About the Editor

Abstract

Dr. Ram B Singh comes from a multidisciplinary background. He began his career with an undergraduate degree in Science, followed by a Medical Science degree, and an MD degree in Internal Medicine with specialization in Cardiology. Dr. Singh further extended his career specializing in the area of Nutritional Science. During the subsequent years, He became much involved in clinical research, integrating nutrition and cardiovascular disease (CVD) along with its risk factors.Dr. Singh's research, especially on magnesium relating to CVD has received a great deal of international recognition. He was first to (a) perform Radioimmunoassay of serum digoxin in relation to digoxin intoxication in the year 1971-73 [1, 2], (b) demonstrate the role of magnesium deficiency in the pathogenesis of arrhythmias in patients with digoxin toxicity [3], (c) develop a concept of magnesium deficiency as a risk factor of digitalis intoxication [4], (d) report magnesium deficiency among patients with pulmonary heart disease [5] and atrial fibrillation (96), and (e) propose that magnesium deficiency is a risk factor for refractory cardiac arrhythmias [6] as well as for the elderly [7]. Furthermore, Dr Singh was first to report the role of magnesium deficiency in the pathogenesis of digoxin toxicity in children [8] with particular emphasis of its role in coronary artery disease (CAD), sudden cardiac death (SCD) [9,10], and ventricular fibrillation [10]. These reports earned him an invitation by the editor of the American Heart Journal to write an annotation [11] and by the editor of the Practical Cardiology to write a review article [12]. Dr Singh proposed that the role of magnesium deficiency and its repairement in the neurons, cardiomyocytes, , arterial endothelial and smooth muscle cells are important factors in predisposing CAD and SCD [12,13]. He reported the association between chronic active hepatitis and cardiomyopathy [14] and magnesium deficiency in the brain predisposing sudden death and the role of magnesium and potassium in hypertension [15][16][17][18][19]. Dr. Singh proposed a hypothesis that calcium channel antagonists modulate calcium by increasing magnesium influx by influencing magnesium ATPase and magnesium channels [20]. It is known that calcium channel blockers do not block the calcium channels, but they simply delay the opening of the channels, resulting in a decreased entry of calcium.