Primary hyperlipidemia is caused by congenital defects in lipid and lipoprotein metabolism (familial) as well as by certain environmental factors, through various mechanisms. These environmental factors include diet and drugs. They are outlined as follows: 1. Genetic factors: Genetics can cause hyperlipidemia through a variety of mechanisms, some of which may occur at the cellular level, mainly in the form of defects in cell surface lipoprotein receptors and defects in certain intracellular enzymes (e.g., defects or deficiencies in lipoprotein lipases), or in molecules of lipoproteins or apolipoproteins, mostly due to genetic defects. Also called familial dyslipidemia, this is an autosomal inherited disorder. All types of hyperlipoproteinemia can occur genetically, but familial hypercholesterolemia is commonly encountered in domestic clinical practice. This is an autosomal dominant disorder, which means that if one parent has this type of hypercholesterolemia, the child must also exhibit familial hypercholesterolemia. Unlike secondary hypercholesterolemia, in familial hypercholesterolemia total plasma cholesterol levels are two to three times higher than normal and LDL is also elevated. coronary heart disease develops between 30 and 40 years of age, and 23% of men die of coronary heart disease before the age of 50, 10 years later in women. An autopsy was performed on a fatal case of familial hypercholesterolemia, and the patient’s aortic intima was found to be covered with atheromatous plaques, just like a thick layer of buttercream, and multiple “relics” of myocardial infarction were found in the patient’s heart. There are reports from abroad that such patients die of myocardial infarction at the age of 3. Familial mixed hyperlipidemia is also an autosomal dominant disorder. It manifests clinically as elevated plasma cholesterol and triglycerides with a family history of early-onset coronary heart disease. Such dyslipidemia is most common in patients with a positive family history of myocardial infarction occurring under the age of 60 years, and in patients with cerebral infarction of unknown cause over the age of 40 years, and also manifests as a decrease in low-density lipoprotein. 2, dietary factors: the role of dietary factors is relatively complex, and a significant proportion of patients with hyperlipoproteinemia are closely related to dietary factors. Consumption of high-fat, high-cholesterol foods, especially animal fat intake, can promote bile secretion, increase the rate of cholesterol and triglyceride synthesis, so that its level in the plasma increases. Saturated fatty acids in the general diet, such as meat, eggs, dairy products and other foods, often accompanied by high cholesterol content, so that cholesterol synthesis increases; unsaturated fats such as cheese, animal offal, etc. are high-calorie nutrients, too much intake directly affects the level of plasma cholesterol and lipoproteins, leading to overweight, obesity. Excessive intake of sugar can affect insulin secretion and accelerate the synthesis of very low density lipoprotein in the liver, which can easily cause hypertriglyceridemia. Excessive intake of cholesterol and animal fat is associated with the formation of hypercholesterolemia, and other dietary components (such as long-term intake of excessive protein, fat, carbohydrates and low dietary fiber intake) are also associated with the occurrence of this disease.