Nutrients That May Assist

Magnesium

Magnesium glycinate dihydrate (MagActive^® Magnesium bisglycinate*)

Taurine

L-Glutamine

Potassium

Potassium citrate

Calcium

Calcium citrate

Vitamin C

Calcium ascorbate

Vitamin B1

Thiamine hydrochloride

Vitamin B2

Riboflavin sodium phosphate

Vitamin B3

Nicotinamide

Vitamin B5

Calcium pantothenate

Vitamin B6

Pyridoxal 5-phosphate

Zinc

Zinc amino acid chelate (Meta Zn ^® - Zinc bisglycinate)

Actions

• · Nervous system support
• · Anxiolytic
• · Reduces the effects of physical and psychological stress
• · Alkalising

Clinical Applications

• · Reduce stress and anxiety
• · Supporting healthy mood

Clinical Overview

Magnesium, taurine and glutamine are key nutrients that reduce the effects of physical and psychological stress on the body. In addition, sufficient amounts of B group vitamins are important for the production of stress-response hormones. Magnesium in particular plays apivotal role in a number of functions in the human body, many of which are brain related. For example, magnesium can reduce the effect of N-methyl-D-aspartate (NMDA) receptor * Contains MagActive®, an exclusive, enhanced absorption magnesium. stimulation, by acting as a voltage-gated antagonist at the glutamate NMDA receptor (Figure1). With chronic stress increasing the hypothalamic NMDA receptor expression, deficiency ofmagnesium can impact mood with symptoms such as depression, apathy and/or anxiety.Furthermore, studies have demonstrated increased rates of depression in individuals with lowerlevels of serum zinc; with an inverse relationship seen between lowered zinc status and higherdepressive scores. Potassium citrate and glutamine, which enhance the acid-alkaline balance of the body, may also be beneficial for low-grade metabolic acidosis.

Figure 1: Magnesium reduces the effect of NMDA receptor stimulation by acting as a voltage-gated antagonist at the glutamate NMDA receptor in the brain.

Background Information

Magnesium, the Mental Mineral

Magnesium regulates neuronal excitability and membrane fluidity and is arguably the most important micronutrient in relation to nerve and mental function. Magnesium is a cofactor for more than 300 enzymatic reactions in the body1,2 and with many of magnesium’s enzymatic processes being brain-related, deficiency has been associated with a large range of symptoms. These include psychological changes such as apathy, depression, confusion, agitation, and delirium.3 Furthermore, low magnesium status has been correlated with other mental health disorders, including anxiety,4 psychosis,5 and stress-related conditions such as phobias, tics, obsessive-compulsive and dissociative disorders, hyperexcitability, hyperemotivity and other negative emotional states.6 Magnesium deficiency is common, with an Australian Health Survey finding 72% of 14 to 18-year-old females, and an average of just under 40% of all Australian adults, consuming inadequate amounts of magnesium daily.7 In addition, dietary factors such as high intakes of fat, calcium, coffee and strong tea can worsen magnesium status, by either reducing absorption or enhancing elimination.8

Magnesium Bioavailability

MagActive®, Magnesium bisglycinate a next-generation magnesium bisglycinate, isengineered for superior potency and absorption, offering up to 35% greater absorption thanconventional magnesium bisglycinate (Figure 2)9 and 4 x times more than magnesium oxide.10

Figure 2. MagActive® 35% greater absorption than other forms of magnesium bisglycinate.11

Its fully chelated structure prevents binding with water molecules and dietary antinutrients suchas phytates, ensuring more magnesium reaches the gastrointestinal membrane for absorptionwhile remaining gentle on the gut (Figure 3).12

Magnesium bisglycinate is absorbed at the epithelial border of the small intestine through bothpassive paracellular pathways (TRMP7) and active transport via the MagT1 transporter.13 Thepresence of glycine enhances passive absorption mechanisms and facilitates uptake throughdipeptide channels (Figure 3).14

Figure 3: MagActive® high potency magnesium bisglycinate with superior absorption.15,16,17,18

Nervous System Support

Magnesium supplementation has been shown to affect all elements of the body’s reactionsto stress, exerting a neuroprotective effect. For example, in the event of deficiency, magnesium repletion reversed the increased stress sensitivity and pharmacological loading of magnesium induced resistance to neuropsychological stressors such as glutamate† excitotoxicity.19

With the ability to inhibit the release of excitatory neurotransmitters, magnesium acts as avoltage-gated antagonist at the glutamate, NMDA receptor.20 When the NMDA receptor isover-activated, it can result in increased cell death and increased excitotoxicity whichultimately results in neurological changes. For example, low levels of magnesium have beenassociated with hippocampal atrophy. Further, supplementation demonstrated an increase inbrain-derived neurotrophic factor (BDNF) along with hippocampal neurogenesis.21
Psychological stress is one of the states that can result in the release of glutamate (which exerts excitatory effects), and appears to be mediated, at least in part, via glucocorticoids, which can both increase glutamate levels and contribute to the neuronal damage.22

In a state of deficiency, the neuronal requirements for magnesium may not be met, causing the neuronal alterations that can result in low mood.23 Acute stress has been associated with increased plasma magnesium levels due to the release of stress hormones (catecholamines and corticosteroids), and increased urinary excretion.24 This results from the body shifting magnesium from the intracellular to extracellular space as a protective mechanism to reduce the effects of stress.25

With extended periods of stress resulting in progressively deficient magnesium levels, a vicious cycle can develop where stress increases cellular magnesium losses, thus resulting in an exaggerated stress response.26 Moreover, magnesium deficiency is itself a stress to the body, as it has been linked to promoting catecholamine release, promoting proinflammatory factors, and disrupting sleep patterns.27 Therefore, it is suitable to say that magnesium deficiency is both a cause and a consequence of stress.

Anxiolytic

The anxiolytic effects of magnesium are similarly attributed to the reduction of glutamate activity, and the increased actions of the gamma-aminobutyric acid (GABA)-ergic systems.28
This results in a soothing effect on the entire stress response system,29 as GABA acts as thebody’s primary calming influence, working to control and balance the effects of glutamate.Magnesium ions regulate calcium ions as part of nerve cell conduction activity (Figure 5).30
However, magnesium deficiency can cause NMDA-coupled calcium channels to remainopened, leading to further neuronal injury and neurological dysfunction.31 The end result isglutamate-induced neuro-excitotoxicity, which may manifest as anxiety and other mood andbehavioural disorders.32

Figure 5: The role of magnesium in regulating calcium ion flow and neurotransmission.33

Moreover, animal studies of zinc deficiency display increased states of aggression and anxiety, with anxiety-like behaviours shown to develop within just two weeks of being fed a zincdeficientdiet.34 Poor stress resilience along with higher corticosterone levels was apparent in zinc deficient animals exposed to stressors compared with controls, suggesting zinc to be an important factor in both the modulation of anxiety and stress responses. Additionally, taurine was found to exert an anxiolytic-like effect in animal models of anxiety.35
Taurine was administered 30 minutes before the stress tests, and was demonstrated to havesignificant anxiolytic-like effects by acting as an anti-anxiety agent in the central nervoussystem.36

Reduces the Effects of Physical and Psychological Stress

Taurine has modulatory effects on the magnitude of the stress response in the brain. Taurine has been described as a unique psychopharmacological compound,37 which can act as a neuromodulator, an osmoregulatory, a regulator of cytoplasmic calcium levels, a neuroprotectant, and a trophic factor in development.38 It is involved in the regulation of calcium movement during depolarisation and maintaining the structural integrity of the neuronal membrane.39 Animal studies indicate taurine exerts anxiolytic40 and antidepressant-like effects, with no alteration of locomotor activity.41

Taurine is found abundantly in the brain.42 It has been shown to act as an inhibitory neurotransmitter or neuromodulator, thus protecting against glutamate excitotoxicity, and may directly interact at the glutamate NMDA receptor to suppress glutamatergictransmission.43 Furthermore, taurine has been shown to be supportive when treating addictions, displaying ability to decrease extracellular basal levels of dopamine and prevent acute increases in the synaptic levels of dopamine within the nucleus accumbens;44 the area of the brain involved in reward, motivation and impulsivity.

Zinc is required throughout the human body for a myriad of chemical reactions necessary for normal body functioning.45 For example, it is well-established that zinc supplementation provides antidepressant-like effects, with zinc deficient diets associated with low moods.46 Zinc has been shown to increase BDNF, which is recognised as a target implicated in the aetiology of depression.47 It has been demonstrated that BDNF plays a significant role in supporting patients with low mood, with a meta-analysis showing depressive patients have decreased serum and plasma BDNF levels.48 Zinc is highly concentrated in the synaptic vesicles of specific neurons, and regulates the release of neurotransmitters. Specific neurons, known as ZEN neurons, which are primarily involved with the regulation of glutamate and GABA transmission have been shown to increase synaptic dopamine levels, thereby allowing dopamine to stay and engage with receptors longer within the synapse. Therefore, zinc is considered an important regulator of dopamine transporter function.49

Additionally, zinc acts as an inhibitory neuromodulator of glutamate release, regulating NMDA receptors.50 The areas of the brain in which functional and structural changes occur in the course of low mood are areas of particularly high concentration of glutamatergic neurons sequestering zinc, and the subsequent NMDA receptors are characterised by a high degree of susceptibility to the inhibitory effects of zinc.51 This reflects a further need for sufficient zinc to reduce the excitotoxicity associated with the pathophysiology of mood disorders.

Moreover, deficiency of thiamine has been associated with decreased glutamate uptake in the brain and increased levels in the cerebrospinal fluid.52 Up to 85% of thiamine content in meat and vegetables is lost with cooking and processing, and there is significant loss with refining of grains.53

L-Glutamine is the most abundant extracellular amino acid and a precursor for glutamate and GABA. It is quantitatively the most important fuel for intestinal tissue, while other functions include its role as a precursor for glutathione production,‡ neurotransmitter synthesis, and its function in controlling acid-base balance.54

Vitamin C (ascorbic acid) is required for the synthesis of neurotransmitters (including noradrenaline and serotonin), as well as the synthesis and catabolism of tyrosine.55 Vitamin C is maintained at elevated levels in the central nervous system and may act as a neuromodulator, facilitating the release of neurotransmitters and inhibiting glutamate binding to receptors.56 The presence of reactive oxygen species (ROS) may result in oxidative damage in the central nervous system, which has been demonstrated to play a role in the development of depressive symptoms. The antioxidant properties of vitamin C can assist in reducing ROS, which have been shown to be elevated during chronic stress.57

There are many forms of vitamin C, with calcium ascorbate being the calcium mineral salt of ascorbic acid. This form is buffered and less acidic than ascorbic acid itself. Therefore, it is better tolerated by those who may experience abdominal pain or diarrhoea with ascorbicacid.58

Riboflavin sodium phosphate (vitamin B2), and its derivative flavin adenine dinucleotide (FAD),functions as a coenzyme for a wide variety of different reactions in intermediary metabolism in the body.59 In particular, riboflavin is involved in the activation of vitamin B6 and folate, which ‡ Glutathione is the most important intracellular antioxidant, protecting cellular organelles, including the nucleus and DNA, from oxidative damage. are essential cofactors for the formation and metabolism of neurotransmitters.60 Due to this, itis likely that the production of stress supporting neurotransmitters will be affected without sufficient vitamin B2, resulting in subsequent changes in mood.

Niacin (vitamin B3) is a generic term for nicotinic acid and nicotinamide (niacinamide).Approximately 200 enzymes in the body require, as coenzymes, the nucleotides of niacin: nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotide phosphate (NADP). Niacin is therefore important for many biosynthetic pathways. The reduced form of NADH is used for folate metabolism,61 with niacin also able to be converted from tryptophan; a deficiency of niacin can likely impact on the production of serotonin, thereby leading to low mood.62

Pantothenic acid (vitamin B5), as part of coenzyme A (CoA) and 4’-phosphopantethiene, participates in nutrient metabolism, resulting in the production of energy and synthetic reactions for the production of many vital compounds within the body. These include bile salts, fatty acids and steroid hormones.63 Vitamin B5’s role in the synthesis of acetylcholine makes it imperative for stress resilience, with CoA also being required for adrenal cortex function and the synthesis of cortisone.64

Pyridoxine (vitamin B6) has many important roles, one of which is in the synthesis of taurine.65 In its coenzyme form, pyridoxal phosphate (PLP), it is associated with over 100 enzymes, the majority of which are involved in amino acid metabolism.66 Vitamin B6 is fundamental to the production of many neurotransmitters67 and is specifically involved in the creation of histidine to histamine, tryptophan to serotonin, glutamate to GABA, and dihydroxyphenylalanine to dopamine,68 as well as the synthesis of adrenaline and noradrenaline.69 Therefore, deficiency in this nutrient is often associated with psychological disturbances such as mood alterations,70 with signs of deficiency including confusion, lethargy and depression.71

Alkalising

The type of diet consumed will alter the acidic/alkaline balance, affecting the body’s metabolic pH buffering mechanism. The typical Western diet produces a net acid load, which is attributed to the relatively high proportion of acid-forming meats, coupled with acid-forming starchy carbohydrates (such as pasta, rice and potato), along with energy-dense, nutrient poor calories from fats and simple sugars. These are consumed at the expense of alkali-forming foods (fruit and vegetables). Additionally, high intake of sodium chloride contributes to thisimbalance, placing the body’s metabolic pH buffering system under tremendous strain. To manage systemic acidosis, diet must be the focus, however supplementation can support the body while dietary changes are being made.

Glutamine is an important regulator of acid-base balance as it is the most important donor of ammonia in the kidney. Glutamine’s metabolism in the kidney helps to excrete excessive hydrogen ions and maintain blood pH.72 Supplementation with glutamine could potentially spare skeletal muscle from acidosis-induced muscle breakdown.

Potassium citrate is an effective alkalising agent that can help maintain an optimal pH in the body. Not only is potassium an alkalising agent,73,74 citrate is metabolised to bicarbonate in the body, and therefore adds to the buffering potential. Additionally, the citrate anion may bebeneficial through its function as an intermediate of the Krebs cycle, with a potential role inenergy production.75

Reducing Stress and Anxiety

Magnesium is highly associated with stress levels, and both stress and hypomagnesaemia potentiate each other’s negative effects.76 With extensive reviews performed on magnesium’s association alongside increased stress, Cuciureanu and Vink77 suggest that magnesium should be evaluated in patients presenting with a variety of mental/emotional symptoms, including hyper-emotionality, generalised anxiety, panic attack disorders, insomnia, fatigue and asthenia. They further suggest that alleviation of clinical manifestations with oral supplementation of 5 mg/kg/d can confirm the diagnosis of suspected hypomagnesemia.

In humans, chronic sleep deprivation is associated with progressively decreasing levels of magnesium, and low magnesium levels are associated with decreased melatonin.78 Additionally, experimental data indicate magnesium deficiency can lead to slightly increased plasma corticosterone levels, increased irritability, aggressive behaviour, disrupted sleep patterns and higher mortality rates in animal studies compared to controls.79

Interestingly, a clinical trial investigated the impact of chronic stress on magnesium and oxidative status. Thirty eight males aged 18 to 38 of military background who were exposed to either chronic stress (>10 years) or sub chronic stress (>three months) were recruited into the trial where blood samples were taken to assess magnesium and oxidative status. These results were then compared to a control group of 10 individuals. Both groups that were exposed to chronic or sub chronic stress revealed a significant decrease (p<0.05) in total plasma magnesium, and significant decreases (p<0.05) in ionised magnesium compared to the level of ionised magnesium in the control group. Similarly, oxidative stress levels were increased in both the chronic and sub chronic stress groups and was negatively associated with magnesium status. The findings of this study support the need for magnesium supplementation for individuals who have exposure to moderate or prolonged stress.80

Supporting a Healthy Mood

Decreased magnesium intake has been strongly associated with depression in a study consisting of over 5,700 community-dwelling middle-aged and older adults, even after adjustments for age, gender, body type, blood pressure, socioeconomic and lifestyle factors.81
In a randomised trial of elderly subjects with type 2 diabetes and hypomagnesaemia (low serum magnesium), magnesium was shown to be as effective as a tricyclic antidepressant(TCA) in the treatment of low mood.82 The elderly participants were given a solution with the equivalent of 450 mg/d elemental magnesium, or the TCA (imipramine), for 12 weeks. At trial conclusion both groups experienced a significantly improved symptoms of depression, demonstrating magnesium to be as effective as the TCA.

Additionally, magnesium and vitamin B6 have both been demonstrated to be beneficial for improving premenstrual mood of women, in isolation83,84 or combination.85 Forty-four women(average age 32) were randomly assigned to take consecutively: 200 mg magnesium (as oxide), 50 mg vitamin B6, a combination of the magnesium and B6, or placebo for one menstrual cycle. The results showed a significant effect of the combination of 200 mg/d magnesium with 50 mg/d vitamin B6 on reducing anxiety-related premenstrual symptoms(nervous tension, mood swings, irritability, or anxiety) (p=0.040) demonstrating that the synergistic effects of the nutrients were greater than the effect of the magnesium or B6 inisolation.86 Interestingly, zinc has been associated with numerous behavioural alterations in both humans and animals (Figure 6),87 with lower levels of serum zinc being possibly associated with depressive symptoms.88

Figure 6: Behavioural alterations reportedly associated with zinc deficiency in animals and humans.89

For example, in a study investigating serum levels of zinc in unipolar depressed subjects, patients with minor depression displayed serum zinc levels approximately 93% lower that of the control group, whereas patients with major depression had serum zinc levels approximately88% lower compared to controls (p<0.001).90

Moreover, in a study of 100 adolescent female students with mood disorders, decreased serum zinc was shown to be inversely correlated with the presenting symptoms of depression andanxiety.91 The subjects were assessed for serum zinc levels, with each 10 µg/dL increment in serum zinc levels leading to 0.3 and 0.01 decrease in depression and anxiety scores respectively (p<0.05). The results indicated that the higher the depression and anxiety scores, the lower the patient’s serum zinc, suggesting zinc may be an important supporting nutrient for patients with (or at risk of) mood disorders.92

Furthermore, zinc supplementation has been shown to be an effective adjuvant agent in the management of patients with schizophrenia, alongside the anti-psychotic risperidone. Thirty inpatients with schizophrenia were randomly allocated to receive risperidone (6 mg/d) plus zinc sulphate (50 mg elemental zinc) three times per day, or risperidone (6 mg/d) plus placebo. Psychotic symptoms and aggression scores were assessed, with the results displaying significantly greater improvements over six weeks in the group receiving zinc sulphate alongside risperidone (p=0.04), compared to the group receiving placebo alongside risperidone (Figure 7).93 The results of this study further confirm the beneficial effects of zinc for the potentially profound mood regulatory activity.

Figure 7: The reduction of negative symptoms in patients with schizophrenia with the combination of risperidone plus zinc.94

Additionally, thiamine and vitamin C have also demonstrated therapeutic potential in the treatment of low mood. In a 12-week randomised double-blind placebo-controlled trial of patients with major depressive disorder (MDD), the combination of thiamine with antidepressant medication resulted in faster improvement of symptoms. Fifty-one inpatients with MDD were prescribed the selective serotonin reuptake inhibitor (SSRI) fluoxetine (20 mg/d),and randomised to receive either thiamine (300 mg/d) or placebo. After six weeks, the remission rates were greater for the patients receiving thiamine compared to placebo(p=0.001) with all patients reaching a similar remission rate after 12 weeks. The results of thestudy indicate that the adjuvant administration of thiamine accelerated the improvement indepressive symptoms in patients taking the SSRI, compared to patients taking placebo withthe SSRI. Furthermore, in an animal model of depression, vitamin C was shown to improvemood as effectively as fluoxetine,95 indicating the potential beneficial effects of vitamin C tosupport states of low mood in patients.

Disclaimer: In the interest of supporting health Practitioners, all safety information provided at the time of publishing (Oct 2025) has been checked against authoritative sources. Please note that not all interactions have been listed.

For further information on specific interactions with health conditions and medications, refer to clinical support on 1800 777 648(AU), 0508 227 744(NZ) or via email, anz_clinicalsupport@metagenics.com, or via Live Chat www.metagenics.com.au, www.metagenics.co.nz

Pregnancy

Insufficient reliable information available; avoid using.

Breastfeeding

Insufficient reliable information available; avoid using.

Prescribing Tips and Notes

Levothyroxine - Calcium reduces levothyroxine absorption, probably by forming insoluble complexes. Advise patients to take levothyroxine and calcium supplements at least 4 hours apart. Be cautious with this combination.

Antibiotics - Calcium seems to reduce the absorption of quinolone and tetracycline antibiotics. Advise patients to take oral quinolones at least 2 hours before or 4-6 hours after calcium supplements or calcium-fortified foods. Magnesium can form insoluble complexes with quinolone antibiotics and tetracycline antibiotics, decreasing their absorption. Advise patients to take these drugs at least 2 hours before, or 4 to 6 hours after, magnesium supplements. Zinc can decrease the levels and clinical effects of quinolones antibiotics and tetracycline antibiotics. Advise patients to take these drugs at least 2 hours before, or 4-6 hours after, zinc supplements. Zinc might decrease cephalexin levels by chelating with cephalexin in the gut and preventing its absorption. To avoid an interaction, advise patients take zinc sulfate 3 hours after taking cephalexin.

Contraindications

• Dolutegravir - Calcium seems to reduce levels of dolutegravir. Do not take this combination.
• Elvitegravir - Calcium seems to reduce levels of dolutegravir. Do not take this combination.
• Levodopa/Carbidopa - Magnesium can reduce the bioavailability of levodopa/carbidopa. Do not take this combination.
• Liver Disease - Theoretically, glutamine intake might increase the risk of hepatic encephalopathy in patients with liver disease. Glutamine is metabolised to ammonia. Monitor ammonia levels in patients with liver disease or impaired liver function who are taking glutamine. Advise patients with severe liver disease to avoid glutamine supplements.

Cautions

• ACE Inhibitors - Concomitant use of these drugs with potassium supplements increases the risk of hyperkalemia.
• Angiotensin Receptor Blockers - Concomitant use of these drugs with potassium supplements increases the risk of hyperkalemia.
• Anticonvulsants - Theoretically, glutamine might antagonise the effects of anticonvulsant medications.
• Antihypertensive Drugs - Theoretically, taurine might increase the risk of hypotension when taken with antihypertensive drugs. Theoretically, vitamin B6 may have additive effects when used with antihypertensive drugs.
• Bleeding Disorders - Theoretically, magnesium might increase the chance of bleeding in patients with existing bleeding disorders.
• Bisphosphonates - Calcium and magnesium can decrease absorption of bisphosphonates.
• Gallbladder Disease - Nicotinamide might exacerbate gallbladder disease, use with caution.
• Kidney Disease - Kidney disease reduces magnesium excretion and increases the risk for hypermagnesemia. Use cautiously in individuals with reduced kidney function and avoid use in those with creatinine clearance <20 mL/min due to an increased risk of hypermagnesemia. Kidney disease affects potassium excretion and increases the risk for elevated potassium levels. Additionally, patients on hemodialysis may experience fluctuations in potassium levels. Use potassium supplements with caution in individuals with kidney disease, including chronic kidney disease (CKD), kidney failure or post-kidney transplant.
• Kidney Stones - Larger amounts of vitamin C can increase the risk of oxalate kidney stones, especially in those prone to oxalate stone formation. People who have a history of oxalate stones seem to be more sensitive to supplemental vitamin C than non-stone formers. In those with a history of oxalate kidney stones (the most common type of nephrolithiasis), supplemental vitamin C 1 gram per day appears to increase stone risk by 40%. Tell patients prone to kidney stone formation to avoid higher doses of vitamin C.
• Monosodium Glutamate (MSG) Hypersensitivity - Theoretically, people who are sensitive to MSG might be sensitive to glutamine. Glutamine is metabolized to glutamate in the body.
• Myasthenia Gravis - Intravenous magnesium might worsen neuromuscular weakness and respiratory failure in patients with myasthenia gravis and contribute to a myasthenic crisis. Magnesium competes with calcium on the presynaptic membrane of the neuromuscular junction, inhibiting release of acetylcholine (ACh) and exacerbating the reduction in postsynaptic ACh function seen in myasthenia gravis.
• Neuropathy - Vitamin B6 has been linked with neuropathic symptoms such as tingling, burning or numbness. If symptoms occur, discontinue use.
• Potassium-sparing Diuretics - Potassium-sparing diuretics decrease excretion of magnesium, possibly increasing magnesium levels. Using potassium-sparing diuretics with potassium supplements increases the risk of hyperkalemia.
• Thiazide Diuretics - Taking calcium along with thiazides might increase the risk of hypercalcemia and renal failure. Patients may need to have their serum calcium levels and/or parathyroid function monitored regularly.
• Seizure Disorders - Theoretically excess amounts of glutamine and its metabolite, glutamate, might increase the risk of seizures. Glutamine is metabolized to glutamate and an excess amount of both might lower the seizure threshold. This effect has not been reported in humans. Until more is known, advise people with seizure disorders to use glutamine with caution.
• Skeletal Muscle Relaxants - Parenteral magnesium alters the pharmacokinetics of skeletal muscle relaxants, increasing their effects and accelerating the onset of effect.
• Warfarin - High-dose vitamin C might reduce the levels and effectiveness of warfarin. Lower doses (< 10 grams daily) may be safe, but the anticoagulation activity of warfarin should be monitored.

Footnotes

* Contains MagActive®, an exclusive, enhanced absorption magnesium.

† Glutamate is an excitatory neurotransmitter important for brain function and development, however, an excess of glutamate can result in neurotoxicity.