Carbohydrates (complex carbohydrates, monosaccharides, disaccharides) are the main components of energy in human diets, mainly derived from polysaccharides and starch in grains.
With the continuous improvement of people’s living standards, the proportion of refined sugars (sucrose, ordinary sugar, fructose) in the total energy intake is increasing. The heat source has changed from refined starch and polysaccharides to processed double sugars and monosaccharides, which are easily absorbed but also lead to the loss of fiber. In addition, sucrose and fructose have high calorie density and are tempting to eat due to their sweet taste, easily causing excessive total calorie intake.
Eating a large amount of carbohydrates enhances carbohydrate metabolism, leading to an increase in ATP within cells. This, in turn, inhibits a series of biochemical reactions such as citrate lyase and activates acylcoa carboxylase, ultimately resulting in increased fatty acid synthesis. Simultaneously, it enhances the activity of various enzymes involved in fatty acid synthesis, leading to increased fat synthesis. Therefore, excessive intake of carbohydrates, particularly high-calorie, fiber-deficient disaccharides or monosaccharides, can increase serum levels of VLDL-C, TG, and LDL-C. High carbohydrate intake can also decrease serum HDL-C levels, and the percentage of carbohydrate intake in total calories is negatively correlated with serum HDL-C levels.
A systematic review and meta-analysis found that individuals with the highest carbohydrate intake had a 1.15-fold increased risk of cardiovascular disease (CVD) compared to those with the lowest intake. Further subgroup analysis revealed that this association was only present in Asia, with a 1.52-fold increased risk, while no associations were observed in the Americas, Europe, and Oceania. The relationship between carbohydrate intake and CVD risk was nonlinear, with a marked increase in risk beyond 60% of total energy from carbohydrates.
In dietary experiments, when the percentage of carbohydrates and heat supply in total dietary calories increases abruptly from 40% to 50% to 80% to 85%, both normal individuals and patients with high blood lipid levels, especially those with insulin resistance, experience a significant increase in serum TG levels. However, there is no significant change in serum TC levels. This indicates that the impact of changes in calorie proportion on serum TG is much greater than on serum TC. The increase in serum TG induced by abrupt carbohydrate increase is temporary. If sucrose is used instead of starch in the experiment, serum TG levels will only increase when the dietary fat is primarily saturated fatty acids.
Generally, when designing a dietary treatment plan for high blood lipid levels, it is recommended to reduce fat intake and correspondingly increase carbohydrate intake to compensate for the reduced calories due to decreased fat. If the increase in carbohydrates is gradual, serum TG levels will not increase. On the contrary, if carbohydrate intake is reduced, fat intake must be increased, and a high-fat diet not only increases serum TC and TG levels but also slows down the elimination of serum TG. Therefore, it is not advocated to significantly reduce carbohydrate intake in patients with high TG levels.
If the carbohydrates in the diet mainly come from grains and excessive high-energy fats are not consumed, it is appropriate for patients with high blood lipid levels.
