Homocystine (Plasma)

- Plasma homocystine, as well as taurine, were significantly lower in insufficient methotrexate therapy responders.

- Plasma homocystine is higher in those with cystathionine-beta-synthase deficiency. Cystathionine beta-synthase deficiency is a rare inherited disorder in the methionine catabolic pathway, in which the impaired synthesis of cystathionine leads to accumulation of homocysteine.

- High levels in body fluids of homocystine have been associated with increased risk of cardiovascular disease as well as ocular, neurological, musculoskeletal and joint abnormalities.

- Meat contains substances that cause an increase in homocystine levels, which in turn is associated with increased risk of heart disease. High homocystine levels irritate the lining of arteries, increasing the likelihood that they will clog, whereas the folate and vitamin b6 found in vegetables and grains reduce homocystine levels.

- It has been shown in epidemiological studies that elevated levels of homocystine in the plasma is one of 3 major risk factors in dementia or Alzheimer’s. The other 2 factors are the APOE4 genotype and a decreased DHA plasma level.

– Homocystine is deemed to be a direct vascular toxin that hastens arterial blockages, not only to the coronary arteries of the heart, but also to the arteries to the brain, leading to almost 2 times higher risk of dementia.

– Moderately elevated levels of homocystine are associated with a significantly increased risk of atherosclerosis.

– Elevated homocystine tends to coincide with high homocysteine.

– The enzyme that converts homocysteine (reduced homocystine) to cystathionine is B6 dependent; remethylation of homocysteine to methionine requires B12, folate and betaine.

– High levels can (very rarely) be due to Homocystinuria: A rare biochemical abnormality characterized by the abnormal presence of homocystine in the blood and urine. It is caused by any of several enzyme deficiencies in the metabolic pathway of methionine to cystine. The disease is inherited as an autosomal-recessive trait. Its clinical signs are similar to those of Marfan’s syndrome, including intellectual disability, osteoporosis leading to skeletal abnormalities, dislocated lenses, and thromboembolism.

Treatment may include a diet low in methionine and supplementation with high doses of vitamin B6. Long-term results of treatment are not available.

Possible treatment options for high levels that are not genetic:

– Follow a strict plant-based (=vegan) diet that is high in green leafy vegetables, fruits, grains and legumes.

– Make sure to have enough B6, Folate, B12, Betaine and magnesium as those are effective for the proper metabolism of homocystine. However, getting your homocystine levels down with vitamins doesn’t reduce your chance of having heart disease.