Biophysical Semeiotic Constitutions, Genomics, and Cardio-Vascular Diseases. Sergio Stagnaro, Private 7 November 2004 Sir,as show GENEQUEST, PROCARDIS, and GENECARD, 3 genome-wide searches for genetic regions that are linked with coronary disease and other CVD (1-3), genome scans for coronary risk factors, such as blood pressure, body weight, lipids, and diabetes, have also been published in recent times (4). There is still, however, a long distance to travel from recognizing chromosomes abnormalities to the particular genes and the specific causative DNA variants (n-DNA and mit-DNA, of course), apart from the expense in doing that. By contrast, doctor can nowadays “clinically” recognize in a “quantitative” way the different biophysical-semeiotics constitutions and, then, the diverse risk factors as well as the diverse “real” risk, like that for CAD (See HONCode site 233738, www.semeioticabiofisica.it). In fact, clinicians are expecting relatively uncomplicated genetic solutions to Mendelian conditions, and, by preference, they are looking for a “clinical” method, that allows them to analyze at the bed side on very large scale modified biological events, caused by genetic alterations, which are usually very numerous, as those underlying CAD, Hypertension, Raynaud’s syndrome, a.s.o.). As a matter of fact, I agree completely with the paper’s authors, who demostrated that a common genetic factor underlies hypertension and other cardiovascular disorders (5). In other words, for both arterial disorders and cancers there is no simple gene test, no unifying genetic hypothesis: such as diseases occur in individuals involved by well-defined constitutions, I described previously, based on a singular mitochondrial cytopatology, i.e., Congenital Acidosic Enzyme-Metabolic Histangiopathy (6, 7, 8, and in above-cited website). In conclusion, thank to Biophysical Semeiotics, doctors can recognize and select since birth individuals with diabetic and/or dyslipidemic and/or hypertensive and/or arteriosclerotic (a.s.o.) constitutions, quantifying them, and finally diagnose the “real” risk of diverse disorders in well-localized biological system.1. Francke S, Manraj M, Lacquemant C. et al. A genome -wide scan for coronary heart diseasesuggests in Indo-Mauritians a susceptibility locus on chromosome 16p13 and replicates linkagewith the metabolic syndrome on 3q27. Human Molecular Genetics 2001;10(24):2751-65.2. Broeckel U, Hengstenberg C, Mayer B, et al. A comprehensive linkage analysis for myocardialinfarction and its related risk factors. Nature Genetics 2002;30(2):210-14.3. Harrap SB, Zammit KS, Wong ZYH, et al. Genome-wide linkage analysis of the acute coronarysyndrome suggests a locus on chromosome 2. Arteriosclerosis Thrombosis & Vascular Biology2002;22(5):874-78.4) Kraus WE. Genetic approaches for the investigation of genes associated with coronary heartdisease. Am Heart J 2000;140:S27-S35.5) Williams FMK., Cherkas LK., Spector LK.and MacGregor AJ.. A common genetic factor underlies hypertension and other cardiovascular disorders. BMC Cardiovascular Disorders 2004, 4:20 doi:10.1186/1471-2261-4-206) Stagnaro Sergio, Stagnaro-Neri Marina. Introduzione alla Semeiotica Biofisica. Il Terreno oncologico”. Travel Factory SRL., Roma, 2004. http://www.travelfactory.it/semeiotica_biofisica.htm7) Stagnaro S., Stagnaro-Neri M., La Melatonina nella Terapia del Terreno Oncologico e del “Reale Rischio” Oncologico. Ediz. Travel Factory, Roma, 2004.8) Stagnaro S., Stagnaro-Neri M., Le Costituzioni Semeiotico-Biofisiche.Strumento clinico fondamentale per la prevenzione primaria e la definizione della Single Patient Based Medicine. Ediz. Travel Factory, Roma, 2004. Competing interests No declared.