Magnesium and Electrolytes for Cramp Prevention

Magnesium is the most common cramp remedy recommended by primary-care doctors and the one whose evidence is most contested. The 2020 Cochrane review concluded that magnesium probably does not meaningfully reduce idiopathic nocturnal cramps in the general adult population — but the same review found a clear signal in pregnancy-associated cramps, and clinical practice consistently sees responders among older adults, athletes, and patients on diuretics or proton pump inhibitors. The disconnect is a measurement problem: serum magnesium is a poor measure of cellular magnesium, the form of magnesium taken matters more than the dose, and the trial populations were mostly already-replete community-dwelling adults. This page maps the physiology of the calcium-magnesium-sodium-potassium quartet that governs muscle relaxation, walks through which magnesium forms actually work, and gives the practical 6-week trial protocol for figuring out whether you personally respond.

Table of Contents

1. Why Electrolytes Matter for Muscle Relaxation
2. Magnesium Physiology — the Cellular Brake on Calcium
3. The Serum-vs-Cellular Paradox
4. Forms of Magnesium — Glycinate, Malate, Citrate, Oxide
5. Dosing & the 6-Week Trial Protocol
6. Potassium — the Second Most Useful Electrolyte
7. Calcium and Sodium — Why They Matter Less Than You Think
8. Drug-Induced Magnesium Depletion
9. The Cochrane Controversy and How to Read It
10. Cautions and Interactions
11. Key Research Papers
12. Connections

Why Electrolytes Matter for Muscle Relaxation

The single most important fact about muscle contraction is that relaxation requires energy. A muscle is not "off" in the absence of an active signal — it is held in the relaxed state by the ATP-dependent active pumping of calcium back into the sarcoplasmic reticulum after every twitch. When ATP runs short, calcium accumulates in the cytosol, the actin-myosin cross-bridges stay engaged, and the muscle stays contracted. That sustained involuntary contraction is a cramp.

Three of the four major intracellular and extracellular electrolytes regulate this calcium-management machinery directly:

• Magnesium (Mg²⁺) is the obligatory cofactor for the ATP-dependent calcium pumps (SERCA pumps in the sarcoplasmic reticulum membrane). ATP-Mg is the actual substrate, not free ATP. Magnesium is also a non-competitive antagonist at the NMDA receptor in the central nervous system, modulating motoneuron excitability upstream.
• Calcium (Ca²⁺) is the trigger ion. Voltage-gated calcium influx through the T-tubule triggers release of stored calcium from the sarcoplasmic reticulum, which binds troponin C and initiates contraction. Both too little and too much extracellular calcium produce cramping.
• Potassium (K⁺) is the dominant intracellular cation. Cellular potassium maintains the resting membrane potential at -90 mV, which keeps voltage-gated sodium channels in their resting (not inactivated) state. Hypokalemia depolarizes the resting membrane, inactivates a fraction of sodium channels, and produces both weakness and cramping in the small remaining excitable pool.
• Sodium (Na⁺) is the dominant extracellular cation and the depolarizing ion that propagates the action potential. Genuine hyponatremia (serum sodium below 130 mmol/L) is associated with seizure and cramping at the severe end, but the role of sodium in athletic cramping is more nuanced and is covered in Hydration Beyond Water.

The interaction matters. Magnesium and calcium compete for some of the same transporters and binding sites — low magnesium effectively unmasks calcium signaling. Magnesium also enables the Na/K-ATPase that maintains the resting membrane potential, so low magnesium produces functional potassium depletion at the cellular level even when serum potassium is normal. This is why magnesium repletion alone often resolves cramps that an unsuccessful potassium-supplementation trial has failed to budge — the patient was magnesium-depleted, with secondary functional potassium depletion.

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Magnesium Physiology — the Cellular Brake on Calcium

The adult human body contains approximately 25 grams of magnesium. About 60% is in bone, 39% is intracellular in soft tissue (predominantly muscle), and less than 1% is in the extracellular space (serum). This distribution explains why serum magnesium is such a poor reflection of total body status — you can have substantial intracellular depletion with completely normal serum levels.

Magnesium serves at least four functions that bear directly on muscle relaxation:

1. ATP-Mg complex — ATP only acts as a phosphoryl donor when complexed with Mg²⁺. The SERCA calcium pump, the Na/K-ATPase, and the myosin ATPase all require Mg-ATP, not free ATP. In magnesium-depleted cells, all three ATPase systems run at reduced capacity, and calcium accumulates in the cytosol after each twitch.
2. NMDA receptor block — in the central and peripheral nervous system, Mg²⁺ sits in the NMDA receptor channel as a voltage-dependent block. Low magnesium increases NMDA-mediated excitatory neurotransmission and raises motoneuron excitability, the same axis that contributes to chronic pain syndromes and migraine.
3. Calcium channel modulation — Mg²⁺ is a natural calcium-channel antagonist. The clinically used calcium channel blockers (verapamil, diltiazem) work via the same fundamental mechanism that magnesium uses constitutively. Low magnesium effectively un-blocks voltage-gated calcium channels, increasing calcium influx during each depolarization.
4. Smooth muscle and vascular tone — chronic magnesium depletion is associated with vasoconstriction (one mechanism behind the magnesium-hypertension link) and bronchoconstriction (the IV magnesium sulfate response in severe asthma). These are largely tangential to skeletal muscle cramps but illustrate the breadth of magnesium-dependent smooth-muscle relaxation.

Because the body buffers serum magnesium tightly &mdash and because chronic mild depletion is largely silent — magnesium deficiency is one of the most under-recognized nutritional issues in adult clinical medicine. NHANES survey data suggest 40-50% of US adults consume less than the Estimated Average Requirement for magnesium, and the figure is higher in adults over 70.

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The Serum-vs-Cellular Paradox

The standard "serum magnesium" lab test runs from 1.7 to 2.2 mg/dL in most reference ranges. A patient with a serum magnesium of 1.9 will be reported as "normal" by the lab and is unlikely to receive supplementation from a primary-care physician.

The problem is that less than 1% of body magnesium is in the serum. The serum compartment is actively maintained by mobilization from bone — the body will deplete its own skeleton to keep serum magnesium "normal" right up to the point where bone stores are exhausted. A serum magnesium in the lower half of the reference range is consistent with substantial intracellular depletion, particularly in the presence of any of the chronic depletion risk factors (proton pump inhibitor use, loop or thiazide diuretic, alcohol intake, type 2 diabetes, malabsorption, age over 70).

Better tests exist but are less widely used:

• Red blood cell magnesium — reflects intracellular content better than serum. Reference range is approximately 4.2-6.8 mg/dL. Available through specialty labs (Genova, LabCorp, Quest with the right test code).
• 24-hour urinary magnesium excretion — low excretion (<80 mg/24h) in the face of normal dietary intake suggests intracellular depletion driving renal reabsorption. Combined with serum, gives a more complete picture.
• Magnesium loading test (parenteral) — an IV magnesium load followed by 24-hour urine collection. Retention >25% of the load is considered diagnostic of depletion. The gold-standard test but rarely done outside research.
• Ionized magnesium — only the unbound ionized fraction is biologically active. Measurable on blood-gas analyzers in some hospital labs but rarely ordered for outpatient cramp evaluation.

The practical takeaway is that a "normal" serum magnesium does not rule out functional deficiency, and a therapeutic trial of oral magnesium is reasonable in any adult with idiopathic cramping, particularly nocturnal cramps in older adults or pregnancy cramps. The risk of a 6-week trial of 350 mg elemental magnesium glycinate is essentially zero in adults with normal renal function.

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Forms of Magnesium — Glycinate, Malate, Citrate, Oxide

The form of magnesium matters enormously, and most over-the-counter "magnesium" sold in pharmacies is the form with the poorest absorption. The relative bioavailability and clinical profile of the major forms:

• Magnesium glycinate (bisglycinate) — magnesium bound to two glycine amino acids. Highest bioavailability of common forms, minimal laxative effect, neutral taste, well tolerated. The preferred form for cramp prevention, sleep, and any application where you want the magnesium to reach tissue rather than the toilet. Typical product: 200-250 mg elemental per capsule. The glycine itself has mild inhibitory neurotransmitter activity and may contribute to the sleep effect.
• Magnesium malate — magnesium bound to malic acid (a Krebs cycle intermediate). Well absorbed, gentle on the gut, often promoted for fibromyalgia and chronic fatigue (the malate component is thought to support ATP production). A reasonable alternative to glycinate, particularly for daytime dosing because the malate has a slightly energizing effect that some find incompatible with the bedtime dose.
• Magnesium citrate — magnesium bound to citric acid. Well absorbed but has a moderate-to-strong osmotic laxative effect at doses above ~250 mg elemental. Useful when constipation is co-occurring with cramps (the laxative effect is then a feature). Often the cheapest reasonably bioavailable form.
• Magnesium L-threonate — a proprietary form developed at MIT designed to cross the blood-brain barrier. Studied primarily for cognitive applications. Substantially more expensive than glycinate and the data for cramps specifically are thin; glycinate is a better cost-per-elemental-mg choice for cramp prevention.
• Magnesium taurate — magnesium plus the amino acid taurine. Promoted for cardiovascular applications. Reasonable but expensive for cramp prevention compared to glycinate.
• Magnesium chloride — well absorbed; available as liquid drops, as a topical "magnesium oil" (which has limited transdermal absorption despite marketing claims), and in Epsom-alternative bath flake form (magnesium chloride flake baths versus magnesium sulfate Epsom salt; both have minimal transdermal contribution but provide relaxation effects).
• Magnesium oxide — the cheapest and most commonly sold form. Bioavailability is approximately 4% per the Coudray et al. comparative rat study and Walker et al. human study — an order of magnitude worse than the organic chelates. Its primary clinical role is as an osmotic laxative. The single negative magnesium-for-cramps RCT (Maor et al. 2016) used magnesium oxide, which goes a long way toward explaining the negative result.
• Magnesium sulfate (Epsom salt) — useful as IV preparation in obstetric eclampsia and severe asthma. Oral magnesium sulfate is strongly cathartic and not used for cramp prevention. Transdermal absorption from Epsom salt baths is real but small; the warm-water immersion itself probably contributes more to muscle relaxation than the magnesium uptake.

The single most common reason a patient "tried magnesium and it didn't work" is that they bought magnesium oxide at the grocery store, took 250 mg total (representing about 10 mg of actually absorbed magnesium), and concluded the supplement was useless. Switching to 350 mg elemental magnesium glycinate often produces a different result. See our Magnesium overview for the broader supplement landscape.

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Dosing & the 6-Week Trial Protocol

For idiopathic nocturnal cramps or exercise-related cramping in adults with normal renal function, a reasonable trial protocol:

1. Form: magnesium glycinate, 350-500 mg elemental magnesium per day. Read the supplement label carefully — "1,000 mg magnesium glycinate" usually delivers ~140 mg elemental magnesium, because the glycine accounts for the rest of the molecular weight. The elemental amount is what counts.
2. Timing: 30-60 minutes before bedtime. Magnesium glycinate's mild calming effect synergizes with sleep and gives overnight tissue concentration its best chance to rise.
3. Duration: 6 weeks minimum before declaring failure. Tissue magnesium repletion is slow because the deficit accumulated over years, not weeks. Many responders report partial benefit at 2-3 weeks and fuller benefit at 4-6 weeks.
4. Co-intervention: simultaneously start the calf-stretch protocol (3 times daily, 10 seconds hold × 3 reps). This is the only intervention with consistent RCT evidence for nocturnal cramps, and combining it with magnesium gives the best chance of success without confounding the trial — if both work, you do both indefinitely.
5. Diet: add magnesium-rich foods — pumpkin seeds (~150 mg per 30 g), almonds (~80 mg per 30 g), spinach (~80 mg per cup cooked), dark chocolate (~65 mg per ounce 70% cocoa), avocado (~60 mg per medium fruit). Real food magnesium is absorbed at similar efficiency to supplements but comes with additional cofactors.
6. Adjuncts to consider: potassium (food first, supplement only with clinician guidance), Vitamin D (deficiency can present with cramping — check 25-OH-vitamin D and replete if <30 ng/mL), Vitamin B6 (a magnesium-transport cofactor; 50 mg P5P daily for 4 weeks is a reasonable adjunct).

If cramps persist unchanged after 6 weeks of 500 mg elemental glycinate plus calf stretching, magnesium is unlikely to be your problem. Move to evaluating drug causes, neurology referral for ALS/peripheral neuropathy screening if other red flags exist, sleep study for restless legs / Willis-Ekbom disease, and (if exercise-associated) the neural reflex remedies.

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Potassium — the Second Most Useful Electrolyte

After magnesium, potassium is the next most commonly implicated electrolyte in cramping. Most adults consume less than half the recommended 4,700 mg/day of potassium. The Modern Diet Problem is the inversion of the ancestral sodium:potassium ratio — hunter-gatherer diets provided approximately 1:10 sodium-to-potassium, while a typical processed-food modern diet runs 2:1 or worse. Almost any switch toward more whole-food vegetables and fruits and less processed food improves the ratio.

Food sources, with approximate potassium per typical serving:

• Beans, white (1 cup cooked): 1,000 mg
• Potato with skin, baked (medium): 925 mg
• Salmon (6 oz): 800 mg
• Avocado (medium): 700 mg
• Yogurt, plain (1 cup): 550 mg
• Banana (medium): 420 mg
• Orange juice (1 cup): 500 mg
• Coconut water (1 cup): 600 mg
• Tomato sauce (1 cup): 800 mg
• Spinach (1 cup cooked): 840 mg

For supplementation, the FDA limits OTC potassium supplements to 99 mg per pill because of the risk of localized GI irritation and the cardiac risk of sudden hyperkalemia (particularly in patients on ACE inhibitors, ARBs, potassium-sparing diuretics, or with renal insufficiency). This is far below a therapeutic dose. For genuine potassium repletion above what diet can provide, prescription potassium chloride (10-40 mEq) under physician supervision is needed.

The much safer general approach is to add 2-3 of the food-source list above to the daily diet. A patient eating one banana plus one cup of beans plus one avocado per day is adding roughly 2,100 mg of potassium — substantially more than any non-prescription supplement can deliver. For more on potassium specifically, see our Potassium page.

Coconut water deserves special mention: it provides approximately 600 mg of potassium per cup along with sodium, magnesium, and natural sugars, making it a reasonable peri-exercise rehydration choice particularly for endurance athletes who cramp.

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Calcium and Sodium — Why They Matter Less Than You Think

Most patients (and many clinicians) overestimate the role of calcium and sodium in routine cramp prevention. Calcium deficiency severe enough to cause cramping (latent tetany, Trousseau's and Chvostek's signs) is genuinely uncommon outside of post-surgical hypoparathyroidism, severe vitamin D deficiency, or chronic kidney disease. Pregnancy was historically thought to be a calcium-cramp setting, but the 2015 Cochrane review on pregnancy cramps found that calcium supplementation did not consistently outperform placebo — magnesium had better evidence in this setting.

The sodium story is more nuanced. Sodium depletion can cause cramping when genuine, but in modern populations most adults consume too much sodium, not too little. The exception is the endurance athlete or outdoor worker who sweats heavily in heat for several hours, replaces with plain water or low-sodium sports drinks, and develops exercise-associated hyponatremia with secondary cramping. That specific scenario is addressed in Hydration Beyond Water.

For the average adult with nocturnal or non-athletic cramps, neither calcium nor sodium supplementation is a high-yield intervention. Vitamin D repletion (which improves calcium handling) is more useful than direct calcium supplementation. Reducing processed food intake (which lowers sodium) is more useful than salt supplementation.

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Drug-Induced Magnesium Depletion

A surprising number of common medications deplete magnesium and/or potassium and produce cramping as a side effect. Review the patient's medication list before starting a cramp work-up:

• Proton pump inhibitors (omeprazole, esomeprazole, pantoprazole, lansoprazole) — the FDA issued a 2011 safety communication on PPI-associated hypomagnesemia after long-term use (typically >1 year). The mechanism is impaired intestinal magnesium absorption via the TRPM6/M7 channels. Stopping the PPI (or switching to H2 blocker) plus magnesium repletion typically resolves the cramping over weeks.
• Loop diuretics (furosemide, bumetanide, torsemide) — aggressively waste both potassium and magnesium via the loop of Henle. Patients on chronic loop diuretics almost universally need supplementation of both.
• Thiazide diuretics (hydrochlorothiazide, chlorthalidone, indapamide) — deplete potassium and (less consistently) magnesium. The combination of a thiazide for hypertension plus an undiagnosed magnesium deficit is a classic cramp scenario.
• Beta-2 agonists (albuterol, salmeterol) — drive potassium intracellularly via beta-2 receptor stimulation of the Na/K-ATPase. Acute bronchodilator-induced cramping is usually transient; chronic use can produce more sustained shift.
• Statins (atorvastatin, simvastatin, rosuvastatin) — the classic "statin myalgia" includes cramping in some patients. Mechanism involves CoQ10 depletion (statins block the same mevalonate pathway), mitochondrial dysfunction, and rarely autoimmune statin-induced necrotizing myopathy. CoQ10 100-200 mg daily plus dose reduction or switch to a different statin is the typical approach.
• Calcium channel blockers — nifedipine in particular has reported cramping as a side effect (though it's also paradoxically used for cramps in some settings).
• Lithium — chronic therapeutic lithium can cause cramping.
• Donepezil — the Alzheimer's cholinesterase inhibitor has nocturnal leg cramps as a recognized side effect.
• Alcohol — chronic alcohol intake depletes magnesium via increased renal excretion. Cramping is one of the lesser-recognized features of subclinical alcohol-related magnesium deficiency.

The Garrison et al. 2012 pharmacoepidemiology study found that statins, diuretics, beta-agonists, and several other drug classes were associated with newly prescribed cramp remedies in older adults, supporting the causal direction. If a patient's cramps began within weeks of starting a new medication, that medication is the place to start the investigation.

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The Cochrane Controversy and How to Read It

The 2020 Cochrane systematic review of magnesium for skeletal muscle cramps (Garrison, Allan, Sekhon, Musini, and Khan) is the most cited source for the position that "magnesium does not work for cramps." A more careful reading is needed.

The review pooled 11 randomized trials (735 participants total). For idiopathic nocturnal cramps in community-dwelling adults, the pooled effect estimate showed no statistically significant reduction in cramp frequency from magnesium supplementation versus placebo. The 95% confidence interval included the null but also allowed for a modest benefit (the effect could not be definitively excluded).

For pregnancy-associated cramps, the review found a different picture — a clear and statistically significant reduction in cramp frequency and severity from magnesium supplementation. The pregnancy context was the strongest signal in the entire review.

Several reasons to interpret the negative idiopathic-cramps result cautiously:

1. Most trials used magnesium oxide, the form with the worst bioavailability. The single trial in the review that used magnesium citrate (Roffe 2002) had a non-significant trend toward benefit. No trial in the Cochrane analysis used magnesium glycinate, the form clinically preferred for cramps.
2. The community-dwelling adult population was largely already replete. Cramp trials recruited people with frequent cramps but did not specifically select for low magnesium status. A repletion trial in a population that does not need repletion is destined to underestimate the effect.
3. Trial durations were 4-6 weeks, which is at the lower end of what may be needed for cellular repletion in chronically depleted individuals.
4. Outcome measures varied widely — some counted cramp frequency, others severity, others a subjective "improvement" score. Pooling heterogeneous outcomes attenuates effects.
5. The review's own authors note that the evidence base is limited and that "future trials should use bioavailable forms of magnesium and target populations with documented or suspected magnesium insufficiency."

The honest clinical position is: magnesium glycinate is not a guaranteed cramp fix in the average community-dwelling adult, but it is high-probability-of-benefit in pregnancy cramps, plausibly beneficial in older adults with risk factors for depletion, low-risk to try, and the alternative therapies have their own limitations (quinine is FDA-restricted for cramps due to thrombocytopenia risk, calcium channel blockers and benzodiazepines have systemic side effects, no other supplement has better evidence). A 6-week trial of 350-500 mg elemental magnesium glycinate at bedtime is a reasonable first-line intervention even acknowledging the Cochrane uncertainty.

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Cautions and Interactions

• Renal insufficiency — the kidneys excrete excess magnesium. Patients with eGFR <30 mL/min/1.73 m² (CKD stage 4-5) are at risk of hypermagnesemia from supplementation and should not take magnesium supplements without nephrology guidance. For most adults with normal renal function, the upper limit of supplemental (non-dietary) magnesium is 350 mg elemental per day per the NIH ODS; doses above this are widely used clinically but raise the risk of loose stools.
• Diarrhea — any form of magnesium can cause loose stools at sufficient dose; oxide and citrate are the most prone to this, glycinate the least. If diarrhea develops, reduce the dose or switch form.
• Drug interactions with absorption — magnesium chelates with tetracycline and fluoroquinolone antibiotics, bisphosphonates (alendronate, risedronate), and levothyroxine. Separate dosing by at least 2 hours.
• Magnesium and digoxin — hypomagnesemia increases digoxin toxicity (the K/Mg-ATPase digoxin binds is more sensitive when Mg is low). Magnesium repletion is part of standard care for digoxin-treated patients.
• Pregnancy — oral magnesium glycinate is considered low risk and is the recommended first-line cramp remedy in pregnancy. IV magnesium sulfate is standard for eclampsia and preterm labor neuroprotection. The cautions in pregnancy are around IV use, not routine oral supplementation.
• Pediatric — pediatric dosing should be guided by a pediatrician.
• Acute severe hypermagnesemia — signs are loss of deep tendon reflexes (occurs at ~4 mg/dL), respiratory depression (~10 mg/dL), and cardiac arrest (>15 mg/dL). Functionally impossible to reach with oral glycinate in a patient with normal renal function but a real risk of IV use.

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Key Research Papers

1. Garrison SR, Allan GM, Sekhon RK, Musini VM, Khan KM (2020). Magnesium for skeletal muscle cramps. Cochrane Database of Systematic Reviews. — PubMed 32956536
2. Roffe C, Sills S, Crome P, Jones P (2002). Randomised, cross-over, placebo controlled trial of magnesium citrate in the treatment of chronic persistent leg cramps. Medical Science Monitor. — PubMed 12011773
3. Frusso R, Zarate M, Augustovski F, Rubinstein A (1999). Magnesium for the treatment of nocturnal leg cramps: a crossover randomized trial. Journal of Family Practice. — PubMed 10399051
4. Dahle LO, Berg G, Hammar M, Hurtig M, Larsson L (1995). The effect of oral magnesium substitution on pregnancy-induced leg cramps. American Journal of Obstetrics and Gynecology. — PubMed 7847532
5. Maor NR, Alperin M, Shturman E et al. (2017). Effect of Magnesium Oxide Supplementation on Nocturnal Leg Cramps: A Randomized Clinical Trial. JAMA Internal Medicine. — PubMed 27214001
6. Walker AF, Marakis G, Christie S, Byng M (2003). Mg citrate found more bioavailable than other Mg preparations in a randomised, double-blind study. Magnesium Research. — PubMed 14596323
7. Coudray C, Rambeau M, Feillet-Coudray C et al. (2005). Study of magnesium bioavailability from ten organic and inorganic Mg salts in Mg-depleted rats. Magnesium Research. — PubMed 16548135
8. Lindberg JS, Zobitz MM, Poindexter JR, Pak CY (1990). Magnesium bioavailability from magnesium citrate and magnesium oxide. Journal of the American College of Nutrition. — PubMed 2407766
9. Costello R, Wallace TC, Rosanoff A (2016). Perspective: The Case for an Evidence-Based Reference Interval for Serum Magnesium. Advances in Nutrition. — PubMed 27170592
10. Schwalfenberg GK, Genuis SJ (2017). The Importance of Magnesium in Clinical Healthcare. Scientifica. — PubMed 29093983
11. FDA Drug Safety Communication (2011). Low magnesium levels can be associated with long-term use of proton pump inhibitor drugs. — PubMed: FDA PPI hypomagnesemia
12. Garrison SR, Dormuth CR, Morrow RL, Carney GA, Khan KM (2012). Nocturnal leg cramps and prescription use that precedes them: a sequence symmetry analysis. Archives of Internal Medicine. — PubMed 22550113

PubMed Topic Searches

• PubMed: Magnesium nocturnal cramp RCTs
• PubMed: Magnesium glycinate bioavailability
• PubMed: Intracellular magnesium assessment
• PubMed: PPI hypomagnesemia
• PubMed: Pregnancy cramps and magnesium

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Connections

• Cramp Prevention Main Page
• Cramp Benefits Hub
• Pickle Juice & Neural Reflex
• Hydration Beyond Water
• Stretch & Reset Techniques
• Magnesium
• Potassium
• Calcium
• Sodium
• Vitamin D3
• Vitamin B6
• Pumpkin Seeds
• Spinach
• Almonds
• All Remedies

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