Magnesium and the Brain: Which Form Actually Works?

TL;DR: Magnesium is a gatekeeper of NMDA receptor function and synaptic plasticity — two processes at the core of learning, memory, and neuroprotection. Subclinical deficiency is remarkably common, driven by declining soil mineral content, processed food consumption, and chronic stress. Among supplement forms, magnesium L-threonate (developed at MIT) is the only one demonstrated to meaningfully increase brain magnesium concentrations in animal research, with emerging human data showing cognitive benefits. Magnesium glycinate and taurate are well-absorbed alternatives with strong calming and sleep-promoting properties. Magnesium oxide and citrate are poorly suited for cognitive goals. Prioritize magnesium-rich whole foods, but targeted supplementation — especially with threonate or glycinate — is a reasonable strategy for most adults.

Introduction

Magnesium is involved in over 600 enzymatic reactions in the human body, yet when it comes to brain health, it rarely receives the same attention as omega-3 fatty acids or B vitamins. This is a significant oversight. Magnesium sits at the intersection of several processes that are foundational to cognitive function: it regulates the activity of NMDA receptors (the molecular switches that govern synaptic plasticity and memory formation), it modulates neurotransmitter release, it protects neurons from excitotoxic damage, and it is essential for the sleep architecture that consolidates learning.

The scale of the problem is not trivial. Data from the National Health and Nutrition Examination Survey (NHANES) consistently show that roughly 48 percent of the U.S. population consumes less magnesium than the Estimated Average Requirement. In Europe, surveys paint a similar picture. This is not outright clinical deficiency in most cases — it is chronic subclinical inadequacy, the kind that does not produce dramatic symptoms but may quietly erode cognitive performance, stress resilience, and sleep quality over years and decades.

Adding complexity to the issue is the fact that not all magnesium supplements are the same. The form of magnesium you take determines how much is absorbed, how much reaches the brain, and what additional effects (if any) come along with the carrier molecule. The difference between magnesium oxide and magnesium L-threonate, for example, is not a minor nuance — it is the difference between a supplement that largely stays in the gut and one that was specifically engineered to cross the blood-brain barrier.

This article covers what magnesium does in the brain, how widespread deficiency has become, which supplement forms actually deliver on their promises, the key research, and practical guidance for food sources, dosing, and sleep.

How Magnesium Works in the Brain

NMDA Receptor Regulation

The NMDA (N-methyl-D-aspartate) receptor is one of the most important molecular players in learning and memory. It is a type of glutamate receptor — a gate that opens in response to the brain’s primary excitatory neurotransmitter — and it has a unique feature: a voltage-dependent magnesium block.

At resting membrane potential, a magnesium ion physically sits inside the NMDA receptor channel, preventing calcium from flowing through. When a neuron is sufficiently depolarized (indicating that meaningful input is being received), the magnesium ion is expelled, the channel opens, and calcium floods in. This calcium influx triggers a cascade of intracellular signaling that strengthens the synapse — a process known as long-term potentiation (LTP), which is widely considered the cellular basis of learning and memory.

This means magnesium serves a dual role. It prevents the NMDA receptor from firing in response to background noise — protecting neurons from excessive calcium entry and excitotoxic damage. But it also allows the receptor to fire decisively when genuine signals arrive, enabling synaptic strengthening. Without adequate magnesium, this gating function degrades. NMDA receptors become more prone to tonic activation by ambient glutamate, leading to excessive calcium influx, oxidative stress, and neuronal damage — a process implicated in neurodegenerative diseases, anxiety, and chronic pain.

Synaptic Plasticity and Memory

The connection between magnesium and synaptic plasticity extends beyond the NMDA receptor mechanism alone. Magnesium influences the density and function of synapses, the release probability of neurotransmitters, and the structural remodeling of dendritic spines — the tiny protrusions on neurons where most excitatory synapses are located.

The groundbreaking work from Inna Bhatt, Guosong Liu, and colleagues at MIT (discussed in detail below) demonstrated that increasing brain magnesium levels in rats led to measurable increases in synapse density in the hippocampus and prefrontal cortex — two regions central to memory and executive function. These were not subtle effects. The treated animals showed enhanced short-term memory, improved long-term memory, and greater learning capacity on multiple behavioral tests.

Neurotransmitter Balance

Beyond NMDA receptor regulation, magnesium influences the broader balance of excitatory and inhibitory neurotransmission. It modulates the release of glutamate (the brain’s main excitatory neurotransmitter) and supports the function of GABA (the main inhibitory neurotransmitter). When magnesium levels are low, the brain shifts toward a more excitatory state — which may manifest as anxiety, difficulty relaxing, insomnia, heightened stress reactivity, and, in extreme cases, seizures.

This excitatory-inhibitory imbalance is one reason magnesium deficiency so often co-occurs with anxiety and sleep disturbances. It also explains why magnesium supplementation can have calming effects even in individuals without clinically diagnosed deficiency — it restores a balance that modern diets and lifestyles have subtly disrupted.

Neuroinflammation and Neuroprotection

Magnesium has well-documented anti-inflammatory properties in the brain. Low magnesium levels are associated with elevated C-reactive protein, increased NF-kB signaling, and higher levels of pro-inflammatory cytokines — all of which contribute to neuroinflammation, a process increasingly recognized as a driver of cognitive decline, depression, and neurodegeneration.

Mazur et al. (2007) demonstrated in animal models that magnesium deficiency triggered a systemic inflammatory response involving elevated substance P, TNF-alpha, and IL-6 — the same inflammatory mediators implicated in neurodegeneration. Adequate magnesium helps maintain the anti-inflammatory tone that protects neurons from chronic low-grade damage.

The Deficiency Epidemic

How Common Is Magnesium Inadequacy?

The numbers are striking. Analysis of NHANES data by Rosanoff, Weaver, and Rude (2012), published in Nutrition Reviews, found that approximately 48 percent of the U.S. population consumes less magnesium than the Estimated Average Requirement (EAR). The Recommended Dietary Allowance (RDA) is 420 mg/day for adult men and 320 mg/day for adult women; the EAR (the level estimated to meet the needs of 50 percent of the population) is lower still, meaning that nearly half of Americans do not even meet this more conservative threshold.

In Europe, the situation is comparable. A systematic review by Olza et al. (2017), published in Nutrients, found inadequate magnesium intake across multiple European countries, with particularly low intakes in adolescents and older adults.

Why Is Deficiency So Widespread?

Several converging factors explain the modern magnesium gap:

Soil depletion. Intensive agricultural practices have reduced the mineral content of soil in many regions. Studies comparing crop mineral content over the past 50 to 70 years — including a widely cited analysis by Thomas (2007) — have documented declines in the magnesium content of vegetables and grains. The food supply delivers less magnesium per calorie than it did for previous generations.

Processed food consumption. Magnesium is concentrated in whole grains, nuts, seeds, and leafy greens — precisely the food categories displaced by ultra-processed foods, which typically have very low magnesium content. Grain refining alone strips approximately 80 percent of the magnesium from wheat.

Chronic stress. Stress drives magnesium excretion through the kidneys. Cortisol and catecholamines increase urinary magnesium loss, creating a vicious cycle: stress depletes magnesium, and low magnesium reduces the body’s ability to buffer the physiological effects of stress, which in turn drives further depletion. Seelig (1994) described this feedback loop in detail in the Journal of the American College of Nutrition.

Medications. Proton pump inhibitors (PPIs), commonly prescribed for acid reflux, are well-established causes of magnesium depletion with chronic use. Diuretics, certain antibiotics, and some diabetes medications can also reduce magnesium levels.

Water softening. Hard water historically contributed meaningful magnesium intake. Modern water treatment and widespread use of filtered or softened water have eliminated this source for many populations.

Measuring Magnesium Status

One of the challenges with magnesium is that standard blood tests are poor indicators of true status. Serum magnesium — the most commonly ordered test — reflects less than one percent of total body magnesium, since 99 percent is stored intracellularly (in bone, muscle, and soft tissue). A person can have normal serum magnesium while being significantly depleted at the cellular and tissue level. This means that the true prevalence of magnesium inadequacy is almost certainly higher than what dietary intake surveys alone suggest.

More sensitive measures, such as red blood cell (RBC) magnesium, ionized magnesium, or magnesium loading tests, exist but are not routinely ordered in clinical practice. This diagnostic gap contributes to the widespread under-recognition of the problem.

The Slutsky/MIT Threonate Research

The most significant scientific contribution to the magnesium-cognition conversation came from the laboratory of Guosong Liu at MIT and Tsinghua University. In a landmark 2010 paper published in Neuron, Slutsky et al. reported on a newly developed compound — magnesium L-threonate (MgT) — that was specifically engineered to increase magnesium concentrations in the brain.

The Problem MgT Was Designed to Solve

Previous research had established that raising brain magnesium levels could enhance synaptic plasticity and cognitive function. However, conventional magnesium supplements had a fundamental limitation: they raised serum magnesium, but brain magnesium levels did not increase proportionally. The blood-brain barrier tightly regulates magnesium transport, and simply flooding the bloodstream with magnesium (via oxide, citrate, or other common forms) did not effectively increase cerebrospinal fluid or brain tissue concentrations.

Slutsky, Liu, and colleagues systematically tested multiple magnesium compounds for their ability to increase intracellular magnesium in neuronal cultures. They found that L-threonate, a metabolite of vitamin C, served as an exceptionally effective carrier that enhanced magnesium transport into neurons. They then developed magnesium L-threonate and tested it in vivo.

Key Findings

The results published in Neuron were remarkable:

Increased brain magnesium. Oral supplementation with MgT raised cerebrospinal fluid magnesium levels in rats by approximately 15 percent — a significant increase that other magnesium forms failed to achieve at equivalent doses.

Enhanced synaptic density. MgT-treated rats showed increased density of functional synapses in the hippocampus and prefrontal cortex, measured by both electrophysiology and structural imaging.

Improved short-term and long-term memory. On multiple behavioral tests — including novel object recognition, T-maze, and fear conditioning — MgT-treated rats outperformed controls. Notably, both young and aged rats showed improvements, though the magnitude of benefit was greater in aged animals.

Enhanced synaptic plasticity. NMDA receptor signaling and long-term potentiation were significantly enhanced in the treated animals, consistent with the known role of magnesium in NMDA receptor gating.

Human Evidence

Following the animal work, human studies began to appear. A randomized, double-blind, placebo-controlled trial by Liu et al. (2016), published in the Journal of Alzheimer’s Disease, examined the effects of the proprietary MgT formulation (marketed as Magtein or MMFS-01) in older adults (ages 50 to 70) with subjective cognitive complaints. Over 12 weeks, participants receiving MgT showed significant improvements on a composite of cognitive tests assessing executive function and working memory compared to placebo. Brain age, as estimated by cognitive performance, was effectively reversed by an average of approximately nine years in the treatment group.

While this study was modest in size and funded by the company behind the compound, the effect sizes were large enough to attract attention from the broader research community. Additional studies and independent replications are ongoing.

Supplement Forms Compared

This is where practical decision-making gets critical. Magnesium supplements vary enormously in their elemental magnesium content, bioavailability, ability to reach the brain, and side effect profiles.

Magnesium L-Threonate

Elemental magnesium: Low (~8% by weight, meaning you need approximately 2,000 mg of the compound to get 144 mg of elemental magnesium). Bioavailability: High, with uniquely high brain penetration. Key evidence: The only form with published evidence (Slutsky et al., 2010; Liu et al., 2016) demonstrating increased brain magnesium levels and cognitive benefits. Best for: Cognitive enhancement, memory support, age-related cognitive concerns. Downsides: Expensive. Low elemental magnesium content means it is not the most efficient way to address total body magnesium deficiency. Should ideally be combined with another form if overall magnesium status is a concern.

Magnesium Glycinate (Bisglycinate)

Elemental magnesium: ~14% by weight. Bioavailability: High. The glycine chelate protects magnesium from binding to phytates and other inhibitors in the gut, resulting in excellent absorption with minimal gastrointestinal side effects. Key evidence: Strong absorption data. Glycine itself is an inhibitory neurotransmitter co-agonist at the NMDA receptor and has well-documented calming and sleep-promoting effects. Bannai et al. (2012) showed that glycine supplementation improved subjective sleep quality and reduced daytime sleepiness in a randomized, double-blind, placebo-controlled study published in Sleep and Biological Rhythms. Best for: General magnesium repletion, anxiety, sleep quality, and individuals with sensitive stomachs. Downsides: No specific evidence for raising brain magnesium above baseline (as opposed to correcting deficiency). More expensive than oxide or citrate, though much cheaper than threonate.

Magnesium Taurate

Elemental magnesium: ~9% by weight. Bioavailability: Good. Taurine, the carrier amino acid, has independent neuroprotective and anxiolytic properties. It modulates GABAergic neurotransmission and has been shown to stabilize cell membranes. Key evidence: Limited clinical trials specific to cognition, but taurine’s neuroprotective effects are well-established in preclinical research. Some cardiologists favor magnesium taurate for cardiovascular applications due to taurine’s role in cardiac electrophysiology. Best for: Combined cardiovascular and nervous system support, anxiety, and individuals seeking a calming magnesium form. Downsides: Limited direct cognitive research. Low elemental magnesium content.

Magnesium Citrate

Elemental magnesium: ~16% by weight. Bioavailability: Moderate. Better absorbed than oxide, but known for its osmotic laxative effect, which makes it poorly tolerated at higher doses. Key evidence: Widely studied for general magnesium repletion and constipation relief. Walker et al. (2003) demonstrated improved absorption compared to oxide in a direct comparison study published in Magnesium Research. Best for: General magnesium repletion, constipation. Downsides: Gastrointestinal side effects (loose stools, diarrhea) at doses that would be needed for meaningful repletion. Not specifically brain-targeted.

Magnesium Oxide

Elemental magnesium: ~60% by weight (highest of all forms). Bioavailability: Poor. Studies consistently show absorption rates of only 4 to 5 percent. Firoz and Graber (2001) published a direct comparison in Magnesium Research showing that magnesium oxide had the lowest fractional absorption among common oral forms. Best for: It is cheap and widely available. Primarily useful as a laxative or antacid. Downsides: Poorly absorbed, poorly tolerated at meaningful doses, and essentially useless for raising intracellular or brain magnesium levels. Despite being the most commonly sold form, it is the worst choice for anyone with cognitive or neurological goals.

Quick Comparison

Magnesium and Sleep

The connection between magnesium and sleep is one of the most practically relevant aspects of this mineral for cognitive health. Sleep is not a passive state — it is the period during which the brain consolidates memories, clears metabolic waste (including beta-amyloid, via the glymphatic system), repairs cellular damage, and rebalances neurotransmitter systems. Anything that impairs sleep quality directly undermines cognitive function, a relationship explored in our guide on sleep and diet.

Magnesium supports sleep through multiple mechanisms. It enhances GABAergic tone (promoting relaxation and reducing neural excitability), it helps regulate the hypothalamic-pituitary-adrenal (HPA) axis (reducing cortisol-driven wakefulness), and it is involved in the synthesis and regulation of melatonin.

A randomized, double-blind, placebo-controlled trial by Abbasi et al. (2012), published in the Journal of Research in Medical Sciences, studied magnesium supplementation (500 mg/day of magnesium oxide, despite its poor bioavailability) in elderly participants with insomnia. Even with this suboptimal form, the supplemented group showed significant improvements in sleep time, sleep efficiency, serum melatonin, and serum cortisol levels compared to placebo.

Held et al. (2002) demonstrated that magnesium supplementation increased slow-wave sleep (deep sleep) and reduced nocturnal cortisol levels in a study published in Pharmacopsychiatry. Slow-wave sleep is the phase most critical for memory consolidation and growth hormone release.

Given these findings, magnesium glycinate — which combines well-absorbed magnesium with glycine’s independent sleep-promoting effects — is arguably the optimal form for individuals whose primary concern is sleep quality. Magnesium L-threonate may also improve sleep, though through its central nervous system effects rather than direct GABAergic modulation.

Food Sources of Magnesium

Before reaching for supplements, it is worth understanding which foods deliver the most magnesium per serving:

1. Pumpkin seeds (1 oz / 28 g): ~156 mg The single most concentrated commonly available food source. A small handful provides roughly 37 to 49 percent of the RDA. Also rich in zinc, iron, and healthy fats.

2. Almonds (1 oz / 28 g): ~80 mg A convenient and widely available source. Cashews are comparable at approximately 74 mg per ounce.

3. Spinach (1 cup cooked): ~157 mg Leafy greens are excellent sources, with Swiss chard (~150 mg per cooked cup) close behind. The magnesium is part of chlorophyll — the molecule that makes plants green — which is why dark leafy greens are consistently the best vegetable sources.

4. Dark chocolate (1 oz / 28 g, 70%+ cacao): ~65 mg A legitimately good source, provided it is high-cacao dark chocolate. Milk chocolate is not comparable.

5. Black beans (1 cup cooked): ~120 mg Legumes broadly are strong magnesium sources. Lentils and chickpeas provide roughly 70 to 80 mg per cooked cup.

6. Avocado (1 medium): ~58 mg Also provides potassium, fiber, and monounsaturated fats.

7. Whole grains (1 cup cooked quinoa): ~118 mg Brown rice (~84 mg per cooked cup), oats, and other intact whole grains contribute meaningfully. Refined grains do not — the refining process strips the magnesium-rich bran and germ.

8. Fatty fish (3 oz / 85 g cooked salmon): ~26 mg Modest per serving, but fish also provides omega-3 fatty acids, making it a multifunctional brain food.

The key dietary pattern is clear: whole foods, especially seeds, nuts, leafy greens, legumes, and whole grains, are the foundation of adequate magnesium intake. Ultra-processed diets, which displace these foods, are a recipe for chronic insufficiency.

Who Needs More Magnesium

Older Adults

Magnesium absorption decreases with age while urinary excretion increases. Intestinal absorption in adults over 60 can be 20 to 30 percent lower than in younger adults. Simultaneously, age-related declines in NMDA receptor function and synaptic plasticity make adequate magnesium even more critical for preserving cognitive function. Older adults are the population most likely to benefit from both dietary optimization and targeted supplementation.

People Under Chronic Stress

The stress-magnesium depletion cycle is one of the most underappreciated feedback loops in nutritional neuroscience. Chronic psychological or physiological stress increases magnesium excretion, and the resulting low magnesium reduces the body’s capacity to dampen the stress response. Boyle, Lawton, and Dye (2017) published a systematic review in Nutrients reporting that magnesium supplementation had a beneficial effect on subjective anxiety in anxiety-prone populations, though the overall evidence base was graded as modest.

Athletes and Physically Active Individuals

Intense exercise increases magnesium requirements through sweat losses and elevated metabolic demand. Nielsen and Lukaski (2006) published a comprehensive review in Magnesium Research documenting the relationship between exercise-induced magnesium depletion and impaired performance. Athletes who fail to replace magnesium losses may experience not only physical performance decrements but also impaired sleep and cognitive recovery.

People Taking Magnesium-Depleting Medications

Chronic PPI use (omeprazole, esomeprazole, and related drugs) is one of the most common causes of iatrogenic magnesium depletion. Loop diuretics and thiazide diuretics also increase urinary magnesium loss. Anyone on these medications long-term should discuss magnesium monitoring and supplementation with their physician.

Individuals with High Alcohol Intake

Alcohol increases renal magnesium excretion and reduces intestinal absorption. Chronic heavy drinking is a well-established cause of magnesium depletion, contributing to the neurological complications associated with alcohol use disorder.

Dosing Recommendations

For general magnesium repletion, the goal is to reach or modestly exceed the RDA: 420 mg/day for adult men, 320 mg/day for adult women. This includes magnesium from both food and supplements.

For targeted supplementation:

• Magnesium L-threonate: The dose used in the Liu et al. (2016) human cognitive trial was approximately 1,500 to 2,000 mg of the compound per day (providing 144 mg of elemental magnesium), typically divided into two doses — one in the morning and one in the evening. Because of the low elemental magnesium content, many people pair threonate with glycinate or another well-absorbed form to address total body magnesium needs simultaneously.

• Magnesium glycinate: 200 to 400 mg of elemental magnesium per day, often taken in the evening due to its calming and sleep-promoting effects. Glycinate is well tolerated even at higher doses and rarely causes GI distress.

• Magnesium taurate: 200 to 400 mg of elemental magnesium per day. Similar dosing to glycinate, with the added benefit of taurine’s cardiovascular and neuroprotective effects.

The Tolerable Upper Intake Level (UL) for supplemental magnesium (from supplements and pharmacological agents, not food) is 350 mg/day, as established by the National Academy of Medicine. This limit was set based on the osmotic diarrhea threshold for poorly absorbed forms (primarily oxide and citrate). Well-absorbed chelated forms (glycinate, threonate, taurate) are generally tolerated at doses exceeding this threshold without GI effects, though it is reasonable to use the UL as a general guideline.

A practical combined protocol for cognitive goals might include: magnesium L-threonate (1,500 to 2,000 mg of the compound, taken as two divided doses) plus magnesium glycinate (200 mg elemental, taken in the evening). This provides brain-targeted magnesium through the threonate while ensuring adequate total body repletion through the glycinate.

Practical Takeaway

Magnesium is not a luxury supplement — it is a foundational mineral that most adults are not consuming in adequate amounts. Its role in NMDA receptor function, synaptic plasticity, sleep, and stress resilience makes it one of the most directly relevant nutrients for brain health. Here is what to do:

1. Build your diet around magnesium-rich whole foods. Pumpkin seeds, almonds, dark leafy greens, legumes, whole grains, and dark chocolate should feature regularly. Every meal that displaces processed food with whole food moves the needle.

2. Choose the right supplement form for your goal. Magnesium L-threonate is the top choice for cognitive enhancement and memory support. Magnesium glycinate is the best all-around option for repletion, anxiety, and sleep. Magnesium oxide is essentially worthless for cognitive or systemic goals despite being the most commonly sold form.

3. Consider combining forms. Threonate for the brain plus glycinate for overall repletion and sleep is a well-reasoned combination that covers multiple bases without excessive cost.

4. Take magnesium in the evening if sleep is a priority. The calming, GABAergic, and cortisol-lowering effects of magnesium (particularly glycinate) are best leveraged when taken one to two hours before bed.

5. Address depletion drivers, not just intake. If you are under chronic stress, taking PPIs, exercising intensively, or consuming significant alcohol, your magnesium needs are elevated beyond what the standard RDA reflects. Adjust accordingly.

6. Do not rely on serum magnesium testing to rule out inadequacy. Standard blood tests miss the vast majority of magnesium-depleted individuals. RBC magnesium is a somewhat better measure, but clinical context (symptoms, dietary history, medication use) is more informative than any single lab value.

Frequently Asked Questions

Can magnesium help with anxiety?

There is meaningful evidence supporting this. Boyle, Lawton, and Dye (2017) conducted a systematic review suggesting magnesium supplementation may reduce subjective anxiety, though the evidence was stronger for individuals with existing anxiety vulnerability than for the general population. The mechanism is plausible: magnesium promotes GABAergic tone, dampens HPA axis activity, and reduces NMDA receptor overactivation — all of which counteract the neurobiological profile of anxiety. Magnesium glycinate and taurate are the best-suited forms for this application.

How long does it take for magnesium supplementation to show effects?

For sleep and relaxation effects, many people notice improvements within the first one to two weeks. For cognitive benefits from magnesium L-threonate, the human trial by Liu et al. (2016) assessed outcomes at six and twelve weeks, with significant differences emerging by week six. Correcting systemic magnesium depletion, depending on severity, can take four to eight weeks of consistent supplementation.

Can I take too much magnesium?

The primary symptom of excessive magnesium supplementation is osmotic diarrhea — loose stools caused by unabsorbed magnesium drawing water into the intestines. This is self-limiting and resolves with dose reduction. It is most common with oxide and citrate forms and rare with glycinate or threonate. True magnesium toxicity (hypermagnesemia) is essentially impossible with oral supplementation in individuals with normal kidney function. It is a concern only with intravenous magnesium or in patients with renal failure.

Is magnesium L-threonate worth the price?

If your primary goal is cognitive enhancement or you are concerned about age-related memory decline, the evidence supporting threonate’s unique ability to increase brain magnesium levels makes a reasonable case for the premium. If your main concerns are sleep, general repletion, or anxiety, magnesium glycinate delivers excellent results at a fraction of the cost. The two forms are complementary rather than competing — many people benefit from using both.

Should I take magnesium with or without food?

Magnesium supplements can be taken with or without food. Taking them with a meal may slightly improve absorption and reduce the small risk of GI upset. Chelated forms (glycinate, threonate, taurate) are well absorbed regardless of food intake. Oxide and citrate are more likely to cause GI issues on an empty stomach.

Does magnesium interact with any medications?

Magnesium can reduce the absorption of certain antibiotics (tetracyclines, fluoroquinolones) and bisphosphonates if taken simultaneously. Separate magnesium supplementation from these medications by at least two hours. Magnesium can also potentiate the effects of muscle relaxants and blood pressure medications. Anyone on prescription medications should discuss magnesium supplementation with their physician.

Sources

• Slutsky, I., Abumaria, N., Wu, L. J., Bhatt, I., Bhatt, C. P., Bhatt, D. H., … & Liu, G. (2010). Enhancement of learning and memory by elevating brain magnesium. Neuron, 65(2), 165–177.

• Liu, G., Weinger, J. G., Lu, Z. L., Xue, F., & Sadeghpour, S. (2016). Efficacy and safety of MMFS-01, a synapse density enhancer, for treating cognitive impairment in older adults: a randomized, double-blind, placebo-controlled trial. Journal of Alzheimer’s Disease, 49(4), 971–990.

• Rosanoff, A., Weaver, C. M., & Rude, R. K. (2012). Suboptimal magnesium status in the United States: are the health consequences underestimated? Nutrition Reviews, 70(3), 153–164.

• Abbasi, B., Kimiagar, M., Sadeghniiat, K., Shirazi, M. M., Hedayati, M., & Rashidkhani, B. (2012). The effect of magnesium supplementation on primary insomnia in elderly: a double-blind placebo-controlled clinical trial. Journal of Research in Medical Sciences, 17(12), 1161–1169.

• Held, K., Antonijevic, I. A., Kunzel, H., Uhr, M., Wetter, T. C., Golly, I. C., … & Murck, H. (2002). Oral Mg(2+) supplementation reverses age-related neuroendocrine and sleep EEG changes in humans. Pharmacopsychiatry, 35(4), 135–143.

• Boyle, N. B., Lawton, C., & Dye, L. (2017). The effects of magnesium supplementation on subjective anxiety and stress — a systematic review. Nutrients, 9(5), 429.

• Seelig, M. S. (1994). Consequences of magnesium deficiency on the enhancement of stress reactions; preventive and therapeutic implications. Journal of the American College of Nutrition, 13(5), 429–446.

• Mazur, A., Maier, J. A., Rock, E., Gueux, E., Nowacki, W., & Rayssiguier, Y. (2007). Magnesium and the inflammatory response: potential physiopathological implications. Archives of Biochemistry and Biophysics, 458(1), 48–56.

• Bannai, M., Kawai, N., Ono, K., Nakahara, K., & Murakami, N. (2012). The effects of glycine on subjective daytime performance in partially sleep-restricted healthy volunteers. Frontiers in Neurology, 3, 61.

• Firoz, M., & Graber, M. (2001). Bioavailability of US commercial magnesium preparations. Magnesium Research, 14(4), 257–262.

• Walker, A. F., Marakis, G., Christie, S., & Byng, M. (2003). Mg citrate found more bioavailable than other Mg preparations in a randomised, double-blind study. Magnesium Research, 16(3), 183–191.

• Nielsen, F. H., & Lukaski, H. C. (2006). Update on the relationship between magnesium and exercise. Magnesium Research, 19(3), 180–189.

• Olza, J., Aranceta-Bartrina, J., Gonzalez-Gross, M., Ortega, R. M., Serra-Majem, L., Varela-Moreiras, G., & Gil, A. (2017). Reported dietary intake and food sources of zinc, selenium, and vitamins A, E and C in the Spanish population: findings from the ANIBES study. Nutrients, 9(7), 697.

• Thomas, D. (2007). The mineral depletion of foods available to us as a nation (1940–2002) — a review of the 6th edition of McCance and Widdowson. Nutrition and Health, 19(1-2), 21–55.