MethylPlus

AOR04260

Agents de méthylation et cofacteurs

  • Diminue les taux dangereux d’homocystéine
  • Réduit le risque de maladies cardiovasculaires
  • Prévient l’endommagement des vaisseaux sanguins.
  • Ralentit le processus de vieillissement
Sans Gluten
Sans OGM
Végétalien

$37.44

En stock

La méthylation est un processus clé indispensable au bon fonctionnement de toutes les cellules de l’organisme et permettant d’éviter le vieillissement et les maladies. La méthylation réduit l’homocystéine, un acide aminé toxique qui augmente considérablement le risque de maladie cardiaque, de cancer, de perte osseuse, de dégradation articulaire, de déséquilibre de l’humeur et de déclin cognitif.

MethylPlus contient tous les cofacteurs et donneurs de méthyle requis dans les processus de méthylation et pour la convertion de l’homocystéine en acides aminés utiles : vitamine B6, vitamine B12, folate et triméthylglycine (TMG). Il a été démontré que cette combinaison de nutriments réduit significativement les taux d’homocystéine après seulement 6 semaines de supplémentation. La TMG seule peut réduire les taux plasmatiques d’homocystéine jusqu’à 30 %. De plus, il a été démontré que les vitamines B, en particulier B6, B12 et le folate, réduisent le risque d’AVC en raison de leur capacité à réduire l’homocystéine.

Il a été récemment découvert qu’une grande partie de la population présente une mutation du gène MTHFR qui l’empêche de convertir le folate en sa forme utilisable, L-5-MTHF. Cela entraîne une carence en folate et une diminution de la méthylation conduisant à des taux élevés d’homocystéine. Le folate utilisé dans MethylPlus est sous forme de L-5-MTHF, ce qui en fait un complément idéal pour les personnes présentant la mutation MTHFR.

La grande majorité de personnes n’obtient pas les nutriments spécifiques favorisant la méthylation de son alimentation. MethylPlus est un excellent complément pour le vieillissement en général, pour les personnes ayant des taux élevés d’homocystéine et pour celles qui sont à la recherche d’un soutien contre les maladies dégénératives des os, articulations, nerfs et fonctions cognitives liées au vieillissement.

Avantage AOR

La formule de MethylPlus d’AOR réunit un maximum de cofacteurs et de donneurs de méthyle nécessaires à la convertion de l’homocystéine en acides aminés utiles, aidant ainsi à la réduction du risque de maladie cardiaque.

NPN

80026949

Discussion

MéthylPlus offre des nutriments qui favorisent la formation des tissus, des globules rouges et le métabolisme des glucides, des matières grasses et des protéines.

Certifie

AOR™ certifie que tous les ingrédients sont mentionnés sur l’étiquette. Ne contient ni blé, ni gluten, ni maïs, ni noix, ni arachide, ni graine de sésame, ni sulfite, ni moutarde, ni soja, ni produit laitier, ni œuf, ni poisson, ni mollusque, ni crustacé ou produit d’origine animale.

Posologie Adulte

Prendre une capsule trois fois par jour avec ou sans nourriture, ou selon les recommandations d’un professionnel de la santé.

Mises en Garde

Consulter un professionnel de la santé avant d’utiliser ce produit si vous êtes enceinte, si vous allaitez, ou si vous souffrez d’une maladie hépatique ou cardiovasculaire.

Main Applications
  • Methylation
  • Homocysteine
  • Detoxification
  • Cardiovascular health
  • Healthy blood pressure
  • Anti-aging
Avertissement

Les renseignements sur les produits contenus dans ce site web, y compris la description des produits, leurs effets potentiels et leurs avantages sont destinés à des fins d’information uniquement. Ils ne sont pas destinés à donner ou remplacer les renseignements médicaux ou l’avis d’un professionnel qualifié. Consulter votre médecin pour tout problème de santé

Portion: une capsule
Vitamine B6 (Pyridoxal-5-Phosphate)
17 mg
Folate (L-5-méthyltétrahydrofolate de calcium)
267 mcg
Vitamine B12 (méthylcobalamine)
216 mcg
Triméthylglycine (bétaïne anhydre)
500 mcg

Ingrédients non médicinaux : stéarylfumarate de sodium.

Capsule : hypromellose.

Background

Protect yourself against elevated homocysteine levelsHomocysteine is a toxic amino acid. It is naturally produced in the body as a byproduct of several metabolic pathways, such as the metabolism of the amino acid methionine to produce essential nucleic acids, fats and high-energy bonds. When methionine loses a methyl group, homocysteine is produced. If homocysteine levels increase, blood vessels are damaged and collagen formation is impeded. There are two pathways in the human body that can lead to the elimination of homocysteine: it can be methylated to methionine or condensed into cysteine. The former process requires folate and vitamin B12, while the latter is vitamin B6 dependant.Why is Homocysteine Harmful? Elevated blood levels of homocysteine (Hyperhomocysteinemia) have been associated with higher incidences of coronary artery disease and increased risk of mortality from cardiovascular diseases. Hyperhomocysteinemia is an independent factor for peripheral vascular, cerebrovascular and coronary heart disease. High homocysteine levels have a variety of injurious effects and are thought to damage blood vessel walls and lead to cardiovascular complications. Impairment in the conversion of homocysteine to cysteine might also lead to higher blood cholesterol levels because cysteine is required for the metabolism of cholesterol. It is also possible that the amino acid affects blood coagulation.What causes elevated homocysteine levels? Elevations can arise from genetic defects, or from poor consumption of nutritional factors involved in homocysteine metabolism, particularly vitamins B12, B6 and folic acid. Insufficient intake of folate, vitamin B12 and B6 are common in the elderly. However, even young, healthy adults who exercise have been found to have elevated levels of homocysteine.

Research

  • A study of over 1000 people showed that as dietary folate intake decreases, homocysteine level, narrowing of arteries, heart attacks and death due to cardiac disease increase.
  • It is estimated that over 40% of the population is not consuming enough folate to keep homocysteine levels low.
  • Hyperhomocysteinemia is believed to cause 60% of peripheral vascular disease.
  • The Physician’s Health Study showed that men with higher homocysteine levels had a threefold risk of coronary events.
  • Elevated homocysteine levels lead to structural defects in collagen and may play a role in osteoporosis. In vitro studies have demonstrated that homocysteine increases the activity of bone breaking cells, leading to bone resorption.
  • Folic acid supplementation reduces homocysteine levels even if the individual is not folate deficient. Simple supplementation can reduce mild homocysteine elevation in virtually all cases. Folic acid supplementation is more effective than dietary folate at lowering homocysteine levels.

The ingredient combination included in AOR’s MaxMethyl was tested in a randomized, double-blind, controlled study from the University of East London. Participants who took this combination had a significant decrease in their homocysteine levels regardless of their initial levels. Those whose initial levels of homocysteine were high enough to put them in the “at risk” category experienced a dramatic homocysteine drop, indicating that these participants reduced their risk of cardiovascular disease in only 6 weeks of supplementation.How can homocysteine levels be reduced? The enzymes that metabolize homocysteine into methionine and cysteine use folate, vitamin B12, and vitamin B6 as cofactors. Trimethylglycine is a methyl group donor and has been shown to reduce plasma homocysteine levels by as much as 30%! Trimethylglycine is the most effective homocysteine lowering substance known.  AOR’s MaxMethyl has been formulated to include the cofactors and methyl donors necessary for the methylation of homocysteine into other harmless amino acids, and is therefore an effective supplement for the support of cardiovascular health.

Market Trends

For many consumers, methylation products are not well understood in terms of their importance. Methylation is not a process that is talked about in the media or in health circles. However, proper methylation processes are the basis for health in so many areas including joint health, mood, heart disease, and more! Without adequately functioning methylation, aging and disease arrive quickly.

AOR Advantage

MaxMethyl is formulated to include all the cofactors and methyl donors needed to convert homocysteine into useful amino acids, thereby helping to reduce the risk of heart disease.

References

Cashman KD. Homocysteine and osteoporotic fracture risk: a potential role for B vitamins. Nutr Rev. 2005 Jan;63(1):29-36.Herrmann M, Widmann T, Herrmann W. Homocysteine – a newly recognised risk factor for osteoporosis. Clin Chem Lab Med. 2005;43(10):1111-7.Jellin JM, Gregory P, Batz F, Hitchens K, et al. Pharmacist’s Letter/Prescriber’s Letter Natural Medicines Comprehensive Database. 3rd ed. Stockton, CA: Therapeutic Research Faculty; 2000Sato Y, Honda Y, Iwamoto J, Kanoko T, Satoh K. Homocysteine as a predictive factor for hip fracture in stroke patients. Bone. 2005 Apr;36(4):721-6.Shils M. E., Olson J.A., Shike M., Ross A. C., Modern Nutrition in Health and Disease, 1998, 9th Edition, Baltimore, Lippincott Williams & WilkinsVerhoef P, de Groot LC. Dietary determinants of plasma homocysteine concentrations. Semin Vasc Med. 2005 May;5(2):110-23. Review.

Abstract

Vitamin B supplementation, homocysteine levels, and the risk of cerebrovascular disease: A meta-analysis.Neurology. 2013 Sep 18.Ji Y, Tan S, Xu Y, Chandra A, Shi C, Song B, Qin J, Gao Y.OBJECTIVE: To perform a meta-analysis on the effect of lowering homocysteine levels via B vitamin supplementation on cerebrovascular disease risk.METHODS: Using clinical trials published before August 2012 to assess stroke events, we used relative risks (RRs) with 95% confidence intervals (95% CIs) to measure the association between B vitamin supplementation and endpoint events using a fixed-effects model and χ2 tests. We included 14 randomized controlled trials with 54,913 participants in this analysis.RESULTS: We observed a reduction in overall stroke events resulting from reduction in homocysteine levels following B vitamin supplementation (RR 0.93; 95% CI 0.86-1.00; p = 0.04) but not in subgroups divided according to primary or secondary prevention measures, ischemic vs hemorrhagic stroke, or occurrence of fatal stroke. There were beneficial effects in reducing stroke events in subgroups with ≥3 years follow-up time, and without background of cereal folate fortification or chronic kidney disease (CKD). Some trials that included CKD patients reported decreased glomerular filtration rate with B vitamin supplementation. We conducted detailed subgroup analyses for cyanocobalamin (vitamin B12) but did not find a significant benefit regarding intervention dose of vitamin B12 or baseline blood B12 concentration. Stratified analysis for blood pressure and baseline participant medication use showed benefits with >130 mm Hg systolic blood pressure and lower antiplatelet drug use in reducing stroke risk.CONCLUSIONS: B vitamin supplementation for homocysteine reduction significantly reduced stroke events, especially in subjects with certain characteristics who received appropriate intervention measures. Orally administered betaine has an acute and dose-dependent effect on serum betaine and plasma homocysteine concentrations in healthy humans.J Nutru. 2006 Jan;136(1):34-8.Schwab U, Torronen a, Meririnne E, Saarinen M, Alfthan G, Aro A, Uusitupa M.Betaine, i.e., trimethylglycine, is linked to homocysteine metabolism. A 3-mo daily betaine supplementation decreased even normal plasma total homocysteine (tHcy) concentrations in humans. The pharmacokinetic characteristics and metabolism of betaine in humans have not been investigated in detail. The aim of this study was to assess the pharmacokinetics of orally administered betaine and its acute effect on plasma tHcy concentrations. Healthy volunteers (n = 10; 3 men, 7 women) with normal body weight (mean /- SD, 69.5 /- 17.0 kg), 40.8 /- 12.4 y old, participated in the study. The betaine doses were 1, 3, and 6 g. The doses were mixed with 150 mL of orange juice and ingested after a 12-h overnight fast by each volunteer according to a randomized double-blind crossover design. Blood samples were drawn for 24 h and a 24-h urine collection was performed. Orally administered betaine had an immediate and dose-dependent effect on serum betaine concentration. Single doses of 3 and 6 g lowered plasma tHcy concentrations (P = 0.019 and P < 0.001, respectively), unlike the 1-g dose. After the highest dose, the concentrations remained low during the 24 h of monitoring. The change in plasma tHcy concentration was linearly associated with betaine dose (P = 0.006) and serum betaine concentration (R2 = 0.17, P = 0.025). The absorption and elimination of betaine were dose dependent. The urinary excretion of betaine seemed to increase with an increasing betaine dose, although a very small proportion of ingested betaine was excreted via urine. In conclusion, a single dose of orally administered betaine had an acute and dose-dependent effect on serum betaine concentration and resulted in lowered plasma tHcy concentrations within 2 h in healthy subjects.