Decreases dangerous levels of homocysteine
Lowers the risk of cardiovascular disease
Protects against damaged blood vessels
Slows the aging process
Methylation is a key process that is essential for the function of every cell in the body, keeping aging and disease at bay. Methylation reduces homocysteine, a toxic amino acid that dramatically increases the risk of heart disease, cancer, bone loss, joint degradation, mood imbalances and cognitive decline.
MaxMethyl contains all the cofactors and methyl donors needed to promote methylation and convert homocysteine into useful amino acids: vitamin B6, vitamin B12, folate and trimethylglycine (TMG). This combination of nutrients was shown to significantly reduce homocysteine levels after just 6 weeks of supplementation. TMG alone can reduce homocysteine plasma levels by as much as 30%. Additionally, B vitamins, specifically B6, B12 and folate, have been shown to reduce the risk of stroke due to their ability to reduce homocysteine.
Recently it was discovered that a large portion of the population has a mutation of the gene MTHFR, which prevents them from converting folate into its usable form, L-5-MTHF. This leads to folate deficiency and decreased methylation, resulting in high homocysteine levels. The folate used in MaxMethyl is in the form of L-5-MTHF, which makes it an ideal supplement for those with the MTHFR mutation.
Most people do not get enough of the specific nutrients that support methylation in their diets. MaxMethyl is an excellent supplement for aging in general, for those who know they have high homocysteine levels, and those looking for support against age-related degenerative conditions of the bones, joints, nerves and cognitive function.
MaxMethyl provides nutrients that help in tissue formation, the formation of red blood cells, and in the metabolism of carbohydrates, fats, and proteins.
|Serving Size: 1 Capsule||Amount|
|Trimethylglycine (betaine anhydrous)||500 mg|
|Folic acid (calcium L-5-MTHF)||267 mcg|
|Vitamin B6 (Pyridoxal-5’-phosphate)||17 mg|
|Vitamin B12 (Methylcobalamin)||216 mcg|
|Non-medical ingredients: |
sodium stearyl fumarate. Capsule : hypromellose.
AOR™ guarantees that all ingredients have been declared on the label. Contains no wheat, gluten, corn, nuts, peanuts, sesame seeds, sulphites, mustard, soy, dairy, eggs, fish, shellfish or any animal byproduct.
Take 1 capsule three times daily with/without food, or as directed by a qualified health care practitioner.
Consult a health care practitioner prior to use if you are pregnant, breastfeeding, or if you have liver or cardiovascular disease.
Healthy blood pressure
The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide or replace medical advice to individuals from a qualified health care professional. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes.
Protect yourself against elevated homocysteine levels
Homocysteine 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.
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.
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.
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.
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; 2000
Sato 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 & Wilkins
Verhoef P, de Groot LC. Dietary determinants of plasma homocysteine concentrations. Semin Vasc Med. 2005 May;5(2):110-23. Review.
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.
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