What makes LDL bad, and HDL good cholesterol?
Clinical Nutrition • • 1 minute to read • By Dr Akshay Alawani, INFS Faculty
Author- Dr Akshay Alawani ANutr, Faculty Head, INFS
‘High cholesterol’ sets a scare in a patient’s heart because everyone understands that it is a future invitation to dreaded health conditions like cardiovascular disorders and diabetes. Very often, doctors’ worrying remarks on these reports nudge the working-age population towards a healthy lifestyle. Yet, such individuals often have little clarity about why their cholesterol report is so concerning, and how bad it is. This article will unfold the reality of – Good and Bad Cholesterol.
Like oil cannot mix up with water, fats cannot freely move around and get transported in the blood. They require specialized vehicles to get shipped. These vehicles are known as lipoproteins. They can move these water-repelling molecules around in blood by enclosing them inside the water-friendly shell. The passengers (fats) travel to different destinations (cells) using these vehicles, and there they either get used up or stored.
Each of these lipoprotein particles has its own properties. Levels of different lipoproteins such as VLDL (Very Low-Density Lipoprotein), LDL (Low-Density Lipoprotein) and HDL (High-Density Lipoprotein) are stated in an individual’s lipid-profile report. If the doctors see elevated LDL and lower HDL, they often show concern and advise the patient to exercise, eat better, and lose weight. On the contrary, if they notice the opposite trend, they encourage the patient. Let’s understand answers to the crucial question - What makes LDL bad, and HDL good?
LDL particles originate from VLDL particles which come from the liver. VLDL particles are quite larger and full of triglycerides (the storage form of fat). Triglycerides can be thought of as the fuel that cells need. As VLDL knocks on the door of each cell and donates its fuel storage, it gets smaller and smaller and eventually becomes an LDL particle. LDL particles mainly contain cholesterol (and very less triglycerides). They are innately not bad, but when the lifestyle choices are poor and an individual has pre-existing conditions like insulin resistance, LDL particles become even smaller and denser. This happens because, with insulin resistance, the body is unable to deal with the fuels efficiently. So, these particles act as irritants to arteries and can damage their internal walls. Now, these arteries are like multi-layered pipes. With the internal layer damaged, such LDL particles make their way inside the layers and start blocking the artery diameter. This is the start of the ‘artery block’ that doctors warn against. The development of this fat blockage (‘atheroma’ in medical terms) has many other components to it, but as discussed so far, these LDL particles play a definitive role in its development. On the other hand, HDL particles pick up the extra cholesterol and have the capacity to cleanse the arterial fat (plaque) deposition. Unsurprisingly, this makes HDL a good guy.
Naturally, lower LDL and high HDL in reports indicate a relatively active lifestyle and cautious dietary choices. However, there are also some debates in the area. While following certain diets such as low-carb high fat (discussed in the Good and Bad Fat article in detail), observed high LDL is often claimed to be non-damaging as it is hypothesized to be larger and less dense. Plus, such a diet often leads to optimal weight loss which is great for overall health. But, there is no conclusive evidence that indicates a specific rise in a good type of LDL with weight loss during such a diet.
Concisely put, the vascular damage and obliteration that qualitatively and quantitatively compromised LDL can create make it a bad guy. The anti-plaque properties of HDL make it the good guy.
Lee Y, Siddiqui WJ. Cholesterol Levels. [Updated 2020 Jul 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan
Ivanova, E. A. et al. (2017) ‘Small Dense Low-Density Lipoprotein as Biomarker for Atherosclerotic Diseases’, Oxidative Medicine and Cellular Longevity, 2017. doi: 10.1155/2017/1273042.
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