Magnesium deficiency is one of the most common mineral deficiencies in North America. It can contribute to a multitude of symptoms and long term health concerns. Magnesium is an essential mineral for the optimal functioning of the cardiovascular, nervous and musculoskeletal systems. It also plays a role in mood stabilization and has been shown to be an effective treatment for major depression. Magnesium deficiency can also contribute to symptoms such as migraines, PMS, dysmenorrhea, muscle cramping, and insomnia. This deficiency is also commonly seen in alcoholics and patients with diabetes mellitus. There are many different forms of magnesium, but magnesium bisglycinate found in Magnesium SAP has been demonstrated to be more readily absorbed and utilized by the body versus other ion forms.
INCREASED BIOAVAILABILITY Magnesium SAP takes the mineral magnesium and naturally binds (chelates) it to 2 molecules of glycine. Because of the low molecular weight of glycine, it is readily absorbed across the intestinal membrane. It does not need to be digested and broken down to release the mineral like other magnesium ions. Once absorbed into the bloodstream, the mineral is released and can then be used by the body. Magnesium SAP is supplied in a vegetarian capsule for easy digestion
PURITY, CLEANLINESS and STABILITY Third party testing on finished products ensure Magnesium SAP is free of heavy metals, volatile organics and other impurities. electrolyte of great importance in metabolic function. Magnesium is a cofactor in more than 300 enzymatic reactions and is critically involved in energy metabolism, glucose utilization, protein synthesis, fatty acid synthesis and breakdown, and ATPase functions. It is also involved in hormonal reactions and is essential in both the central and peripheral nervous systems. It is a critical ion as it helps to maintain ionic balance of other minerals such as sodium, potassium and calcium. Magnesium deficiency is most commonly caused by increased urinary output and reduced intestinal absorption. It should be of concern when considering the elderly and those with inflammatory bowel disease; hypomagnesemia must be suspected in any patient with alcoholism, chronic diarrhea or on diuretics. Magnesium deficiency is commonly found in chronic diseases leading to inflammation of various pathologies. Altered magnesium balance is seen in diabetes mellitus, chronic renal failure, nephrolithiasis, osteoporosis, and heart and vascular disease.
METABOLIC SYNDROME Metabolic syndrome is a cluster of pathologies that includes hypertension, hyper-insulinemia of insulin resistance, dyslipidemia, HDL:cholesterol ratio >3, and increased visceral fat. These are also the risk factors for both cardiovascular disease and diabetes mellitus, both of which are implicate subclinical chronic inflammation. Adipose tissue has been linked to the development of insulin resistance as it releases proinflammatory molecules. Magnesium is a natural calcium antagonist, and it is suggested that magnesium has an anti-inflammatory effect by altering intracellular calcium concentration.
• A magnesium deficient diet has been shown to induce heart arrhythmias, impairs glucose homeostasis, and alters cholesterol and oxidative metabolism in post menopausal women.
• Serum Mg and intramononuclear Mg level means were significantly lower in patients with metabolic syndrome than in controls: 1.80?0.18 mg/dL vs. 2.43?0.43 mg/dL and 0.98?0.55 μ g/mg vs. 1.67?0.64 μ g/mg of protein (P<0.001).
• Inverse correlation was observed between, SMg and MMg with BMI; SMg with systolic blood pressure and waist circumference in women.
CARDIOVASCULAR • Supplementation of magnesium has been found to be beneficial in treating hypertension, congestive heart failure, arrhythmia, myocardial infarction, diabetes mellitus, and preeclampsia(1).
• Animal models show that magnesium deficiency releases substance P. This initiates a cascade of inflammatory, oxidative and nitrosative events, which lead to cardiomyopathy and other CVD(6, 7). The release of substance P consumes antioxidants, and promotes the formation of lesions.
• Postmenopausal women show that high magnesium intake is associated with lower concentrations of certain markers of systemic inflammation (hs-CRP, IL-6, sVCAM-1, TNF-alpha-R2) and endothelial dysfunction in postmenopausal women.
• Post-menopausal women exhibited atrial fibrillation and flutter that responded quickly to magnesium supplementation(4).
OSTEOPOROSIS • Epidemiologic studies have linked magnesium deficiency to osteoporosis(6). Studies involving magnesium deficiency show low serum parathyroid hormone (PTH) and 1,25(OH)(2)-vitamin D levels, which contribute to reduced bone formation(6).
• Magnesium deficiency resulted in inflammatory markers substance P, TNFalpha and IL1beta. Further research shows magnesium deficiency may alter bone mineral metabolism increasing the risk of osteoporosis(6).
DEPRESSION AND PMS Studies show low intracellular magnesium concentration in women with PMS, and improved symptoms with magnesium supplementation. Inflammatory PMS symptoms include altered moods (depression, anxiety and irritability), insomnia, headaches and migraines. Depression can be caused by magnesium deficiency which can be further exacerbated by calcium excess and/or stress. Supplementation with magnesium glycinate show rapid recovery from major depression.
ABSORPTION, BIOAVAILABILITY AND LESS GASTRIC IRRITATION Magnesium is absorbed by the intestines, and under ideal basal conditions the small intestine absorbs 30-50% of its intake. This percentage declines with age and IBD. Magnesium repletion is difficult to accomplish because of the cathartic action of most oral magnesium supplements at therapeutic doses. A common use for high doses of oral magnesium supplementation is to treat constipation.
• Unabsorbed magnesium and sulphate ions exert an osmotic effect and cause water to be retained in the intestinal lumen. This increases the fluidity of the intraluminal contents and results in a laxative action.
• Oral magnesium citrate acts locally in the colon as an osmotic laxative and is a component in a precolonoscopy bowel preparation. Studies show that in is not absorbed in any detectable quantities. Magnesium bisglycinate is a stable compound and is readily absorbed across the intestinal membrane as a dipeptide. Therefore, the release of magnesium in the intestine is not required for absorption.
• Magnesium amino acid chelates have shown significantly higher bioavailability than magnesium oxide.
• Magnesium bisglycinate was 2x more readily absorbed than magnesium oxide in patients with severe impairment (ileal resection) of magnesium absorption (23.5% vs 11.8%).
90 capsules per bottle
1-4 capsules daily with food, or as directed by your health care practitioner.
1. Gums JG. 2004. “Magnesium in cardiovascular and other disorders.” American Journal of Health-System
Pharmacy, Vol 61, Issue 15, 1569-1576.
2. Kaze Foleafack F, and Stoermann Chopard C. 2007 “Magnesium metabolism disturbances.” Rev Med Suisse Mar
7;3(101):605-6, 608, 610-1.
3. Musso CG. 2009. Magnesium metabolism in health and diease.” Int Urol Nephrol. 41(2):357-62. Epub 2009 Mar 10.
4. Nielson FH, Milne DB, Klevay LM, Gallagher S, Johnson L. 2007. “Dietary magnesium deficiency induces heart
rhythm changes, impairs glucose tolerance, and decreases serum cholesterol in postmenopausal women.” Am
Coll Nutr. Apr;26(2):121-32.
5. Lima Mde L, Cruz T, Rodrigues LE, Bomfim O, Correia R, Porto M, Cedro A, Vicente E. 2009. “Serum and
intracellular magnesium deficiency in patients with metabolic syndrome--evidences for its relation to insulin
resistance.” Diabetes Res Clin Pract. Feb;83(2):257-62.
6. Rude RK, Singer Fr, Gruber HE. 2009. “Skelatal and hormonal effects of magnesium deficiency.” Am Coll Nutr.
7. Kramer JH, Spurney C Iantorno M, Tziros C, Mak IT, Tejero-Taldo MI, Chmielinska JJ, Komarov AM, Weglicki WB.
2009. “Neirogenic Imflammation and cardiac dysfunction due to hypomagnesia.” Am J Med Sci. Jul;338(1):22-7.
8. Kramer JH, Mak IT, Phillips TM, Weglicki, WB. 2003. Exp Biol Med. “Dietary magnesium intake influences
circulatingpro-inflammatory neuropeptide levels and loss of myocardial olerance to posischemicstress.” Eep Biol
Med (Maywood). Jun;228(6):665-73
9. Chacko SA, Song Y, Nathan L, Tinker L, de Boer IH, Tylavsky F, Wallace R, Liu S. 2010. “Relations of dietary
magnesium intake to biomsarkers of inflammation and endothelial dysfunctionin an ethnically diverse cohort of
postmenopausal women.” Diabetes Care. Feb;33(2):304-10.
10. Quaranta S, Buscaglia MA, Meroni MG, Colombo E., Cella S. 2007. “Pilot study of the efficacy and safety of a
moodified-release magnesium 250 mg tablet (Sincronag) fo rthe treatment of prementrual syndrome.” Clin Drug
11. Eby Ga, Eby KL. 2006. “Rapid recovery form major deprssion using magnesium treatment.” Med Hypothesis
12. Izzo AA, Gaginella TS, Capasso F. 1996. “The osmotic and intrinsic mechanisms of the pharmacological laxative
action of oral high doses of magnesium sulphate. Importance of the release of digestive polypeptides and nitric
oxide.” Magnes Res. Jun;9(2):133-8.
13. Love J, Bernard EJ, Cockeram A, Cohen L, Fishman M, Gray J, Morgan D. 2009. “ A multicentre, observational
study of sodium picosulfate and magnesium citrate as a precolonoscopy bowel preparation.” Can J Gastroentrerol.
14. Hoy SM, Scott LJ, Wagstaff AJ. 2009. “Sodium picosulfate/magnesiumcitrate: a review of its use as a colorectal
cleanser.” Drugs. 69(1):123-36.
15. Firoz M, Graber M. 2001. “Bioavailability of US commercial magnesium preparations.” Magnes Res. Dec;14(4)257-62.
16. Schuette SA, Lashner BA, Janghorbani M. 1994. “Bioavailability of magnesium digycinate vs magnesium oxide in
patients with ileal resection.” J Parenter Enteral Nutr. Sep-Oct;18(5):430-5.
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