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What is hyperlipidemia?

Blood lipids, blood contains lipids collectively, include: triglyceride (TG), cholesterol (TC), β- lipoprotein, phospholipids and free fatty acid, etc. They are effected by age, sex, diet content, composition, lipid metabolism, genetic factors, mental activity, and disease, and many other factors, and in dynamic equilibrium. Under normal circumstances, the majority of lipids can penetrate the arterial wall artery intima, then discharge from the adventitia lymphatic vessels, so not deposite on the arterial wall. Normal fasting plasma concentrations (mg/100 mL): TG 20~ 110, cholesteryl and its esters 110~ 220 (including cholesterol ester 70% ~ 75%), Phospholipid 110~ 120. Clinically called Hyperlipidemia (Hyperlipidemias), mainly refers to the cholesterol is higher than 220~ 230 mg/100 mL, triglycerides above 130~ 150 mg/100mL.

Hyperlipidemia can speed up a process called atherosclerosis, or hardening of the arteries. Your arteries are normally smooth and unobstructed on the inside, but as you age, a sticky substance called plaque forms in the walls of your arteries. Plaque is made of lipids and other materials circulate in your blood. As more plaque builds up, your arteries can narrow and stiffen. Eventually, enough plaque may build up to reduce blood flow through your arteries.

Atherosclerosis increases your risk of heart disease, stroke, and other vascular diseases. Fortunately, you may be able to reduce high lipid levels and, therefore, prevent or slow the progression of atherosclerosis. Lifestyle changes like exercising and eating a healthy diet can also lower your lipid levels and are often the first step in treatment.

Blood lipids-lowering can be categorized into the following seven main mechanisms;

1, Inhibit biosynthesis pathway of cholesterol through one or several ways;

2, Block bile or cholesterol absorption by the intestine, promote excretion of Cholic acid or cholesterol in feces and promote the degradation of cholesterol;

3, Inhibit biosynthesis and absorption of triglycerides;

4, Activate the lipoprotein metabolic enzymes, promote the hydrolysis and metabolism of triglyceride;

5, Inhibit the Adenylate Cyclase, decrease the content of cAMP in the fat cells, inhibit the hydrolysis of adipose tissue, then decrease serum non-esterified fatty acids, resulting in the reduction of VLDL(very low density lipoprotein) synthesis in liver, and the further reduction of LDL(low density lipoprotein) and IDL(intermediate density lipoprotein);

6, Improve the activity of lipoprotein lipase and lecithin cholesterol acyltransferase, increase HDL (high density lipoprotein) level, thereby promoting lipid catabolism and inhibition of lipid synthesis, transportation and deposition in the arteries;

7, Through antioxidation to reduce plasma fat. Free radicals exist in reactive oxygen species, soluble in membrane. High oxygen concentrations cause lipid peroxidation free radical chain reaction, resulting in membrane lipid damage, disorder of lipid metabolism and atherosclerosis. Clearing the extra free radicals in the body can achieve the purpose of reducing blood lipid.

What can be used to treat hyperlipidemia?


Mechanisms: 1, 4, 5, 6

Niacin is also known as vitamin B3 and nicotinic acid. When the dose exceeds dose as vitamin, there is a clear role in regulating blood lipid. Niacin readily absorbed from the gastrointestinal tract, peak serum concentration of 30-60 minutes after oral administration and widely distributed in body tissues with a half-life of about 45 minutes. Metabolism in the liver. When high-dose oral, major metabolite is nicotinoylglycine (Nicotiuric Acid),N-methyl nicotinamide and 2-pyridone derivatives. 2/3 from urine in unchanged form. The major mechanism of Niacin adjusts blood lipids is inhibit the formation of cAMP, then result in decrease of triglyceride enzyme activity, adipose tissue lipolysis in slow, decrease of serum non-esterified fatty acids (NEFA)concentration, decrease of hepatic VLDL synthesis, IDL and LDL is also decreased.

In addition, the Niacin can synthesis nicotinoylglycine and glycine under the action of Coenzyme A (CoA), then prevent liver cells using CoA cholesterol synthesis. Niacin can cause elevated blood levels of HDL-C's mechanism is unknown. Blood lipid regulation of Niacin efficacy and dose associated with lipid levels before taking. When the abnormal lipid levels significantly, the dosage should be big, the curative effect is also more obvious.

Oral niacin, 3-6g/d, 1-4, TG after taking declined, 5-7, LDL-C began to decline. Average decline: TC10%-15%, LDL-C15%-20%, TG 20%-80%,HDL-C with mild to moderately elevated. Long-term treatment, yellow tumors visible fading. Hold for 5 years take Nicotinic Acid daily 3g reported that average down TC 15%, TG 26%, total mortality is not lower than the control group, but can make survivors of acute myocardial infarction myocardial infarction incidence again decreased 29%. Nicotinic Acid can be used in addition to homozygous Familial Hypercholesterolemia and I high outside the lipoprotein blood of any type of hyperlipidemia.

Vitamin E

Mechanisms: 7

Vitamin E refers to a group of compounds that include both tocopherols and tocotrienols. As a fat-soluble antioxidant, it stops the production of reactive oxygen species formed when fat undergoes oxidation, then delay the ageing of the cells due to oxidation. It can also prevent cancer, prevent liver disorders and liver detoxification,lower cholesterol, prevent stroke, promote the blood circulation.


Mechanisms: 5, 6, 7

Coenzyme Q10 can reduce the harmful low-density lipoprotein levels, prevent LDL to penetrate through endothelial cells and reduce the formation of arterial inner wall lipids. It can also increase level of HDL, known as the "vascular scavenger", and remove the waste, toxins and plaque formed in blood vessel inner wall. The two-ways regulation of blood lipids can achieve in preventing atherosclerosis.

Coenzyme Q10 is a kind of important intracellular antioxidant, which has the function of anti-LDL oxidation, reversing the atherosclerotic plaque and protecting vascular endothelial cells.


Mechanisms: 1, 2, 3, 4, 5, 6

DHA can promote plasma lipids (TC, TG and LDL) metabolism, has been hailed as "vascular scavenger", has played the role of prevention and treatment of hyperlipidemia, hypertension, coronary heart disease.

DHA has the effect of preventing and controlling the diseases of circulatory system such as atherosclerosis,and its mechanism is that they inhibit the synthesis of endogenous TC and endogenous TG, so as to reduce the total TC, TG, LDL and VLDL, which are atherogenic factors.

Furthermore, DHA can significantly increase the lecithin-cholesterol acyltransferase phthalidyl, increase the liver endothelial lipase activity and inhibit lipoprotein lipase activity so that HDL (anti-arteriosclerotic factor) is increased.


Mechanisms: 1, 2, 7

Silymarin, via its antioxidant properties, helps to prevent damage of LDL cholesterol and thereby reduce the amount of monocyte adhesion. Silymarin not only acts as a scavenger of the free radicals that induce lipid peroxidation, but also influences enzyme systems associated with glutathione and superoxide dismutase.

Both binding bile acid in the gut and limiting its synthesis from cholesterol, and its selective inhibition of intestinal absorption of cholesterol through blocking mucosal transport are the mechanism that might be involved for the effect of silymarin.

Intracellular esterification of cholesterol, catalyzed by acyl-CoA enzyme, the silymarin slow down this enzyme and lead to hypocholestrolaemia and be due to inhibition of HMG-CoA reductase enzyme, are found to decrease the cholesterol synthesis by liver in vitro.

Gamma Oryzanol

Mechanisms: 2, 6, 7

Cholesterol-lowering activity of Oryzanol can result from the enhanced catabolism of LDL-C through hepatic receptors for final elimination in the form of bile acids. The underlying mechanism may be attributed to the enhancement of lecithin cholesteryl acyl transferase (LCAT), which plays a key role in incorporating the free cholesterol into HDL and transferring back to VLDL or IDL, which is taken back by the liver cells. Additional mechanism may involve an inhibition of hepatic triglyceride lipase (HTL) on HDL which may lead to a rapid catabolism of blood lipids through extrahepatic tissues.

Oryzanol’s antihypercholesterolemic effect is partially due to its sterol moiety, which is partly split off from the ferulic acid structure in the small intestine by cholesterol esterase. The antiatherogenic action of OZ could also be based on the inhibition of the accumulation of cholesterol-esters within the macrophages or by the modulation of cholesterol acid esterase and acyl-CoA-cholesterol-acyltransferase.

Red yeast rice

Mechanisms: 1

Red yeast rice is reputed for its hypolipidemic properties. A study shows that red yeast rice may lower total cholesterol (TC) by 13–26%, low-density lipoprotein cholesterol (LDL-C) by 21– 33%, and TG by 13–34%, in humans.

Nine types of active compounds in Red yeast rice known as monacolins (polyketides), are reported to exhibit a cholesterollowering action by inhibiting the HMG-CoA reductase.

The ability of an aqueous extract of red yeast rice to induce vascular relaxation by stimulating endothelial enzyme nitric oxide synthase to release nitric.

By researching, the intake of red yeast rice could lead to a compromise: a moderate reduction in cholesterol levels compared to more efficient statins, but with less several adverse reactions.

Ginkgo biloba leaf extract

Mechanisms: reduce the harm caused by hyperlipidemia.

Ginkgo biloba leaf extract can promote blood circulation, Reduce plasma lipids, prevention of cardiovascular and cerebrovascular diseases, boost brain function, improve brain function, enhance blood flow to the brain, prevent stroke, improve peripheral false barrier, keep foot and normal movement, slow down the Alzheimer.

The main components of Ginkgo biloba leaf extract flavonoids is a potent platelet activating factor (PAF)inhibitors, PAF is a media release from the cells, which leads to platelet aggregation (stacked together). This feature may suffer from strokes the role of adjuvant therapy of patients. In addition to inhibiting platelet adhesion, a Ginkgo biloba extract regulates vascular tone and elasticity. In other words, it can make the blood circulation more efficiently. Efficiency of the promotion through effects on the circulatory system of the large blood vessels (arteries) and small blood vessels (capillaries) has the same effect.

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