Homocystinaemia

Homocysteine in high levels is a major culprit in the process of atherosclerosis and heart attack. Unfortunately the majority of doctors have overlooked the importance of homocysteine’s role as a major risk factor in CHD. The best evidence to that is that in conventional medicine measuring homocysteine levels is not part of recommended testing in diagnosis of CHD. This, despite homocysteine being a major risk factor in CHD as is high cholesterol, hypertension and smoking.

Homocysteine is an amino acid, which is derived from the breakdown of another essential amino acid called methionine.

Homocysteine as indicated is the bad guy but our clever body breaks it down into cysteine, which is a harmless metabolite. It is interesting to note that Vitamin B6 is essential for conversion of homocysteine into cysteine. Homocysteine can also convert back into methionine for which vitamin B12 and folic acid are required.

Homocystinuria is an inborn disease in which methionine metabolism is impaired. These children are born with enzyme deficiency causing high levels of homocysteine in their blood (homocystinaemia) and urine (homocystinuria). The children have mental retardation, dislocated optic lenses resulting in acute glaucoma, osteoporosis by age 15, and most importantly, vascular disease. Vascular disease is the major cause of death due to premature and relentless atherosclerosis resulting in heart attack before the age of 30. Twenty five per cent of these children die before the age of 30 due to vascular damage to the heart, kidney or brain.

How does homocysteine cause atherosclerosis?

Homocysteine has an irritative effect on the inner lining of the arteries like oxidised LDL-cholesterol. This is as a result of oxidative stress and inflammatory response, which can create a tear in the intima. Damaged and unsmooth arterial lining is ready to attract waste material, debris, LDL-cholesterol, calcium and so on which is the beginning of the process of atherosclerosis and atheroma formation. As time passes by the atheroma gets larger and fibrous causing narrowing of the arterial lumen, which results in less blood flow to the vital organs such as the heart, brain and kidneys. The patient may develop heart attack, stroke or hypertension.

Homocysteine also triggers LDL oxidation and increases the risk of blood clotting and as such is thrombogenic.¹⁹

Is there any research on the adverse effect of homocysteine?

Yes, there have been more than 40 clinical studies.

There were 15,000 physicians who took part in the Physicians’ Health Study had their homocysteine levels checked. Professor Meir Stampfer supervised the study. He concluded that those with high levels of homocysteine were three times more in danger of developing a heart attack.

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