Abnormalities of lipid metabolism Lipids are the general term for lipids in the blood, with a total lipid amount of about 600 mg/dl. The components of lipids are complex, mainly total cholesterol (tc, of which 2/3 is cholesterol lipid and 1/3 is free cholesterol), triglycerides (tg), phospholipids (pl), free fatty acids (ffa), fat-soluble vitamins, steroid hormones and so on. They are fat-soluble and must be bound to proteins in the blood to exist and function as water-soluble substances, of which all are bound to globulins as lipoproteins (lp) except ffa which is bound to plasma albumin.
Lipoproteins can be separated by ultracentrifugation or lipoprotein electrophoresis into high-density lipoproteins (hdl), which are alpha-lipoproteins (alpha-lp), low-density lipoproteins (ldl), which are beta-lipoproteins (beta-lp), very-low-density lipoproteins (vldl), which are pre-beta-lipoproteins (prebeta-lp), and celiac particles (cm), which are immobile at the origin. The part of the protein bound to lipoproteins is called apolipoprotein (apo), and there are 10 major classes of a, b, c, d, e, f, g, h, j and (alpha) that have been discovered and have their structures clarified.
Various lipoproteins and apolipoproteins can be divided into several subtypes (such as hdl can have hdl2, hdl3 and other subtypes, apo-a can be divided into apo-a i, apo-a ii, etc., apo-b can be divided into apo-b100 and apo-b48, etc., apo-c has apo-ci, apo-c, apo-c, etc.), lipids, lipoproteins, apolipoproteins play an important role in human metabolism. play an important role in human metabolism. Elevation or decrease of one or several components of lipids in the blood of human body is called dyslipidemia. Dyslipidemia predisposes to atherosclerosis (as) and coronary heart disease (chd) and damages the health of the body. The elevation of certain lipid components in the blood is called hyperlipidemia or hyperlipoproteinemia.
I. Criteria for the classification of dyslipidemia
Since the 1980s, scholars at home and abroad have advocated that it is appropriate to determine the criteria for dyslipidemia based on the relationship between abnormal lipid levels and increased risk of chd and the need for treatment.
In the second report of the U.S. National Cholesterol Education Program (nep) in 1993, plasma tc <200mg/dl for adults without chd is the ideal level, 200-239mg/dl is the critical high level, and over 240mg/dl is the rapidly increasing risk of chd; hdl-c <35mg/dl as the low value, and low level of hdl-c constitutes one of the chd One of the risk factors; tg level is divided into four levels, namely, normal level <200mg/dl, critical high level 200-400mg/dl, high level 400-1000mg/dl, very high level >1000mg/dl; ldl-c <30mg/dl is the appropriate level, 130-159mg/dl is the high risk level.
In Beijing region of China, with reference to the analysis of survey data of Beijing brain workers, if the upper limit of 90% distribution of lipids in middle-aged people (35-50 years old) is taken as the dyslipidemia, serum tc>250mg/dl and tg><200mg/dl are taken as the classification criteria of chd risk level, and serum hdl-c<35mg/dl is the low hdl-c hypo. In Shanghai area, according to statistical analysis combined with clinical, serum tc>220mg/dll and tg>160mg/dl are determined as the criteria of excessive lipid.
Second, the danger of dyslipidemia
Numerous epidemiological survey data prove that abnormal lipid metabolism is an important lipid risk factor causing cardiac and macrovascular as. The conclusion that serum tc is positively correlated with the development of chd has been confirmed by many studies at home and abroad. The results of the Multifactorial Intervention Trial (mrfit), a prospective study of 356,222 men aged 35-57 years with a 6.5-year follow-up, suggest that the relative risk of premature chd death is 1.0 if plasma tc is 200 mg/dl, and the relative risk is 0.7, 2.0 and 2.0 if tc is 150 mg/dl, 250 mg/dl and 300 mg/dl, respectively. were 0.7, 2.0 and 4.0, respectively.
The results of the cumulative follow-up of a group of 5298 male workers with a mean age of 45 years in Shougang, Beijing, with a cox regression line analysis of the factors affecting the onset of chd showed that after controlling for age and systolic blood pressure, the incidence of chd in the groups with serum tc ≥ 240 mg/dl and 200-239 mg/dl was 3.2 and 1.9 times higher than that in the group with tc < 200 mg/dl, respectively. This shows that plasma tc concentration was significantly and positively correlated with chd incidence. Serum cholesterol is present in 67%-80% of ldl, and elevated serum tc must lead to an increase in its ldl-c.
In one study, plasma ldl-c of 4086 subjects was divided into four groups according to <135 mg/dl, 135-154 mg/dl, 155-195 mg/dl, and >195 mg/dl, and the incidence of chd was 1.6%, 3.1%, 5.4%, and 12%, respectively, indicating that the incidence of chd was also positively correlated with plasma ldl-c, and the magnitude of the increase was 1.6%, 3.1%, 5.4%, and 12% in each group. The latter was two times higher than the former. Serum hdl binds cholesterol from surrounding tissues, including the arterial vessel wall, to the bile ducts for catabolism, where it protects the arteries from atherosclerosis.
The results of a 6-year prospective study showed that the incidence of chd was 1.8%, 0.5%, and 0.26% when hdl-c was grouped as <35 mg/dl, 35-55 mg/dl, and >55 mg/dl, respectively, showing that serum hdl-c concentration was negatively correlated with the development of chd.
The relationship between elevated serum tg levels and chd incidence is not a simple single relationship, but through a series of changes in lipoprotein metabolism such as increased cm and vldl residual particles, small dense ldl particles and decreased hdl-c levels due to elevated serum tg, and the resulting hyperinsulinemia, insulin resistance and hypercoagulability of blood in the body can cause as and make chd increased risk of disease onset.
Some studies have found coronary event rates of 2.6% and 16.5% for ldl-c/hdl-c ratios <5 and >5, respectively, and moderate and significant elevations in serum tg levels at values >5 increase the risk of chd. Lipoprotein(a) [lp(a) is a lipoprotein that was proposed in the 1980s to be associated with the development of chd. It consists of two parts, ldl and apo(a), and has a high degree of structural homology with fibrinolytic zymogen. Several groups of studies have shown that lp(a) is an independent risk factor for the development of chd.
The lp(a) concentration is positively correlated with the incidence of early-onset chd, and the relative risk of early-onset chd can increase up to 6-fold if lp(a) is elevated with elevated ldl. lp(a) concentration is also valuable in predicting the prognosis of chd. lp(a) concentrations have been reported to be significantly higher in reoccurring myocardial infarction than in first-onset, and it has also been reported that the lp(a) ≥480 mg/dl group is more likely to die from chd than the <480 mg/dl group. Recently, it was found that patients with acute myocardial infarction with higher lp(a) had lower success rate of thrombolytic therapy or larger infarct size and higher mortality; coronary angiography confirmed that serum lp(a) concentration was positively correlated with the severity of coronary lesions.
The relationship between intercepted lipoproteins and as has received increasing attention from clinical workers. apo-ai and apo-a ii are important in preventing the occurrence and development of as by reducing cholesterol deposition in the arterial vessel wall and accelerating its catabolism in the liver through different pathways: apo-b is mainly present in ldl, and its elevation plays an important role in the itinerary of as; it has been reported that serum apo- ai/apo-b ratio has been reported to be more sensitive and specific for the evaluation of coronary artery stenotic lesions. As research continues, the effects of abnormal lipid metabolism on blood coagulation, fibrinolysis, platelets, prostacyclin and vascular endothelial cell function are gaining increasing attention.
The increased activity of some coagulation factors in blood injection is also positively correlated with serum tc and tg levels, serum tg and tc levels are positively correlated with fibrinogen content, fibrinolytic activity is significantly reduced in those with elevated tg, and platelet aggregation is increased in patients with hyperlipidemia. Vascular endothelial cell function is affected in those with abnormal lipid metabolism. As an extensive and major tissue organ in the organism, abnormal function of endothelial cells can be involved in the occurrence and development of a variety of diseases. Elevated serum tc reduces prostacyclin synthesis in endothelial cells, which can also have a series of adverse effects on the organism.
In addition, severe hypertriglyceridemia can trigger recurrent episodes of abdominal pain and pancreatitis, obesity, hepatosplenomegaly and yellow tumors of the skin.
Third, the factors affecting blood lipids
1, genetic factors Generally speaking, people with a family history of dyslipidemia have a higher chance of having dyslipidemia in their offspring. Therefore, for this group of people, they should check their blood lipids frequently and pay attention to the influence of environmental factors on blood lipid metabolism.
2.Environmental factors
(1)Obesity. Simple obesity, especially central obesity with the increase in body mass index, so that serum tc, ldl, tg, apo-b increased, hdl and apo-ai reduced, tc / hdl-c ratio increased.
(2) Dietary structure
1) Foods containing mainly saturated fatty acids can raise serum tc, ldl: each 1% increase in the percentage of total calories consumed by such foods can increase serum tc by 2mg/dl, and studies have shown that only foods containing saturated fatty acids with 12 (lauric acid c12:0), 14 (myristic acid c14:0), 16 (palmitic acid 16:0) even carbon chains can raise serum tc, while foods containing 18 carbon atoms and 10 and more carbon atoms of saturated fatty acids food has little effect on serum tc concentration.
2) foods with monovalent unsaturated fatty acids: olive oil and other vegetable oils that replace dietary saturated fat with oil acid (c18:1) can reduce serum ldl-c levels while maintaining hdl-c levels.
3) Foods containing polyunsaturated fatty acids are mainly e-6 polyunsaturated fatty acids and e-3 polyunsaturated fatty acids; the former mainly has linoleic acid (c18:2), which contains about 50%-60% in corn oil, cottonseed oil and soybean oil, and 75% in safflower seed oil; the latter is mainly in seafood fish, and commonly has epq (c20:5, e3) dha (c22:5, e3). In addition, walnuts also contain high levels of polyvalent unsaturated fatty acids. Replacing those containing saturated fatty acids with such foods can reduce serum tc, especially ldl-c and tg. Generally polyvalent unsaturated fatty acid supplementation can account for 7% of total calories.
(4) dietary cholesterol intake of 300-600mg per day can increase serum tc; every 100g/1000kcal increase in cholesterol in food can cause serum ldl-c to rise 8-10mg/dl.
(3) Smoking. Daily smoking was positively correlated with serum tc, ldl-ctg, tc/hdl-c, ratio, and negatively correlated with hdl-c. This may be related to the thiocyanate contained in tobacco.
(4) Alcohol consumption. Appropriate alcohol content (about 50g/d of white wine) was positively correlated with serum tc and hdl-c levels and negatively correlated with tg and tc/hld-c ratios. Moderate amounts of alcohol have a protective effect on the arterial vessel wall, mainly through increased serum hdl2-c and hdl3-c concentrations.
(5) Tea and coffee. Have the habit of drinking tea can make serum tc level decrease, foreign reports coffee can increase serum tc level.
(6) Exercise and physical activity. Foreign research that exercise can make serum tc, tg lower and hdl-c higher. Our survey shows that serum tc and ldl-c levels of heavy manual laborers are lower than those of light manual laborers, while hdl-c and tg are not significantly different.
(7) Drugs. Thyroid hormone can lower serum tc, dihydrocoumarin can increase serum tc and tg levels, tachyphylaxis can lower serum hdl-c levels, tretinoin can increase serum tg and lower hdl-c, reserpine can increase serum tc and lower hdl-c, prazosin can lower serum tg and increase hdl-c, postmenopausal women taking female hormone replacement therapy can lower serum tc and hdl-c levels increase.
(8) Seasonal fluctuations in lipids. Serum tc peaks in winter and decreases in summer, with seasonal differences of up to 12 mg/dl, and seasonal changes are greater in men than in women. Serum tg is also highest in winter, especially in women, and lower in summer, with a seasonal variation of 20 mg/dl. Serum hdl-c is highest in late winter and early spring, and lower in summer, with a seasonal variation of 6.19 mg/dl. Serum ldl-c is higher in fall and winter than in spring and summer, with a seasonal variation of 10.5 mg/dl, especially in men in winter. hdl-c/tc ratio is highest in late winter and early spring.
(9) Mood swings. Stress can increase the level of serum tc and tg.
3.Other factors
(1) Age. Serum tc and tg levels increase with age, and the tendency to increase gradually decreases after the age of 60-70.
(2) Gender. Premenopausal women have higher serum hdl-c levels than men of the same age; tc is lower than men, after menopause, hdl- levels are similar in both sexes of the same age, and serum tc levels are higher in women than in men.