It is generally recognized that serum total cholesterol (TC) levels are easily influenced by dietary cholesterol intake.
High-cholesterol diets are the main culprit for elevated serum TC levels. However, the sensitivity of dietary cholesterol to induce hypercholesterolemia varies among different animal species, racial groups, and individuals within the population. It is generally believed that the impact of cholesterol intake on individual serum TC levels is influenced by two aspects.
First, the weakening factors:
- The absorption of cholesterol in food is not complete, with an average absorption rate of about 30%.
- Decreased bile acid secretion or excretion disorders can affect cholesterol absorption (cholesterol in food needs to be emulsified by bile acids before it can be absorbed in the small intestine).
- Consuming cholesterol can inhibit cholesterol synthesis in the liver, thereby reducing the total serum TC level. However, this intracellular feedback inhibition is incomplete; even with a large amount of cholesterol intake, 60% of plasma TC still originates from endogenous biosynthesis.
- Plant foods do not contain cholesterol, but plant sterols have a similar structure to cholesterol and are not easily absorbed. Excessive intake of plant sterols can also inhibit cholesterol absorption.
- Food fibers can bind with bile acids, promoting their excretion through the feces, thereby indirectly reducing cholesterol absorption.
Second, enhancement factors.
Mainly include the following aspects:
- Fat can not only promote bile secretion but also act as a medium for the digestion and absorption of cholesterol, thereby increasing the absorption rate of cholesterol.
- Fat can accelerate the conversion of cholesterol and free fatty acids, enhancing the synthesis rate of cholesterol and triglycerides and the level of plasma triglycerides.
- Excess fat stimulates the liver to synthesize more cholesterol to adapt to the increased need for fat transport (the biological chemical function of cholesterol is to assist the solidification and transport of fat).
- Fat increases the synthesis of cholesterol by increasing the number of cholesterol synthesis rate-limiting enzymes (HMG-CoA reductase) (when high-fat food is fed to rats, the liver HMG-CoA reductase increases 12 hours later, and cholesterol synthesis increases 2-4 times).
- Fat and free fatty acids can stimulate cholesterol generation (when dogs fed high-fat diets are injected with adrenaline or noradrenaline, plasma free fatty acids increase, and serum TC increases more than with high-fat diets alone).
It can be seen from this that the influence of dietary cholesterol on serum TC levels is complex, and multiple factors may be involved simultaneously. Therefore, it is not simple to achieve the ideal serum TC levels in all patients with hypercholesterolemia by limiting dietary cholesterol intake. Moreover, since dietary cholesterol intake can be partially compensated for by endogenous synthesis, additional measures to inhibit cholesterol synthesis are needed to significantly reduce serum TC levels.
