Cardiovascular disease (CVD) is the leading cause of death worldwide. Many factors have been identified as potential causes for CVD development, such as smoking, obesity, hypertension, sedentary lifestyle, and unhealthy diet.

However, there is increasing evidence that levels of homocysteine, an amino acid produced during methionine metabolism, may also contribute to CVD development.

What is Homocysteine?

Homocysteine is a sulfur-containing amino acid produced through the metabolism of methionine, an essential amino acid found in many types of food.

Methionine is converted to homocysteine in a biochemical pathway that requires various enzymes and nutrients, including vitamin B6, vitamin B12, and folate. After being formed, homocysteine can either be remethylated back to methionine or converted to cystathionine and then to cysteine, another amino acid.

Abnormally high levels of homocysteine, known as hyperhomocysteinemia, can be caused by genetic mutations, nutritional deficiencies, or certain medical conditions.

For example, mutations in the genes that encode for the enzymes catalyzing the conversion of homocysteine to methionine can cause hyperhomocysteinemia. Deficiencies in vitamin B6, vitamin B12, or folate can lead to homocysteine accumulation as these nutrients are required for the homocysteine metabolism pathway to work properly.

Medical conditions that can cause hyperhomocysteinemia include chronic kidney disease, hypothyroidism, and psoriasis.

The Relationship between Homocysteine and CVD

Studies have shown that high levels of homocysteine in the blood are associated with an increased risk of developing CVD. One of the mechanisms by which homocysteine could contribute to CVD development is by promoting oxidative stress and inflammation.

High levels of homocysteine have been shown to induce endothelial dysfunction, a condition in which the cells lining the blood vessels lose their ability to regulate vascular tone and permeability. This can lead to the development of atherosclerosis, a condition in which cholesterol and other substances accumulate in the arterial walls, narrowing and hardening the arteries and increasing the risk of heart attack and stroke.

Homocysteine can also contribute to blood clotting, a process that can trigger heart attack and stroke.

High levels of homocysteine have been shown to promote the formation of clots in the blood vessels by damaging the endothelium and activating platelets, the small blood cells that help in the clotting process. In addition, homocysteine can interfere with the conversion of plasminogen to plasmin, an enzyme that dissolves blood clots.

Assessing Homocysteine Levels

Homocysteine levels can be measured with a simple blood test. Fasting blood samples are usually taken for the test, as homocysteine levels can increase after a meal.

The normal range for homocysteine levels varies depending on age and sex, but generally ranges from 4 to 15 micromoles per liter (μmol/L). Levels above 15 μmol/L are considered high and may require further investigation and treatment.

Treatment and Prevention of Hyperhomocysteinemia

Treatment for high homocysteine levels depends on the underlying cause of hyperhomocysteinemia.

For individuals with a genetic mutation causing hyperhomocysteinemia, medication, such as pyridoxine (vitamin B6), may be prescribed to help lower homocysteine levels. For individuals with nutritional deficiencies, supplementation with vitamin B6, vitamin B12, or folate can be used to reduce homocysteine levels.

In addition, lifestyle interventions, such as healthy diet modifications, regular exercise, and smoking cessation, can also reduce homocysteine levels and lower the risk of developing CVD.

Conclusion

High homocysteine levels can contribute to CVD development, although the relationship between the two is complex and not fully understood.

Measurement of homocysteine levels in the blood can be used to assess the risk of developing CVD, and interventions to lower homocysteine levels, including nutritional supplementation and lifestyle modifications, can be used to prevent CVD development. Further research is needed to fully understand the relationship between homocysteine and CVD and to develop effective prevention and treatment strategies.