The interplay between cholesterol, triglycerides, and insulin forms a crucial nexus in understanding metabolic health. As we delve into the intricate processes within our bodies, we discover how the food we consume, sets off a cascade of events involving chylomicrons, insulin, and lipoproteins. This intricate dance impacts the absorption and transformation of triglycerides, shaping our metabolic landscape. Unraveling the connections between cholesterol, triglycerides, and insulin provides key insights into conditions like diabetes, and cardiovascular health, where imbalances in this delicate equilibrium can have profound implications for overall well-being.

From the food we eat (mostly from fats?), chylomicrons are formed in the intestines (composed of triglycerides, cholesterol, and apolipoproteins/Apo B48, Apo E, Apo C2) (fats from the food are absorbed in the intestines!!). Chylomicrons circulate in the blood, and with the help of insulin, they convert triglycerides into fatty acids that are absorbed into cells. When there is insufficient insulin in the body, such as in diabetes type 1 or hyperthyroidism, a person is losing weight because the body does not absorb fats without insulin. When there is high insulin, as in the initial stages of insulin resistance, the opposite occurs. From this point on, easy weight gain occurs, making weight loss difficult. The remnants of chylomicrons go to the liver, and from them, with the help of sugar (triglycerides are made from high sugar in the liver) and Apo B100 lipoprotein, very-low-density lipoprotein (VLDL) is created. (Sugar and proteins are absorbed in the liver.) Then VLDL from the liver goes through the blood vessels. It gives part of the triglycerides to the cells (with the help of HDL) and becomes intermediate-density lipoprotein (IDL). IDL then gives triglycerides to HDL and takes from it cholesterol, becoming low-density lipoprotein (LDL) cholesterol. (HDL is formed with the help of Apo A1 lipoprotein.) LDL remains only with Apo B100. The main purpose of LDL is to transport cholesterol to cells for hormone production and other needs, or, if it doesn’t achieve that (in excess), to return it to the liver with the help of HDL. (LDL gives cholesterol to cells with the help of ApoB100, which attaches to receptors on the cells. Statins reduce cholesterol by increasing the number of these receptors.)

Now, mainstream medicine considers high LDL in the blood vessels (high LDL) as the main cause of damage/narrowing of the arteries (high LDL and toxins from smoking, etc., damage the walls of the arteries (endothelium); the body oxidizes LDL, and other toxins, calcium, collagen stick to the walls and narrow them. This is a brief explanation). HOWEVER… Half of the people who have a heart attack do not have high cholesterol!! And approximately 75% of patients admitted to the hospital with some heart condition do not have high cholesterol! Here, the medical explanation is: there are other factors that play a role, such as high blood pressure, diabetes, obesity, etc. Now, the other (more specific) explanation is that, during circulation in the blood, part of LDL (due to high sugar, plant oils/olive oil) is converted into small dense LDL (sdLDL). sdLDL particles more easily enter the endothelium (they are smaller) and more easily become oxidized. Also, in sdLDL, the ApoB100 lipoprotein (which is damaged by sugar) is present, with the help of which receptors in the cells and liver remove LDL from circulation. So, sdLDL remains in the blood. This means that someone can have high cholesterol, can have high LDL, but still have a lower risk of cardiovascular diseases, and vice versa (have normal cholesterol but larger sdLDL particles). Of course, if the level of LDL is extremely elevated, it is normal to have an increased number of sdLDL, and with that, an increased risk. There is a test for the number of sdLDL, but it is not widely available. However, a good indicator for the number of sdLDL is the ratio between the levels of triglycerides and HDL. It should be a maximum of 2 to 1. For example: triglycerides 4 — HDL 2. If the number of triglycerides is lower than the number of HDL, the number of sdLDL is low, and the risk of cardiovascular diseases is minimal!