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Magnesium for Sleep and Anxiety: Which Form Works and What the Research Shows

27 March 2026 · 21 min read

Magnesium for Sleep and Anxiety: Which Form Works and What the Research Shows

Magnesium is the fourth most abundant mineral in the human body and is involved in over 300 enzymatic reactions — yet surveys consistently find that a substantial proportion of Australians fail to meet the recommended dietary intake. In the context of sleep and anxiety, this matters considerably: magnesium sits at the intersection of GABA signalling, NMDA receptor regulation, and HPA axis (stress response) modulation. When magnesium status is suboptimal, the biological machinery underpinning calm, restorative sleep and appropriate anxiety responses is working with impaired inputs.

This article covers the neuroscience of why magnesium is so relevant to sleep and anxiety, why deficiency is so prevalent in the modern Australian context, which forms of supplemental magnesium are actually supported by evidence for these specific applications, what dosing the clinical trials used, how to test your own magnesium status accurately, and the key nutrient interactions that affect how well magnesium works.

Magnesium's Role in the Nervous System

To understand why magnesium supplementation affects sleep and anxiety, it helps to understand what magnesium is doing in the nervous system at a mechanistic level. There are three primary pathways.

GABA Receptor Modulation

GABA (gamma-aminobutyric acid) is the central nervous system's primary inhibitory neurotransmitter. GABAergic signalling reduces neuronal excitability — it is the molecular mechanism of calm. Benzodiazepines, Z-drugs (zopiclone, zolpidem), and alcohol all exert their sedative and anxiolytic effects by enhancing GABA-A receptor activity.

Magnesium contributes to GABAergic tone through two mechanisms. First, magnesium ions support the function and sensitivity of GABA-A receptors directly. Second, magnesium regulates glutamate — the primary excitatory neurotransmitter — through NMDA receptor blockade (see below). Since the GABAergic and glutamatergic systems are reciprocally regulated, reducing glutamatergic excitability indirectly amplifies GABAergic inhibitory tone.

Suboptimal magnesium status is associated with reduced GABA synthesis and impaired GABA-A receptor sensitivity — creating a neurological environment that is biased toward excitability, anxiety, and difficulty transitioning into sleep onset.

NMDA Receptor Blockade

NMDA (N-methyl-D-aspartate) receptors are a class of glutamate receptor critical for synaptic plasticity, memory consolidation, and — when overactivated — excitotoxicity and anxiety. Magnesium ions act as a voltage-dependent blocker of the NMDA receptor ion channel: at resting membrane potentials, magnesium physically occupies the channel pore and prevents calcium ion influx.

This is a critical regulatory function. Without adequate magnesium, NMDA receptors become easier to activate — lowering the threshold for neuronal excitation and effectively turning up the nervous system's gain. This manifests clinically as heightened anxiety reactivity, racing thoughts at bedtime, hypervigilance, and difficulty downregulating arousal in the evening. The NMDA receptor blocking property of magnesium is also a proposed mechanism behind some of magnesium's observed antidepressant-adjacent effects in low-dose research.

HPA Axis Regulation

The hypothalamic-pituitary-adrenal (HPA) axis is the body's central stress response system, governing cortisol production. There is a bidirectional relationship between magnesium and the HPA axis with significant practical implications.

Magnesium helps regulate the HPA axis by limiting the release of ACTH (adrenocorticotropic hormone) from the pituitary and modulating glucocorticoid receptor sensitivity. In low magnesium states, the HPA axis shows increased reactivity to stressors — producing larger, longer cortisol spikes in response to the same stimulus load. Elevated evening cortisol is one of the most reliable disruptors of sleep onset and sleep architecture.

Critically, the relationship runs in both directions: acute stress increases urinary magnesium excretion significantly. People under chronic psychological, occupational, or physiological stress therefore deplete their magnesium more rapidly than the general population — creating a feedback loop where stress depletes magnesium, depleted magnesium amplifies HPA reactivity, which drives more cortisol and more magnesium loss.

This relationship is explored in detail in the context of ashwagandha's HPA axis modulation — a complementary approach that addresses the cortisol side of the same feedback loop through a different mechanism.

Why Many Australians Are Deficient

Magnesium deficiency in the broad clinical sense — symptomatic hypomagnesaemia — is relatively uncommon. But suboptimal magnesium status, where serum levels are within the "normal" range but intracellular and total body magnesium is insufficient for optimal function, is substantially more prevalent. Several factors drive this in the Australian context.

Dietary Depletion

The primary dietary sources of magnesium are green leafy vegetables, legumes, nuts and seeds, and whole grains. The magnesium content of these foods is dependent on soil mineral content, and agricultural intensification over the past 60 years has reduced the magnesium concentration of many crops significantly compared to mid-20th century data.

Processed food diets, which characterise a large proportion of Australian eating patterns, are substantially lower in magnesium than traditional whole-food diets. Alcohol consumption — common in the Australian cultural context — directly increases renal magnesium excretion, further reducing body stores.

Stress-Driven Excretion

As described above, the HPA axis-magnesium relationship means that chronically stressed individuals excrete more magnesium in urine than people in lower-stress states. The modern occupational and lifestyle environment — high cognitive load, disrupted sleep, sedentary work, financial pressure — creates a structural demand for magnesium that dietary intake often cannot meet.

PPI Medications and Proton Pump Inhibitor-Induced Hypomagnesaemia

Proton pump inhibitors (PPIs) — omeprazole, pantoprazole, esomeprazole — are among the most commonly prescribed medications in Australia, used for reflux, gastric ulcers, and NSAID-related gastric protection. Long-term PPI use (typically beyond 12 months) impairs intestinal magnesium absorption through a mechanism involving the TRPM6 and TRPM7 transient receptor potential channels in the gut epithelium. The result is a well-documented clinical phenomenon called PPI-induced hypomagnesaemia, which can be severe enough to cause tetany, cardiac arrhythmia, and seizures in extreme cases, but more commonly manifests as fatigue, muscle cramps, anxiety, and sleep disturbance at moderate levels.

TGA product information for all major PPI brands in Australia includes warnings about hypomagnesaemia risk with long-term use. Notably, serum magnesium is what is typically checked — which means borderline intracellular deficiency may be missed.

Insulin Resistance and Type 2 Diabetes

Magnesium is reabsorbed from urine in the kidney tubules; this process is impaired in insulin-resistant and diabetic states, leading to increased renal magnesium wasting. Given the prevalence of insulin resistance and prediabetes in Australia, this represents a significant contributor to population-level suboptimal magnesium status.

Forms of Magnesium: Which One for Sleep and Anxiety

Not all magnesium supplements are equivalent — the form of magnesium determines its bioavailability, tissue distribution, and which physiological effects are most pronounced.

Magnesium Glycinate — Best for Sleep and Anxiety

Magnesium glycinate (magnesium bound to the amino acid glycine) is the form with the strongest evidence base for sleep and anxiety applications, and the form recommended most consistently in functional medicine and naturopathic practice for these specific indications.

The rationale is dual:

Magnesium component: Glycinate form achieves good elemental magnesium absorption (bioavailability estimated at 80%+ in comparative studies) and efficiently raises intracellular magnesium, which is more relevant to nervous system function than serum magnesium alone. It is gentle on the gut — unlike citrate or oxide, glycinate does not draw osmotic water into the bowel, so it is generally well tolerated even at higher doses.

Glycine component: Glycine is itself a significant neurotransmitter. It acts as an inhibitory neurotransmitter in the brainstem and spinal cord, and has separate but complementary effects on sleep: studies have shown that 3g of glycine taken before bed reduces sleep onset latency, improves sleep efficiency, and reduces daytime fatigue after shortened sleep. Glycine also reduces core body temperature by promoting peripheral vasodilation, which is a well-established physiological trigger for sleep onset. In magnesium glycinate, you receive both the magnesium and a meaningful dose of glycine with each serving.

For someone whose primary goals are improved sleep onset, reduced nighttime anxiety, and better sleep quality, magnesium glycinate is the evidence-aligned first choice.

Magnesium L-Threonate — For Brain and Cognitive Function

Magnesium threonate (magnesium bound to L-threonic acid) is a newer form specifically developed to cross the blood-brain barrier more efficiently than other magnesium salts. Animal research has demonstrated that magnesium threonate significantly raises brain magnesium levels — cerebrospinal fluid magnesium and hippocampal magnesium — to a greater extent than equivalent elemental doses of other forms.

The proposed clinical applications are primarily cognitive: synaptic density, working memory, and the NMDA receptor regulation relevant to memory consolidation during sleep. A human RCT published in Journal of Alzheimer's Disease (2016) found that magnesium threonate improved cognitive performance measures in older adults compared to placebo.

Magnesium threonate is the appropriate choice when primary goals are cognitive function and brain magnesium specifically, rather than general sleep and anxiety. It is substantially more expensive per dose of elemental magnesium than glycinate. Some practitioners use threonate for daytime cognitive support and glycinate in the evening for sleep — a rational combination given the different tissue distribution profiles.

Magnesium Citrate — Practical for General Use

Magnesium citrate is highly bioavailable, generally well tolerated, widely available, and affordable. It is an effective general-purpose magnesium supplement that will reliably raise magnesium status. Its limitation for sleep and anxiety applications relative to glycinate is the absence of the glycine component, and the fact that at higher doses citrate can have a mild laxative effect due to its osmotic properties in the gut. For people needing to raise magnesium status generally without specific sleep or anxiety targets, citrate is a practical and cost-effective choice.

Magnesium Oxide — Largely Ineffective for Supplementation Goals

Magnesium oxide has very low bioavailability — absorption studies suggest as little as 4% of elemental magnesium content is absorbed, compared to 80%+ from glycinate and 30–40% from citrate. Despite containing a high percentage of elemental magnesium by weight, the actual amount absorbed is poor, and most passes through the gut with significant osmotic laxative effect.

Magnesium oxide appears frequently in budget supplements and multivitamins, primarily because it is inexpensive. For sleep, anxiety, or any goal requiring meaningful tissue magnesium elevation, oxide is the form to avoid. If a supplement lists magnesium oxide as its primary magnesium source, selecting an alternative is worthwhile.

Other Notable Forms

  • Magnesium malate: Bound to malic acid; good bioavailability; often recommended for muscle function and fatigue. Less specific evidence for sleep/anxiety than glycinate.
  • Magnesium taurate: Bound to taurine; both magnesium and taurine have cardiovascular and GABA-modulatory properties; some interest for blood pressure and cardiac rhythm.
  • Magnesium chloride (topical): Topical magnesium oil or flakes are popular but evidence for transdermal absorption contributing meaningfully to systemic status is weak.

Clinical Evidence for Sleep and Anxiety

Insomnia Evidence

A double-blind, placebo-controlled trial published in the Journal of Research in Medical Sciences (Abbasi et al., 2012) enrolled 46 elderly adults with insomnia and randomised them to receive 500mg magnesium or placebo daily for 8 weeks. The magnesium group demonstrated statistically significant improvements in:

  • Sleep onset latency (time to fall asleep)
  • Sleep duration (total sleep time increased)
  • Sleep efficiency (proportion of time in bed spent asleep)
  • Serum melatonin (increased in the magnesium group — consistent with magnesium's role as a cofactor in the enzymatic conversion of serotonin to melatonin)
  • Serum cortisol (significantly reduced in the magnesium group)

The finding that magnesium supplementation raised serum melatonin is particularly clinically relevant — magnesium is a cofactor in the enzyme HIOMT/ASMT that converts serotonin to melatonin. Low magnesium may impair endogenous melatonin production independently of the GABA and NMDA mechanisms, adding another pathway through which magnesium deficiency disrupts sleep.

A 2021 systematic review of magnesium supplementation for sleep quality (Mah and Pitre, BMC Complementary Medicine and Therapies) examined 7 clinical trials and found consistent trends toward improved subjective sleep quality, sleep efficiency, and sleep onset latency with magnesium supplementation, with the caveat that trial quality was variable and sample sizes were small. The authors concluded that the evidence was promising but required larger, higher-quality RCTs — a fair characterisation of where the literature currently stands.

Anxiety Evidence

A 2017 systematic review by Boyle, Lawton, and Dye (Nutrients) examined 18 human studies on magnesium and anxiety across various populations. The review found consistent evidence of an association between lower magnesium status and higher anxiety scores, and preliminary evidence that supplementation improved anxiety measures in populations with suboptimal magnesium status — including people with mild-to-moderate anxiety, premenstrual syndrome-related anxiety, and stress-related anxiety.

An important nuance: the evidence is strongest in populations with documented or likely magnesium insufficiency. The anxiolytic effect of magnesium supplementation in people who are already replete is less established. This is consistent with the mechanism — if GABA and NMDA receptor function are already fully supported by adequate magnesium, additional supplementation offers diminishing returns.

A well-controlled 8-week trial by Boyle et al. found that magnesium supplementation (300mg daily) significantly reduced trait anxiety scores on validated assessment tools in healthy adults with low dietary magnesium intake at baseline, compared to placebo. The effect was most pronounced in participants with the lowest baseline magnesium intake — consistent with a repleting rather than pharmacological mechanism.

Dose Protocols and Timing

Recommended Dietary Intake and Supplemental Dosing

The Australian RDI for magnesium is:

  • Men 19–30: 400mg/day elemental magnesium
  • Men 31+: 420mg/day
  • Women 19–30: 310mg/day
  • Women 31+: 320mg/day

Supplemental doses used in the sleep and anxiety clinical literature generally range from 200–400mg elemental magnesium daily. This is the elemental magnesium content — not the total weight of the magnesium salt. A label that says "Magnesium Glycinate 600mg" contains approximately 60–70mg of elemental magnesium (glycinate is roughly 10–14% elemental by weight), so label reading requires attention to the elemental figure, not the total salt weight.

Practical Dosing for Sleep

For sleep specifically, the evidence and clinical convention supports:

  • 200–400mg elemental magnesium taken 30–60 minutes before bed
  • Magnesium glycinate is the preferred form for this application
  • Starting at the lower end (100–200mg elemental) for the first week or two allows adaptation; titrate upward to 300–400mg elemental based on individual response

Timing Considerations

For anxiety as the primary goal, splitting the dose morning and evening keeps magnesium availability more consistent across the day and mirrors the continuous NMDA receptor modulation needed for ongoing anxiolytic effect. Many practitioners prescribe the larger portion of the dose in the evening regardless of primary goal, as this aligns with the sleep-onset benefit and supports the natural evening reduction in cortisol.

Cofactors: Vitamin B6 and Intracellular Uptake

Vitamin B6 (pyridoxine and its active form pyridoxal-5-phosphate, P5P) significantly enhances intracellular magnesium uptake and retention. B6 facilitates the transport of magnesium ions across cell membranes, increasing the proportion of absorbed magnesium that actually enters cells rather than remaining in circulation.

A 2021 randomised trial published in PLOS ONE found that high-stress individuals supplementing with both magnesium and B6 showed significantly greater reductions in anxiety and stress scores than those taking magnesium alone, despite both groups receiving identical magnesium doses. The practical implication: if you are supplementing magnesium for anxiety or sleep and not seeing the expected benefit, assessing and supplementing B6 status (particularly in its active P5P form) is worth considering. Doses of B6 used in magnesium co-supplementation trials are typically 10–25mg P5P daily — well below levels associated with B6 toxicity (which occurs at sustained intakes above 200mg/day).

Magnesium-Rich Foods

While supplementation is often necessary to achieve therapeutic levels, dietary magnesium remains the foundation. The highest-magnesium foods per serving:

  • Pumpkin seeds (pepitas): 150mg per 30g serving — one of the densest food sources available
  • Hemp seeds: 90mg per 30g
  • Dark chocolate (70%+ cacao): 65mg per 30g
  • Almonds: 75mg per 30g
  • Spinach (cooked): 80mg per half cup
  • Cashews: 75mg per 30g
  • Black beans: 60mg per half cup cooked
  • Edamame: 50mg per half cup
  • Avocado: 44mg per whole medium avocado
  • Tofu (firm): 50mg per 100g

A diet anchored in green leafy vegetables, legumes, nuts and seeds, and whole grains provides a substantially better magnesium baseline than a processed food diet, reducing the supplemental dose required to achieve adequate status.

How to Test Magnesium Status

This is an area where the common test and the most accurate test diverge significantly.

Serum Magnesium: Commonly Ordered, Poorly Sensitive

Serum magnesium measures magnesium in the liquid portion of blood. The problem is that serum magnesium represents only about 1% of total body magnesium — the vast majority is stored intracellularly in muscle and bone. The body tightly regulates serum magnesium within a narrow range by drawing on bone stores as a buffer, which means serum magnesium can be "normal" while total body magnesium is substantially depleted.

A serum magnesium result in the normal reference range does not rule out clinically significant functional deficiency. A low serum magnesium reliably indicates significant deficiency — but the test misses many people in the grey zone of suboptimal status.

RBC Magnesium: Superior but Underutilised

Red blood cell (RBC) magnesium measures magnesium content within red blood cells — making this a more accurate reflection of cellular magnesium status than serum. RBC magnesium is the test most consistently used in magnesium research and recommended in functional medicine practice for assessing status relevant to sleep, anxiety, and metabolic function.

RBC magnesium is not routinely ordered on standard GP blood panels in Australia, but can be requested specifically from most major pathology providers. Understanding what each marker on a blood panel actually measures is covered in more detail in the guide to reading a blood panel.

Functional medicine reference ranges typically consider RBC magnesium values below 5.5–6.0 mg/dL as indicating suboptimal status, even where serum magnesium is normal.

Interactions with Calcium and Zinc

Calcium

Calcium and magnesium compete for intestinal absorption via shared transporter proteins. Taking high doses of calcium supplements simultaneously with magnesium can reduce magnesium absorption. For people supplementing both calcium and magnesium (common in bone health protocols), separating the doses by 2+ hours optimises absorption of both minerals. Dietary calcium from food does not significantly impair magnesium absorption in the same way that high-dose calcium supplements can.

The calcium-to-magnesium ratio in Western diets has shifted substantially over the past century — calcium fortification of processed foods has increased calcium intake while magnesium intake has declined, creating a ratio that some researchers argue contributes to elevated cardiovascular disease risk and more excitable nervous system states. Prioritising magnesium alongside calcium — rather than treating calcium alone as the bone mineral of concern — reflects the current evidence more accurately.

Zinc

Zinc and magnesium also compete for intestinal absorption when taken together in supplemental doses. High-dose zinc supplementation (above 25–30mg elemental) can reduce magnesium absorption. Taking zinc with food and magnesium before bed — or separating them by several hours — avoids the absorption competition in most practical contexts.

Reishi and NAD+ as Complementary Supports

Magnesium is a foundational support for sleep and anxiety, but it operates within a broader system. Two commonly combined additions are worth noting.

Reishi mushroom has its own sleep-relevant mechanisms — adenosine content that augments sleep pressure, and ganoderic acid-mediated HPA axis modulation that reduces evening cortisol. Reishi combined with magnesium glycinate in an evening protocol addresses sleep from both the mineral and neurotransmitter side (magnesium) and the adaptogenic and adenosinergic side (Reishi), without pharmacological interaction concerns.

NAD+ and cellular longevity pathways are increasingly relevant to sleep quality — NAD+ is required for SIRT1-dependent regulation of circadian rhythm genes (CLOCK, BMAL1), and age-related NAD+ decline contributes to circadian dysregulation and poorer sleep architecture in older adults. For anyone managing sleep issues alongside broader ageing and cellular health goals, addressing both magnesium status and NAD+ levels represents a mechanistically coherent protocol.

Selecting a Quality Magnesium Supplement

For sleep and anxiety applications, the criteria for a quality magnesium product are straightforward:

  • Form: Magnesium glycinate or bisglycinate as the primary magnesium source
  • Elemental magnesium declared: Look for the elemental magnesium content per dose, not just the total salt weight
  • Absence of magnesium oxide as a filler: Check the supplement facts panel — oxide is a common cost-reduction strategy in combination products
  • Third-party testing: Certificate of Analysis from an independent laboratory confirming elemental content and absence of heavy metals
  • B6 inclusion: Products combining magnesium glycinate with pyridoxal-5-phosphate (P5P) form of B6 offer the intracellular uptake advantage without requiring separate supplementation

Practitioner-grade magnesium glycinate formulations — the kind dispensed through integrative medicine practitioners and available through select health platforms like third-party-tested practitioner-grade supplement suppliers — offer consistent elemental content and verified form quality that is not always guaranteed in mass-market products. The difference between a well-formulated practitioner-grade magnesium glycinate and an underdosed or oxide-containing supplement is meaningful for clinical outcomes.

Frequently Asked Questions

Does magnesium actually help with sleep?

The research evidence is positive and mechanistically coherent, though the human RCT base is smaller than ideal. Magnesium supports sleep through at least three parallel mechanisms: enhancing GABA-A receptor sensitivity, blocking NMDA glutamate receptors to reduce neuronal overactivation, and reducing cortisol via HPA axis regulation. Clinical trials have demonstrated improvements in sleep onset latency, total sleep time, and sleep efficiency with supplementation, with the strongest effects in populations likely deficient at baseline. For most people with suboptimal magnesium status — common in the modern Australian diet and lifestyle context — supplementation with the right form (glycinate) at an effective elemental dose (200–400mg) is a well-supported first-line non-pharmaceutical sleep support strategy.

What is the best form of magnesium for anxiety?

Magnesium glycinate is the most evidence-aligned form for anxiety applications. The glycine component has independent inhibitory neurotransmitter activity at glycine receptors in the brainstem and spinal cord, complementing magnesium's GABA and NMDA mechanisms. Magnesium threonate is the preferred form if cognitive function and brain-specific magnesium levels are the primary goal alongside anxiety support. Magnesium citrate is a reasonable second-line option if glycinate is unavailable. Magnesium oxide should be avoided — its poor bioavailability means it is unlikely to meaningfully raise the intracellular magnesium levels relevant to anxiety mechanisms.

How long does magnesium take to work for sleep and anxiety?

Some people notice improved sleep quality within the first week, particularly if significantly deficient. The full benefit of magnesium supplementation — raising intracellular stores adequately to optimise GABA, NMDA, and HPA axis function — typically takes 4–6 weeks of consistent daily supplementation. Clinical trials showing significant anxiety and sleep improvements generally run for 6–8 weeks. Assessing magnesium on a one or two week trial is insufficient.

What dose of magnesium should I take for sleep?

200–400mg of elemental magnesium daily is the range used in clinical trials and most commonly recommended by naturopathic and functional medicine practitioners for sleep applications. The elemental figure is what matters — not the total weight of the magnesium salt. Start at the lower end and increase gradually. Take the dose 30–60 minutes before bed for sleep-specific applications. Magnesium glycinate is the preferred form.

Should I take magnesium with food?

Magnesium glycinate can be taken with or without food — it is generally well tolerated either way. Taking with a small amount of food may slightly improve absorption for some people. Avoid taking high-dose calcium or zinc supplements simultaneously — separate them by 2+ hours to avoid absorption competition.

Can I test my magnesium levels?

Serum magnesium is the standard test ordered on GP blood panels in Australia, but it is a poor measure of functional magnesium status because the body maintains serum levels at the expense of intracellular stores. Red blood cell (RBC) magnesium is substantially more accurate and reflects cellular magnesium status. It can be requested specifically from most Australian pathology providers. If you are experiencing symptoms consistent with magnesium insufficiency (muscle cramps, sleep disturbance, anxiety, fatigue) despite a normal serum magnesium result, asking specifically for RBC magnesium is a clinically appropriate next step.

Key Takeaways

Magnesium occupies a unique position in natural sleep and anxiety support — it operates through well-characterised neuroscientific mechanisms (GABA receptor modulation, NMDA receptor blockade, HPA axis regulation) that directly address the biology of poor sleep and heightened anxiety. Deficiency or suboptimal status is genuinely common in Australia, driven by dietary depletion, stress-driven excretion, and PPI medication use.

Form selection is clinically important: magnesium glycinate is the evidence-aligned choice for sleep and anxiety, delivering both elemental magnesium and sleep-supportive glycine with excellent bioavailability and gut tolerability. Magnesium threonate is the alternative when brain-specific magnesium and cognitive function are primary goals. Magnesium oxide is the form to avoid. Dosing at 200–400mg elemental daily, with vitamin B6 (P5P form) as a cofactor, optimises intracellular uptake and clinical outcomes. Testing via RBC magnesium rather than serum magnesium gives a more accurate picture of functional status.

For most Australians experiencing sleep difficulty or anxiety with no identified primary psychiatric cause, magnesium glycinate at an adequate elemental dose is a rational, well-evidenced, and safe starting point.

This article is for educational purposes and does not constitute medical advice. Always consult a qualified healthcare practitioner before starting any new supplement protocol, particularly if you have kidney disease, are taking medications, or have a pre-existing medical condition. Magnesium is generally well tolerated but can interact with certain medications including antibiotics, bisphosphonates, and diuretics.