Ortho-Methyl

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Ortho•Methyl supports optimal methylation and healthy metabolism of the toxic amino acid homocysteine.

Recent research suggests that methylation plays a central role in human health, supporting normal cell differentiation, gene expression, bone structure, and cardiovascular function. Research strongly suggests that elevated homocysteine is plays a negative role in cardiovascular health.

Ortho•Methyl provides orthomolecules with proven methylation-enhancing abilities, at doses supported by published human studies.*

60 Servings 185 G AOR04015

SUPPLEMENT FACTS:
Serving Size: 1 Teaspoons %DRI

Trimethylglycine (TMG Anhydrous) .......... 3000 mg *
Folic acid ........................................... 400 mcg 200
Pyridoxamine (B6 vitamer) .................... 12.5 mg 735
Riboflavin ............................................. 6.5 mg 500
Methylcobalamin (B12 Coenzyme) ............ 250mcg 1042

*Dietary Reference Intake not established.
Other ingredients: Silicon dioxide.

AOR guarantees that no ingredients not listed on the label have been added to the product. Contains no wheat, gluten, corn, nuts, dairy, soy, eggs, fish or shellfish.

Suggested Use
Take one and a half teaspoons twice daily, or as directed by a qualified health practitioner.

Main Applications
* Aging
* Elevated homocysteine levels
* Cardiovascular health
* Inflammation
* Osteoporosis
* Neurodegenerative diseases
* Macular degeneration
* Cancer

Pregnancy / Nursing
None, best to avoid.

Cautions
Avoid moisture e.g. using a wet spoon as the powder is hygroscopic and will tend to clump together into a hardened mass.

Methylation is a metabolic process that involves the addition of methyl groups. Methylation is essential for over 100 different metabolic reactions including the methylation of nucleic acids, DNA, RNA, proteins, phospholipids, myelin, polysaccharides, melatonin, creatine, catecholamines and other molecules.

Impaired methylation is thought to be a risk factor for neural tube defect, impairs DNA repair and may be a risk factor for cancer, and can lead to reduced myelination in the aging brain. If methylation is impaired, homocysteine levels increase.

What is Homocysteine?

Homocysteine is a toxic amino acid. It is normally present in the body and is part of several metabolic pathways. Homocysteine is produced when methionine looses a methyl group. The transfer of methyl groups (CH3) from methionine is essential for the production of nucleic acids, fats and energy. Furthermore, methylation is responsible for the conversion of homocysteine to useful methionine and SAMe. When homocysteine levels increase, blood vessels are damaged and collagen formation is impeded.

Why is Homocysteine harmful?

Elevated homocysteine levels are indicative of a reduced methylation capacity.

Elevated blood levels of Homocysteine (Hyperhomocysteinemia) have been associated with an increase in the incidence of coronary artery disease and an augmentation in the 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 on endothelial and smooth muscle cells and are thought to damage blood vessel walls and lead to complications such as premature occlusive arterial disease. Impairment in the methylation of homocysteine to cysteine might also lead to higher blood cholesterol levels because cysteine is required for the metabolism of cholesterol. In addition, it is possible that the amino acid directly affects blood coagulation leading to increases in blood clot formation.

What causes elevations in homocysteine levels?

There are two different metabolic pathways in the human body that lead to the elimination of homocysteine. Homocysteine can be methylated to methionine or it can be condensed into cysteine.

The transmethylation of homocysteine into methionine requires methyltetrahydrofolate (the active form of folate) and vitamin B12. The transsulfuration pathway is vitamin B6 dependent and leads to the condensation of serine and homocysteine for the production of cysteine. The powerful antioxidant glutathione is also produced through the transsulfuration of homocysteine. Vitamin B6 and folic acid reduce homocysteine levels through different mechanisms and supplementation with a B6 vitaminer is especially important for those with a defective folate-metabolizing enzyme. Elevations in homocysteine levels can arise from multiple causes. Genetic defects leading to deficiencies and reduced activity of the enzymes required for the metabolism of homocysteine play a major role in cases of elevated homocysteine levels. Several different defects can impair the uptake, transfer, and conversion of dietary vitamin B12 into the active form of the vitamin. Defects in the enzyme known as 5-methyltetrahydro-folate-homocystinuria are the most common form of hyperhomocysteinemia. More than 20 mutations for the gene responsible for the production of the enzyme have been identified, with some responding to vitamin B6 supplementation while others do not.

Poor consumption of nutritional factors involved in homocysteine metabolism lead to hyperhomocysteinemia; of particular importance are vitamins B12, B6 and folic acid. For instance, low folate levels we shown to contribute to persistent elevations in homocysteine levels. Insufficient intake of folate, vitamin B12 and B6 are common in the elderly.

Research

• A study of over a thousand people showed that, as dietary folate intake decrease, homocysteine levels and stenosis of the carotid arteries increase. Similar results have related folate intake to coronary artery stenosis, heart attacks and death due to cardiac disease.
• 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.
• Homocysteine levels reached a stable low with 400?g of folate per day leading to a 20-25% reduction. It is estimated that over 40% of the population is not consuming enough folate to keep homocysteine levels low.
• Elevated homocysteine levels are thought to interfere with collagen cross-linking and may have an important role in osteoporosis. ?-homocysteine interacts with aldose groups found on collagen and leads to structural defects in collagen. In vitro studies have demonstrated that homocysteine increases osteoclastic activity, which leads to bone resorption.
• In the Framingham study, men with high homocysteine levels had a 4-fold increase in their risk of hip fractures.
• In a study published in The New England Journal of Medicine, Dutch researchers showed that men and women with high homocysteine levels were twice as likely to have suffered form a broken hip or have fractured other bones commonly injured in the elderly.
• Folic acid supplementation reduces homocysteine levels even if the person is not 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.

How can homocysteine levels be reduced?

The enzyme that metabolizes homocysteine into methionine uses folate and B12 as cofactors. Vitamin B6 is also an important cofactor for methylation and transsulfuration enzymes. Ortho Methyl contains pyridox-amine, one of three different forms of vitamin B6. Pyridox-amine is superior at preventing glycation, a detrimental reaction between proteins and sugars that impairs function and plays a significant part in the aging process. Trimethylglycine, also present in Ortho Methyl, is a methyl group donor and can reduce homocysteine plasma levels by as much as 30%. Trimethylglycine is the most effective homocysteine lowering substance known.

OrthoMethyl is AOR’s superior formulation to up regulate methylation. It has been designed with generous amounts of highly absorbable cofactors and methyl donors necessary to enhance methylation and to promote the transformation of homocysteine into harmless metabolites. OrthoMethyl is supported by research and improves methylation - a metabolic process important for health and crucial for the prevention of disease and premature aging.

References

• Shils M. E., Olson J.A., Shike M., Ross A. C., Modern Nutrition in Health and Disease, 1998, 9th Edition, Baltimore, Lippincott Williams & Wilkins

• 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

• Herrmann M, Widmann T, Herrmann W. Homocysteine - a newly recognised risk factor for osteoporosis. Clin Chem Lab Med. 2005;43(10):1111-7.

• Verhoef P, de Groot LC. Dietary determinants of plasma homocysteine concentrations. Semin Vasc Med. 2005 May;5(2):110-23. Review.

• 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.

• Cashman KD. Homocysteine and osteoporotic fracture risk: a potential role for B vitamins. Nutr Rev. 2005 Jan;63(1):29-36.

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