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If your blood pressure, blood sugar, blood lipids are not very high, you are also a young man.
, but during the physical examination, I was told that there is a risk of stroke (stroke). Please don’t be surprised, you are not alone.
According to statistics from some studies, the phenomenon of stroke is gradually becoming younger , which is all related to an indicator - homocysteine (hcy).
Although most people don’t take this indicator seriously, I hope you all take it seriously today!
What is homocysteine ?
homocysteine (Hcy), which is a sulfur-containing amino acid in the body, is an intermediate metabolite of methionine and cysteine .
Under normal circumstances, homocysteine can be catabolized in the body, and the concentration remains at a low level .
reduces homocysteine levels and is a key way for to improve brain health, mental health and overall health , especially in the presence of inflammation.
Various reasons will affect blood homocysteine metabolism, leading to accumulation and increase of homocysteine concentration, referred to as hyperemia.
The high blood and Hcy will damage cells, tissues, and organs and have an impact on the body.
clinical research found that in addition to being closely related to blood pressure, blood sugar , etc., Hcy is also related to stroke, dementia, cardiovascular disease, kidney disease, skeletal system disease, and even cancer .
Therefore, the level of Hcy should be the same as blood sugar, blood pressure, and blood lipids, and it has become the focus of clinicians and an important item in our physical examination.
internationally recognized measurement standards are:
Hcy6.3µmol/L is the security range ; Hcy6.3µmol/L.
enters the high-risk area of cardiovascular and cerebrovascular events in ; Hcy≥10µmol/L, and the incidence of cardiovascular and cerebrovascular events in reaches 3 times normal .
The only way for our human body to obtain homocysteine is to consume foods containing methionine , and animal protein contains higher methionine.
Isn’t that just can’t eat meat? ? Of course not.
vitamins B6, B12 and folate , betaine can help metabolize homocysteine, so the rise in homocysteine levels may be a sign of these vitamin deficiency .
There are two factors that have high homocysteine:
, genetic factors , such as mutations in mthfr and cbs, which reduces the activity of enzyme , etc., can all cause hcy to accumulate in the body.
How homocysteine blocks blood vessels
After the discovery of homocysteine in 1931, it has been very little known about it for decades.
In the 1960s, Dr. McCully of Harvard proposed that abnormally advanced atherosclerosis observed in heart attacks and strokes, children and adolescents, is due to high excess of Hcy.
In the blood of these children, the Hcy level is as high as 300μmol/L, which is so high that it is easily detected in the urine, so the initial wrong name was "homocystinuria".
Despite strong opposition in the years following his initial observation of children, Dr. McCully believes that Hcy is also the main risk factor for heart disease in the wider population.
Subsequent studies confirmed Dr. McAlley's view, an epidemiology study showed that Hcy10 μmol/L was associated with a three-fold increase in the risk of heart attack . This high level is very common, with 5-10% of the U.S. population and 40% of the patients with vascular diseases.
Hcy risk is "continuous", and there is no risk of suddenly developing to the threshold level ; the higher the level of Hcy , the greater the risk of for cardiovascular disease .
Hcy is related to multiple stages of the process that leads to the growth and activity of coronary plaques. The most important destructive effects observed include:
→Hcy promotes plaque formation and makes blood vessels stiff
Hcy is an important marker of increased risk of carotid and aortic plaques, both of which indicate an increased risk of stroke ; the higher the level of Hcy, the greater the range of plaques in the aorta.
In various in vitro studies, Hcy has been shown to induce the value-added of vascular smooth muscle cells, which is the main component of atherosclerotic plaques .
In a mouse experiment, Hcy can activate the macrophage ERK signaling pathway through , significantly upregulating the expression of MMP-9.
thus causes an increase in extracellular matrix degradation and promotes the proliferation and migration of vascular smooth muscle cells, and leads to endovascular thickening and vascular remodeling of .
serum Hcy concentration was also related to arterial stiffness. In one study, carotid artery-femoral PWV (an index for evaluating arterial stiffness) was significantly higher than that of the normal Hcy group.
The study also pointed out that elevated Hcy levels may enhance vascular endothelial cells oxidative stress and inflammation vascular endothelial cells , and hrefore endothelial cells production and utilization of nitric oxide (NO, a factor that relaxes blood vessels) .
In addition, Hcy has a strong binding ability to procollagen , and can cut off the binding of procollagen to lysine residue, thereby causing collagen fibers to break and lose tensile effect.
And the blood vessels are supported by collagen and extracellular matrix. Hcy causes collagen fibers to break, which will reduce the elasticity of the blood vessels .
→Promote oxidative stress and induce inflammation
Hcy level, which can stimulate the production of interleukin-8 (IL-8) and monocyte chemotaxis protein-1 (MCP-1), both of which are responsible for attracting inflammatory cells to the arterial wall .
Inflammation of the arterial wall can lead to damage to the blood vessel wall and rupture of the plaque, which in turn leads to heart attacks.
Hcy can also self-oxidize, produce reactive oxygen free radicals, promote the oxidation of low-density lipoprotein (LDL) particles, leading to increased deposition in arterial blood vessels and promoting the formation of foam cells.
In addition, during Hcy metabolism, hydroxyl radicals, hydrogen peroxide radicals, etc. will also be produced, inducing oxidative stress reactions, thereby destroying the morphology and functional integrity of endothelial cells, and inducing endothelial cell apoptosis.
→Promote the formation of blood clots and increase the risk of thrombosis
Hcy can promote the formation of blood clots through various mechanisms, promotes the formation of blood clots , and has the effect of increasing the coagulation factor , tissue factor expression, platelet aggregation, and inhibiting thrombomodulin (an anticoagulant protein).
- Hcy can change the level of coagulation factors, causing the aggregation of platelets at the atherosclerosis of the blood vessel wall, and puts the body in a pre-thrombotic state .
- Hcy can inhibit protein kinase C and its activated cofactors, thrombosis regulates the activity of protein , and reduces the inactivation of thrombin .
- Hcy produces hydrogen peroxide , interfering with endothelial cells to synthesize heparin , reducing the binding ability of thrombin and heparin, reducing the anticoagulant activity, and destroys the balance between the body's coagulation and fibrinolytic .
- high Hcy and its derivatives can increase platelet adhesion, promote the generation of platelet-derived growth factor , and activates coagulation factors V, X, XII, causing coagulation to increase .
The above mechanisms all help the formation of blood clots. It is the last step in the heart attack after the plaque ruptures.
How to reduce homocysteine Hcy
Hcy level not only damages blood vessel health, but also will accelerate the oxidation and aging of the human body, weaken the body's immune system, cause damage to the brain, lead to mental decline, and cause hormone imbalance , etc.
Therefore, it is urgent to reduce the Hcy level.
We mentioned above that high Hcy is mainly related to two factors: genetic factors and nutritional factors.
Genetic factorsWe can do nothing, but we can start from the nutritional aspect to reduce the Hcy level.
can reduce homocysteine, and can provide it with methyl . In the previous article, we talked about this very important principle. This is the principle of betaine reducing homocysteine .
above picture: Betaine reduces homocysteine↑
Commonly used to reduce Hcy are Group B, betaine, choline , etc.
→Folic acid: an important factor in controlling Hcy.
study shows that for most adults, providing an additional 100 μg of folic acid per day can reduce Hcy by about 0.5 μmol/L.
It is difficult to obtain sufficient amount of folic acid from food. The bioavailability of folic acid supplements is twice that of folic acid in food.
If your Hcy level exceeds the normal range, then in addition to supplementing folic acid in your diet, you also need to take folic acid supplements.
daily folic acid dose of 800μg can reduce Hcy by about 25%. Some doctors will prescribe up to 5000μg of folic acid doses to patients with highly elevated Hcy levels.
→Vitamin B12
Vitamin B12 deficiency is very common and can lead to increased Hcy, especially for people over 65 years old.
Generally speaking, vitamin B12 should be supplemented with folic acid to maximize the effect of reducing Hcy.
→Vitamin B6
Vitamin B6 Take with folic acid can effectively prevent the post-meal surge of Hcy, especially when the meat rich in methionine in the diet.
Low B6 levels are very common in people with high Hcy levels. There has been controversy in the dose of B6 required to minimize Hcy. Currently, the commonly used doses in clinical studies are 2-50 mg.
In terms of reducing Hcy treatment, Dutch researchers with extensive experience often use 250mg of B6 without adverse effects.
→betaine (TMG)
betaine is a substance present in food and is the most effective nutrient for to inhibit the surge of Hcy after meals of . can reduce the level to 50% .
supplementation with TMG reduces Hcy, starting at a dose of 1000 mg per day, and up to 20% at 6000 mg per day, which is usually used for severe homocysteine diseases.
We usually use a dose of 2000 mg per day as the starting dose to reduce the fasting Hcy level;
When the Hcy level does not respond to the three B vitamins, a higher TMG dose can be used to solve the postprandial surge caused by methionine load .
beet , spinach, fish and beef , etc. are rich food sources for TMG.
→choline
Choline can be directly converted into TMG in the body. Choline is easily obtained in daily foods, such as eggs and various meats.
Like TMG, choline also has an impact on fasting Hcy, which has a greater impact on the postprandial surge of Hcy. The recommended dose is 2000-4000 mg per day.
→Other precautions
In addition to the nutrients I mentioned above, we should also pay attention to exercise moderately in daily life, and exercise can also help reduce Hcy.
For high Hcy, , such as MTHFR gene mutation population, can supplement vitamin B2.
study found that after supplementing with vitamin B2, folic acid and vitamin B12 were not supplemented with, and the homocysteine decline was also obvious.
The key skin dragon says that
hyperhomocysteinemia is an indicator that has gradually received attention in recent years. It is an independent risk factor for stroke and also has potential risks to cardiovascular disease.
Homocysteine is an item that is often included in the "biochemistry" of blood tests, but it is often overlooked.
Hcy can make your blood vessels become brittle, causing cholesterol to be oxidized into oxldl, inflamed , and promote the formation of blood clots and plaques. It must be taken seriously.
For friends with high Hcy, they must actively pay attention to their diet and supplement folic acid, vitamins B6, 12, betaine and choline .
