Smoking Hsas an Effect on Blood Fat. Forward It to Someone Who Smokes around You

Smoking has the following effects on blood fat:

1. Increase serum total cholesterol level.

Epidemiological studies have found that smokers have higher serum total cholesterol levels than non-smokers, and the concentration of carbon monoxide hemoglobin in the blood of smokers is as high as 10% to 20%, which may be related to the concentration of carbon monoxide in the blood.

2. Lower serum HDL cholesterol.

Many studies have linked negative serum HDL cholesterol levels to smoking.

Serum HDL cholesterol levels were 0.13-0.23 nmol/l lower in both male and female smokers than in non-smokers.

A foreign survey of 191 premenopausal women aged 20-40 years found that the average serum HDL cholesterol level of smokers was 0.18 nm/L lower than that of non-smokers, and there was a significant difference between the two groups (P< 0.005), the average serum HDL cholesterol level of those who smoked more than 25 cigarettes a day was lower than that of those who smoked 1-14 cigarettes a day.

But there was a negative correlation between serum HDL cholesterol and triglyceride levels in smokers.

However, the increase of triglyceride could not explain the low level of serum HDL cholesterol. The actual reason is still unclear, and it is thought that carbon monoxide may be related to the inhibition of mitochondrial synthesis of LDL cholesterol in hepatocytes.

3. Increase serum triglyceride.

Cigarettes contain a large amount of nicotine and carbon monoxide, which stimulate the sympathetic nerve and release catecholamines. Catecholamines not only increase serum free fatty acids, resulting in the final intake of free fatty acids by adipose tissue and the formation of triglycerides, but also promote the release of lipids from adipose tissue, thus increasing the level of triglycerides.

4. Promote the oxidative modification of low density lipoprotein.

LDL exposed to smog is susceptible to oxidative modification to form oxidized LDL, possibly because carbon monoxide enhances the sensitivity of LDL to oxidative modification.

Oxidized low-density lipoprotein (LDL) formed by oxidative modification is the main substance that directly leads to atherosclerosis.