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Nutrients That May Assist
Magnesium
Magnesium amino acid chelate (Magnesium bisglycinate)
Zinc
Zinc amino acid chelate (Meta Zn ® – Zinc bisglycinate)
Vitamin B6
Pyridoxal 5-phosphate monohydrate
Chromium
Chromic chloride
Actions
- Antispasmodic
- Neuromuscular support
- Modulates inflammatory response
- Metabolic support
- Nervous system support
Clinical Applications
- Muscle aches, pains, cramps and spasms
- Migraine prevention
- Healthy serum glucose levels
- Reduce stress and anxiety
- Female health
Clinical Overview
Magnesium deficiencies are far more prevalent than generally suspected, with surprising statistics showing that nearly 40% of adult Australians have an insufficient magnesium intake. [1] The therapeutic value of magnesium is far-reaching and considering the multi-system effects of inadequate levels, insufficient magnesium can be suspected as playing a role in many common health complaints presenting in patients. In particular, with effects on neurotransmitters, reducing glutamate excitotoxicity [2] and supporting hippocampal neurogenesis, [3] it is clear to see that magnesium plays a particularly vital role in chronic stress and anxiety – after all, hypomagnesaemia can be seen as both a cause and consequence of stress. [4] For example, figure 1 displays the roles magnesium plays in the management of healthy mood.
Importantly, magnesium can also help to promote healthy musculoskeletal and nervous system function, assisting in the management of muscle cramps and spasms, as well as maintaining healthy serum glucose levels [5] particularly alongside other important nutrients such as chromium. [6] Furthermore, supporting adequate levels of nutrients such as magnesium, zinc and vitamin B6 can be vital to maintain and support female health and wellbeing. For example, premenstrual syndrome [7] and conditions such as pregnancy-induced hypertension [8] and pre-eclampsia [9] are associated with low magnesium.
Figure 1: Magnesium is involved in various mechanisms concerning the modulation of healthy mood. [10]
Background Information
Magnesium – a Vital Mineral
Magnesium is either a structural cofactor or activator of more than 300 metabolic reactions in the body. These processes include protein synthesis, cellular energy production and storage, maintenance of cellular electrolyte composition, DNA and RNA synthesis, and stabilisation of mitochondrial membranes. [11] Magnesium deficiency is not uncommon, with a recent Australian Health Survey finding 72% of 14-18 year old females, and an average of just under 40% of all Australian adults consuming inadequate amounts of magnesium daily. [12] In addition, dietary imbalances such as high intakes of fat, calcium, coffee and strong tea can worsen magnesium inadequacy, by either reducing absorption or enhancing elimination. [13]
Early signs of magnesium deficiency include fatigue, weakness, loss of appetite and/or nausea and vomiting. [14] As magnesium levels decrease, patients may experience muscle contractions and cramps, numbness, tingling, personality changes, abnormal heart rhythms, coronary spasms and seizures. [15] Severe deficiency may lead to hypocalcaemia (low serum calcium) and hypokalaemia (low serum potassium). Although dietary intake is a common factor; conditions that may also lead to hypomagnesaemia include poorly-controlled diabetes mellitus; chronic malabsorptive problems (e.g. Crohn’s disease, gluten-sensitive enteropathy, regional enteritis); medication use (e.g. diuretics, antibiotics); alcoholism; and older age (e.g. decreased absorption of magnesium, increased renal excretion). [16]
Magnesium Bioavailability
Magnesium bisglycinate has demonstrated superior bioavailability when compared to other forms of supplemental magnesium, such as magnesium oxide and magnesium citrate (Figure 2), in both cell line studies [17],[18] and in patients who have compromised magnesium absorption. [19]
The superior bioavailability of magnesium bisglycinate can be explained by several mechanisms:
1. Reduced anti-nutrient binding
Minerals in their ionic (free) form can create complexes with anti-nutrients (phytates, oxalic acid, tannins, etc.) and polyphenols, inhibiting absorption. Magnesium bisglycinate consists of two glycine molecules bound covalently with magnesium. [20],[21] This bond is of sufficient strength so to prevent magnesium from dissociating in the upper gastrointestinal tract, therefore preventing it from creating complexes. [22],[23]
Figure 2: Magnesium bisglycinate demonstrates superior bioavailability when compared to other forms of supplemental magnesium. [24]
2. Enhanced passive transport
The majority of magnesium is absorbed through passive, paracellular, transport, which relies on particular claudin proteins. [25] These proteins are down-regulated as luminal pH increases. [26],[27] Additionally, a more alkaline pH reduces the affinity between magnesium and claudins, further reducing absorption. [28],[29] When glycine dissociates from magnesium ready for absorption, it acts as a buffer, modulating pH and improving passive absorption. [30]
3. High tolerability
Ionic magnesium is densely charged and has a high hydration energy, resulting in a double hydrate shell. This shell must be removed before magnesium is absorbed through the narrow ion channels (Figure 4), a process called dehydration which can be achieved via paracellular claudins and transient receptor potential melastatin 6 (TRPM6) and 7 (transcellular active transport channels). [31] The strong attraction of water to magnesium ions is responsible for the common side effect of diarrhoea in response to magnesium supplementation. In this respect, the benefit of magnesium bisglycinate is two-fold. Firstly, the bond between magnesium and glycine reduces magnesium hydration. [32] Secondly, the reduction in pH, caused by glycine’s buffering capacity improves the dehydration, and therefore absorption, of magnesium. This minimises laxation, and improves the tolerability of magnesium bisglycinate, [33],[34],[35] an effect that has been demonstrated in human clinical trials. [36],[37]
Figure 4: Among the biological cations, magnesium is the most densely charged and has a high hydration energy. [38]
4. Dipeptide transport
A portion of magnesium bisglycinate is absorbed intact into the enterocyte, through the dipeptide channels, [39] further improving absorption.
5. Solubility
Solubility improves both passive, paracellular, and active, transcellular, transport. Magnesium bisglycinate is easily soluble in water. In addition, solubility reduces as pH increases, further highlighting the benefit of glycine’s buffering capacity. [40],[41],[42] While solubility is certainly one factor that impacts absorption, it is important to note that it shouldn’t be conflated with bioavailability. Evidence demonstrating that solubility significantly correlates with bioavailability is lacking. For instance, magnesium citrate, an organic magnesium salt, is over 30,000 times more soluble than the inorganic magnesium salt, magnesium oxide (200 g/L vs 0.006 g/L respectively), however, its bioavailability is nowhere near as superior (Figure 2). [43],[44]
Actions
Antispasmodic
Deficiency of magnesium is associated with muscular cramps, and magnesium has long been recognised for its important therapeutic applications in enhancing muscle relaxation and relieving spasm. [45] Magnesium exerts its muscle-relaxing actions by competing with calcium for binding sites on troponin C, allowing the sarcoplasmic reticulum to actively transport calcium out of the sarcomere, thus inhibiting contraction and allowing relaxation. [46] Additionally, magnesium causes muscle relaxation by decreasing the amount of acetylcholine liberated at motor nerve terminals, reducing depolarisation and depressing the excitability of the muscle fibre membrane. [47]
Furthermore, magnesium is involved in the regulation of a wide variety of enzymatic reactions and phosphorylation-dependent processes essential for neuronal excitability. Therefore, magnesium is required for the correct muscle contractile signalling via motor neurons.
Neuromuscular Support
Amongst magnesium’s many vital roles is its importance in neuromuscular transmission. Magnesium prevents or controls convulsions by blocking neuromuscular transmission and decreasing the release of acetylcholine at the motor nerve terminals. [48] Magnesium deficiency should always be included in the differential diagnosis for a patient who presents with persistent or severe muscle pain. [49]
Fibromyalgia (FM) is a particularly painful neuromuscular condition, which is most common among women aged 30 to 50. [50] This is a common syndrome characterised by long-term, body-wide pain and tenderness in the joints, muscles, tendons, and other soft tissues. The cause is unknown, but FM has also been linked to fatigue, sleep problems, headaches, and anxiety. [51] These same symptoms are also found in patients with low magnesium levels, [52] with red blood cell magnesium levels being found to be low in fibromyalgic patients. [53] People suffering from this condition tend to wake up with body aches and stiffness; with magnesium found to be effective in the reduction of these symptoms. The proposed mechanism of action is via mitochondrial support, as there is evidence of muscle hypoxia and deficient ATP production in FM.
Magnesium can also provide analgesic effects, due to its N-methyl-D-aspartate (NMDA) receptor blocking action. [54] Magnesium deficiency is particularly associated with increased susceptibility to painful migraines due to effects on neuroinflammation, NMDA receptor binding, glutamate and nitric oxide activity as well as serotonin receptor affinity. [55] Migraines have been linked to brain excitability, with magnesium able to block the excitatory NMDA glutamate receptors, thereby inactivating them. [56] Additionally, muscle cramps, muscle strains (and damage) and muscle tension are all associated with magnesium deficiency. Interestingly, approximately 70% of patients who have tension headaches also exhibit muscular tightness and tenderness. It is therefore no surprise that magnesium supplementation is of great benefit for patients presenting with tension-type headaches [57] and migraines. [58]
Modulates Inflammatory Response
Interestingly, it has been shown that after a few days of experimental magnesium deficiency in an animal model that clinical inflammatory syndrome is induced, characterised by leukocyte and macrophage activation, release of inflammatory cytokines and acute phase proteins, and excessive production of free radicals. [59] Research has led to the conclusion that increasing the extracellular magnesium concentration decreases the inflammatory response, while reduction of extracellular magnesium results in cell activation. [60]
Importantly, magnesium acts as a natural calcium antagonist, and the molecular basis for the inflammatory response is essentially the result of modulation of intracellular calcium concentration. The priming of phagocytic cells, the opening of calcium channels and activation of NMDA receptors, and the activation of nuclear factor kappa B (NFkB) have all been considered as potential mechanisms. Moreover, magnesium deficiency induces a systemic stress response by activation of neuro-endocrinological pathways. As nervous and immune systems interact bi-directionally, the role of neurological mediators, such as magnesium, have to be considered. [61]
Figure 5: Magnesium’s many roles in insulin sensitivity including regulating the insulin signalling pathway, with hypomagnesemia affecting many downstream pathways.
Additionally, magnesium deficiency contributes to an exaggerated inflammatory response to immune stress, and oxidative stress is the consequence. Inflammation contributes to the pro-atherogenic changes in lipoprotein metabolism, endothelial dysfunction, thrombosis, and hypertension, and explains the aggravating effect of magnesium deficiency on the development of metabolic syndrome. Further studies are still needed to assess more accurately the role of magnesium in immune response in humans, but these experimental findings in animal models suggest that inflammation may be the missing link to explain the role of magnesium in many pathological conditions. [62]
Metabolic Support
Hypomagnesaemia has been strongly related to type 2 diabetes mellitus (T2DM) due to magnesium’s many roles in insulin and glucose metabolism (Figure 5). [63] Intracellular magnesium regulates glucokinase (an enzyme which plays an important role in the regulation of carbohydrate metabolism),
In addition, chromium plays a significant role in glucose metabolism by potentiating the action of insulin. [64] For example, it facilitates insulin signalling by augmenting insulin binding through increasing the number of insulin receptors on cells. Chromium also improves insulin sensitivity by increasing insulin receptor phosphorylation through modulation of kinase activity. [65] As such, it has important roles not only in glucose but also lipid metabolism. Signs of chromium deficiency in humans consuming standard diets include elevated serum glucose, insulin, cholesterol and triglycerides, and decreased high density lipoprotein (HDL) cholesterol. [66] Supplementation with chromium has demonstrated beneficial effects on people with conditions ranging from mild glucose intolerance to overt T2DM, without side effects. [67]
Nervous System Support
Magnesium supplementation has been shown to affect all elements of the body’s reactions to stress, exerting a neuroprotective effect. For example, in the event of deficiency, magnesium repletion reverses the increased stress sensitivity, with pharmacological loading of magnesium inducing resistance to neuropsychological stressors such as glutamate [*] excitotoxicity. [68]
With the ability to inhibit the release of excitatory neurotransmitters, magnesium acts as a voltage-gated antagonist at the glutamate, NMDA receptor. [69] When the NMDA receptor is over-activated, it can result in increased cell death and increased excitotoxicity which ultimately results in neurological changes. For example, low levels of magnesium has been associated with hippocampal atrophy, with supplementation demonstrating the ability to boost brain derived neurotrophic factor (BDNF) and promote hippocampal neurogenesis. [70] 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. [71]
In a state of deficiency, the neuronal requirements for magnesium may not be met, causing the neuronal damage which can result in low mood. [72] Acute stress has been associated with increased plasma magnesium levels due to the release of stress hormones (catecholamines and corticosteroids), and increased urinary excretion. [73] This is due to the body shifting magnesium from the intracellular to extracellular space as a protective mechanism to reduce the effects of stress. [74] For example, by limiting the rate of inflammation and oxidation experienced at times of stress, as well as supporting extra neurotransmitter requirements.
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. [75] 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. [76] Therefore, it is suitable to say that magnesium deficiency is both a cause and a consequence of stress.
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 [77] (Figure 6). This results in a soothing effect on the entire stress response system, [78] as GABA acts as the body’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, [79] (Figure 7) with magnesium deficiency causing NMDA-coupled calcium channels to be biased towards opening, leading to further neuronal injury and neurological dysfunction. [80] This results in glutamate-induced neuro-excitotoxicity, which may manifest as anxiety and other mood and behavioural disorders. [81]
Magnesium is recommended as a migraine prophylactic for those suffering frequent migraines.
Figure 6: Magnesium’s mechanism of action in anxiety and panic. [82]
In addition, zinc is required throughout the human body for a myriad of chemical reactions necessary for normal body functioning. [83] For example, it is well-established that zinc supplementation provides antidepressant-like effects, with zinc deficient diets associated with low moods. [84] Zinc has been shown to increase BDNF, which is recognised as a target implicated in the aetiology of depression. [85] 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. [86]
Figure 7: The role of magnesium in regulating calcium ion flow and neurotransmission. [87]
Zinc is highly concentrated in the synaptic vesicles of specific neurons, and regulates the release of neurotransmitters. The neurons that contain zinc are known as zinc-enriched neurons (ZEN), with cerebellar ZEN primarily associated with GABA neurotransmission, which produces a calming effect by balancing over-excitability. In other regions, ZEN are found in glutamate-producing neurons. [88] Furthermore, zinc has been shown to increase synaptic dopamine levels, thereby allowing dopamine to stay and engage with receptors longer within the synapse, and is considered an important regulator of dopamine transporter function. [89]
Zinc also acts as an inhibitory neuromodulator of glutamate release, regulating NMDA receptors. [90] 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. [91] This reflects a further need for sufficient zinc to reduce the excitotoxicity associated with the pathophysiology of mood disorders.
Pyridoxine (vitamin B6) has many important roles; in its coenzyme form, pyridoxal phosphate (PLP), it is associated with over 100 enzymes, the majority of which are involved in amino acid metabolism. [92] Vitamin B6 is fundamental to the production of many neurotransmitters [93] and is specifically involved in the creation of histidine to histamine, tryptophan to serotonin, glutamate to GABA, and dihydroxyphenylalanine to dopamine, [94] as well as the synthesis of adrenaline and noradrenaline. [95] Therefore, deficiency in this nutrient is often associated with psychological disturbances such as mood alterations, [96] with signs of deficiency including confusion, lethargy and depression. Up to 40% of food-derived vitamin B6 can be lost with cooking. [97] P-5-P is the main circulating form exported from the liver and may be more beneficial with patients where conversion is compromised (e.g. liver disease or zinc or magnesium deficiency). [98] , [99]
Clinical Applications
Muscle Aches, Pains, Cramps and Spasms
Magnesium is well known as an effective agent to reduce muscle cramps and spasms. In a double-blind randomised placebo-controlled trial on 73 women, it was found that otherwise healthy pregnant patients suffering with leg cramping had a negative magnesium balance. [100] Oral supplementation with three doses of 122 mg magnesium daily (one in the morning, two at night) for three weeks effectively reduced cramping in comparison to controls. [101]
Furthermore, non-pregnant volunteers suffering regular leg cramps were recruited into a randomised, double-blind, cross-over placebo-controlled trial. [102] They were given a supplement equivalent to 300 mg elemental magnesium and matching placebo for six weeks each. The number of cramps was recorded in cramp diaries, with the results showing fewer leg cramps were experienced when the patients received the active treatment of magnesium compared to placebo (Figure 8). [103]
Figure 8: Time course of magnesium supplementation on leg cramps over the 12 week trial period. [104]
Migraine Prevention
Deficiency in magnesium is associated with neuronal dysfunction, such as found in those who suffer migraines. [105] Magnesium is recommended as a migraine prophylactic for those suffering frequent migraines, [106] , [107] with the more bioavailable magnesium forms demonstrating increased efficacy compared to other low-absorbable forms. [108]
Several studies have demonstrated significant benefits in patients with the use of magnesium to prevent headaches and migraines. For example, in a double-blind, placebo-controlled trial in women experiencing menstrual migraine, the use of magnesium pyrrolidone carboxylic acid (360 mg/day) starting on the 15th day of their cycle until the next menses, resulted in a significantly reduced pain score, and a reduction in the number of days with headache. [109]
Further, in another double-blind randomised study, adults suffering migraines aged 18 to 65 years were given oral magnesium at a dose of 600 mg daily (as trimagnesium dicitrate) over 12 weeks. [110] The results demonstrated a substantial 41.6% decrease in migraine attack frequency, compared to only 15.8% in placebo group. Additionally, after three months of oral magnesium citrate (600 mg/day), patients experiencing migraines without aura showed notable reductions in migraine frequency (p=0.005) and severity (p<0.001), [111] further displaying the preventative effect of daily magnesium on the recurrence of debilitating migraines.
Healthy Serum Glucose Levels
Hypomagnesaemia is a prominent feature of T2DM, with many studies having been performed to show the effects of magnesium supplementation on patients with prediabetes and diabetes. For example, a recent systematic review and meta-analysis of 18 randomised controlled trials concluded that magnesium supplementation can improve glucose parameters in people with diabetes, and also improves insulin-sensitivity parameters in those at high risk of T2DM. [112] Compared with placebo, magnesium treatment was shown to reduce fasting plasma glucose in those with diabetes, and improve plasma glucose levels after a glucose tolerance test in those at high risk of diabetes.
Additionally, a meta-analysis of 13 cohort studies with over 500,000 participants found a significant decrease in the incidence of diabetes with higher magnesium intake. [113] Moreover, a 2017 cohort study of 395 patients with T2DM showed 30.6% of patients suffered from hypomagnesaemia, with both plasma triglyceride (p<0.001) and actual glucose levels (p<0.001) negatively correlated with plasma magnesium concentration. [114] The patients in this study who were using metformin, proton pump inhibitors or β-adrenergic receptor agonists displayed even further reduced plasma magnesium levels.
Furthermore, the combination of magnesium with chromium has been shown to decrease IR more effectively than either alone. [115] One hundred and twenty subjects with IR were randomly divided to receive either placebo, chromium (160 µg/day), magnesium (200 mg/day) or chromium plus magnesium for three months. The results indicated the combination of chromium with magnesium improved the IR more effectively than either alone, with significant decreases in fasting serum glucose (0.37 mmol/L; p<0.01), fasting insulin (2.91 µIU/mL; p<0.01) and IR index (0.60; p<0.01) displayed in the combination group only. Additionally, significant changes in glucose-transporter-4 (2.9-fold increase; p<0.05) and glycogen-synthase-kinase-3β (2.2-fold decrease; p<0.05) mRNA levels in activated T-lymphocytes were observed with the combination of the two minerals, but not in the other groups.
Reduce Stress and Anxiety
Magnesium is highly associated with stress levels, and both stress and hypomagnesemia potentiate each other’s negative effects. [116] With extensive reviews performed on magnesium’s association alongside increased stress, Cuciureanu and Vink [117] 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/day can confirm the diagnosis of suspected hypomagnesemia.
In humans, chronic sleep deprivation is associated with progressively decreasing levels of magnesium, with low magnesium being associated with decreased melatonin. [118] Additionally, experimental data indicates 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. [119]
Interestingly, magnesium and oxidative status were investigated in young military volunteers exposed to chronic stress (>10 years) or subchronic stress (>3 months). [120] Both of the stress situations caused a significant decrease (p<0.05) in total plasma magnesium, with chronic and subchronic stress causing significant decreases in ionised magnesium compared to the level of ionised magnesium in the control group. The findings of this study supports the need for magnesium supplementation in people living in conditions of stress. Additionally, this study shows that chronic stress of long duration but moderate intensity, as well as subchronic exposure to intense stress, can significantly alter magnesium homeostasis and initiate increased oxidative stress.
Additionally, zinc has been associated with numerous behavioural alterations in both humans and animals (Figure 5). [121] Notably, serum zinc levels have been correlated with severity of depression, with zinc supplementation used in the augmentation therapies as a treatment for depression. [122] It has been confirmed in multiple studies that the more severe the depressive symptoms in patients, the lower the serum zinc, compared to non-depressed controls. [123]
Animal studies of zinc deficiency show increased states of aggression and anxiety, with anxiety-like behaviours shown to develop within just two weeks of being fed a zinc-deficient diet. [124] The animal models of zinc deficiency have also demonstrated a lowered stress response, with lower zinc levels correlating to higher corticosterone levels following stress in comparison to controls, suggesting zinc to be an important factor in the modulation of anxiety and stress responses.
Female Health
Another aspect of magnesium’s many roles is its impact on female health. Through its effects on energy production, neuromuscular function and inflammation, magnesium deficiency can be seen to contribute to premenstrual syndrome (PMS), infertility, and problems associated with pregnancy. Deficiencies of magnesium have been implicated in various reproductive events such as congenital anomalies, pregnancy-induced hypertension, placental abruption, premature rupture of membranes, still births and low birth weight. [125]
Pregnancy has been shown to induce a significant (15%) decrease in serum magnesium levels, due primarily to increased renal excretion. Pregnant women with hypomagnesaemia have been found to be 47 times more likely to experience pre-eclampsia than predicted by their body mass index (BMI). [126] In addition, vaginal (but not caesarean) delivery results in significant decreases in magnesium; most probably due to the participation of skeletal and uterine muscles during labour. [127] Magnesium supplementation during pregnancy has been shown to improve maternal health and foetal outcome, and intravenous magnesium sulphate has been used as a tocolytic agent, to reduce uterine contractility in preterm labour. [128]
Additionally, magnesium and vitamin B6 have both been demonstrated to be beneficial for improving premenstrual mood of women, in isolation [129],[130] or combination. [131] 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/day magnesium with 50 mg/day vitamin B6 on reducing anxiety-related premenstrual symptoms (nervous tension, mood swings, irritability, or anxiety) demonstrating that the synergistic effects of the nutrients were greater than the effect of the magnesium or B6 in isolation. [132]
Safety Information
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
- Avoid use. Safety has not been conclusively established during pregnancy.
Breastfeeding
- Appropriate for use.
Prescribing Tips and Notes
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.
Contraindications
- Heart block: magnesium supplements should be avoided.
- Levodopa/Carbidopa - Magnesium can reduce the bioavailability of levodopa/carbidopa. Do not take this combination.
Cautions
- Bleeding Disorders - Theoretically, magnesium might increase the chance of bleeding in patients with existing bleeding disorders.
- Bisphosphonates - Magnesium can decrease absorption of bisphosphonates.
- 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.
- Neuropathy - Vitamin B6 has been linked with neuropathic symptoms such as tingling, burning or numbness. If symptoms occur, discontinue use and investigate all causes of symptoms, including elevated B6.
- Potassium-sparing Diuretics - Potassium-sparing diuretics decrease excretion of magnesium, possibly increasing magnesium levels.
Footnotes
[*] Glutamate is an excitatory neurotransmitter important for brain function and development; however, an excess of glutamate can result in neurotoxicity.
References
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