Cholesterol is a fatty substance that can build up on the walls of your heart and arteries. The excess can cause high blood pressure, heart disease, and an increased risk of stroke.
Cholesterol is a fatty substance that is produced in the liver, and it helps the body use oxygen and fat-based energy. One of the effects of too much cholesterol is that it clogs the arteries, which can lead to a heart attack or stroke. The most common type of cholesterol in the blood is called “low-density lipoprotein (LDL),” and a large amount of it can lead to a heart attack or stroke.
What is the effect of carbohydrates on cholesterol levels, particularly triglycerides?
The liver is the hub of metabolism and circulation of nutrients, especially carbohydrates and proteins. These nutrients, located just below the absorbent surface of the intestine, enter the bloodstream with the portal circulation and go directly to the liver. The main exception is dietary fat, which is absorbed directly into the lymphatic system in the form of chylomicrons, from where it enters the bloodstream via the liver.
As the main energy storage and distribution organ, it is of course the main site of action of the hormone insulin. During the digestion of carbohydrates and proteins, the pancreas releases insulin. It passes through the portal vein to reach the liver directly. Glucose and insulin concentrations are often 10 times higher in portal and liver blood than in the rest of the body and systemic circulation.
Insulin helps store energy from food for later use. This is crucial for the survival of the species, as food is not constantly available. We must be able to store enough food to survive the periods of famine inherent in human history. In the liver, glucose molecules from carbohydrates in the diet are assembled into long chains to form a glycogen molecule. Glycogen is easily broken down into its constituent glucose molecules for rapid energy production.
Proteins from food are broken down to their individual amino acids during intestinal absorption. Some amino acids are necessary for the formation of new proteins and for the general renewal of proteins. However, the surplus may not be stored directly. They must be converted to glucose in the liver and then stored as glycogen. Since dietary fats do not need to be processed by the liver, they do not require insulin. Insulin secretion is minimal in response to dietary fat intake.
Glycogen is the preferred form of glucose storage because it is readily available. However, the storage space in the liver is limited. Glycogen is the equivalent of a refrigerator. Food brought into the house can simply be placed in the refrigerator and removed. However, it can only absorb a certain amount of food.
Production of new fat
Once saturated, excess glucose requires another form of storage. The liver converts this glucose into newly formed triglyceride molecules, also known as fats. This process is called the Novo Lipogenesis (DNL). De Novo means again, and lipogenesis means fat formation. So DNL literally means to create new fat. It is not clear that this newly formed fat is made from a glucose substrate and not from dietary fat. This distinction is important because DNL-derived fats are highly saturated, which can be confusing. Consumption of excessive amounts of carbohydrates can lead to increased levels of saturated fats in the blood.
If necessary, the triglyceride molecule in fat can be broken down into three fatty acids, most of which can be used directly by the body for energy. Compared to glycogen, converting fat into energy and vice versa is a much more laborious process. However, fat storage offers the unique advantage of unlimited storage space.
This body fat is like a freezer in the basement. Although it is more difficult to get food in and out of the freezer, you can store large quantities in the freezer. It is also possible to buy a second or third freezer in the basement if needed. These two forms of storage have different and complementary functions. Glycogen (refrigerator) is readily available, but its capacity is limited. Body fat (frozen) is hard to find, but its capacity is unlimited.
There are two main activators of DNL. The first is insulin. High dietary carbohydrate intake stimulates insulin secretion and also provides a substrate for DNL. The second major factor is an excess of fructose in the diet.
When the DNL is running at full capacity, large quantities of new fat are produced. But the liver is not the right place to store this new fat. Normally the liver should only contain glycogen. What are all these new fats?
What happens to the newly formed triglycerides?
First of all, you can try to burn fat for energy. But if your body is all glucose supplies after a meal, it simply has no reason to burn new fat. Imagine you’re at Costco and you bought too much stuff to keep in the fridge. One option is to eat it, but there are too many. If you don’t get rid of it, most of the food will stay on the countertop where it will rot. Therefore, this option is not practical.
The only remaining option is to transfer this newly formed triglyceride to another location. This pathway is called the endogenous lipid transport pathway. Triglycerides are full of special proteins called VLDL (Very Low Density Lipoproteins). These packages can now be exported to relieve an overloaded liver.
The amount of VLDL produced depends mainly on the presence of hepatic triglycerides. The large amount of newly formed fat triggers the production of more of these triglyceride-filled VLDL packets. Insulin plays a key role in VLDL production by increasing the number of genes required for DNL. Experimental administration of large amounts of carbohydrates increases the release of VLDL from the liver by a factor of 3.4. This massive increase in triglyceride-rich VLDL particles is the primary cause of the elevated plasma triglyceride levels found in all standard blood tests for cholesterol.
Excess DNL can overload this export mechanism, resulting in abnormal storage of new fat in the liver. When more and more fat accumulates in the liver, it becomes visibly enlarged and an ultrasound may detect fatty liver.
After leaving the liver, VLDL particles circulate in the bloodstream. The hormone lipoprotein lipase (LPL), which is present in the small blood vessels of muscles, adipocytes and the heart, cleaves VLDL. This releases the triglycerides and breaks them down into fatty acids that can be used directly for energy production. When VLDL releases triglycerides, the particles become smaller and denser, called VLDL residues. They are absorbed by the liver and released as low-density lipoproteins (LDL). This level is measured by a standard cholesterol blood test and is classically considered bad cholesterol.
A high-carbohydrate diet increases VLDL secretion and increases blood triglyceride levels by 30-40%. This phenomenon is called carbohydrate-induced hypertriglyceridemia and can occur after as little as five days of ingesting large amounts of carbohydrates. Similarly, increased consumption of fructose has been associated with hypertriglyceridemia.
In 1967, Dr. Riven described the important role of hyperinsulinemia in increasing blood triglyceride levels, explaining 88% of the variability. An increase in insulin levels leads to an increase in blood triglyceride levels.
So it’s no surprise that reducing carbohydrates and fructose in the diet is effective in lowering blood triglyceride levels. The landmark DIRECT study found that the Atkins diet reduced triglyceride levels by 40%, compared to 11% in the low-fat group.
Frequently Asked Questions
Is a low carb diet good for cholesterol?
A low carb diet is not good for cholesterol.
What type of carbohydrate helps lower cholesterol?
A low-glycemic index carbohydrate, such as oatmeal, is a good choice.
What reduces cholesterol quickly?
A diet that is low in saturated fat and cholesterol.
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