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Coronary heart disease is the single greatest cause of death in the Western world. Its incidence even in the developing countries is growing at an alarming rate. This is widely believed to be linked to some secondary habits, rich fatty diet, high blood pressure, diabetes, smoking, alcohol and increased serum cholesterol. It has, however, been observed that in more 50% of the patients of coronary heart disease, some factors other than cholesterol and the said factors are affecting their health. This is explained further, later in this document.
In your blood, three types of cholesterol affect your coronary heart condition – low-density lipoproteins (LDLs), high-density lipoproteins (HDLs), and very-low-density lipoproteins (VLDLs). LDLs are ‘bad’ cholesterol molecules: they can accumulate on the walls of your arteries, forming plaques which disturb the flow of blood. This is called atherosclerosis.
This is what happens. If LDL particles are in excess, then there are some left over from cells that would have taken them up. These stay in the blood. If there are too many LDL particles in your blood, if your liver cells (LDL receptors) do not receive LDL particles normally, or, if there are too few LDL receptors in your liver, your body's cells become saturated with cholesterol from the LDL particles. Cholesterol is then deposited in your artery walls.
At this point your high-density lipoproteins (HDLs) play their "good" role. They actually pick up cholesterol deposited in your artery walls and transport it to your liver for disposal. If too much cholesterol from LDL particles remains deposited in your artery walls, you have a problem. Your arteries will develop plaques and begin to narrow.
This is why a high HDL level relative to an LDL level is good. It can
help protect you from developing atherosclerosis. This can be achieved by cutting down your consumption of fat from
dairy products, meats and partially hydrogenated oils, eat less sugar and highly
refined starch. It is also advisable to replace saturated fats with
monounsaturated fats (e.g. olive oil).
But scientists have argued that this theory does not sufficiently explain mortalities. Increasing HDLs in a group of people does not directly imply that less of the specimen die. The same is true for the opposite. It is argued that dietary trials are not accurate as not enough people are tested, and that something else other than LDL must be affecting heart condition.
This other factor is thought to be homocysteine. Mildly raised homocysteine levels are associated with an increased risk of vascular disease. High levels can arise from inherited disorders of the enzymes involved in methionine metabolism, a high intake of methionine, or deficiency of vitamins B6, B12 and folic acid. It is still unclear whether all forms of mild homocysteinaemia increase vascular risk or whether normalising the homocysteine level reduces the risk.
This hypothesis that mildly elevated levels of homocysteine contribute to vascular disease was raised early in Australia. Since then several international studies have confirmed higher mean homocysteine levels in patients with coronary, cerebral and peripheral vascular disease, particularly in those with vascular disease not readily explained by the conventional risk factors. When animals are infused with large amounts of homocysteine, platelets are activated and there is evidence of damage to the endothelial lining of blood vessels.
Homocysteine in cells arises from the metabolism of methionine, an essential sulphur-containing amino acid. On the usual Australian diet approximately 50% of the homocysteine undergoes transformation to cystathionine and then to cysteine, with vitamin B6 as a cofactor for the enzyme cystathionine-b-synthetase (CbS); the remainder is remethylated to methionine in a series of reactions involving the enzyme methyltetrahydrofolate reductase (MTHFR) and the cofactors methyltetrahydrofolate and vitamin B12.
Classical homocysteinuria is the consequence of an inherited deficiency or absence of CbS activity. In the homozygous state, vascular events occur in 50% of affected individuals by age 30 (3). The heterozygous state has been estimated to have a frequency of about 1% in the general population; in this case, however, the homocysteine levels are only slightly elevated.
A common polymorphism of the MTHFR gene has been found to affect about 12% of Australians and is associated with elevated homocysteine levels. Two Australian studies attempting to link the genotype directly with coronary disease have been negative, although neither of these studies measured homocysteine levels. It has been suggested that subjects with this genotype have elevated homocysteine levels only when there is an accompanying deficiency of dietary folate.
It has been estimated that a 5umol/L reduction in homocysteine levels would achieve a reduction in cardiovascular events equivalent to that achieved by a 0.5mmol/L lowering of cholesterol. Some have proposed folate fortification of commonly used foods to reduce the incidence not only of spina bifida but also to reduce cardiovascular risk. Between 0.5 and 5mg of folate daily lowers homocysteine levels in most subjects.
So it is not just diet that affects your health. However, it is still advisable that you have a balanced diet and stay away from saturated fats.
Ronald Kam
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