Dr. Kulick received his undergraduate and medical degrees from the University of Southern California, School of Medicine. He performed his residency in internal medicine at the Harbor-University of California Los Angeles Medical Center and a fellowship in the section of cardiology at the Los Angeles County-University of Southern California Medical Center. He is board certified in Internal Medicine and Cardiology.
Dr. Lee was born in Shanghai, China, and received his college and medical training in the United States. He is fluent in English and three Chinese dialects. He graduated with chemistry departmental honors from Harvey Mudd College. He was appointed president of AOA society at UCLA School of Medicine. He underwent internal medicine residency and gastroenterology fellowship training at Cedars Sinai Medical Center.
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
Homocysteine is metabolized (chemically transformed) into methionine and
cysteine with the help of the B vitamins; folic acid, B12, and B6 (pyridoxine).
Therefore, insufficient amounts of these B vitamins in the body can
theoretically hamper the metabolic breakdown of homocysteine, and hence increase
its blood levels. High levels of homocysteine in the blood
(hyperhomocysteinemia) can damage the inner surface of blood vessels, promote
blood clotting, and accelerate atherosclerosis.
The current state of knowledge regarding folic acid, homocysteine, and
heart
attacks is as follows:
The level of blood folate is an important determinant
of the blood homocysteine level. Low blood folate levels are associated with
high blood levels of homocysteine.
Low blood folate is common among individuals who do
not take multivitamins, but unusual among those who do.
The consumption of folic acid supplements or folic
acid fortified cereals can increase blood folate levels and decrease blood
homocysteine levels.
In a
large population study involving women, those who had the highest consumption of
folic acid (usually in the form of multivitamins) had fewer heart attacks than
those who consumed the least amount of folic acid.
Even though current
scientific evidence suggests that taking folic acid and vitamin B supplements to
lower homocysteine levels should help prevent atherosclerosis and heart attacks,
conclusive proof is still lacking because:
There are no conclusive controlled studies (discussed
at the beginning of this article) demonstrating that increasing folic acid
intake actually prevents atherosclerosis and heart attacks.
There is no clinical study demonstrating that lowering blood levels
of homocysteine actually prevents atherosclerosis and heart attacks.
There is
also no official recommendation as to who should be tested for
hyperhomocysteinemia. The optimal doses of the B vitamins, folic acid, B12, and
B6, required to prevent and treat hyperhomocysteinemia are also uncertain. For
folic acid, a daily dose of 0.8-1.0 mg is probably adequate.
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