Please note: The content of this post is my own, unless the technical terms is too hard to explain, then the content is copy and pasted. I am not a medical professional and thus the post is my point of view. But the content is science-based and credible. Just because it is a new science, does not necessarily make it quackery. Always consult your doctor first before trying a new treatment.

Homocysteine is a sulfur-containing amino acid that can be converted to cystathionine and further to cysteine via the transsulfuration pathway or remethylated to methionine. The latter reaction is catalyzed by methionine synthase in most tissues. In this reaction, vitamin B₁₂ (cobalamin) serves as cofactor and folate (5-metyltetrahydrofolate) as substrate. In the liver and kidney, an additional pathway for homocysteine remethylation exists, requiring betaine as a methyl donor. Choline is the immediate metabolic precursor of betaine. Choline is involved in membrane biosynthesis and acetylcholine formation and is regarded as a critical nutrient in fetal development and neuro-transmission.

An interesting read: Add brain assault to homocysteine’s rap sheet

There are two major conditions too high or too low homocysteine levels can cause:

1. Hyperhomocysteinemia – When the levels are high. This is the more come of the two. a person more prone to [simple_tooltip content=’The endothelium lines the inside of the blood and heart vessels. It is a thin membrane which helps regulate blood clotting, immune function and controls vascular relaxation. When endothelial dysfunction occurs, the ability to perform these tasks is reduced due to the blood vessels not functioning properly.’]endothelial cell injury[/simple_tooltip], which leads to inflammation in the blood vessels, which in turn may lead to [simple_tooltip content=’The process of forming atheromas, plaques in the inner lining (the intima) of arteries.’]atherogenesis[/simple_tooltip], which can result in [simple_tooltip content=’Condition caused by a restriction in blood supply to tissues, causing a shortage of oxygen that is needed for cellular metabolism (to keep tissue alive).’]ischemic injury[/simple_tooltip]. Hyperhomocysteinemia is therefore a possible risk factor for coronary artery disease.

1.2. Homocystinuria – Homocystinuria is more severe than Hyperhomocysteinemia. This is when level of Homocysteine is dangerously high. It is much rarer than Hyperhomocysteinemia, it is autosomal recessive disorder characterized by severe elevations in plasma and urine homocysteine concentrations. Clinical manifestations of homocystinuria include developmental delay, osteoporosis, ocular abnormalities, thromboembolic disease, and severe premature atherosclerosis. This condition is mainly recognized in childhood.

2. Hypohomocysteinemia – This is when your homocysteine level are low. Lower than normal homocysteine levels can be a result of a metabolic insult which prompts the body to produce more glutathione  than normal, low intake of the amino acids methionine and cysteine, an inherently low level of the enzyme MTHFR, low intake of vitamins folate and B12, or increased detoxification of xenobiotics through the phase II liver reaction sulfation.

Hypohomocysteinemia has been shown to play a role in the malnutrition-inflammation-cachexia syndrome with which low dietary intake of methionine would lead to worsening of chronic kidney disease, with which homocysteine can be a variable in determining survivability of the patient.

If there is a low level of antioxidants, the body will steal cysteine from homocysteine to support glutathione production. So low homocysteine may be a sign of oxidative stress. Formation of more cysteine from homocysteine would then deplete the homocysteine pool to support the formation of glutathione to combat the free radicals.

Another factor that would deplete homocysteine levels would be the detoxification pathway sulfation – CBS. Cysteine is also employed in the formation of bile acids such as taurine. Taurine is especially synthesized when the body takes in fat and alcohol. Synthesis of taurine would also deplete homocysteine levels by promoting the Transulfuration pathway in the formation of cysteine.

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