Continuing the theme that the misinformation that we are given that cholesterol is somehow toxic is wrong....
By "toxic" I mean that a chemical substance that causes damage to us in a way that is related to dose and time-span of exposure. We are told that he greater the amount of cholesterol in the blood, and for a longer period of time, the more damaging it is. This assertion is not just over-simplistic but it is in defiance of the evidence. It is clear but generally unstated that it is only in men below the age of 50 that blood cholesterol is an indicator of risk of future manifestations of coronary heart disease (CHD). Above the age of 60, the age after which the vast majority of the deaths from CHD occur, a high blood cholesterol is a positive indicator of better survival.
Therapy is aimed at reducing the cholesterol level in the blood, but can this really be expected to be of any benefit? It does not appear to help.
Nature supplies us with a natural experiment by which we can investigate the effect of a high level of cholesterol in the blood. It is a liver disease called primary biliary cirrhosis (PBC).
PBC is a chronic disease of the liver that affects mainly middle-aged women. It has nothing to do with alcohol. The cause is unknown but it is generally classified as an auto-immune disease. In older women it tends to be a curiosity that is picked up incidentally from "routine" blood tests, but in younger women it is likely to be progressive and serious. There is no cure for this condition but it might lead to liver transplantation.
In PBC there is characteristically a very high level of cholesterol in the blood, and this has been recognised for more than half a century. This has given plenty of time for research.
The large amount of cholesterol in the blood in PBC might be deposited in the skin, creating fat patches that are called xanthomas, or xanthelasma if there are many of them. They tend to occur on the inner parts of the eyelids, on the knees and in the creases of the palms of the hands.
According to what we are told this would make people with PBC particularly susceptible to early death from CHD. They might be expected to have a large amount of cholesterol deposited in the walls of the arteries causing blockage, but this does not happen.
People with an exceptionally high level of cholesterol can be recognised as having familial hypercholesterolaemia (FH), of which we learn more in a Post to follow shortly. It is however interesting to compare the fortunes of those with PBC and those with FH as both have similarly high levels of blood cholesterol.
Those with PBC have a fundamental disadvantage in that they have a serious liver disease. It is only in recent years that liver transplantation has become available as otherwise the younger ones would die early because of liver failure. Transplantation has proved to be every effective in this condition although it can sometimes recur in the new liver.
During the 20th century people with FH have been at a considerable disadvantage in respect of CHD with premature death. However it is now clear that in contrast people with PBC are not at any disadvantage. They do not develop premature CHD and this has been demonstrated in a number of studies. The conclusion of one study is that "(in people with primary biliary cirrhosis) marked hypercholesterolaemia ....is not associated with an excess risk of cardiovascular disease."
If CHD were due to a high blood cholesterol with simple deposition of cholesterol from the blood then we would expect people with PBC to be very much at risk. But we can see that this is not so. This natural experiment casts serious doubt on the widely-accepted model of CHD. It indicates that CHD is not simply due to large amounts of cholesterol in the blood being deposited in the tissues.
We have seen in a recent Post that cholesterol in the wall of the arteries is not the result of simple deposition from the blood. It is an integral part of body defence mechanism and an important part of the inflammatory reaction.
Longo M et al.
Hyperlipidaemic state and cardiovascular risk in primary biliary cirrhosis.
GUT 2001 51 265-269.