27 March, 2024

Blood Cholesterol: Good, Bad, and Ugly

Introduction:
Blood cholesterol is a term often used to describe the circulating fat content in our blood. Circulating fat molecules combine with certain proteins to produce various fat-protein structures, which are labelled based on their size, weight, and role in overall metabolism. A standard blood test, called a “Lipid Profile,” typically lists all the major formations of fat-protein complexes.

This write-up aims to familiarize the reader with the concept of circulating fat and its effect on humans, develop a basic understanding of the Lipid profile test, and explain how treatment strategies are decided.

Fat, cholesterol, and lipids are different terms used to describe various forms of fatty acids. Body fat comes from two sources: one that we consume in the form of oil, ghee etc. and the other that the body makes due to positive energy balance. The second form is important to understand. If we consume too many calories, either in the form of carbohydrates, protein or fat, the body stores this excess energy by converting it into fat. The body fat can be found as stored units like the one seen with love handles, make up for essential body structures, or found circulating in the blood. The circulating fat, aka total cholesterol, is composed of various fat-protein formations, each serving a specific function. Needless to say, these fat molecules are vital for healthy living. It’s only when they become too abundant or go off balance that they start causing problems.

A typical blood report for cholesterol (called ‘Lipid Profile’) mentions ‘total cholesterol’ and its components. A lipid profile blood sample should be taken after 14 hours of fasting. Also, a person should be on his/her routine diet at least 2-3 days prior. This is done to minimize erroneous blood reports due to recent changes in dietary patterns. While this is the ideal format for obtaining a lipid profile, there are scenarios when a cardiologist may provide different instructions based on individual clinical scenarios.

There are 3 main components of a lipid profile that are extensively studied concerning clinical outcomes. They are:
Triglycerides (TG)
Low-density lipids (LDL), and
High-density lipids (HDL).

There are a few other components as well which I will skip for the time being.

Triglycerides (TG):
TG is the basic fat configuration found in animal fat, vegetable oil, and circulating blood. They are typically elevated in blood temporarily after food intake. TG can also be elevated in Diabetes, Thyroid dysfunction, Kidney disease etc. Although high TG is implicated in blockage formation, its association is not as strong as that of LDL or HDL. Nevertheless, attempts should be made to reduce TG levels to below 150 mg/dl (<100 mg/dl in high-risk subjects). It is important to note that very high TG levels (>500) can damage the pancreas which can be life-threatening. Ways to reduce TG levels include exercise, weight loss, reduced carbohydrate intake (sugar, potato etc), alcohol cessation, blood sugar control, and normal thyroid status. There are medications that, added to lifestyle modifications, can further reduce TG levels if required.

Low-density lipids (LDL)
LDL is the bad fat configuration. High LDL levels cause blockages of the blood vessels and can involve any part of the human body. The clinical outcome depends upon which organ’s blood vessel is affected. If the blockages involve blood vessels of the heart, it may cause a heart attack. Similarly, blockages involving blood vessels of the brain may cause stroke or paralysis; kidneys may lead to kidney dysfunction and uncontrolled blood pressure; legs may lead to ulcers or leg amputation and so on.
Lowering LDL has been shown to reduce the risk of heart disease significantly. Various LDL cutoffs are recommended for subjects with different risk profiles for heart disease. While an LDL level of below 55 mg/dl is recommended for the highest-risk patient, an LDL level of below 130 is acceptable for routine subjects.  Lifestyle modifications are an important aspect of LDL management. A class of drugs called ‘statins’ have been shown in multiple trials to decrease heart attack chances and improve survival. For this reason, statins are the most commonly prescribed drug for high LDL across the globe. Based on a person’s risk profile and lipid values, a cardiologist decides whether he/she should be started on a statin. If an optimal target is not achieved by statins and lifestyle modifications, other drugs can be added to get LDL to the desired goal.

High-density lipids (HDL)
HDL is a good fat configuration. For HDL, higher is better. A level above 40 mg/dl for men and above 50 mg/dl for women is considered normal.  Low HDL level is associated with an increased risk of blockages. To a certain degree, HDL level is genetically determined. Lifestyle, particularly exercise, plays an important role in increasing HDL levels. Limiting the amount of alcohol intake has been shown to increase HDL levels although the causative effect remains unproven. Certain medications had been tried in the past to increase HDL levels with varied clinical success. At this point, medications are rarely used to increase HDL levels.

Other forms of fat configurations which are reported in ‘advanced’ or ‘extended’ lipid profile tests:
ApoB
ApoB (also called ApoB 100) is a protein affiliated only with bad lipid types. The level of ApoB rises or falls along with those of bad lipid molecules. Hence, the ApoB level can be used as a surrogate for ‘total’ bad lipid molecules circulating in the blood. Like LDL, the optimal ApoB level depends on an individual’s risk profile. Treatment for high ApoB is in line with that of LDL. A brief overview of ApoB can be read on the Cleveland Clinic website.

Lp(a)
It is a variant of LDL and is found to be highly atherogenic, with a high likelihood of causing blockages. Lp(a) is genetically determined and doesn’t change much with diet, lifestyle or other routine measures. A level of more than 50 is considered high risk. Traditional cholesterol-lowering drugs, including statins, have been shown to have minimal or no effect on reducing Lp(a) levels. A newer class of drugs called PCSK9-inhibitors are tried with variable success. PCSK9 inhibitors are injectable drugs and are cost-prohibitive to many. We generally aim to lower LDL levels to below 55 in patients with high Lp(a) to offset the risk.

As you can see, blood cholesterol levels have different components, each with its own role. A comprehensive review of lipid profiles involves looking at all the parameters, including the risk profile of a particular individual, before taking the next course of action.

I am sure I didn’t answer all your questions on this topic. Feel free to message me with your queries; I will happily answer them.

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