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From cramps to cell power — magnesium does far more than we thought

In this presentation, Dr Hudson explored magnesium as a fundamental element in human physiology, extending well beyond its traditional neuromuscular role to include key functions in immunity, metabolism, and cellular energy production. Drawing on decades of clinical experience, he shared practical insights into how magnesium status influences disease patterns and patient outcomes across multiple organ systems.

Magnesium is not just a metal, but a medical multitasker

Dr Hudson, reframed magnesium not as a simple supplement, but as an ‘ubiquitous, universal metabolic’ driver of human physiology. Drawing on decades of clinical experience, his perspective is grounded in observation — from early neurology cases in the 1980s, where magnesium improved dystonia and seizure-like activity, to its role during the HIV pandemic, where it was used to support immunity and patient longevity.

Magnesium, element number 12, is far from ordinary. It is the second most abundant intracellular cation and functions as a macrometal, comparable in importance to iron. Despite this, deficiency remains common, while excess is rare. This imbalance reflects its predominantly intracellular distribution, with only 1% measurable in extracellular fluid, complicating diagnosis.

The intracellular influencer behind the scenes

At a cellular level, magnesium is inseparable from life itself. It is central to adenosine triphosphate production in the mitochondria, supports enzymatic reactions, regulates receptors and transport proteins, and contributes to DNA and RNA processes. In essence, it connects intracellular systems — what Dr Hudson described as ‘joining the dots’. This explains its wide-ranging clinical manifestations when deficient, spanning neuromuscular, cardiovascular (CV), metabolic, and immune systems.

Hypomagnesaemia presents subtly. Symptoms are often non-specific and may include irritability, tremors, seizures, arrhythmias, headaches, and neuromuscular excitability. Importantly, deficiency frequently coexists with low calcium and potassium. Despite its clinical significance, up to 90% of cases remain undiagnosed.

Right patient, right mineral — the art of selection

A key emphasis in Dr Hudson’s approach is patient selection. Magnesium is not a universal intervention, rather, it requires targeted, clinically reasoned use. Identifying the right patient is therefore central to effective management.

One practical tool is the magnesium depletion score (see Table 1 and 2), which integrates common clinical risk factors. Patients receive points for diuretic use, proton pump inhibitor therapy, alcohol intake, and declining renal function. Even a modest score is associated with increased risk of CV,  neurodegenerative, and metabolic disease, with risk increasing exponentially at higher scores.

High-risk groups are diverse and commonly encountered. Gastrointestinal conditions such as malabsorption syndromes — including inflammatory bowel disease, coeliac disease, and chronic pancreatitis — impair magnesium uptake. Poor dietary intake, particularly diets high in processed foods, further increases vulnerability.

Renal losses represent another major category. Patients with renal tubular disorders, chronic kidney disease, or those receiving loop and thiazide diuretics frequently exhibit depletion. Medication-related causes are particularly relevant: Proton pump inhibitors, certain antibiotics, chemotherapy agents such as cisplatin, and newer immune therapies all contribute to magnesium loss.

Endocrine and metabolic conditions refine selection further. Individuals with metabolic syndrome, type 2 diabetes, obesity, and insulin resistance are at increased risk. Magnesium plays a role in insulin signalling, and deficiency exacerbates metabolic dysfunction. Even therapies such as insulin and glucagon-like peptide-based treatments influence magnesium balance through intracellular shifts or reduced intake.

Critically ill patients form another key subgroup. More than 70% of intensive care patients are magnesium depleted, with consequences for cardiac rhythm, neurological status, renal function, and immune competence. Transplant recipients on immunosuppressive therapy frequently develop deficiency, contributing to metabolic complications. Oncology patients are particularly vulnerable, with up to 90% demonstrating abnormalities driven by both disease and treatment.

Ageing populations also require attention, as frailty, sarcopenia, osteoporosis, and polypharmacy all contribute to declining magnesium levels. Pregnancy, particularly the third trimester, represents an additional high-risk period.

Importantly, symptoms alone are insufficient for selection. Many patients remain asymptomatic until levels are significantly reduced. Clinicians must therefore actively consider magnesium in at-risk individuals rather than waiting for overt clinical signs.

Table 1: Magnesium depletion score (MDS)^1p2a 

Table 2: Interpretation of MDS^1p2b 

From nerves to the heart — magnesium everywhere

The breadth of magnesium’s clinical impact reflects its intracellular role. In the neuromuscular system, deficiency leads to hyperexcitability, manifesting as cramps, spasms, neuralgias, migraines, and seizures. These symptoms arise at the neuromuscular junction rather than the muscle itself.

CV effects are equally significant. Magnesium deficiency contributes to arrhythmias, prolonged QT interval, vascular tone dysregulation, and hypertension. It is also linked to atherosclerosis, dyslipidaemia, and coronary artery spasm, with preventative potential in perioperative settings.

Metabolically, magnesium is integral to insulin function and glucose regulation. Deficiency promotes oxidative stress, inflammation, and the development of metabolic syndrome. It also contributes to osteoporosis through impaired vitamin D activation and parathyroid dysfunction.

The immune glue you did not know you needed

Magnesium plays a critical structural and functional role in immunity. It supports immunoglobulin synthesis, complement activation, and T-cell activity. Crucially, it enables immune cell adhesion via lymphocyte function-associated antigen, allowing effective antigen targeting. Without sufficient magnesium, immune responses are structurally impaired, reducing the body’s ability to fight infection and respond to therapy.

Conclusion

Dr Hudson’s perspective reframed magnesium as far more than a simple micronutrient. It is a central regulator of cellular function, influencing systems as diverse as neurology, cardiology, metabolism, and immunity. Yet its value lies not in indiscriminate supplementation, but in careful patient selection. By identifying at-risk individuals — those with metabolic disease, medication exposure, critical illness, or age-related decline — clinicians can intervene early and effectively. Magnesium deficiency is common, underdiagnosed, and clinically significant, but also modifiable. A structured, risk-based approach positions magnesium as a precise, practical tool in modern patient care.

Reference

Costello RB, Fan Z, Wallace TC. Magnesium Depletion Score as an Indicator of Health Risk and Nutritional Status-A Scoping Review. Nutrients, 2025. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC12566843/#:~:text=An%20MDS%20%3E2%20has%20been,health%20risk%20and%20nutritional%20status?

Dr Gary Hudson is a specialist physician in Internal Medicine with a particular interest in immunology, metabolic syndromes, and electrolyte disorders, including magnesium. He runs a busy private practice and has extensive experience in the management of complex chronic conditions such as hypertension, type 2 diabetes, and cardiometabolic disease. Dr Hudson is an experienced medical educator, having delivered numerous lectures to healthcare professionals on immune function, metabolic health, and the clinical relevance of micronutrient deficiencies. He has also contributed to expert discussions on avitaminosis and electrolyte disorders, with a strong focus on magnesium. His combined clinical and academic experience enables him to translate emerging evidence into practical, patient-centred strategies for everyday clinical practice.

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