Metagenics CalmX
Product Video: Metagenics CalmX
Directions: Metagenics CalmX
Adults:
Add 2 level scoops (12.7g) to 200 mL of water, twice daily.
Clinical Benefits: Metagenics CalmX
- Provides 350 mg of highly bioavailable Meta Mag magnesium to be of benefit during stress. Magnesium, B vitamins, vitamin C and zinc are all nutrients required to be able to cope with stress effectively and may be depleted in chronic stress.4 The adrenergic effects of stress induce a shift of magnesium to the extracellular space, increasing urinary excretion and depleting body stores (Figure One). Magnesium deficiency adversely affects excitatory neurotransmitters such as serotonin and acetylcholine and is associated with stress.
- A double-blind, placebo controlled trial using 6.0 g of taurine per day investigated its impact on stress symptoms and biochemistry. This study showed taurine to inhibit the stress-induced release of adrenaline.8 Magnesium, B vitamins, vitamin C and zinc are required to regulate the stress response as co-factors in neurotransmitter synthesis.
- Zinc is essential in modulating the stress response.9 Zinc levels have been found to be deficient in people with generalised anxiety disorder.10 Exposure to acute stress increases serum glycocorticoids and induces metallothionein synthesis which consequently decreases serum zinc.11
Figure One: Magnesium and the Stress Response.
Ingredients: Metagenics CalmX
Each 12.7 g dose contains: | |
Magnesium amino acid chelate (Meta Mag® - Magnesium bisglycinate) | 3.5g |
Equivalent Magnesium | 350mg |
Taurine | 3.0g |
Glutamine | 2.0g |
Potassium citrate | 1.0g |
Equivalent Potassium | 362mg |
Calcium ascorbate dihydrate | 605mg |
Equivalent Ascorbic acid (Vitamin C) | 500mg |
Thiamine hydrochloride (Vitamin B1) | 25mg |
Equivalent Riboflavin sodium phosphate | 34mg |
Riboflavin (Vitamin B2) | 25mg |
Nicotinamide (Vitamin B3) | 25mg |
Calcium pantothenate (Vitamin B5) | 25mg |
Pyidoxal 5-phosphate monohydrate (Vitamin B6) | 25mg |
Zinc amino acid chelate (Meta Zn® - Zinc bisglycinate) | 50mg |
Equivalent Zinc | 10mg |
Metagenics CalmX is free from animal products, dairy protein, lactose, eggs, gluten, wheat, nuts, yeast and soy protein.
Metagenics CalmX is free from artificial colours, sweeteners, flavours and preservatives. Sweetened with steviol glycosides. Contains 362 mg of potassium per 11.9 g dose.
Excipients: Metagenics CalmX
Citric acid, Colloidal anhydrous silica, Flavour, Hypromellose, Malic acid, Silicon dioxide, Steviol glycosides and Tartaric acid.
Warnings: Metagenics CalmX
Not all cautions and contraindications are listed. For full details, references or more information contact HealthMasters in Australia by email: reception@healthmasters.com.au
Storage: Metagenics CalmX
Store below 30° C
Magnesium Bisglycinate: Metagenics CalmX
MAGNESIUM BISGLYCINATE
Metagenics CalmX contains evidenced-based ingredients to support the natural metabolic pathways for gamma-aminobutyric acid (GABA) production and activity, indicated to promote relaxation during times of stress. MetaMag Magnesium bisglycinate is scientifically designed to provide a highly bioavailable form of magnesium. Magnesium may act as a GABA receptor agonist and also has a binding site on the glutamate receptors helping to regulate the activity of this main excitatory neurotransmitter.1 Glycine functions as an inhibitory neurotransmitter in the nervous system while glutamine is a precursor to GABA production.2 Pyridoxal (vitamin B6) is a cofactor for the enzyme Glutamate decarboxylase that synthesises GABA from glutamate.4 Zinc also has a binding site on the glutamate receptor and may act as a modulator for both excitatory and inhibitory neurotransmission.5
Magnesium
Magnesium is predominantly located intra-cellular in bone, muscles and non-muscular soft tissues while only 1% of total magnesium is found in serum and red blood cells. Magnesium needs to be consumed in the diet regularly to prevent the risk of magnesium deficiency and due to the increased consumption of processed foods; magnesium intake in the western world is decreasing. Magnesium is a cofactor in more than 300 enzymatic reactions, critically stabilising enzymes, including many ATP-generating reactions. ATP metabolism, muscle contraction and relaxation, normal neurological function and release of neurotransmitters are all magnesium dependent.6 While evidence generally does not support the use of magnesium for skeletal muscle cramps with many studies producing null effect7,8, there is evidence to suggest oral magnesium supplementation can improve anaerobic metabolism in athletes, decreasing lactate production9 and improving physical performance in healthy elderly women involved in an exercise program.10
Magnesium may function as a GABA receptor agonist promoting the effects of GABA. Further, in the central nervous system (CNS), magnesium ions block NMDAR channels at resting membrane potentials. The binding site for magnesium ions is deep within the channel. This block is voltage-dependent but ion flux occurs when the membrane potential is depolarized. NMDAR receptors are glutamate-binding sites, being the major excitatory neurotransmitter in the CNS.11 See Figure 1.
Figure 1. Neurotransmitter signalling12
Glycine
Glycine functions as one of the major inhibitory neurotransmitters in the CNS with a high density of glycine containing neurons being found in spinal cord and brain stem. When glycine binds to its receptor it opens the anion channel allowing an influx of chloride ions into the postsynaptic neuron causing hyperpolarization that raises the threshold for neuronal firing and thereby inhibits the postsynaptic neuron.2,13
Glutamine
Glutamine and glutamate are amino acids. Several studies show that concentrations of serum glutamine in the body are diminished during times of physical or psychological stress and further that patients presenting with exhaustion, anxiety, sleeplessness and lack of concentration have low serum glutamate concentration. Glutamine and glutamate synthesis occur interchangeably (see figure 2). Glutamine converts to glutamate using NADPH as a cofactor and glutamate is a precursor for GABA production using vitamin B6 as a cofactor.15-19
Figure 2. GABA is synthesized from Glutamine and Glutamate20
Pyridoxal 5-Phosphate (Vitamin B6)
Pyridoxine is the cofactor required by Glutamate decarboxylase to convert glutamate to GABA in the CNS.4 See Figure 2.
Zinc
Approximately 10% of total zinc in the brain is located in synaptic vesicles of certain glutamatergic neurons.5 Zinc may modulate neurotransmission mediated via both excitatory and inhibitory amino acid receptors at specific synapses for example the NMDA glutamate receptor is directly inhibited by zinc whereas GABA release from the presynapse can be potentiated (see Figure 1).28
Clinical Summary:
- To naturally increase GABA production to induce relaxation
- Helps relieve symptoms of nervous tension, stress and mild anxiety
- For the symptomatic relief of stress disorders.
- Herbal blend which helps relieve stress of study or work
- May help reduce the frequency of migraines.
Who will benefit:
- Those with symptoms of anxiety and nervous tension
- Those who are experiencing mild stress and associated disorders
- Those who are experiencing stress associated with work and/or study
- Those with magnesium deficiency
- Those who are experiencing frequent migraines
- Those who wish to improve their cognitive performance and mood.
References:
- Held K, Antonijevic IA, Künzel H, et al. Oral Mg(2+) supplementation reverses age-related neuroendocrine and sleep EEG changes in humans. Pharmacopsychiatry 2002;35(4):135-143
- Legendre P. The glycinergic inhibitory synapse. Cell. Mol. Life Sci 2001;58:760–793
- Kimura K1, Ozeki M, Juneja LR, et al. L-Theanine reduces psychological and physiological stress responses. Biol Psychol 2007;74(1):39-45
- Qu K, Martin DL, Lawrence C. Motifs and structural fold of the cofactor binding site of human glutamate decarboxylase. Protein Sci 1998;7:1092-1105.
- Takeda A, Minami A, Seki Y, et al. Differential effects of zinc on glutamatergic and GABAergic neurotransmitter systems in the hippocampus. J Neurosci Res 2004; 15;75(2):225-9.
- Jahnen-Dechent W, Ketteler M. Magnesium basics. Clin Kidney J 2012;5 (1);i3–i14.
- Nygaard IH, Valbo A, Oethick SV, et al. Does oral magnesium substitution relieve pregnancy-inducede leg cramps? Eur J Obstet Gynecol Reprod Biol 2008;141:23-6.
- Garrison SR, Birmingham CL, Koehler BE, et al. The effect of magnesium infusion on rest cramps: a randomized controlled trial. J Gerontol A Biol Sci Med Sci 2011;66:661-6.
- Setaro L, Santos-Silva PR, Nakano EY, et al. Magnesium status and the physical performance of volleyball players: effects of magnesium supplementation. J Sports Sci 2014;32:438-45.
- Veronese N, Berton L, Carraro S, et al. Effect of oral magnesium supplementation on physical performance in healthy elderly women involved in a weekly exercise program: a randomized controlled trial. Am J Nutr 2014;100:974-81.
- Monaghan DT, Jane DE. Pharmacology of NMDA receptors. In: Van Dongen AM, editor. Biology of the NMDA receptor. Boca Raton (FL): CRC Press/Taylor & Francis; 2009. Chapter 12.
- Gecz, J. Glutamate receptors and learning and memory. Nat. Genet 2010;42:925
- Berger AJ, Dieudonne S, Ascher P. Glycine uptake governs glycine site occupancy at NMDA receptors of excitatory synapses. J. Neurophysiol 1998;80: 3336–3340.
- Hubner CA, Stein V, Hermans-Borgmeyer I, et al. Disruption of KCC2 reveals an essential role of K-Cl cotransport already in early synaptic inhibition. Neuron 2001;30:515–524.
- Chen SW, Kong WX, Zhang YJ, et al. Possible anxiolytic effects of taurine in the mouse elevated plus-maze. Life Sci 2004;75(12):1503-1511.
- Hertz L, Kvamme E, McGeer, EG, et al. Glutamine, Glutamate, and Gaba in the Central Nervous System. Alan R Liss Inc. New York; 1983.
- Bowtell JL, Gelly K, Jackman ML, et al. Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise. J.Appl Physiol 1999:1770-1777.
- Welbourne TC. Increased plasma bicarbonate and growth hormone after an oral glutamine load. Am J Clin Nutr 1995;61(5):1058-1061.
- Hasler G, Van der Veen JW, Tumonis, T, et al. Reduced Prefrontal Glutamate/Glutamine and Aminobutyric Acid Levels in Major Depression Determined Using Proton Magnetic Resonance Spectroscopy. Arch Gen Psych 2007;64 (2):193-200.
- Owens DF, Krieg Stein AR. Is there more to GABA than synaptic inhibition? Nat. Rev. Neurosci 2002;3:715
- Kakuda T, Nozawa A, Sugimoto A, et al. Inhibition by Theanine of binding of [3H]AMPA, [3H]Kainate and [3H]MDL 105,519 to glutamate receptors. Biosci Biotechnol Biochem 2002;66:2683-86.
- Kimura R, Murata T. Influence of alkylamides of glutamic acid and related compounds on the central nervous system I. Central depressant effect of theanine. Chem Pharm Bull 1971;19:1257–1261.
- Nathan PJ, Lu K, Gray M, et al.; The neuropharmacology of L-theanine (N-ethyl-L-glutamine): a possible neuroprotective and cognitive enhancing agent. J Herb Pharmacother 2006;6(2):21-30.
- Heese T, Jenkinson J, Love C, et al.& Anxiolytic effects of L-theanine - a component of green tea - when combined with midazolam, in the male Sprague-Dawley rat. AANA J 2009;77(6):445-449.
- Ito K, Nagato Y, Aoi N, et al. Effects of L-theanine on the release of alpha brain waves in human volunteers. Nippon Nogeikagaku Kaishi 1998;72:153-157.
- Lu K., Gray MA, Oliver C, et al. The acute effects of L-theanine in comparison with alprazolam on anticipatory anxiety in humans. Hum Psychopharmacol 2004;19(7):457-465.
- Lardner AL. Neurobiological effects of the green tea constituent Theanine and its potential role in the treatment of psychiatric and neurodegenerative disorders. Nutr Neurosci 2014;17:145-55.
- Smart TG, Hosie AM, Miller PS. Zn2+ ions: modulators of excitatory and inhibitory synaptic activity. Neuroscientist 2004;10(5):432-42.
- Gröber U. Magnesium. In: Gröber U., editor. Micronutrients: Metabolic Tuning-Prevention-Therapy. 1st ed. MedPharm Scientific Publishers; Stuttgart, Germany: 2009:159–166.
- Foca FJ. Motor and sensory neuropathy secondary to excessive pyridoxine ingestion. Arch Phys Med Rehabil 1985;66(9):634-6.
- Dalton K, Dalton MJ. Characteristics of pyridoxine overdose neuropathy syndrome. Acta Neurol Scand 1987;76(1):8-11.