Homocysteine

Overview

Homocysteine is an amino acid found in the body’s blood; however, if levels are too high, it becomes very dangerous. It may be a participant in 90% of heart disease.

Homocysteine elevation leads to plaque build-up, smooth muscle proliferation, intimal-medial wall thickening, increased thrombosis and decreased nitric oxide formation, meaning less vessel wall pliability). This condition also speeds up the oxidation of cholesterol, taken up by macrophages, which leads to foam cells in plaques.

Nitric Oxide reacts with homocysteine forming S-nitroso homocysteine, which protects endothelial cells.

A level greater than 6.3 micromoles/l reflects a steep, progressive increase in the risk of heart disease. Medications to treat congestive heart failure often result in depletion of B vitamins which disrupt the metabolism of homocysteine.

Levels are kept reduced by:

Remethylation of Methionine
Transulfuration

Homocysteine is catabolized to Cysteine, Glutathione and Taurine.

In remethylation - the methyl groups are supplied by folate (5-methyltetrahydrofolate is needed for normal function of methionine synthetase)

Homocysteine may be converted into:

Cysteine
Methionine
SAMe (donates methyl groups to form creatine, phosphatidylcholine, and carnitine)

Genetic Defects may be:

Remethylation issue
Catabolic issue

Supplemental use of sidebar creatine diminishes the need for SAMe, and therefore reduces the need for homocysteine.

Choline, converted in the liver to phosphatidylcholine via methylation of phosphatidylethanolamine, reduces the need for SAMe.

Transulfuration is homocysteine to cysteine, taurine and sulfate.

There may be a deficiency of B6, or genetic def/dysfunction of cystathionine-B-synthase

B6 is converted to active cofactor pyridoxyl-5-phosphate. Too high doses of B6 (300-500 mg/day, chronically) may lead to peripheral neuropathy. Pyridoxyl-5-phosphate is used instead.

Cysteine/taurine are important nutrients for cardiac health, hepatic detoxification, cholesterol excretion, bile-salt formation, and glutathione production.

Methylation is fundamental in maintaining healthy DNA.

Homocysteine:

Blocks production of nitric oxide
Stimulates smooth muscle proliferation
Lipid abnormalities
Thromboxane A2 activity
Binding of Lp (a) to fibrin for increased clotting
Intimal-medial wall thickening.

Homocysteine and Associated Disorders:

Extracranial carotid artery disease
Predisposition to deep vein thrombosis
Hyperhomocysteinemia, hypercholesterolemia, or hypothyroidism
Increased with elevated creatinine (Renal Disease)
Impaired metabolism in type 2 diabetes
Associated eye problems, depression, liver disease, Crohn's, ulcerative colitis, pernicious anemia, and Parkinson’s

Clinically, 30-40% of elderly people have high levels (same as healthy individuals)

Also raised in impaired renal function, use of drugs i.e. diuretics and malnutrition

Treatment Options

Homocysteine-Lowering Nutrients:

Specific vitamins & minerals
SAMe
TMG
Avoid foods rich in methionine like flesh foods and dairy products
Chronic inflammation, high intensity exercise and age while putting the brakes on methylation
Choline (methyl donor) can act independent of cofactors to lower homocysteine. It operates in the liver and kidneys where it is converted to TMG.

Chemical component in black tea and coffee—which contains chlogenic acid—can raise homocysteine levels.

Diet rich in fresh fruit and vegetables may decrease levels.

Niacin may increase levels of homocysteine by depleting SAMe.

High levels of homocysteine can be extremely dangerous. The doctor first will do the appropriate testing to get an accurate indication level so that a treatment plan can be constructed depending on the severity. At the wellness center, the treatment plan is extremely individualized depending on each patient's body. It is our mission to treat the cause of the problem, not just the symptoms, so that optimal health can be achieved.

Learn more about how the Houston Wellness Clinic treats Homocysteine.

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