five types of diets: regular, 1% cholesterol, and 1% cholesterol diets supplemented with either 300, 600, or 900 mg (as Mg) of Mg sulfate. Diets with the additional Mg decreased both the area of the aortic atherosclerotic lesions and the cholesterol content of the aortas in a dose-dependent manner. The 1% cholesterol diet significantly increased plasma cholesterol and triglyceride concentrations and decreased high density lipoprotein (HDL) cholesterol concentration…These results indicate that dietary Mg prevents the development of atherosclerosis in cholesterol-fed rabbits. (12)

In 2001, Dr. Ravn studied ApoE-Deficient Mice: Oral magnesium supplementation reduced atherosclerotic plaque area in the aortic root by 66% in female mice, (p<0.02).  (13)

In 2009, Dr. King studied rabbits on an atherogenic diet: Higher dietary magnesium (+Mg group) significantly reduced aortic plaque formation and intimal thickness compared with magnesium-deficient animals. Aortas from Mg deficient rabbits had significantly more plaque, with an intima thickness 42% greater than controls. The authors write:

Our study demonstrates that inadequate intake of Mg results in a marked increase in atherosclerotic plaque development in rabbits fed a hypercholesterolemic diet. …Our findings support the epidemiological and in vivo observations that adequate Mg intake can help to decrease incidence of atherosclerotic disease and that assessment of adequate Mg status or dietary intake of Mg might be a good addition to therapy and prevention of CVD. Our findings suggest that serum Mg levels do not correlate with degree of atherosclerotic plaque development and that erythrocyte Mg [Magnesium RBC] levels might be of interest when assessing Mg status clinically. Note: This is why we use the RBC magnesiun test instead of the serum magnesium test  (14)

In 2012 Dr. Kupetsky-Rincon studied genetically modified mice with accelerated atherosclerosis. Magnesium supplementation slowed carotid intima-media thickness progression by nearly 50% (from 8.3 μm/month untreated to 4.5 μm/month treated). (15)

In 2023, Dr. López-Baltanás studied a Rat Model of Metabolic Syndrome and Renal Failure: Dietary magnesium supplementation reduced oxidative stress, inflammation, and vascular dysfunction, preventing progression of atherosclerosis-related pathology. (16)

Díaz-Tocados et al. 2017 (Uremic Rat Model): Magnesium supplementation prevented and reversed vascular calcification and atherosclerotic changes in a uremic rat model of chronic kidney disease. (17)

Magnesium Useful for Cardiac Arrhythmia/ Atrial Fibrillation/PVCs

A shocking number of Americans suffer from heart rhythm disorders experiencing palpitations and skipped beats indicating premature ventricular contractions (PVCs), premature atrial contractions (PACs), and even worse, atrial fibrillation with a racing heart. When severe, these symptoms patients end up in the emergency room treated by cardiologists with beta blockers, anti-arrhythmic drugs, blood thinners and even electrical shock cardioversion. Despite best efforts by our medical system, cardiac arrythmias are increasing. What if the solution to cardiac arrhythmia lies in magnesium, a simple, inexpensive mineral that most cardiologists overlook? Many have low magnesium levels when properly tested with the RBC magnesium, not the serum magnesium which is the wrong test. When magnesium deficiency is corrected with diet and supplementation, the results are often dramatic: fewer palpitations, more stable rhythms, and patients who finally feel in control again. Why does magnesium work so well for heart rhythm disorders? It is not one single effect. It works through multiple mechanisms that directly stabilize the heart’s electrical system.

Important Point: Magnesium is not a drug. It is a natural mineral cofactor for hundreds of enzymes in the body, including those that control the heart’s electrical conduction. Deficiency is widespread because modern diets are low in magnesium-rich foods, and many common medications (diuretics, proton pump inhibitors, and some blood pressure drugs) deplete it further. Low magnesium is a hidden trigger for arrhythmia that most doctors never check. (22) (34-36)

In 2022, Dr. Alina Negru reviewed the role of magnesium in cardiac arrythmias, writing:

The importance of magnesium (Mg2+), a micronutrient implicated in maintaining and establishing a normal heart rhythm, is still controversial. It is known that magnesium is the cofactor of 600 and the activator of another 200 enzymatic reactions in the human organism. Hypomagnesemia can be linked to many factors, causing disturbances in energy metabolism, ion channel exchanges, action potential alteration and myocardial cell instability, all mostly leading to ventricular arrhythmia. This review article focuses on identifying evidence-based implications of Mg2+ in cardiac arrhythmias. The main identified benefits of magnesemia correction are linked to controlling ventricular response in atrial fibrillation, decreasing the recurrence of ventricular ectopies and stopping episodes of the particular form of ventricular arrhythmia called torsade de pointes. Magnesium has also been described to have beneficial effects on the incidence of polymorphic ventricular tachycardia and supraventricular tachycardia. The implication of hypomagnesemia in the genesis of atrial fibrillation is well established; however, even if magnesium supplementation for rhythm control, cardioversion facility or cardioversion success/recurrence of AF after cardiac surgery and rate control during AF showed some benefit, it remains controversial. Although small randomised clinical trials showed a reduction in mortality when magnesium was administered to patients with acute myocardial infarction, the large randomised clinical trials failed to show any benefit of the administration of intravenous magnesium over placebo. (25)

Here are the key reasons magnesium is so effective for heart rhythm disorders:

1. Membrane Stabilization and Ion Channel Regulation

Magnesium acts as a natural calcium channel blocker and stabilizes cardiac cell membranes. It helps regulate potassium, sodium, and calcium movement across heart cells. Low magnesium leads to increased excitability, early after-depolarizations, and re-entrant circuits that trigger PVCs, PACs, and atrial fibrillation. Restoring magnesium calms this electrical instability.

2. Na/K ATPase Pump Function

Magnesium is an essential cofactor for the sodium-potassium ATPase pump that maintains the heart’s resting membrane potential. Without enough magnesium, the pump fails, potassium leaks out of cells, and arrhythmias become more likely. This is why low magnesium and low potassium often occur together and why fixing magnesium is crucial even when potassium levels look “normal.”

3. Anti-Inflammatory and Antioxidant Effects in the Heart

Chronic low-grade inflammation and oxidative stress damages the heart’s conduction system and promote atrial fibrillation. Magnesium reduces inflammation and oxidative damage, thus protecting the sensitive electrical pathways.

Clinical Evidence from Human Studies

The medical literature is clear. Magnesium supplementation (especially when deficiency is present) reduces the incidence of serious arrhythmias in multiple settings.

Post-Acute Coronary Syndrome Arrhythmias 

In 2018, Dr. Salaminia did a systematic review and meta-analysis of randomized trials showed that magnesium supplementation significantly reduced both ventricular and atrial arrhythmias after acute coronary syndrome compared with placebo. The effect was consistent across studies and provides strong evidence for magnesium’s role in preventing dangerous rhythm disturbances in high-risk heart patients. (19)

Postoperative Atrial Fibrillation After Cardiac Surgery

Multiple meta-analyses of randomized controlled trials have shown that magnesium supplementation (intravenous or oral) significantly reduces the risk of new-onset atrial fibrillation following heart surgery. A large review in 2017 by Dr. William Baker confirmed magnesium lowers the incidence of postoperative atrial fibrillation without increasing adverse events. This benefit is now widely recognized in cardiac surgery protocols. (20)

Premature Ventricular and Atrial Contractions (PVCs and PACs)

Randomized trials have shown that oral magnesium supplementation can reduce the frequency and symptoms of premature atrial and ventricular cardiac contractions. In my practice, patients with bothersome PVCs often see dramatic relief once magnesium levels are optimized. (26-28)

Torsades de Pointes and Drug-Induced Arrhythmias

Intravenous magnesium is very effective and is the standard of care for torsades de pointes (a dangerous polymorphic ventricular tachycardia often triggered by QT-prolonging drugs). Magnesium rapidly suppresses early after-depolarizations and restores normal rhythm even when serum levels appear only mildly low. The list of QT prolonging drugs is lengthy and can be found HERE (requires free registration) (29-31)

RBC Magnesium is Preferred Form

Important Point: Serum magnesium levels are a poor indicator of total body stores. Red blood cell (RBC) magnesium or ionized magnesium testing is far more accurate. Most patients with arrhythmias have low intracellular magnesium even when the serum magnesium blood test is “normal.” (33)

Conclusion: Magnesium addresses the core problems of coronary artery disease: inflammation, oxidative stress, mitochondrial dysfunction, endothelial impairment, and disordered lipid metabolism. In cardiac arrythmia, magnesium addresses the core electrical and metabolic problems that cause heart rhythm disorders. Magnesium is safe, inexpensive, and available without prescription. Dietary sources include leafy greens, nuts, seeds, and dark chocolate, but most patients with arrhythmias benefit from targeted supplementation (typically 300–400 mg elemental magnesium daily, using well-absorbed forms such as glycinate, taurate, or citrate). The magnesium glycinate is considered the “high end’ product because it is the most absorbable and biologically active, because of the amino acid chelate, glycine.

Patients often ask me, “Why doesn’t my cardiologist talk about magnesium?” The answer is simple: it is not a patented pharmaceutical, yet the medical literature is clear. Correcting magnesium deficiency is one of the most powerful, evidence-based steps you can take for preventing and reversing atherosclerotic plaque, preventing arrhythmia, and can be taken with existing blood pressure medication. Feel free to share this with your doctor. Knowledge is power.

Above left Image: Image: food sources of magnesium (clockwise from top left): bran muffins, pumpkin seeds, barley, buckwheat flour, low-fat vanilla yogurt, trail mix, halibut steaks, garbanzo beans, lima beans, soybeans, and spinach. Link to photo on Wikimedia Commons.
This image was released by the United States Department of Agriculture, with the ID K11083-1.Public domain. 

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Complete List of References.

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21) Veronese, Nicola, et al. “Effect of Magnesium Supplementation on Inflammatory Parameters: A Meta-Analysis of Randomized Controlled Trials.” Nutrients, vol. 14, no. 3, 2022, p. 679. https://doi.org/10.3390/nu14030679

22) Zhang, Weiguo, and Youyou Zhao. “Global Dietary Magnesium Deficiency: Prevalence, Underlying Causes, Health Consequences, and Strategic Solutions.” International Journal for Vitamin and Nutrition Research 95.6 (2025).

Magnesium is an essential mineral required for energy metabolism, glucose regulation, cardiovascular function, bone integrity, and neural activity. Despite the vital physiological roles of magnesium, dietary magnesium deficiency remains a widespread and underrecognized global public health concern. The recommended dietary allowance (RDA) for adults in the United States is approximately 420 mg/day for men and 320 mg/day for women, yet large proportions of the population fail to meet these levels with national nutrition surveys consistently documenting inadequate intake. For instance, 64.4% of Chinese adults consume less than the estimated average requirement (EAR) of 270 mg/day for both males and females. Globally, an estimated 2.4 billion people, or roughly 31% of the global population, fail to meet the recommended magnesium intake levels. This deficiency reflects multiple converging factors, including modern dietary patterns low in whole grains and vegetables, soil nutrient depletion from intensive agriculture, food processing losses, aged populations, chronic diseases, and socioeconomic disparities. The health implications are substantial, as magnesium deficiency is associated with elevated risks of cardiovascular disease, metabolic disorders, bone loss, and neuropsychiatric conditions. This review synthesizes current evidence on the biological importance of magnesium, global intake patterns, and determinants of deficiency, and discusses strategic interventions (such as dietary diversification, food fortification, biofortification, supplementation, and public health policies) to enhance magnesium nutrition and reduce the burden of noncommunicable diseases worldwide.

23) Houston, Mark. “The Role of Magnesium in Hypertension and Cardiovascular Disease.” Journal of Clinical Hypertension (Greenwich, Conn.), vol. 13, no. 11, 2011, pp. 843-47.
Full text (free): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8108907/ or
https://onlinelibrary.wiley.com/doi/10.1111/j.1751-7176.2011.00538.x.

24) Rosanoff, Andrea, and Michael R. Plesset. “Oral Magnesium Supplements Decrease High Blood Pressure (SBP > 155 mmHg) in Hypertensive Subjects on Anti-Hypertensive Medications: A Targeted Meta-Analysis.” Magnesium Research, vol. 26, no. 3, 2013, pp. 93-99.
https://doi.org/10.1684/mrh.2013.0337. PMID: 24134861.
PubMed: https://pubmed.ncbi.nlm.nih.gov/24134861/.

25) Negru, Alina. G., et al. “The Role of Hypomagnesemia in Cardiac Arrhythmias.” Biomedicines, vol. 10, no. 10, 2022, p. 2356.
https://doi.org/10.3390/biomedicines10102356

26) De Falco, Cristina Nádja Muniz Lima, et al. “Successful Improvement of Frequency and Symptoms of Premature Complexes after Oral Magnesium Administration.” *Arquivos Brasileiros de Cardiologia*, vol. 98, no. 6, 2012, pp. 480-487. PubMed, https://pubmed.ncbi.nlm.nih.gov/22584491/. DOI: 10.1590/s0066-782×2012005000043.
https://www.scielo.br/j/abc/a/XZs5VBHTn68M9dGckNWmHss/?lang=en

27) De Falco, Cristina Nádja M. Lima, et al. “Late Outcome of a Randomized Study on Oral Magnesium for Premature Complexes.” *Arquivos Brasileiros de Cardiologia*, vol. 103, no. 6, 2014, pp. 468-475. PMC, https://pmc.ncbi.nlm.nih.gov/articles/PMC4290737/. DOI: 10.5935/abc.20140171. PMID: 25590926.
https://pmc.ncbi.nlm.nih.gov/articles/PMC4290737/

28) Lutsey, Pamela L., et al. “A Pilot Randomized Trial of Oral Magnesium Supplementation on Supraventricular Arrhythmias.” *Nutrients*, vol. 10, no. 7, 2018, p. 884. PubMed, https://pubmed.ncbi.nlm.nih.gov/29996476/. DOI: 10.3390/nu10070884. PMCID: PMC6073799.
https://pmc.ncbi.nlm.nih.gov/articles/PMC6073799/

29) Tzivoni, Dan, Andre Keren, Amos M. Cohen, et al. “Magnesium Therapy for Torsades de Pointes.” *American Journal of Cardiology*, vol. 53, no. 4, 1984, pp. 528-30. https://pubmed.ncbi.nlm.nih.gov/6695782/
DOI: 10.1016/0002-9149(84)90025-0

30) Tzivoni, Dan, Shmuel Banai, Claudio Schuger, et al. “Treatment of Torsade de Pointes with Magnesium Sulfate.” *Circulation*, vol. 77, no. 2, 1988, pp. 392-97. https://pubmed.ncbi.nlm.nih.gov/3338130/
DOI: 10.1161/01.cir.77.2.392 (full text often available via AHA Journals)

31) Bailie, D. S., H. Inoue, S. Kaseda, J. Ben-David, and D. P. Zipes. “Magnesium Suppression of Early Afterdepolarizations and Ventricular Tachyarrhythmias Induced by Cesium in Dogs.” *Circulation*, vol. 77, no. 6, 1988, pp. 1395-402. https://pubmed.ncbi.nlm.nih.gov/3370776/
DOI: 10.1161/01.cir.77.6.1395

32) Workinger, Jayme L., Robert P. Doyle, and Jonathan Bortz. “Challenges in the Diagnosis of Magnesium Status.”Nutrients, vol. 10, no. 9, 1 Sept. 2018, p. 1202.
https://doi.org/10.3390/nu10091202. PMC6163803.
https://pmc.ncbi.nlm.nih.gov/articles/PMC6163803/

33) Simşek, Enver, Meltem Karabay, and Kenan Kocabay. “Assessment of magnesium status in newly diagnosed diabetic children: measurement of erythrocyte magnesium level and magnesium tolerance testing.” The Turkish Journal of Pediatrics 47.2 (2005): 132-137.

34) Cundy T, Dissanayake A. Severe hypomagnesaemia in long-term users of proton-pump inhibitors. Clinical Endocrinology (Oxford), vol. 69, no. 2, Aug. 2008, pp. 338-41. doi:10.1111/j.1365-2265.2008.03194.x. Epub 2008 Jan 23. PMID: 18221401.
URL: https://pubmed.ncbi.nlm.nih.gov/18221401/ (or full text via Wiley: https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2265.2008.03194.x)

35) Danziger J, William JH, Scott DJ, et al. Proton-pump inhibitor use is associated with low serum magnesium concentrations. Kidney International, vol. 83, no. 4, Apr. 2013, pp. 692-9. doi:10.1038/ki.2012.452. PMID: 23325090.
URL: https://pubmed.ncbi.nlm.nih.gov/23325090/ (or full text: https://www.kidney-international.org/article/S0085-2538(15)55797-9/fulltext)

36) Kuller LH, Farrier N, Caggiula A, Borhani N, Dunkle S. Relationship of diuretic therapy and serum magnesium levels among participants in the Multiple Risk Factor Intervention Trial. American Journal of Epidemiology, vol. 122, no. 6, Dec. 1985, pp. 1045-59. PMID: 4061439.
URL: https://pubmed.ncbi.nlm.nih.gov/4061439/ (full text often via academic libraries or Oxford Academic).

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Magnesium Inhibits Vascular Calcification

37)  Hruby A, O’Donnell CJ, Jacques PF, et al. Magnesium intake is inversely associated with coronary artery calcification: the Framingham Heart Study. JACC Cardiovasc Imaging 2014;7:59-69.
In community-dwelling participants free of cardiovascular disease, self-reported magnesium intake was inversely associated with arterial calcification, which may play a contributing role in magnesium’s protective associations in stroke and fatal coronary heart disease.

Animal study

38) Pen, Ji-Xia, et al. “The effect of the magnesium supplementation on vascular calcification in rats.” Zhongguo Ying Yong Sheng li xue za zhi= Zhongguo Yingyong Shenglixue Zazhi= Chinese Journal of Applied Physiology 28.1 (2012): 20-23.

To observe the role of magnesium sulfate in vascular calcification, to explore the role and the mechanism of magnesium sulfate in vascular calcification.
METHODS:The vascular calcification model was established by administration of vitamin D3 plus nicotine (VDN) in SD rats. To estimate the extent of calcification by Von Kossa staining, calcium content and alkaline phosphatase activity, osteopontin (OPN) mRNA were determined by using semi-quantitative reverse-transcription polymerase chain reaction.The malondialdehyde (MDA) and nitric oxide (NO) content and activities of superoxide dismutase(SOD) were measured by biochemistry.
RESULTS:A strong positive staining of black/brown areas among the elastic fibers of the medial layer in calcified aorta by Von Kossa staining, calcium content and ALP activity in calcified arteries increased by 3.9-and 3.4-fold as compared with the controls. The expression of OPN mRNA was up-regulated by 40% (P < 0.01). The lipid peroxidation products MDA in vascular were increased 2.0-fold (P < 0.01). The NO content and SOD activity were greatly decreased by 64% and 72% (P < 0.01), respectively, compared with controls. However, calcium content and ALP activity in VDN plus magnesium sulfate group were lower than those in VDN group. Low and high dosage magnesium sulfate obviously relieved degree of calcification in the cardiovascular tissues in a dosage-dependent manner (P < 0.01).
CONCLUSION:Magnesium sulfate plays a role in the pathogenesis of vascular calcification by reducing vascular calcification and decreasing vascular injury.

39) Nagase, N., et al. “Myocardial disorders caused by magnesium deficiency in diabetic KK mice.” Magnesium 8.5-6 (1989): 307-315.

40) Hénaut, Lucie, and Ziad A. Massy. “Magnesium as a calcification inhibitor.” Advances in Chronic Kidney Disease 25.3 (2018): 281-290.
Vascular calcification (VC) is associated with elevated cardiovascular mortality rates in patients with CKD. Recent clinical studies of patients with advanced CKD have observed an association between low serum magnesium (Mg) levels on one hand and elevated VC and cardiovascular mortality on the other. These findings have stimulated interest in understanding Mg’s impact on CKD in general and the associated VC in particular. In vitro and preclinical in vivo data indicate that Mg has the potential to protect vascular smooth muscle cells against calcification via several different molecular mechanisms. Accordingly, data from pilot interventional studies in the clinic suggest that oral Mg supplementation reduces VC in patients with CKD. The present review provides an overview of our current understanding of the impact of Mg on the development of VC in patients with CKD.

41) Sakaguchi, Yusuke, et al. “Association between density of coronary artery calcification and serum magnesium levels among patients with chronic kidney disease.” PLoS One 11.9 (2016): e0163673.
The Agatston score, commonly used to quantify coronary artery calcification (CAC), is determined by the plaque area and density. Despite an excellent predictability of the Agatston score for cardiovascular events, the density of CAC has never been studied in patients with pre-dialysis chronic kidney disease (CKD). This study aimed to analyze the CAC density and its association with serum mineral levels in CKD.
Methods

We enrolled patients with pre-dialysis CKD who had diabetes mellitus, prior cardiovascular disease history, elevated low-density lipoprotein cholesterol levels, or smoking history. The average CAC density was calculated by dividing the Agatston score by the total area of CAC.
Results

The mean estimated glomerular filtration rate (eGFR) of 109 enrolled patients was 35.7 mL/min/1.73 m2. The correlation of the Agatston score with density was much weaker than that with the total area (R2 = 0.19, P < 0.001; and R2 = 0.99, P < 0.001, respectively). Multivariate analyses showed that serum magnesium level was inversely associated with the density, but not with the total area, after adjustment for demographics and clinical factors related to malnutrition-inflammation-atherosclerosis syndrome and mineral and bone disorders including fibroblast growth factor 23 (P = 0.006). This inverse association was pronounced among patients with higher serum phosphate levels (P for interaction = 0.02).
Conclusion

CAC density was inversely associated with serum magnesium levels, particularly in patients with higher serum phosphate levels.

42)  Massy, Ziad A., and Tilman B. Drüeke. “Magnesium and cardiovascular complications of chronic kidney disease.” Nature Reviews Nephrology 11.7 (2015): 432.

Cardiovascular complications are the leading cause of death in patients with chronic kidney disease (CKD). Abundant experimental evidence suggests a physiological role of magnesium in cardiovascular function, and clinical evidence suggests a role of the cation in cardiovascular disease in the general population. The role of magnesium in CKD-mineral and bone disorder, and in particular its impact on cardiovascular morbidity and mortality in patients with CKD, is however not well understood. Experimental studies have shown that magnesium inhibits vascular calcification, both by direct effects on the vessel wall and by indirect, systemic effects. Moreover, an increasing number of epidemiologic studies in patients with CKD have shown associations of serum magnesium levels with intermediate and hard outcomes, including vascular calcification, cardiovascular events and mortality. Intervention trials in these patients conducted to date have had small sample sizes and have been limited to the study of surrogate parameters, such as arterial stiffness, vascular calcification and atherosclerosis. Randomized controlled trials are clearly needed to determine the effects of magnesium supplementation on hard outcomes in patients with CKD.

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Last updated on July 3rd, 2026 by Jeffrey Dach MD