Recently, many outpatients and patients with lower extremity venous thrombosis have found high homocysteine in their blood test results, and they do not understand what this indicator is and what the risk is. Compared to triglycerides and cholesterol, which are household names, homocysteine is a relatively unknown term, but it is one of the biochemical items that is closely related to atherosclerosis, hypertension and thrombosis risk. Therefore, it is necessary to learn more about homocysteine. 1.What is homocysteine? Homocysteine (Hcy) is a sulfur-containing amino acid that is an important intermediate in the metabolism of methionine. Homocysteine in human body is derived from the methionine in animal protein (such as pork, beef, lamb, chicken, fish, eggs, etc.), so it is a by-product of the digestive system in the process of converting protein in food into energy, that is, homocysteine should be present in everyone’s body, only the content varies. Normal human levels are low, higher in men than in women, and increase with age. Normal plasma levels are generally 5-15 μmol/L, and levels above this range are called elevated (hyperhomocysteinemia). Mild elevation of homocysteine (15-30 μmol/L) is mainly due to poor dietary habits, MTHFR C 677T gene polymorphism, mild folate and vitamin B12 deficiency, mild renal impairment, and medications. Moderate elevation (30-100 μmol/L) is mainly due to moderate to severe folic acid and vitamin B12 deficiency and renal insufficiency. Severe elevations (>100 ?mol/L) are mainly due to severe vitamin B12 deficiency and cystinuria. Overall the majority of people with hyperhcythaemia are due to folic acid, vitamin B12 deficiency and renal insufficiency. Under normal conditions, the body self-regulates the metabolic process of homocysteine in the body through two pathways to maintain its relative balance in the body without producing harm to the body. One way is to reconvert it into methionine with the regulation of vitamin B12 and folic acid; the other way is to break down homocysteine into non-toxic cystathionine with the help of cystathionine beta-synthase and vitamin B6, which is then excreted from the urine for the purpose of detoxification by itself. If the lack of cystathione-β-synthase caused by congenital genetic factors makes its detoxification ability absent; or if people eat too much protein and exceed their own detoxification ability, it will cause the increase of homocysteine content in the body, which will lead to hyperhomocysteinemia after accumulation to a certain extent. 2.What is the harm of high homocysteine? The pathogenic mechanism of high homocysteine is believed to be mainly through damage to vascular endothelial cells, causing NO metabolism disorder, resulting in increased elasticity and stiffness of large arteries, causing the formation of hypertension, promoting the proliferation of vascular smooth muscle, increasing the adhesion of platelets in the blood, stimulating the vascular wall and causing damage to the arterial vessels, leading to inflammation and plaque formation on the vessel wall. Patients with high homocysteine are prone to thrombotic diseases, associated with cardiovascular risk factors and cardiovascular diseases, and are independent risk factors for peripheral and cerebrovascular atherosclerosis, neurological and hypertensive heart diseases. The higher the level of homocysteine in the blood, the greater the risk of atherosclerosis and thrombosis, and the higher the incidence of cardiovascular disease. Hyperhomocysteinemia is a risk factor for many diseases. 34.1% of patients with lower extremity venous thrombosis have elevated plasma homocysteine levels, and hyperhomocysteine increases the relative risk of venous thrombosis by 2.44 times. Atherosclerosis is associated with elevated homocysteine in 13-47% of cases. 10% of coronary heart disease is associated with elevated homocysteine, and a mild to moderate increase in homocysteine levels can increase the risk of cardiovascular death by 4-6 times, with each 5ummol/L increase in plasma homocysteine levels increasing the risk of coronary heart disease by 60% in men and 80% in women. This is equivalent to the risk of 20 mg/dL increase in total cholesterol, so it has become a recognized risk factor for cardiovascular disease, and has the name of “cholesterol of the 21st century”. 3, how to reduce homocysteine The main method of treatment for hyperhomocysteinemia is to supplement folic acid, vitamin B6 and vitamin B12, which are essential nutrients that can be obtained from the daily diet, such as green leafy vegetables, fruits, nuts, eggs, beans and so on. Animal liver and kidney are rich in folic acid, lean meat, peanuts, brown rice, green leafy vegetables, bananas and other foods are rich in vitamin B6, meat, animal offal, fish, poultry, eggs, shellfish are rich in vitamin B12. eat less fatty meat, seafood, etc., because these foods are rich in methionine, which will be converted into homocysteine after entering the body. Specifically, a daily intake of 500 grams of vegetables, 200 grams of fruit, especially to eat more leafy greens; strict control of meat intake, not fatty meat, eat lean meat not more than 100 grams per day; eat animal liver and kidney once or twice a week, about 25 to 50 grams each time; eat more brown rice, whole wheat food and other coarse grains. In addition, you should quit smoking and limit alcohol, and eat a low-salt diet (no more than 6 grams per day), etc. For moderate to severe hyperhomocysteinemia, in addition to dietary adjustments, “medication” can be administered under medical supervision, i.e., folic acid, vitamin B6, and vitamin B12 supplements. These are essential nutrients and therefore safe and reliable to take in appropriate amounts over a long period of time. Oral administration of 0.8m g of folic acid per day can reduce homocysteine levels by 8μmol/L. The CSPPT study confirmed that folic acid supplementation was effective in reducing the risk of stroke in 20702 patients. The CSPPT study is the first to demonstrate that concomitant folic acid supplementation with antihypertensive therapy in Chinese hypertensive patients has a more favorable stroke prevention effect. The Chinese hypertensive population differs particularly from the West, with a much higher incidence of stroke and heart attack than in Europe and the United States, an important reason for which is high plasma homocysteine levels. The prevalence of homocysteine in the hypertensive population in China is as high as 75%, so simultaneous intervention of blood pressure and homocysteinemia is very important for stroke prevention and treatment in China.