When it comes to cholesterol, there is no normal cholesterol level. Instead, there is a cholesterol level that predict higher exposure to death and disease if deposited beneath the internal lining of our blood vessels. And there is a cholesterol value that is associated with less likelihood of heart and blood vessel disease.
Cholesterol is carried in blood by three major carriers or lipo-proteins : High Density Lipo-proteins (HDL) which means that they contain a lot of the protein portion, which means also that they have high affinity to carry fat, which makes them the good guys who are able to carry fat to the liver away from blood vessels. The second carriers are the Low Density Lipo-proteins (LDL), which means – unlike above - that they are not able to carry much fat away from blood vessels, so their abundance in blood is dangerous and harmful and associated with deposition under the internal linings of blood vessels. The third class of carriers are the Very Low Density Lipo-proteins (VLDL). Most laboratories measure the total cholesterol, total triglycerides (TG) and the HDL fraction, leaving the measurement of the rest of your lipid profile to your doctor, based on the fact that the amount of cholesterol found in the VLDL fraction can be estimated by dividing the triglyceridesby 5, and also based on the fact that LDL fraction can by calculated by subtracting HDL and VLDL from the total cholesterol value.
Total cholesterol is relatively stable over time, and doesn’t depend on whether the patient is fasting. However, the TG fraction and HDL vary considerably depending on the fasting status of the patient. That’s why the National Cholesterol Education Program (NCEP), Adult Treatment Panel (ATP III) guidelines recommend that only fasting measurements be used to guide management decisions.
Two persons with the same total cholesterol level of 275 mg/dl may have very different lipid profiles. One may have a HDL cholesterol of 110 mg/dl, with a TG of 150 mg/dl, giving an estimated LDL cholesterol of 135 mg/dl. The other may have a HDL cholesterol of 25 mg/dl, with a TG level of 200 mg/dl, giving a LDL cholesterol of 210 mg/dl. Given all other risk factors are equal , the second person would have more than 10-fold higher risk to develop coronary heart disease than the first.
Basic science studies have shown that deposition of cholesterol in arteries is an inflammatory disease. One of the key factors triggering this inflammation is LDL. When LDL is taken up by certain cells in the blood stream, it triggers the release of certain signals, the end results of which is thickening or rupture of a plaque lining the vessel walls, which in turn leads to the events of coronary artery blockade leading to angina , or carotid artery blockade leading to stroke. So, cholesterol lowering via diet or drugs can therefore be thought of as an anti-inflammatory and plaque stabilizing therapy.
Since the advent of statin drugs ( a group of drugs used to lower cholesterol and the most recent of which is crestor ) around 1980s, several studies highlighted their role in reducing the risk of development of cholesterol related diseases on the heart, blood vessels and brain. Five of these studies were specifically significant.
In 1994, the Scandinavian Simvastatin Survival Study (4S) studied 4444 patients for 5.4 years after treating them with 20-40 mg/day of simvastatin. The patients were high risk in terms of both presence of diseases and unfavourable cholesterol profile. The results were a decrease of coronary artery disease deaths by 34%, a decrease in revascularization procedures by 37%, and all-cause death rate by 30%.
In 1995, the West Of Scotland Coronary Prevention Study (WOSCOPS), treated 6569 patients with markedly elevated cholesterol levels with 40 mg/day of pravastatin for 5 years. Coronary events were reduced by 31%. Coronary artery disease deaths were reduced by 28%. Coronary revascularization reduced by 37%, and all-cause deaths reduced by 22%.
In 1996 and 1998, the Cholesterol And Recurrent Events (CARE) study, and the Long term Intervention with Pravastatin in Ischemic Disease (LIPID) study, respectively, showed reduced incidences of bad clinical outcomes too.
Another later study was done in 1998. The Air Force / Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TEXCAPS) treated 6605 patients with the usual range of cholesterol for the US population with 20-40 mg/day of lovastatin. Remarkably even in this low risk group of patients, after 5 years of therapy, there was reduced coronary artery disease and death rate by 25%, reduced myocardial infarction events by 40% and decreased revascularization by 33%.
Non-favourable fat profiles are usually detected by routine laboratory screening in an asymptomatic person. That’s because except for rare patients whose high cholesterol may present with yellowish skin lesions called xanthomas especially related to eye lids or deposited in tendon bodies like the patellar tendon over the knee joint or the Achilles tendon behind the ankle, the majority of patients have no signs or symptoms of diseae.
So, the NCEP guidelines advise that screening for non-favourable lipid profile be done in adults aged 20 years or older with a fasting lipo-protein levels once every 5 years. The profile is categorized based on the LDL, HDL, and total cholesterol values:
LDL Cholesterol (mg/dl)
< 100 Optimal.
100-129 Near optimal.
130-159 Borderline high.
160-189 High.
>190 Very high.
HDL Cholesterol (mg/dl)
< 40 Low.
> 60 High.
Total cholesterol (mg/dl)
< 200 Desirable.
200-239 Borderline high
> 240 High.
After putting yourself in a category, you’ve already started yourself on the right track to prevent the unwanted effects of high cholesterol – if present - or to maintain your current healthy cholesterol status, also if present.
On the next post ( 2 of 9 ), we’ll continue our advice to you on what to do to save yourself from being pulled into the ever growing maze of not knowing what to do with my lipid profile. Stay tuned.
