The Types Of Cholesterol

Published Date: 02 Nov 2017

Cholesterol travels in the blood stream by attaching itself to a protein. The proteins are known as apolipoprotiens. The combination of cholesterol plus the protein attached to it is called as "lipoprotein". Cholesterol is classified in to various types based on the type of cholesterol the lipoprotein carries. So, depending on how much protein is present in relation to the fat, cholesterol is classified in to various types.

Chylomicrons.

Low density lipoprotein (LDL)

High density lipoprotein (HDL)

Very low density lipoprotein (VLDL)

Triglycerides.

Chylomicrons: Chylomicrons are assembled in the intestinal lining as a means to transport dietary cholesterol and triglycerides to the rest of the body. They are therefore molecules to transport exogenous lipids. Triglycerides are the main component of the Chylomicrons.

The Chylomicrons leave the small intestine through the lymphatic system and then get into the general blood circulation. In the liver they acquire apolipoprotein. After distribution to peripheral tissues fatty acids are removed from them for use in the body cells. The Chylomicrons remnants are then transported back to the liver where they are further broken down.

Low density lipoprotein: LDL is also named as "bad cholesterol". The exclusive apolipoprotein of LDLs is apoB-100. LDLs are the primary plasma carriers of cholesterol for delivery to all tissues. LDL has two types of particles. The lipoprotein particles vary in diameter size between 18-25 nm.

Type-A LDL; this pattern has more of the larger and less dense LDL particles

Type-B LDL; this pattern has more of the small dense LDL particles. Because of their smaller size they easily penetrate in to the endothelium.

Research has shown that higher levels of type-B LDL are more dangerous as opposed to type-A LDL. Type-B LDL is responsible for cardiovascular problems. The more the LDL in the blood, the greater is the risk of cardiovascular disorders.

LDL is produced in the liver and it carries cholesterol and other fats from the liver to muscles, different organs, heart and tissues. At the cell level the LDLs interact with their receptors on the cell membrane and are engulfed. In the cell the protein component is cleaved off and the cholesterol esters are hydrolyzed to yield free cholesterol which is then incorporated into the cell wall. Any excess cholesterol is then stored in the cell. Insulin and tri-iodothyronine (a thyroid hormone) hormone increase the binding of LDLs to liver cells while glucocorticoids for example steroids have the opposite effect.

LDL levels should always remain low in our body. High levels of LDL indicate that there is excess amount of cholesterol than that which is needed for healthy functioning of our body. This thereby increases the risk of heart disorders. LDL leads to plaque formation in the walls of the arteries. As LDL can transport cholesterol into the walls of the artery, it gets retained there by the arterial proteoglycans. They attract macrophages which invade the area and engulf LDL particles and initiate plaque formation. This leads to the narrowing and thickening of the arteries which over a period of time might lead to cardiovascular problems. If this continues for a long time, the plaques rupture. This leads to blood clotting and thereby produces arterial stenosis or total arterial occlusion. If this stenosis is severe or occlusion occurs it leads to heart attack and other cardiovascular problems.

LDL’s become oxidized by the free radicals when they enter the endothelium. Oxidized forms are more dangerous as they are easily retained by the proteoglycans. Hereditary form of high LDL is called as "familial hypercholesterolemia" (FH). Increase in the levels of LDL is called as "hyperlipoproteinemia type 2".

Familial hypercholesterolemia is a genetic condition which is inherited in the autosomal dominant manner. The affected individuals are unable to remove LDL from the bloodstream and these results in the buildup of the bad cholesterol in the blood. Therefore they are at higher risk of cardiovascular disease.

The condition is characterized by;

Heart attacks early in life. Most occur in the fifth decade.

Xanthomas- deposition of fat in the skin and tendons.

Xanthelasmas-fat deposits in the eyelids.

High levels of total cholesterol and LDL cholesterol.

Corneal arcus-deposition of cholesterol around cornea of the eye.

In hyperlipoproteinemia type 2, there is a deficiency of LDL receptors which the LDL cholesterol binds to and gets engulfed into body cells. The condition exists in two types. In type IIa, only LDL cholesterol is elevated. Type IIb has elevated triglycerides and cholesterol. Symptoms are similar to those of familial hypercholesterolemia.

Standard fasting blood tests for cholesterol and lipid profiles will include values for Total cholesterol, HDL, LDL and triglycerides.

According to the National Cholesterol Education Program, LDL can be calculated as follows:

LDL= TC- (triglycerides/5) + HDL

TC= Total cholesterol.

All the other values (i.e. TC, HDL, Triglycerides) are measured directly in the blood.

Interpretation

Levels of LDL

Optimal level; seen in young children much before the start of plaque formation in the arterial walls.

25 - <50 mg/dL (1.3 mmol/L)

Optimal level; might lead to slow progression of the plaque formation.

<70 mg/dL (1.8 mmol/L )

Optimal level

< 100 mg/dL (2.6mmol/L)

Near normal or above optimal; corresponds to higher rate for developing symptomatic cardiovascular disease

100-129 mg/dL (2.6-3.34 mmol/L)

Borderline high; corresponds to even higher rates for developing cardiovascular disorders.

130-159 mg/dL (3.36-4.13 mmol/L)

High; much higher rates

160-189 mg/dL (4.14-4.90 mmol/L)

Very high; corresponds to highest and increased rate of developing a cardiovascular problem.

>190 mg/dL (4.91 mmol/L)

High Density Lipoproteins: HDL is also known as "good" cholesterol. It is also produced by the liver. It carries cholesterol and other lipids from the organs and the peripheral tissues back to the liver via the reverse cholesterol transport pathway for the recycling procedure. The HDLs achieve this by interacting with macrophages found in the peripheral blood vessels and by extracting cholesterol directly from the cell membranes.

High levels of HDL translate to a better and healthy heart. When HDL is higher, it helps in reducing the excess cholesterol and thereby reduces the chance of developing atherosclerotic lesions in the blood vessels. This in turn reduces the risk of heart diseases.

HDLs have both anti-inflammatory and antioxidant properties. HDLs carry numerous enzymes that participate in anti oxidant activities for example glutathione peroxidase. They also dilate the blood vessels and this contributes to their atheroprotective function.

Evidence further suggests that HDLs have anti-apoptotic, anti-thrombotic and anti-infectious properties further affirming their position as the good cholesterol.

It is not necessary to be fasting before HDL levels in blood are determined.

According to the National Cholesterol Education Program:

Interpretation

HDL levels

High HDL; this corresponds to a healthy heart. As high HDL guards against heart diseases.

>60 mg/dL (1.56 mmol/L)

Acceptable HDL

40-60 mg/dL (1.04-1.5mmol/L)

Undesirable; corresponds to weak heart. As low HDL may contribute to heart diseases.

<40 mg/dL (1.04 mmol/L)

Non HDL cholesterol is calculated by subtracting HDL cholesterol from the total cholesterol. Since both HDL and total cholesterol can be measured without fasting, so can non HDL cholesterol. Non HDL cholesterol is a good predictor of cardiovascular risk. It is a better predictor of risk than LDL cholesterol in women and people with type 2 diabetes.

Very Low Density Lipoproteins: Excess dietary intake of fat and carbohydrates results in their conversion to triglycerides. These triglycerides are then packaged into the VLDL’s for distribution from the liver to tissues especially the muscles and adipose .In the tissues they are stored or oxidized to produce energy. In a nutshell, VLDL’s carry endogenously produced triglycerides out of the liver.

VLDL’s are lipoproteins that have a similar function like LDL. VLDL’s are a combination of cholesterol + triglycerides. They weigh more than the LDL. Through the action of Lipoprotein lipase (LPL), LDL particles lose triglycerides and form intermediate density lipoproteins (IDLs). IDLs are also called VLDL’s remnants. The IDLs are either taken up by the liver directly or converted to LDLs by extraction of more triglycerides. VLDL’s are smaller and denser than the LDL’s.

VLDL= Triglycerides/5

Triglycerides: Triglycerides are a type of lipids which are transported in the blood by VLDL. Our body stores them for energy. Triglycerides in the right amount are good for our health. The triglycerides and are stored in various fat cells throughout our body. High triglycerides like VLDL and LDL increase the risk of heart diseases. High triglyceride levels are related with low HDL and high LDL. High triglyceride levels are associated with another heart disorder called as "Metabolic syndrome". This syndrome is usually seen in people who have Type-2 Diabetes, High blood pressure, low levels of HDL and too much fat around the waist line.

Increased triglycerides in the body can be attributed to inherited disorders or acquired causes.

Inherited causes include;

Familial hypertriglyceridemia.

Familial combined hyperlipidemia.

Familial dysbetalipoproteinemia.

The acquired causes are as listed below.

Obesity.

Uncontrolled diabetes. In an effort to generate glucose, the body breaks down fat stores with release of triglycerides.

Hypothyroidism; thyroid hormone influences all aspects involved in the metabolism of lipids. It plays a key role in the synthesis, mobilization and degradation of lipids. For instance, thyroid hormones affect lipoprotein lipase activity. Thyroid dysfunction is associated with increased incidence of cardiovascular disease.

Cushing’s syndrome is characterized by elevated cortisol. Cortisol hormone promotes breakdown of peripheral fat stores to make glucose. This results in increased triglycerides in the blood stream.

Kidney disorders especially chronic renal failure. This is due to impaired maturation of HDL’s and down regulation of lipoprotein and hepatic lipases.

The liver as mentioned earlier plays a central role in the metabolism of cholesterol and lipids in the body and if it is dysfunctional it will result in deranged levels of these compounds in the body.

Excess calorie intake. In excess intake there is a situation of too few calories expended for the amount of calories consumed .The excess is then converted to triglycerides for storage.

Excess alcohol intake. Alcohol promotes accumulation of fat in the liver resulting in a fatty liver. The fatty liver will be less efficient in the breakdown and transport of lipids to tissues.

Medications including beta blockers, birth control pills, diuretics and steroids.

Triglycerides are tested after fasting for 12-14 hours. This is because their levels usually remain higher for some time after eating. Levels fall down when we sit down or lie down. Alcohol can cause falsely elevated results and it is recommended to abstain from alcohol far at least 24 hours before the test.

Interpretation

Triglyceride levels

Normal range, low risk

<150 mg/dL (<1.70 mmol/L)

Slightly above normal

151-199 mg/dL (1.70-2.25 mmol/L)

Some risk

200-499 mg/dL (2.26-5.65 mmol/L)

Very High, High risk

>500 mg/dL (> 5.65 mmol/L)