Updated 20 July 2018

High cholesterol and the fat from your diet

About 20% of the cholesterol in your body come from the food you eat. Here’s how dietary cholesterol can contribute to an excess of cholesterol in the bloodstream.

In terms of diet, cholesterol and triglycerides come mainly from eating animal products, fish, dairy products and various oils, which are then absorbed through the gut.

Eggs and shrimp have a very high cholesterol content. For practical purposes, plants have no cholesterol. Instead, plant products have cholesterol-like substances called phytosterols, which may compete with cholesterol for absorption. When consumed in very large amounts, they can lower cholesterol absorption and consequently lower blood cholesterol by about 5-10%.

In the intestine, the ingested cholesterol and triglycerides are assembled into special spherical packages called chylomicrons. These travel through the bloodstream to distribute triglycerides to muscle and adipose (fat) tissue, and to return the remainder to the liver.

Most of the cholesterol in the diet stays in the chylomicrons and is taken up by the liver where it mixes with newly made cholesterol, made by the liver itself. Chylomicrons only remain in the bloodstream for a short while.

VLDL and LDL cholesterol

The liver is also where fats are broken down and made from metabolic products of sugars and proteins. Not only does the liver make cholesterol, it also makes fatty acids, and incorporates these into triglycerides and phospholipids for export to the rest of the body.

The fats made in the liver are assembled with protein compounds called apolipoproteins to make a new, fat-rich lipoprotein called VLDL – very-low-density lipoprotein.

Again, the VLDLs lose most of their triglycerides as fatty acids to muscle and adipose tissue, where they’re either used or stored. Some of these triglycerides are taken up by the muscles as fuel while the rest is laid down as adipose tissue in the body. The fats in adipose tissue act as energy reserves – all too often never utilised.

Some of the VLDL, after losing an initial amount of triglyceride, are converted in the plasma (the liquid, non-cellular part of the blood) into a new form of lipoprotein called low-density lipoprotein (LDL). This lipoprotein is very rich in cholesterol. It’s these particles which, in excess, can lead to atherosclerosis and coronary artery disease (CAD).

LDL remains in the bloodstream for around three days before it’s removed by the liver. The mechanism whereby it’s removed is important. LDL comprises of cholesterol and a protein called apolipoprotein B (apoB). This protein recognises a specific receptor on the liver cell – the apoB-receptor (also known as the LDL receptor) – which allows LDL to “dock” at the receptor and so be taken up by the liver.

If the receptor is faulty (as happens in the case of familial hypercholesterolaemia, a genetic disorder), the LDL isn’t taken up. When this happens, an excess of LDL circulates in the bloodstream, penetrating the vascular wall and leading to CAD.

HDL cholesterol

There’s another lipoprotein in this story – high-density lipoprotein (HDL). Of all the lipoproteins, only high-density lipoprotein (HDL) doesn’t deposit cholesterol in the tissues. Instead, it removes cholesterol, taking it back to the liver for excretion.

HDL has the ability to pick up excess free cholesterol from peripheral (non-liver) cells, including those accumulating in the arterial wall, which predispose us to CAD.

HDL returns the excess cholesterol directly to the liver. It also carries important protective antioxidant enzymes and other molecules, which lessen the risk of CAD. HDL seems also to limit the adverse response of the arterial lining to lipoproteins, cells and clotting processes.

These properties make HDL an effective anti-coronary disease agent. The cholesterol measured in HDL is therefore called "good" cholesterol because of the association with a lowered risk for heart disease. Unfortunately, medication that raises HDL concentrations haven’t proven effective in combating atherosclerosis.

Following a healthy diet is key

All of this means that not only are your levels of cholesterol and triglycerides important, but also your levels of LDL and HDL. The latter two lipoproteins are most easily measured by their cholesterol content. High levels of LDL and low levels of HDL mean that you have a greater risk of CAD; the opposite means that you’re better protected.

The amount of cholesterol and triglycerides made in the liver is influenced by your total energy (kilojoule) intake, and the quantity and kind of fat you consume. This is one reason why following a healthy diet is so important. When you eat too much in general, and ingest too much of the wrong kinds of fat, your cholesterol levels may shoot up.

Take note of the following:

  • Eating saturated fats raises levels of LDL (“bad”) cholesterol; hence too much of these fats in the diet is harmful. Sources of saturated fats include meat, butter, milk and cheese.
  • Mono- and polyunsaturated fats (found in plant-based foods and fish) are viewed as better than saturated fats. In fact, eating more of certain kinds of unsaturated fats can actually decrease your total cholesterol levels.
  • When unsaturated vegetable fats are partially hydrogenated to change the consistency from liquid to solid, the process produces yet another type of fatty acid as a side product. These so-called trans fatty acids raise LDL levels, and so total cholesterol levels, but they also lower HDL levels – known to protect against CAD. These fats are often found in processed foods and brick margarine, and should be avoided.

Reviewed by Prof David Marais, FCP(SA), Head of Lipidology at Groote Schuur Hospital and the University of Cape Town. January 2018.


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