| Overall,
estimates suggest that 30% of patients with CHD and 42% of patients
with cerebrovascular disease have hyperhomocysteinemia, and
some 50% of those with congenital hyperhomocysteinemia experience
a thromboembolic event before they are 30 years old (20% do
not survive).7,9 To date, many studies
have investigated a possible contributory role for homocysteine,
and many do indicate that as homocysteine levels rise, so does
the risk for atherosclerotic vascular disease.
A
landmark meta-analysis found that each 5-µmol/L rise
in fasting homocysteine levels increased the likelihood of
CHD by 1.6 times in men and 1.8 times in women.10 This was
comparable in magnitude to the extra risk imposed by lipid
risk factors. Another study suggested that each additional
5-µmol/L rise in homocysteine levels was equivalent,
risk-wise, to a 20-mg/dL increase in total cholesterol level;
still another found the same increment to be analogous to
an 86-mg/dL rise in total cholesterol.7,11
However,
the findings do not always support a strong tie, particularly
when researchers examine the information from some prospective
trials.12,13 One possible explanation
is that added risk may be mainly limited to people with particularly
high levels of the amino acid. Note, too, that researchers
continue to wait for data proving that lowering homocysteine
levels truly reduces the incidence of vascular events. Such
clinical studies, now in progress, may evaluate as many as
50,000 patients.11
Among
its purported ill effects, homocysteine is believed to injure
the arterial wall, triggering inflammation and endothelial
dysfunction. For example, vasodilation may be hindered. This
damage may create more opportunities for LDL to infiltrate
blood vessels. Homocysteine also fosters LDL oxidation, permitting
it to become atherogenic. When present in abundance, homocysteine
enhances platelet aggregation and activates clotting factors,
major culprits in thrombus formation.
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