Since the mid-1980s there have been campaigns, throughout the industrialised world, to bring attention to the problem of raised lipid levels, in an increasingly overweight population, as the root cause of coronary heart disease. Manufacturers and the media, through aggressive advertising and “documentary” campaigns, using grossly oversimplified claims about diet and “therapeutic” food products, have fuelled consumer concern. Such is this level of concern, that individual “cholesterol numbers” have become a popular topic of the “wellness” debate.
| Cholesterol has been largely portrayed as the “villain” although its presence in the bloodstream is vital to a number of functions especially the synthesis of steroid hormones (including the sex hormones), the production of bile acids needed in digestion and the synthesis of cell membranes. Problems occur when cholesterol is present in excess leading to its deposition upon the walls of the arteries as plaque in a process known as atherosclerosis (hardening of the arteries). Atherosclerosis leads to a narrowing of the arteries, restricting the flow of blood, and thus oxygen, to the heart or brain resulting in coronary heart disease(CHD) and cerebro-vascular accidents (strokes). |  |
In England and Wales CHD affects 3.5% of the population and accounts for 128,000 deaths annually – that is 22% of all deaths. In the USA, 4.8 million Americans are affected by CHD with 287,000 dying annually. This leading cause of death claims more lives than the next seven leading causes combined. In Europe, it is estimated that 45 million people (10% of the population) have dangerously elevated lipid levels whilst in the USA the figure is in excess of 60 million (25% of the population).
In the UK the National Service Framework for Coronary Heart
Disease has called for a reduction of CHD and stroke in the over 75 age
group of 40% by 2010 saving a predicted 200,000 premature deaths in total.
The Department of Health has made an additional £230 million available
annually to fund this initiative.
Routine assessment of blood lipid values has been recommended
in the following high risk groups:
a. Patients over the age of 70 years
b. Asymptomatic men and women under 69 years of age who have one of more
of the Coronary Artery Disease (CAD) risk factors (eg smoking)
c. Patients under 65 years of age who have a history of CAD – angina,
tendinous xanthomata, premature arcus senilis or first degree relatives
with such disease.
d. Diabetics.
In the UK alone such risk factors would apply to approximately 12 million
people.
Cholesterol is a fatty substance that does not mix with water and must, therefore, be “packaged” to be transported in the blood. The “packages” consist of lipoproteins formed as a water-soluble coat around the cholesterol content. There are six classes of lipoprotein distinguished by the protein to lipid ratio, which in turn gives rise to differences in particle density (the higher the ratio the greater the density). In increasing order of density these are:
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Each of these classes exerts a different risk in the parthogenesis
of CHD.
1. HDL (known as “good cholesterol”) is cholesterol-rich and
contains apolipoprotein A and levels are inversely related to the risk of
CHD (high is good, low is bad).
2. LDL (“bad cholesterol”) is cholesterol rich and contains
apolipoprotein B as its sole protein. High levels of LDL are directly related
to the risk of atherosclerosis.
3. IDL is TG rich and contains apo B. It is a breakdown product of VLDL
from which most of the TG has been removed to leave cholesterol. It may
be more atherogenic than LDL.
4. VLDL is the main carrier of TG in the bloodstream and in its most dense
sub-class may be an independent risk factor for CHD.
5. Chylomicrons contain 86% TG and result from the absorption of fats from
the intestine. High levels tend to be transitory immediately after meals.
Most important in diagnosing Type 1 hyperlipidaemia.
6. Lp(a) (“heart attack” cholesterol) consists of LDL bound
to apo A. It is thought that high levels may alter the thrombogenic system
and increase the risk of myocardial infarction.
The varying proportions of each of these components, in any particular patient’s bloodstream, allows classification of their disease and dictates the therapeutic regime needed to manage their health.
Essentially there are six types of hyperlipidaemia which demand
different therapeutic regimes.
1. Type l – often secondary to systemic lupus erythematosus –
showing elevation of the chylomicrons, small elevation of total cholesterol
and large elevation of triglycerides. It is classically treated by a low
fat diet.
2. Type lla. – hypothyroidism, nephrotic syndrome, Cushing’s
syndrome and corticosteroid therapy – shows elevated LDL, some elevation
of total cholesterol and normal triglycerides. Usual treatment is a diet
low in saturated fats and cholesterol and drug therapy – colestipol,
lovastatin and clofibrate.
3. Type llb. – Copathology as Type lla but with LDL and VLDL elevation
and small to medium elevation of total cholesterol and triglycerides. Treatment
requires a diet low in saturated fats, cholesterol and carbohydrates and
drug therapy – cholestyramine, lovastatin or cholestipol.
4. Type lll. – Hypothyroidism and SLE – elevation of intermediate
density lipids, total cholesterol and triglycerides. Treatment includes
a diet low in fats and carbohydrate plus clofibrate, niacin gemfibrozil
or lovastatin.
5. Type lV – diabetes, obesity, alcoholism, nephrotic syndrome, renal
failure, corticosteroid or oestrogen therapy. Elevated VLDL, normal total
cholesterol and triglycerides Treated by low carbohydrate diet and weight
loss programmes together with clofibrate or, rarely, niacin and gemfibrozil.
6. Type V - copathology as Type lV – chylomicrons, VLDL, total cholesterol
and triglycerides all showing elevation. Treated by diet low in fat and
carbohydrate, weight reduction and sometimes gemfibrozil and niacin therapy
The detailed management of hyperlipidaemia requires diagnostic
assessment of the various lipid fractions on a regular basis.