Essential Mineral · Chelated Form · Mg²⁺

Magnesium
Glycinate

Magnesium chelated to two glycine molecules — a dual supplement that corrects the most widespread mineral deficiency in the Western diet while delivering a calming amino acid with its own evidence for sleep, without the gastrointestinal issues that limit magnesium oxide at therapeutic doses.

600+ Enzymatic Roles
48% US Adults Deficient
∼12% Elemental by Weight
14 Days to Sleep Effect
Updated
Clinical Trial Dose 200–250 mg elemental / day
Primary Sources NCBI PubMed · NIH ODS
Multiple RCTs · Meta-Analyses Available

Biological Overview

Magnesium glycinate (bisglycinate) is elemental magnesium chelated to two glycine molecules. It is not simply a convenient delivery vehicle — it is a dual supplement: you receive both the mineral and a therapeutically relevant dose of glycine, an inhibitory amino acid with independent sleep-promoting, collagen-supporting and anti-inflammatory properties. Magnesium itself participates in over 600 enzymatic reactions, acts as an NMDA receptor channel blocker in the CNS, and is a required cofactor for activating thiamine, maintaining intracellular potassium, and converting ATP to its biologically active form.

Chemical FormulaC&sub4;H&sub8;MgN&sub2;O&sub4;
Elemental Mg%~10–14% by weight
Primary CNS TargetsNMDA · GABA · Glycine-R
Strongest EvidenceSleep · Blood Pressure · Glucose
Supplement Classification

Overview & Classification

Also Known As
Magnesium bisglycinate · Magnesium diglycinate · Chelated magnesium
Molecular Weight
172.42 g/mol (anhydrous)
Elemental Mg Content
~10–14% of compound weight
Chelating Amino Acid
Glycine (two molecules per Mg ion)
Absorption Pathways
Passive diffusion + dipeptide transport (PEPT1)
NIH RDA (Adults)
310–420 mg elemental Mg/day
NIH UL (Supplemental)
350 mg elemental Mg/day
Pregnancy Status
Generally considered safe at RDA; consult provider
The Question Nobody Answers

How to Read a Magnesium Glycinate Label

The single most common source of confusion with magnesium supplements: the number on the front of the bottle is not your magnesium dose. Here is the complete guide to calculating what you are actually taking.

A "500 mg Magnesium Glycinate" capsule contains approximately 56–70 mg of elemental magnesium

The rest is the weight of the two glycine molecules. This is not a scam — it is chemistry. Here is what the numbers mean.

500 mg magnesium glycinate compound The figure listed as the capsule weight or serving size. This is the total compound, not elemental magnesium.
× 0.12 →
~60 mg elemental magnesium Your actual dose. Magnesium bisglycinate is approximately 10–14% elemental magnesium by molecular weight.

Step-by-step: reading the Supplement Facts panel correctly

Label Reading Protocol
Step 1: Find the “Magnesium” line, not the serving size In the Supplement Facts table, look for the row that reads Magnesium (as magnesium glycinate) or Magnesium (as bisglycinate). The milligram figure on that line is your actual elemental magnesium dose. Ignore the capsule weight.
Step 1
Step 2: Verify the mathematics for pure bisglycinate Divide the elemental magnesium figure by the compound weight. The result should be between 0.10 and 0.14 (10–14%). If a label claims 200 mg elemental magnesium from a 500 mg compound, the ratio is 40% — which is impossible for pure bisglycinate (molecular weight ~172 g/mol, Mg component ~14%). This product likely contains magnesium oxide blended in.
Step 2
Step 3: Watch for oxide blending Some products labelled “magnesium glycinate” blend pure bisglycinate with cheaper magnesium oxide to hit a higher elemental number while keeping costs low. Oxide has approximately 60% elemental magnesium by weight but very poor intestinal absorption compared to organic chelates. A ratio above 14% elemental is your indicator. Check the full ingredient list for “magnesium oxide” separately listed.
⚠ Watch
Step 4: Compare to clinical trial doses The most relevant human RCT for sleep (Schuster et al. 2025, n=155) used 250 mg elemental magnesium as bisglycinate daily. The NIH RDA for magnesium from all sources is 310–420 mg elemental per day for adults. Supplemental doses in blood pressure meta-analyses ranged from 82–637 mg elemental, median 365 mg. The NIH supplemental upper tolerable limit (UL) is 350 mg elemental per day.
Step 4
Step 5: Glycinate = bisglycinate? Yes, in practice Both terms refer to the same compound. “Glycinate” is the informal name; “bisglycinate” is technically precise, specifying two (bis) glycine molecules per magnesium ion. Magnesium structurally requires two glycine molecules for a stable chelate, so virtually all commercial “magnesium glycinate” products are in fact bisglycinate. You can confirm this with the 10–14% elemental ratio check above.
Step 5

Quick reference: common compound weights and their elemental Mg content

200 mg compound → ~24 mg elemental  |  400 mg compound → ~48 mg elemental  |  500 mg compound → ~60 mg elemental  |  1,000 mg compound → ~120 mg elemental  |  2,000 mg compound → ~240 mg elemental (common 4-capsule dose). Always verify against the Supplement Facts panel — the elemental figure listed there is the definitive number.

Forms & Absorption Evidence

Bioavailability & Forms Comparison

The marketing claim that glycinate is the “most bioavailable” form of magnesium is not as simple as supplement labels suggest. Here is what the primary evidence actually shows.

Organic vs Inorganic Forms — Primary Evidence
Walker et al. 2003 (PMID: 14596323) 46-participant double-blind RCT, 60 days, 300 mg elemental Mg daily. Organic forms (citrate and amino acid chelate) demonstrated significantly greater absorption than magnesium oxide, measured by 24-hour urinary excretion (p=0.033). This is the most-cited head-to-head absorption RCT for organic versus inorganic forms.
RCT
Schuette et al. 1994 (PMID: 7815675) Double-blind, randomized crossover in 12 ileal-resection patients. Absorption of magnesium diglycinate vs oxide: 23.5% vs 22.8% — not statistically different in this specific population. Ileal resection alters the anatomy relevant to chelate absorption (proximal small intestine dipeptide transport) — this finding applies to a narrow clinical population, not healthy adults.
Nuance
Honest verdict Organic forms (glycinate, citrate) are better absorbed than magnesium oxide in healthy adults. The evidence supports this. What is not established by head-to-head RCTs is that glycinate is meaningfully superior to citrate in clinical outcomes for sleep, mood, or cardiovascular endpoints. No such comparative trial exists in humans.
Assessment
Why Glycinate Has a Clinical Advantage for Sleep
Dual mechanism unique to the glycinate form Magnesium glycinate delivers both elemental magnesium and a therapeutically relevant glycine dose. Glycine independently promotes sleep via glycine receptors in the suprachiasmatic nucleus, reduces core body temperature, and modulates NMDA receptors — the same target as magnesium. This dual convergence on sleep architecture is what distinguishes glycinate from citrate or malate.
Unique
Glycine dose in a typical serving A 250 mg elemental magnesium dose from bisglycinate delivers approximately 1,750–2,000 mg of glycine (the two glycine molecules represent ~86% of the compound weight). Clinical sleep trials of glycine alone have used 3 g/night, suggesting the glycine in bisglycinate contributes a meaningful but sub-threshold sleep-promoting effect.
Key Data
GI tolerability advantage vs citrate and oxide Magnesium oxide and high-dose citrate cause osmotic diarrhea by drawing water into the colon. Glycinate's chelated form is absorbed more proximally and completely, leaving less ionic magnesium in the distal bowel to exert osmotic effects. Clinically, this makes bisglycinate substantially better tolerated at equivalent elemental doses.
Evidence
Form Elemental Mg% Absorption GI Tolerance Unique Advantage
Magnesium Glycinate / Bisglycinate 10–14% High Excellent Dual Mg + glycine mechanism; best tolerated form
Magnesium Citrate 16% High Moderate (laxative at high dose) Good absorption at lower cost; useful for constipation
Magnesium Malate 15% High Good Malic acid supports energy production (citric acid cycle)
Magnesium L-Threonate 8% Moderate Good Only form with evidence for CNS penetration; limited human RCTs
Magnesium Oxide 60% Very Low (~4%) Poor Cheapest; effective as antacid/laxative but not for systemic repletion
Pharmacodynamics

Mechanisms of Action

Magnesium glycinate acts through multiple converging pathways. Understanding them explains why it helps sleep, blood pressure, mood, and glucose — and why glycine's own mechanisms compound the effects beyond magnesium alone.

🧠

NMDA Receptor Channel Blockade — Primary CNS Mechanism

Magnesium ions (Mg²⁺) occupy the ion channel pore of NMDA (N-methyl-D-aspartate) receptors in a voltage-dependent manner, blocking calcium influx at resting membrane potentials. This “pore block” reduces neuronal excitability, glutamate-driven excitotoxicity, and the hyperactivated stress response that characterizes both anxiety and poor sleep. The structural basis was confirmed in X-ray crystallography studies (ScienceDirect, 2025). This mechanism is pharmacologically analogous to memantine, used in Alzheimer’s disease — except magnesium is physiological and concentration-regulated by dietary intake. [1],[2]

🡲

GABA-A Receptor Potentiation

Magnesium enhances sensitivity of GABA-A receptors — the primary inhibitory receptors in the CNS — reducing neuronal firing rates throughout the limbic system, hypothalamus, and cortex. Critically, this mechanism converges with vitamin B6: pyridoxal-5-phosphate (the active form of B6) is the cofactor for glutamate decarboxylase (GAD), the enzyme that synthesizes GABA from glutamate. Magnesium and B6 therefore act in series on the same pathway — B6 generating more GABA, magnesium making the receptor more sensitive to it. This explains the clinical synergy documented in RCTs combining both nutrients for stress reduction. [3]

💤

Glycine Receptor Agonism — The Second Sleep Mechanism

The glycine delivered by magnesium glycinate activates glycine receptors (GlyR) in the suprachiasmatic nucleus, the brain’s master circadian clock. This reduces core body temperature — the same physiological process that naturally initiates sleep onset. The reduction in core temperature by glycine supplementation (measured at 1–1.5°C in clinical sleep trials) is mechanistically equivalent to the drop in body temperature that normally precedes deep sleep. This pathway is entirely independent of magnesium’s NMDA and GABA mechanisms, making bisglycinate a genuinely triple-pathway sleep supplement. [4]

⚡

ATP Activation — Cofactor in 600+ Enzymatic Reactions

Magnesium is required for all enzymatic reactions involving ATP (adenosine triphosphate). ATP does not function as an energy currency in its free ionic form — it functions as Mg-ATP, a complex. This means magnesium deficiency creates a functional energy deficit at the cellular level even when caloric intake is adequate. The 600+ enzymatic reactions requiring magnesium include protein synthesis, DNA replication and repair, RNA transcription, all glycolytic enzymes, and the Na-K-ATPase pump that maintains cellular ion gradients. [5]

💊

Vascular Smooth Muscle Relaxation — Blood Pressure Pathway

Magnesium functions as a physiological calcium channel antagonist in vascular smooth muscle cells. By competing with calcium for entry through voltage-gated channels, magnesium promotes vasodilation and reduces peripheral vascular resistance. This is the primary mechanism behind its blood pressure-lowering effects documented in meta-analyses. The effect is most pronounced in hypertensive individuals and those with concurrent hypomagnesemia — normotensive people with adequate magnesium status do not show clinically significant BP reductions. [6],[7]

🧮

Insulin Sensitivity — GLUT4 and Glucose Transport

Magnesium deficiency is associated with impaired insulin signalling at the receptor level. Mg²⁺ is a cofactor for insulin receptor tyrosine kinase, the first step in insulin’s intracellular signalling cascade. When magnesium is deficient, receptor autophosphorylation is impaired, reducing GLUT4 translocation to cell membranes and therefore peripheral glucose uptake. This explains the NHANES-confirmed inverse correlation between serum magnesium and HOMA-IR (Spearman r=−0.44, p<0.05) and why magnesium supplementation reduces fasting blood glucose in T2DM patients with baseline hypomagnesemia. [8],[9]

Clinical Applications

Clinical Indications by Evidence Tier

Each indication listed below is supported by human RCT or meta-analysis data. Evidence limitations are stated explicitly alongside findings.

💤
Sleep Quality & Insomnia
1 high-quality RCT (2025) · Small effect size
  • Best available trial (Schuster et al. 2025): 155 adults, 4-week double-blind RCT, 250 mg elemental Mg as bisglycinate daily. Significant ISI score reduction vs placebo (−3.9 vs −2.3, p=0.049). Most improvements emerged within the first 14 days. Effect size small (Cohen’s d=0.2). [4]
  • Important caveat: Authors explicitly noted the glycine content may have independently driven or substantially contributed to the observed effects. This is not a weakness — it confirms the dual-mechanism advantage of bisglycinate specifically over other forms. [4]
  • Prior systematic review: Mixed results across earlier RCTs (only 247 total participants combined before the 2025 trial). Two found improvements in sleep efficiency or onset latency; three found no significant effect. The 2025 trial is the largest and best-designed to date. [4]
  • Mechanism confidence: High. NMDA antagonism, GABA potentiation, and glycine receptor agonism all have well-established physiological roles in sleep initiation and maintenance.
💉
Blood Pressure Reduction
38-RCT Meta-Analysis · Condition-Dependent
  • 2025 meta-analysis (Argeros et al., Hypertension): 38 RCTs, 2,709 participants. SBP reduction −2.81 mmHg (95% CI: −4.32 to −1.29); DBP −2.05 mmHg (95% CI: −3.23 to −0.88) vs placebo. [6]
  • Critical subgroup finding: Hypertensive individuals with concurrent hypomagnesemia showed SBP reductions of −7.68 mmHg and −5.97 mmHg respectively — clinically meaningful. Normotensive groups did not show statistically significant reductions. Magnesium lowers blood pressure primarily in people who are hypertensive and/or deficient. [6]
  • Glycinate-specific BP RCT (NCT03688503, 2020): 59 participants, 480 mg/day elemental Mg as glycinate, 12 weeks. Result: no significant reduction in seated or 24-hour ambulatory BP in adults with elevated but untreated BP. Underlines that glycinate’s BP effects follow the same population-dependent pattern as magnesium broadly. [7]
🕵
Depression & Mood
7-RCT Meta-Analysis · Preliminary
  • Moabedi et al. 2023 (Frontiers in Psychiatry, PMC10783196): Meta-analysis of 7 RCTs, 325 total participants. Significant reduction in depression scores (SMD: −0.919, 95% CI: −1.443 to −0.396, p=0.001). Effect size is moderate. [10]
  • Epidemiological basis is strong: A 2025 dose-response meta-analysis (12 studies, 50,275 participants) found individuals with highest vs lowest dietary Mg intake had a 34% lower risk of depression (RR: 0.66). Each 100 mg/day increment in Mg intake associated with 7% lower depression risk. [11]
  • Honest limitation: 7 RCTs with 325 participants is a small base. Effect sizes were heterogeneous. The RCT evidence base for depression is preliminary; the epidemiological evidence is more robust. High-quality large trials are needed before clinical guidance can be issued.
🧮
Blood Glucose & Type 2 Diabetes
23-RCT Meta-Analysis · Deficiency-Dependent
  • Al Maqrashi et al. 2025 (PMC12244252): Meta-analysis of 23 RCTs, 1,345 participants. Magnesium supplementation significantly raised serum Mg and reduced fasting blood glucose (WMD: −0.58 mmol/L, 95% CI: −0.87 to −0.28). Serum insulin not significantly altered across pooled data. [8]
  • Hypomagnesemia prevalence in T2DM: Between 13.5–47.7% of patients with type 2 diabetes have hypomagnesemia (vs 2.5–15% of healthy controls). Magnesium’s glycaemic benefits are substantially larger in individuals with documented low serum magnesium. [8]
  • HbA1c evidence: Conflicting across meta-analyses. A 2023 analysis of 24 trials showed significant HbA1c reduction; others have not. The glucose effect is more consistent than HbA1c. Best evidence supports benefit when serum magnesium is documented to be low. [9]

Additional Indication: Migraine Prevention

The American Headache Society and American Academy of Neurology give magnesium a Level B recommendation for migraine prevention (probably effective). Magnesium deficiency is documented in migraine patients; cortical spreading depression (the wave underlying aura) is inhibited by adequate Mg²⁺. Doses used in prevention trials: 400–600 mg elemental magnesium daily. See a neurologist for personalized guidance. Glycinate is the preferred form due to tolerability at these higher doses.

Additional Indication: PMS / Dysmenorrhoea

An RCT by De Souza et al. (2000) found that 200 mg elemental magnesium combined with 50 mg vitamin B6 for one month produced synergistic reduction in anxiety-related PMS symptoms compared to either nutrient alone — a double-blind, crossover design (J Womens Health). Uterine smooth muscle spasm in dysmenorrhoea is directly inhibited by magnesium’s calcium antagonism in smooth muscle. Glycinate is well suited for this use given its tolerability profile.

Clinical Protocols

Dosage, Timing & How Long Until It Works

All doses below refer to elemental magnesium — not compound weight. Confirm the elemental figure on your product’s Supplement Facts panel before calculating your dose.

Goal Elemental Mg Dose Timing Evidence Base
Sleep quality 200–250 mg 1–2 hours before bed Schuster et al. 2025 RCT (250 mg, 155 adults) [4]
General deficiency correction 200–350 mg Any time, consistency > timing NIH RDA guidance — target total daily intake 310–420 mg from all sources [12]
Blood pressure support 300–400 mg Divided dose or evening Argeros et al. 2025 meta-analysis (median 365 mg/day, 38 RCTs) [6]
Blood glucose (T2DM with low Mg) 200–400 mg With meals Al Maqrashi et al. 2025 meta-analysis [8]
Migraine prevention 400–600 mg Divided dose (AM/PM) AHS/AAN Level B recommendation — consult neurologist
NIH Supplemental Upper Limit 350 mg — Established 1997, IOM. Diarrhea as limiting factor. Under re-evaluation in current literature. [13]

How long until magnesium glycinate works?

Based on the 2025 Schuster RCT (the only adequately powered bisglycinate sleep trial): most sleep improvements appeared within the first 14 days. For blood pressure, significant changes appear at 4–8 weeks. For blood glucose, 8–12 weeks. For mood, existing trials ran 4–8 weeks with effects emerging across that period. Tissue magnesium saturation (particularly in bone and muscle, which hold 99% of the body’s magnesium) takes weeks to restore from deficiency, explaining why effects are not immediate. [4]

Morning or night — which is better?

For sleep, anxiety reduction, or muscle recovery: 1–2 hours before bed. The NMDA antagonism and glycine receptor agonism both promote central nervous system quieting, which is counterproductive if taken early in the day when alertness is needed. For general repletion, blood pressure, or glucose management: timing is less critical than consistency. If you feel excessively drowsy after morning doses, the CNS-calming effects of Mg + glycine are likely at play — switch to evening dosing.

Pharmacology

Nutrient–Nutrient Interactions

Magnesium does not work in isolation. Six other nutrients have documented biochemical relationships with magnesium — some amplifying its effects, some depending on adequate magnesium status to function at all, and one directly competing with it for absorption.

Nutrient Interaction Type Mechanism Clinical Relevance Evidence Quality
Vitamin B6 (Pyridoxine / P5P) Synergistic B6 facilitates cellular uptake of Mg²⁺, reducing urinary excretion and improving intracellular concentrations. B6 also increases GABA production (as cofactor for glutamate decarboxylase) while magnesium increases GABA-A receptor sensitivity — dual convergence on the same inhibitory pathway. [3] High: especially relevant for stress, anxiety, and PMS. The combination showed superiority over magnesium alone in severely stressed adults with low magnesemia (Pouteau et al. 2018 Phase IV RCT, n=264, EudraCT:2015-003749-24). Overall (non-stratified) population: no superiority, suggesting the synergy is most pronounced at high stress levels and low baseline magnesium. [3] Phase IV RCT + mechanistic studies
Thiamine (Vitamin B1) Mg Required The enzyme thiamine pyrophosphokinase (TPK) converts dietary thiamine into thiamine pyrophosphate (TPP) — the biologically active form that serves as a cofactor for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, and transketolase. TPK requires Mg²⁺ for catalytic activity. Without adequate magnesium, thiamine cannot be phosphorylated to TPP regardless of thiamine intake or supplementation. [14] High for B1 supplementers: the growing use of high-dose thiamine for fatigue, POTS, fibromyalgia, and post-viral syndromes makes this interaction clinically important. Supplementing thiamine while magnesium-deficient may produce suboptimal or absent results. Magnesium glycinate is the recommended co-supplement in B1 repletion protocols. [14] Established biochemistry (PMID: 217454) + enzyme kinetics studies
Potassium (K⁺) Mg Required Magnesium is an obligatory cofactor for Na-K-ATPase (the sodium-potassium pump). Low intracellular Mg²⁺ releases inhibition of ROMK potassium channels in the kidney collecting duct, increasing urinary potassium excretion. The result: potassium supplementation fails to raise serum potassium in magnesium-deficient individuals regardless of dose. [15],[16] Very High: 38–42% of potassium-depleted patients have concurrent magnesium deficiency (Whang et al. 1992, Arch Intern Med PMID: 1728927). Refractory hypokalemia should always prompt magnesium assessment. Common in: loop diuretic users, cisplatin therapy, heart failure, alcoholism. Magnesium must be corrected before potassium repletion becomes effective. [15] Multiple clinical studies (JAMA 1985; Arch Intern Med 1992; J Am Soc Nephrol 2007)
Calcium (Ca²⁺) Competitive Both calcium and magnesium are divalent cations absorbed via TRPM7 channels in intestinal epithelium. High calcium concentrations competitively reduce magnesium absorption in a dose-dependent manner. Competition is most clinically significant at supplemental calcium doses above 200–250 mg taken simultaneously. At dietary (food-based) calcium levels, competition is minimal. [17] Moderate: people taking calcium supplements (particularly for osteoporosis) and magnesium glycinate simultaneously may experience reduced magnesium absorption. Practical solution: take calcium with a meal earlier in the day and magnesium glycinate separately in the evening. A Ca:Mg ratio of 2:1 has been historically associated with optimal cardiometabolic outcomes vs wider ratios common in Western supplementation. [17] Intestinal absorption studies + TRPM7 transporter research
Vitamin E (Tocopherol) Mild Synergistic Magnesium ions contribute to stabilization of the vitamin E radical (tocopheryl radical), facilitating regeneration of active tocopherol via the antioxidant recycling network. Co-supplementation may synergistically reduce lipid peroxidation and inflammatory cascade markers via complementary pathways (Nrf2/CES1 for vitamin E; enzyme regulation for magnesium). [18] Moderate for specific populations: two RCTs in PCOS patients (Jamilian; Shokrpour) found Mg + vitamin E co-supplementation improved total antioxidant capacity, glycaemic control, and inflammatory markers beyond either alone. Clinical evidence in healthy populations is sparse. A 2025 meta-analysis (PMC12433974) stated co-supplementation “may synergistically attenuate oxidative damage” but evidence remains conflicting. High-dose magnesium may theoretically interfere with fat-soluble vitamin absorption. [18] Mechanistic + 2 PCOS RCTs; limited in healthy populations
Vitamin C (Ascorbic Acid) Mild Facilitative Vitamin C creates a more acidic gastric environment, which can improve solubility of some magnesium forms at the point of absorption. Ascorbate co-administration with magnesium has been studied in patent literature (US12496289) as a method of increasing magnesium bioavailability by at least 55%, though peer-reviewed human RCT data is limited. A review of ascorbic acid’s effect on 18 minerals identified a synergistic effect on magnesium absorption. [19] Low–Moderate: the strongest Vitamin C claims derive from patent literature and animal studies rather than peer-reviewed human clinical trials. The interaction is real but less clinically significant than the B6, B1, or potassium relationships above. There is no harmful interaction — taking both together is safe and potentially modestly beneficial. Patent literature + animal studies; limited human RCT data
Key Clinical Evidence — Pouteau et al. 2018, PLOS ONE, PMC6298677

Magnesium + B6: superior to magnesium alone — but only under high stress with low magnesium status

This Phase IV investigator-blinded RCT (n=264, EudraCT 2015-003749-24) randomized stressed adults with low serum magnesium (0.45–0.85 mmol/L) to magnesium alone (300 mg/day) vs magnesium + B6 (300 mg + 30 mg/day) for 8 weeks. In the overall population, the combination was not statistically superior to magnesium alone. However, in the most severely stressed subgroup (highest DASS-42 tertile), the combination produced significantly greater stress score reduction (p=0.018). The mechanistic basis is plausible: B6 increases cellular Mg uptake (reducing urinary excretion) and is the rate-limiting cofactor for GABA synthesis, while magnesium sensitizes GABA-A receptors. For casual supplementation, magnesium alone suffices. For severe stress combined with probable deficiency, adding B6 (preferably as P5P) has primary-source support. [3]

⚠ The potassium interaction: a clinically urgent one

If your potassium supplements are not raising your serum potassium, check your magnesium status before increasing the potassium dose. This is not a theoretical interaction — it is a well-documented clinical phenomenon. Refractory hypokalemia (potassium that will not correct despite supplementation) is one of the classic presentations of magnesium deficiency, because magnesium is the gatekeeper of the sodium-potassium pump. The JAMA Internal Medicine identified this in 1985; it has been re-confirmed in ICU studies showing 38–42% of hypokalemic patients have concurrent hypomagnesemia. Correcting magnesium first is often the only intervention needed to resolve apparent “refractory” potassium deficiency. [15],[16]

Targeted Populations

Who Needs Magnesium Glycinate Most

Over 48% of US adults consume below the estimated average requirement for magnesium. These are the populations with the highest risk of significant deficiency and the clearest evidence of benefit from supplementation.

Medication-Linked

Long-term PPI Users

Proton pump inhibitors (omeprazole, pantoprazole, lansoprazole) impair the TRPM6 channel in intestinal epithelium, reducing active magnesium absorption. Clinically significant hypomagnesemia typically emerges after more than 12 months of daily PPI use. The FDA issued a warning in 2011 requiring PPI labelling to note hypomagnesemia risk. Magnesium glycinate is the preferred supplemental form for PPI users due to superior tolerability at therapeutic doses compared to oxide or sulphate. Inform your prescribing physician — serum magnesium monitoring may be warranted with long-term concurrent use.

Check serum Mg if on PPI >12 months
Medication-Linked

Loop and Thiazide Diuretic Users

Loop diuretics (furosemide, bumetanide) and thiazide diuretics (hydrochlorothiazide) increase renal magnesium excretion by inhibiting tubular reabsorption mechanisms. People on these medications lose significantly more magnesium in urine than non-users. This creates a compounded deficiency risk — dietary intake rarely compensates for the renal losses. These same medications frequently cause hypokalemia, and the magnesium–potassium interaction (Section 07) means that if both electrolytes are low, magnesium must be corrected first. Always notify your prescribing physician before supplementing alongside prescribed diuretics.

Requires medical supervision alongside diuretics
Lifestyle-Linked

Athletes & Heavy Exercisers

Exercise increases urinary and sweat magnesium losses. Athletes engaging in prolonged endurance or high-intensity resistance training can lose 10–15% more magnesium per day than sedentary individuals. A meta-analysis found NHANES data consistently showing lower serum magnesium in athletes vs controls. Muscle cramping, reduced strength output, impaired recovery, and disrupted sleep — all common athlete complaints — have mechanistic links to magnesium deficiency. Glycinate is preferred for athletes over oxide due to the absence of GI distress during training.

Age-Linked

Adults Over 65

NHANES data shows 83.3% of US adults aged 65 and over do not meet the RDA for dietary magnesium. Reduced dietary intake, impaired intestinal absorption, increased renal losses, and polypharmacy (diuretics, PPIs) all compound to create widespread deficiency in older adults. A double-blind RCT found magnesium glycinate supplementation for 12 weeks produced a 9.1% improvement in MoCA cognitive assessment in adults over 65 (p=0.03) — not significant in under-65s. Bone mineral density also correlates positively with magnesium status across ageing populations. [20]

Cognitive benefit: one low-risk-of-bias RCT only
Condition-Linked

Type 2 Diabetes & Insulin Resistance

Up to 47.7% of T2DM patients have hypomagnesemia — three to five times the prevalence in healthy controls. Insulin resistance impairs renal magnesium reabsorption; conversely, low magnesium impairs insulin receptor function, creating a self-reinforcing cycle. This population has the strongest evidence for magnesium supplementation improving fasting glucose, the most consistent finding across 23 RCTs. If you have T2DM or documented insulin resistance, check your serum magnesium — if low, correction should be a clinical priority before assessing supplementation benefit.

Supplement-Linked

High-Dose Thiamine Supplementers

The use of high-dose thiamine (B1) for fatigue, POTS, post-viral syndromes, and fibromyalgia has grown substantially. The activation pathway of dietary thiamine to thiamine pyrophosphate (TPP) — the biologically active form — requires magnesium as a cofactor for the enzyme thiamine pyrophosphokinase. If magnesium stores are inadequate, thiamine supplementation will not produce expected effects regardless of dose, because the activated form cannot be synthesized efficiently. Magnesium glycinate is now routinely co-supplemented in high-dose B1 protocols for exactly this reason. [14]

Pharmacology

Drug Interactions

All interactions below are sourced directly from the NIH Office of Dietary Supplements Health Professional Fact Sheet for Magnesium (ods.od.nih.gov). Unlike berberine, magnesium does not inhibit CYP enzymes — its interactions arise from physical binding, ion competition, and pharmacodynamic additive effects.

Drug / Drug Class Direction Mechanism Recommendation
Oral bisphosphonates (alendronate, risedronate) Mg reduces drug absorption Magnesium forms insoluble complexes with bisphosphonates in the GI tract, reducing their intestinal absorption and therefore their bone-protective effect. Take bisphosphonates at least 2 hours before or after magnesium supplements. This spacing is sufficient to avoid the interaction. [12]
Tetracycline antibiotics (doxycycline, demeclocycline) Mg reduces drug absorption Magnesium chelates tetracyclines, forming insoluble compounds that cannot be absorbed from the GI tract, reducing antibiotic plasma concentrations and potentially compromising efficacy. Take tetracyclines at least 2 hours before or 4–6 hours after magnesium supplements. [12]
Quinolone antibiotics (ciprofloxacin, levofloxacin) Mg reduces drug absorption Same chelation mechanism as tetracyclines. Quinolone absorption can be reduced by 40–90% when taken simultaneously with magnesium-containing products. Take quinolones at least 2 hours before or 4–6 hours after magnesium supplements. Check the antibiotic prescribing label for specific guidance. [12]
Loop diuretics (furosemide, bumetanide) Drug depletes Mg Loop diuretics inhibit magnesium reabsorption in the thick ascending limb of the loop of Henle, increasing urinary magnesium excretion substantially with each dose. Monitor serum magnesium during chronic loop diuretic therapy. Supplementation is often clinically indicated but should be guided by serum levels and physician supervision. [12]
Thiazide diuretics (hydrochlorothiazide, chlorthalidone) Drug depletes Mg Thiazides increase renal magnesium excretion via inhibition of tubular magnesium reabsorption mechanisms, leading to progressive hypomagnesemia with long-term use. Periodic serum magnesium monitoring recommended with long-term thiazide use. Discuss supplementation with prescribing physician. [12]
Proton pump inhibitors (omeprazole, pantoprazole, lansoprazole) Drug depletes Mg (chronic use) Long-term PPI use impairs TRPM6 magnesium transporter function in the intestinal epithelium, reducing active magnesium absorption. Effect is dose-dependent and cumulative over months to years. FDA 2011 label warning. Magnesium glycinate is the preferred form for PPI users due to tolerability. Inform prescribing physician. Serum magnesium monitoring may be warranted. [12]
Potassium-sparing diuretics (amiloride, spironolactone) Additive Mg retention These diuretics reduce renal magnesium excretion, which in combination with magnesium supplementation could theoretically raise serum magnesium into a hypermagnesemia range. Monitor serum magnesium if combining with magnesium glycinate supplements. Risk is low in those with normal kidney function. Consult prescribing physician. [12]

Source: NIH Office of Dietary Supplements, Magnesium Health Professional Fact Sheet. Available at: ods.od.nih.gov. Last reviewed 2024.

Safety & Contraindications

Safety, Upper Limits & Kidney Function Thresholds

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When to Avoid or Use With Caution

  • eGFR below 30 mL/min/1.73m² (Stage 4–5 CKD): Kidneys cannot adequately clear excess magnesium. Supplementation can cause hypermagnesemia, with symptoms including nausea, flushing, hypotension, bradycardia, and at severe levels, cardiac arrest. Do not supplement without direct medical supervision and regular serum magnesium monitoring. [21]
  • eGFR 30–60 mL/min/1.73m² (Stage 3 CKD): Reduced but not absent magnesium clearance. Use the lowest effective dose and discuss with your nephrologist or prescribing physician. Monitor serum magnesium. [21]
  • Heart block or neuromuscular junction disorders (myasthenia gravis): Magnesium is a neuromuscular blocker at elevated plasma concentrations. In individuals with pre-existing conduction abnormalities or NMJ disease, even moderate hypermagnesemia can be clinically significant.
  • Hypermagnesemia symptoms to recognize: Nausea, flushing, warmth, drowsiness, decreased deep tendon reflexes, and hypotension. Stop supplementation and seek medical assessment if these occur.
⚠️

The NIH Upper Limit — What It Actually Means

  • 350 mg elemental Mg/day from supplements: This is the NIH/IOM UL established in 1997, based on the lowest dose producing diarrhea as an adverse event. It applies to supplemental magnesium only — not to magnesium from food, which does not cause adverse effects even at high dietary intakes. [13]
  • Under active re-evaluation: A 2023 perspective article in The Journal of Nutrition (PMID: 37487817) called for re-evaluation of this UL based on more recent and comprehensive data suggesting higher doses are tolerated safely by most healthy adults, particularly bisglycinate which has lower osmotic laxative potential than inorganic forms. [13]
  • Clinical trial doses often exceed 350 mg: Multiple blood pressure RCTs used 400–600 mg elemental Mg without reporting significant adverse events. Migraine prevention protocols recommend 400–600 mg. These doses should only be used under informed clinical guidance.
  • Laxative threshold is form-dependent: Magnesium oxide and citrate cause diarrhea at lower doses than glycinate due to osmotic effects in the colon. The 350 mg UL was originally derived primarily from oxide data — glycinate tolerability at equivalent doses is substantially better.

Common adverse effects and how to manage them

Side Effect Management
Excessive daytime drowsiness NMDA antagonism + glycine receptor agonism can cause sedation in some individuals, particularly at higher doses or when taken in the morning. Switch to evening dosing. If drowsiness persists at bedtime dosing, reduce dose by 50% and titrate back up over 2–4 weeks.
Management: Evening dosing
Loose stool or mild diarrhea Less common with glycinate than oxide or citrate, but possible at doses above the GI tolerance threshold. Reduce dose by half, take with food, and titrate back up slowly. Split into two smaller doses across the day if a single larger dose is not tolerated.
Management: Dose reduction, food
Nausea Usually occurs when taken on an empty stomach or as a single large dose. Always take with food. If nausea persists with food, switch to smaller divided doses rather than one daily dose.
Management: Take with food
No effect perceived after 4 weeks First verify your elemental magnesium dose using the label-reading guide in Section 02. Many people believe they are taking 400 mg elemental but are actually taking 48–60 mg from a compound-weight label. If dose is confirmed adequate, baseline serum magnesium may already be normal — the benefits of supplementation are substantially greater in deficient individuals.
Management: Verify actual dose
Medical disclaimer: This reference is for educational purposes only and does not constitute medical advice, diagnosis, or treatment guidance. All decisions regarding supplementation alongside prescription medications, or in the presence of kidney disease, cardiovascular conditions, or pregnancy, should involve a qualified healthcare provider. Serum magnesium testing is the definitive assessment of individual magnesium status.
Frequently Asked Questions

Magnesium Glycinate FAQ

Answers to the specific dosing, interaction, and label questions most often raised about magnesium glycinate.

How long does magnesium glycinate take to work for sleep?
Based on the 2025 Schuster RCT — the most rigorously designed bisglycinate sleep trial to date (155 adults, double-blind, placebo-controlled, 4 weeks) — most sleep improvements occurred within the first 14 days at 250 mg elemental magnesium bisglycinate daily. The Insomnia Severity Index score reduction was statistically significant vs placebo (−3.9 vs −2.3, p=0.049), though the effect size was small (Cohen’s d=0.2). If you notice no change after 4 weeks at a confirmed adequate dose, your baseline magnesium status may already be sufficient, which means supplementation is unlikely to provide further benefit. [4]
Is magnesium glycinate the same as magnesium bisglycinate?
Yes, in practice they are identical. Both names describe magnesium chelated to two glycine molecules. “Bisglycinate” is the chemically precise term (bis = two); “glycinate” is the informal name used on most product labels. Magnesium structurally requires two glycine molecules for a stable chelate — so virtually all commercial “magnesium glycinate” products are the bisglycinate form. You can verify this: true bisglycinate should contain 10–14% elemental magnesium by weight. If the ratio is significantly higher, the product likely contains magnesium oxide blended in.
My "500 mg magnesium glycinate" capsule — how much magnesium am I actually taking?
Approximately 56–70 mg of elemental magnesium. Magnesium bisglycinate is roughly 10–14% elemental magnesium by weight. The 500 mg figure refers to the total weight of the compound (magnesium plus both glycine molecules). The remaining ~86% is the weight of the two glycine molecules. To find your actual dose: look at the Supplement Facts panel for the line reading “Magnesium (as magnesium glycinate)” — that number is your actual elemental dose. To hit the 250 mg elemental dose used in the 2025 sleep RCT, you would need approximately 4×500 mg capsules, or 2,000 mg of compound weight.
Why does magnesium glycinate make me feel tired during the day?
Two mechanisms converge to cause daytime drowsiness. First, magnesium’s NMDA receptor channel blockade and GABA-A receptor potentiation reduce overall CNS excitability — which is beneficial for sleep initiation but counterproductive for daytime alertness. Second, the glycine in bisglycinate (approximately 1,750–2,000 mg per 250 mg elemental dose) has independent sleep-promoting properties, including core body temperature reduction via glycine receptors in the suprachiasmatic nucleus. The solution is straightforward: move your dose to 1–2 hours before bed rather than daytime, and reduce to the lowest effective dose while you adjust.
Why isn’t my potassium supplement working? Could magnesium deficiency be the cause?
Yes — this is a well-documented clinical phenomenon called refractory hypokalemia. Magnesium is a required cofactor for Na-K-ATPase, the pump that moves potassium into cells. When intracellular magnesium falls, this pump is impaired, and the ROMK potassium channel in the kidney becomes uninhibited, causing increased urinary potassium loss. The result: potassium will not rise despite supplementation until magnesium is corrected first. Between 38–42% of potassium-depleted patients have concurrent magnesium deficiency (Whang et al. 1992). This interaction is most common in people on loop diuretics, after chemotherapy (particularly cisplatin), or with chronic alcoholism. If your potassium is stubbornly low, ask your doctor to check serum magnesium. [15]
Can I take magnesium glycinate if I’m on omeprazole or another PPI?
Yes, with awareness. Long-term PPI use (typically more than 12 months at standard doses) impairs intestinal magnesium absorption via the TRPM6 transport channel. Magnesium glycinate is generally the preferred supplemental form for PPI users because its superior GI tolerability allows adequate dosing without GI side effects. Critically, magnesium glycinate does not significantly raise gastric pH and will not interfere with PPI efficacy — unlike antacids. Inform your prescribing doctor so they can monitor serum magnesium if clinically indicated. The FDA 2011 safety label update for PPIs specifically flagged hypomagnesemia as a risk requiring awareness.
Is magnesium glycinate safe with kidney disease? What eGFR is the threshold?
The critical threshold is an eGFR below 30 mL/min/1.73m² (Stage 4–5 CKD). Below this level, the kidneys cannot adequately excrete excess magnesium, and supplementation carries a real risk of hypermagnesemia. At eGFR 30–60 (Stage 3 CKD), caution is appropriate: use the lowest effective dose and have serum magnesium monitored. At eGFR above 60, normal kidney function handles supplemental magnesium at standard doses without accumulation. This is why the NIH upper limit of 350 mg/day from supplements was established specifically for healthy individuals with normal renal function. Anyone with documented CKD should discuss magnesium supplementation with their nephrologist. [21]
Does taking magnesium glycinate and calcium at the same time reduce absorption?
At supplemental doses, yes. Both minerals compete for TRPM7 intestinal transport channels. Calcium supplementation above approximately 200–250 mg taken simultaneously reduces magnesium absorption in a dose-dependent manner. The practical solution is simple: take calcium supplements with a meal earlier in the day and magnesium glycinate separately in the evening. At food-based calcium levels (not supplemental), competition is minimal and both can be consumed with meals without concern. This interaction does not apply to dietary calcium in food — only to calcium supplements taken at the same time as magnesium.
I’m taking high-dose thiamine (B1). Do I also need magnesium glycinate?
The biochemistry strongly supports co-supplementation. The enzyme thiamine pyrophosphokinase (TPK) converts dietary or supplemental thiamine into thiamine pyrophosphate (TPP) — the only biologically active form. This enzymatic conversion requires Mg²⁺ as a cofactor. If you are magnesium-deficient, TPP synthesis is impaired regardless of how much thiamine you take. This is why high-dose B1 protocols (used for POTS, chronic fatigue, fibromyalgia) consistently co-recommend magnesium glycinate. The glycinate form is specifically preferred because high-dose thiamine protocols often involve therapeutic B1 doses that require the gut to remain functional — oxide-induced diarrhea would undermine the protocol. [14]
Can I take magnesium glycinate while pregnant?
Magnesium is generally considered safe during pregnancy at RDA levels (350–360 mg elemental per day for pregnant women aged 19–30; 360–400 mg for pregnant women under 19 or over 30), and many prenatal vitamins include magnesium. The glycinate form’s superior GI tolerability makes it a suitable option during pregnancy, when GI sensitivity is heightened. However, magnesium supplementation during pregnancy — particularly at doses above the RDA — should always be discussed with an obstetrician or midwife, who can assess individual dietary intake, underlying conditions, and appropriate monitoring.
References

Bibliography

Numbered references for every claim made on this page, drawn from peer-reviewed literature and primary regulatory sources.

↑ 1. Magnesium Matters: A Comprehensive Review of Its Vital Role in Health and Diseases. PMC11557730. Covers cofactor roles in 600+ enzymatic reactions, NMDA receptor function, and mitochondrial activity. PMC11557730 →
↑ 2. Huang SL, et al. Spotting multifaced actions of magnesium on NMDA receptors. Neuron. 2025. Structural basis of Mg²⁺ voltage-dependent pore block and synaptic plasticity role. PubMed PMID: 40179825 →
↑ 3. Pouteau E, Kabir-Ahmadi M, Noah L, et al. Superiority of magnesium and vitamin B6 over magnesium alone on severe stress in healthy adults with low magnesemia: A randomized, single-blind clinical trial. PLoS ONE. 2018;13(12):e0208454. PMC6298677 / PubMed PMID: 30562392 →
↑ 4. Schuster J, Cycelskij I, Lopresti A, Hahn A. Magnesium Bisglycinate Supplementation in Healthy Adults Reporting Poor Sleep: A Randomized, Placebo-Controlled Trial. Nat Sci Sleep. 2025;17. DOI: 10.2147/NSS.S524348. The primary bisglycinate sleep RCT: 155 adults, 4 weeks, 250 mg elemental Mg. PMC12412596 / PMID: 40918053 →
↑ 5. He C, Wang B, Chen X, et al. The Mechanisms of Magnesium in Sleep Disorders. Nat Sci Sleep. 2025;17:2639–2656. DOI: 10.2147/NSS.S552646. Reviews NMDA, GABA, melatonin, and temperature-regulation pathways in sleep. Full text (PDF) →
↑ 6. Argeros Z, Xu X, Bhandari B, Harris K, Touyz RM, Schutte AE. Magnesium Supplementation and Blood Pressure: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Hypertension. 2025. DOI: 10.1161/HYPERTENSIONAHA.125.25129. 38 RCTs, 2,709 participants. PMC12529988 / PMID: 41000008 →
↑ 7. Randomized Trial Of Magnesium Glycinate Supplementation And Blood Pressure In Middle-aged Adults. Hypertension. 2020;76(suppl 1):P161. ClinicalTrials.gov NCT03688503. 59 participants, 480 mg/day elemental Mg glycinate, 12 weeks. Null result in normotensive population. AHA Hypertension 2020 Abstract →
↑ 8. Al Maqrashi N, Al Busaidi S, Al-Rasbi S, Al Alawi AM, Al-Maqbali JS. Effect of Magnesium Supplements on Improving Glucose Control, Blood Pressure and Lipid Profile in Patients With Type 2 Diabetes Mellitus: A systematic review and meta-analysis. 2025. 23 RCTs, 1,345 participants. Significant FBG reduction (WMD −0.58 mmol/L). PMC12244252 →
↑ 9. Association of Serum Magnesium with Insulin Resistance and Type 2 Diabetes among Adults in China. PMC9104014. NHANES-comparable data: lower serum Mg associated with higher HOMA-IR (Spearman r=−0.44, p<0.05). Nonlinear dose-response relationship confirmed. PMC9104014 →
↑ 10. Moabedi M, Aliakbari M, Erfanian S, Milajerdi A. Magnesium supplementation beneficially affects depression in adults with depressive disorder: a systematic review and meta-analysis of randomized clinical trials. Front Psychiatry. 2023;14:1333261. 7 RCTs, 325 participants, SMD −0.919 (p=0.001). PMC10783196 / PMID: 38155649 →
↑ 11. Dietary Magnesium Intake in Relation to Depression in Adults: A GRADE-Assessed Systematic Review and Dose-Response Meta-analysis of Epidemiologic Studies. PMID: 38812090. 12 studies, 50,275 participants. Highest vs lowest Mg intake: 34% lower depression risk (RR: 0.66). PubMed PMID: 38812090 →
↑ 12. National Institutes of Health, Office of Dietary Supplements. Magnesium — Health Professional Fact Sheet. Covers RDAs, drug interactions (bisphosphonates, antibiotics, diuretics, PPIs), safety, and FDA qualified health claim (2022). NIH ODS: ods.od.nih.gov →
↑ 13. Perspective: Call for Re-evaluation of the Tolerable Upper Intake Level for Magnesium Supplementation in Adults. J Nutr. 2023. PMID: 37487817. Reviews the 1997 IOM UL of 350 mg/day, diarrhea as limiting factor, and evidence that the UL needs updating based on contemporary data. PubMed PMID: 37487817 →
↑ 14. Why Thiamine Supplementation Requires Magnesium. Hormones Matter (2026). Reviews the biochemical role of Mg²⁺ as required cofactor for thiamine pyrophosphokinase (TPK). Primary enzyme kinetics data: PMID: 217454 (Artsukevich IM, Biokhimiia 1979). ScienceDirect overview: Thiamine Diphosphokinase. HormonesMatter.com + PMID: 217454 →
↑ 15. Whang R, Whang DD, Ryan MP. Refractory potassium repletion: a consequence of magnesium deficiency. Arch Intern Med. 1992;152(1):40–45. Documents 38–42% concurrent Mg deficiency in hypokalemic patients. PubMed PMID: 1728927 →
↑ 16. Huang C-L, Kuo E. Mechanism of Hypokalemia in Magnesium Deficiency. J Am Soc Nephrol. 2007;18(10):2649–2652. Explains ROMK channel disinhibition and impaired Na-K-ATPase as mechanisms linking hypomagnesemia to potassium wasting. UT Southwestern / J Am Soc Nephrol 2007 →
↑ 17. Intestinal Absorption and Factors Influencing Bioavailability of Magnesium — An Update. PMC5652077. Reviews TRPM7 transport, calcium competition, passive diffusion mechanisms, and factors affecting Mg bioavailability across the GI tract. PMC5652077 →
↑ 18. The effects of magnesium and vitamin D/E co-supplementation on inflammation markers and lipid metabolism. Front Nutr. 2025;12. PMC12433974. Systematic review and meta-analysis of Mg+D/E co-supplementation in obese/overweight populations. Notes synergistic antioxidant effects and that high-dose Mg may interfere with fat-soluble vitamin absorption. PMC12433974 →
↑ 19. ASCORBIC ACID (VITAMIN C) AND ITS EFFECT ON 18 MINERALS BIOAVAILABILITY IN HUMAN NUTRITION. ResearchGate, 2020. Identified synergistic effect of ascorbic acid on magnesium, iron, calcium, zinc, and cobalt absorption. US Patent 12,496,289 (2024): method for increasing magnesium bioavailability by ≥55% via ascorbate co-administration. USPTO Patent 12,496,289 →
↑ 20. Magnesium: Cognitive Vitality for Researchers. Alzheimer’s Drug Discovery Foundation / AlzDiscovery.org. Reviews Chen et al. 2024 meta-analysis and the low-risk-of-bias RCT showing 9.1% MoCA improvement (p=0.03) in adults over 65 receiving Mg glycinate for 12 weeks. AlzDiscovery PDF →
↑ 21. NIH Office of Dietary Supplements — Magnesium Consumer Fact Sheet. Covers kidney disease contraindication, magnesium retention by healthy kidneys, and food vs supplemental intake guidelines. Separate from the Health Professional Fact Sheet (→ ref 12). NIH ODS Consumer Sheet →

Additional Reference Literature

Walker AF, Marakis G, Christie S, Byng M. Mg citrate found more bioavailable than other Mg preparations in a randomized, double-blind study. Magnes Res. 2003;16(3):183–91. Walker et al. absorption RCT (organic vs oxide). PubMed PMID: 14596323 →
Schuette SA, Lashner BA, Janghorbani M. Bioavailability of magnesium diglycinate vs magnesium oxide in patients with ileal resection. J Parenter Enteral Nutr. 1994;18(5):430–5. Ileal-resection-specific comparison — no difference in this narrow population. PubMed PMID: 7815675 →
Ethnic Differences in Magnesium Intake in U.S. Older Adults: NHANES 2005–2016. PMC6316208. 83.3% of US adults ≥65 not meeting dietary Mg RDA; 90.6% of African Americans. Overall ~48% of US adults consume below the EAR. PMC6316208 →
Call for Re-evaluation of the Tolerable Upper Intake Level — ScienceDirect 2023. Over half of US adults aged ≥20 consume below the EAR for Mg. Reviews evidence that current DRIs may underestimate requirements due to unreliable historical balance data. ScienceDirect 2023 →
De Souza MC, Walker AF, Robinson PA, Bolland K. A synergistic effect of a daily supplement for 1 month of 200 mg magnesium plus 50 mg vitamin B6 for the relief of anxiety-related premenstrual symptoms: a randomized, double-blind, crossover study. J Womens Health Gend Based Med. 2000;9(2):131–9. PMS indication evidence base.
Magnesium Depletion as a Cause of Refractory Potassium Repletion. JAMA Internal Medicine. 1985. Original clinical description of the Mg–K relationship in hospital practice. Foundation reference for the potassium interaction section. JAMA Internal Medicine 1985 →
Refractory potassium repletion due to cisplatin-induced magnesium depletion — PubMed 1989. Clinical case series documenting potassium supplementation failure until hypomagnesemia was corrected. PMID: 2818117. PubMed PMID: 2818117 →
Umbrella Meta-Analysis: Impact of Magnesium Supplementation on Blood Pressure. Pharmacol Res. 2024. PMID: 39280209. 10 review papers, 8,610 participants: SBP −1.25 mmHg, DBP −1.40 mmHg overall. PubMed PMID: 39280209 →
Magnesium in neuroses and neuroticism — NCBI Bookshelf. NBK507254. Detailed mechanistic review: NMDA receptor antagonism, catecholamine modulation, GABA systems, and magnesium’s role in anxiety and neuronal hyperexcitability. NBK507254 →

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