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For many years, cholesterol has been the "bad guy" and has been blamed for heart attacks and other illnesses. However, it has been found that this molecule is very important for the body's optimum performance. These recent findings cast doubt on the vilification of cholesterol. In order to prove that cholesterol is not really the "bad guy" we will explore several examples and citations.
Cholesterol as a Building Block:
In order to understand how important cholesterol is as a building block, we will view the foundation of the human body which is the cell. Every cell that exists in the human body contains cholesterol. Within the human cells, cholesterol supports several physiological activities, including hormone production (mainly steroid hormones such as estrogen, cortisol, and testosterone), maintaining the integrity of cell membranes, and enhancing neuron function and conduction.
Misinterpretation of Research and the Lipid Hypothesis:
In the 1950s it was thought that heart disease was caused by increased blood cholesterol which was in turn increased by the consumption of saturated fats. This was coined as the lipid hypothesis which was postulated by Ancel Keys. Through the years, the lipid hypothesis has been put to the test of validity through scientific studies. In order to prove or disprove a causal link between dietary cholesterol and heart disease, studies such as the Multiple Risk Factor Intervention Trial (MRFIT) and the Framingham Heart Study, have been carried out and have failed to confidently prove the causal link.
Furthermore, out of 17 observational studies published in the American Journal of Clinical Nutrition, no conclusive link has been identified between dietary cholesterol consumption and the risk of heart disease. Suggesting that the influence of cholesterol on cardiovascular health may have been made bigger than it seems.
Size and Density of Cholesterol Particles Play a Part:
Depending on the size and density, we can have several types of cholesterol molecules and the lipoproteins that carry them through the blood circulation. The risk factor is scientifically measured using lipoprotein density which includes High-Density Lipoprotein (HDL) known as good cholesterol (low risk) and Low-Density Lipoprotein (LDL) known as bad cholesterol (high risk).
According to research, LDL can further be divided into two cardiovascular disease risk categories which are LDL-C (bigger and less dense) and LDL-P (smaller and more dense). Compared to LDL-C, LDL-P is linked to a greater risk of heart disease. This shows that a sole focus on total cholesterol without considering the size and density might incorrectly indicate cardiovascular risk
Is Inflammation to blame?
Recently it has been thought that inflammation has been quite a major factor in the development of cardiovascular disorders. According to research, inflammation resulting from artery irritation leads to plaque build-up resulting in atherosclerosis and heart disease. In order to patch up the damage caused by inflammation in the vessels cholesterol raises to the occasion, however in the process, it is unfortunately implicated.
Studies such as the INTERHEART trial taken across 52 nations and involving 29,000 people, majorly implicate inflammation in contributing to cardiovascular disease. These studies have found that the link to cardiovascular disease is stronger with inflammatory factors e.g. C-reactive protein than with cholesterol levels
Despite there being evidence that cholesterol is not the primary cause of cardiovascular disease, Cholesterol has been on the receiving end of singled-out vilification. Controlling cholesterol should still be a priority, however, considerations of the link between cholesterol particle size and density, and inflammation to cardiovascular disease should be there.
There also exist other risk factors for heart disease which include smoking, high blood pressure, diabetes, obesity, and physical inactivity according to the American Heart Association. At the end of the day saying that cholesterol is the only factor in heart disease can be disproved by understanding the complexity of cholesterol.
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