probably nothing that will take the place of a healthy, low calorie, nutrient dense diet. It is also important to keep your weight as close to your ideal weight as possible. Obesity contributes dramatically to inflammation and other risk factors that promote atherosclerosis. Everyone knows about the major risk factors - hypercholesterolemia (high cholesterol), hypertension (high blood pressure), smoking, and diabetes. It is time to address the 'novel' or emerging risk factors that may be equally as important if not more important than the risk factors we have focused on for the last 50 years. In general, each factor detailed below is considered 'an independent risk factor' for atherosclerosis. However, when one looks at the actual biochemistry and mechanism of action of the various factors discussed, it will be evident there is a tremendous inter-relationship and inter-dependency of these factors.
Homocysteine Homocysteine (Hey) is an aminoacid produced by the body usually as a byproduct of consuming meat. It is chemically related to the aminoacid
homocysteine
cysteine. In the presence of , high levels of can be adequate levels of vitamin B6, B12, and folic acid; Hey is converted into reduced easily and inexpensively with the neutral aminoacids methionine and (vitamin B6, B12 and cysteine. In addition, any methyl donor such as s-andenosyl-l-methionine (SAMe) Folic acid) Betaine and and betaine will aid in the conversion of this benign amino acid into the innocuous There is also evidence that Hey oxidizes aminoacids. LDL cholesterol which makes cholesterol even more dangerous. High Hey may In 1969, Kilmer McCully suggested that contribute to chronic disease in a more high levels of Hey in the blood contribute insidious way. People with elevated levels to atherosclerosis. He noticed that children of Hey may have a deficiency in the with an inborn error of methionine ability to perform methylating functions. metabolism developed homocysteinuria Methylation of D N A plays a critical role in (high levels of Hey in the urine) or protecting D N A from damage. In fact, homocysteinemia (high levels of Hey in high Hey has been implicated in such the serum). This error in metabolism can diverse conditions as Parkinson's disease, be caused a disruption of any of three Alzheimer's disease, cognitive interrelated pathways: dysfunction, osteoporosis, and peripheral neuropathy. 1) deficiency in cystathionine B- synthase As mentioned above, high levels of enzyme homocysteine can be reduced easily and inexpensively with the B vitamins 2) defective methyl cobalamin synthesis, (vitamin B6, BI2, and folic acid), betaine, and SAMe.
B vitamins
3) an abnormality in methylene tetrahydrofolate reductase (MTHFR).
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Children with homocysteinuria or homocysteinemia died in their 20's with premature atherosclerosis. One does not have to have this inborn error of metabolism to develop high serum levels of Hey. It is now thought that Hey can cause direct damage to the endothelium prompting the atherogenic cascade described above.
MSM - (methylsulfonomethane) which provides dramatic immune enhancing and anti-inflammatory j activities.
TIWIG/Betaine - (Trimethylglycine) which helps keep homocysteine levels (associated with heart attack, cancer and aging) at safe levels.
Ribose - benefits the heart
Bioperine - aids nutrient uptake
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The pathway starts with methionine, progresses to homocysteine, and then to cysteine. This is a transsulfuration pathway. Conversion of Hey back to methionine, catalyzed by methyl tetrahydrofolate and methlycobala in is considered a methylation pathway.
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In addition, homocysteine promotes hypercoagulation of the blood leading to thrombosis. Hey also promotes inflammation. Apparently Hey can interfere with the release of nitric oxide by the endothelium thereby preventing vasodilation, the relaxation of the artery.
SAMe "
Fibrinogen Fibrinogen is a protein that plays a critical role in clot formation. Fibrinogen is the direct precursor to fibrin, a coagulation protein that binds platelets together to form a blood clot. It is important to note that not all clot formation is bad. If we did not have the ability to clot, we could 'bleed out' with a minor cut. Clot formation is completely normal and necessary. It is when the atheroma or plaque that resides in the lining of an artery breaks or ruptures that the blood clot becomes deadly. A plaque ruptures, combines with fibrinogen which then releases fibrin. The fibrin forms scaffolding and releases peptides that draw blood platelets in the matrix. When this process occurs to stop a cut from bleeding it is a scab. When these blood clots form within the circulatory system they can become life threatening. A clot like this can cause a sudden and acute myocardial infarction (when it winds up in a coronary artery) or a devastating stroke (when the clot travels to the carotid arteries). The coagulation cascade is extremely complex and involves at least a dozen proteins, proteases, and enzymes. A defect in any one of those proteins leads to a