L-Homocystine

Contrary to the present practice of measurement of cardio-vascular risk factors or inflammatory risk factors such as C-Reactive Protein (CRP) from a blood sample from the vein of one arm, by using the Bi-Digital O-Ring Test Resonance Phenomena between 2 identical substances, one can non-invasively detect the approximate location on the body of abnormally increased risk factors in just 2 minutes, by detecting the resonance with L-Homocystine, even when blood CRP failed to detect any abnormality. This is performed by projecting a 0.5 to approximately 5mW red spectral laser beam with 560-670nm wavelength, to at least 6 standard parts of the body, when one of the control risk markers placed next to the laser beam also exists in the part of the body tested. It is generally believed that CRP is increased in the presence of acute myocardial infarct, chronic rheumatoid arthritis, ulcerative colitis, metabolic abnormalities such as often detected in diabetes, inflammation and underlying infection of the cardio-vascular system, and in some cancers. However, in our study, when the clinical significance of CRP and L-Homocystine was compared, we found that CRP often was not increased when there was extensive infection of Mycobacterium Tuberculosis as well as asymptomatic infection by Cytomegalovirus, Herpes Simplex Virus Type I, Human Herpes Virus Type 6, Borrelia Burgdorferi, or Chlamydia Trachomatis in the heart (and other parts of the body), particularly when there was liver cell dysfunction such as an increase in ALT. In contrast, L-Homocystine was often increased in the presence of localized infections of the heart and other parts of the body. For screening of Cardio-Vascular diseases by this method, 0.5mg of L-Homocystine as a control marker was found to be the most sensitive and reliable, compared with most effective amount of CRP, 0.5ng, for detecting early Cardio-Vascular problems due to various localized infections. About 0.5ng of cardiac Troponin T and cardiac Troponin I were also useful for detecting early stages of heart disease but they are not as sensitive as L-Homocystine. Once the pathogenic factors were identified, the effective medication was given, and the Selective Drug Uptake Enhancement Method (originally discovered by the first author in 1990) was applied after the effective drug was administered, to selectively deliver the medication to the pathological area, while reducing drug uptake to the normal parts of the body. As a result, the therapeutic effect was markedly accelerated.

L-Homocystine activates Hageman factor, as demonstrated by its capacity to initiate clotting and to induce the evolution of plasma kinins. Perhaps, strategically located deposits of this amino acid are responsible for the unusual frequency of thrombosis in patients with homocystinuria.