Homocysteine: Understanding its Role in Health and Disease

Homocysteine: Understanding its Role in Health and Disease

For several years, this substance has been repeatedly mentioned in the media in connection with vascular calcification, heart attacks and strokes. But very few people know exactly what she is all about. Homocysteine ​​is an intermediate product in human protein metabolism, more precisely in the breakdown of methionine. This amino acid must be supplied daily through food and serves the body, among other things, as an essential source of sulphur. Homocysteine, on the other hand, is a toxic waste product and is, therefore, quickly bound, converted back into methionine with the help of vitamin B12 and folic acid, or broken down further with the help of vitamin B6 and mostly excreted through the kidneys.

Causes of elevated homocysteine ​​levels

The metabolic pathways described are essential for understanding how a potentially dangerous excess of homocysteine ​​in the blood can occur. Here are some of the causes:

  • Kidney function declines as we age, and homocysteine ​​levels naturally rise (about 10% every ten years).
  • If there is insufficient folic acid and vitamins from the B group in the diet, homocysteine ​​cannot be converted and thus eliminated. Excessive coffee consumption impedes the absorption of folic acid and B vitamins in the gastrointestinal tract.
  • Homocysteine levels are increased with a diet rich in methionine (e.g. eggs, fish, offal, Brazil nuts, corn).
  • Numerous drugs affect the methionine metabolism and “consume” the B vitamins or folic acid so that they can no longer adequately fulfil their tasks. These include antibiotics, tuberculosis drugs, antiepileptics, pills, rheumatism drugs, and expectorants.
  • Certain diseases also increase the total requirement for vitamin B and folic acid, e.g. B., diabetes, cancer, liver diseases or nerve diseases (neuropathies).
  • In the case of kidney weakness, homocysteine ​​is no longer sufficiently broken down and excreted.
  • Rarely is there a congenital disorder of amino acid metabolism in which the metabolic pathway is disrupted (homocystinuria).

Lack of exercise also drives up the amount of homocysteine.


Too much homocysteine ​​is dangerous.

Homocysteine ​​damages the body in several ways. It activates blood platelets – and thereby promotes blood clot formation. It damages the cells B. on the inner walls of the vessels directly and indirectly via the activation of various mechanisms. It encourages scavenger cells to migrate into the vessel walls and muscle cells to change. The consequences? Permanently elevated homocysteine ​​levels in the blood (hyperhomocysteinemia) probably promote vascular calcification and thus the development of corresponding diseases: heart attack, stroke, arterial occlusive disease – diseases from which almost every second German citizen dies. It also appears to increase the risk of venous thrombosis. In addition, it is discussed that homocysteine ​​is also a risk factor for Alzheimer’s disease and dementia caused by vascular changes, as well as for age-related macular degeneration (AMD). This shared visual impairment increases with age.

Determine homocysteine

The homocysteine ​​concentration in the blood determines the individual risk of arteriosclerosis and the associated secondary diseases, especially in patients with other risk factors, such as elevated blood lipid levels, and if homocystinuria is suspected. Blood is taken in the morning on an empty stomach, 2-3 days beforehand. You should not eat anything rich in methionine, and you should drink as little coffee as possible. 

The average value is below ten μmol/L (micromoles per litre). If the homocysteine ​​level is elevated, depending on the extent and other risk factors, therapy with folic acid, vitamin B6 and vitamin B12 preparations is recommended over the long term.

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