Nutritional Supplement Program Halts Progression of Early Coronary Atherosclerosis

Documented by Ultrafast Computed Tomography

Matthias Rath, M.D. and Aleksandra Niedzwiecki, Ph.D.



According to the World-Health Organization, over 12 million people die every year from heart attacks, strokes and other forms of cardiovascular disease. The direct and indirect costs for treatment of cardiovascular disease are the single largest health care expense in every industrialized country of the world. Despite modest success in some countries in lowering the mortality rate from heart attacks and strokes, the cardiovascular epidemic is still expanding on a worldwide scale.


Current concepts of the pathogenesis of cardiovascular disease focus on elevated plasma risk factors damaging the vascular wall and thereby initiating atherogenesis and cardiovascular disease. Accordingly, drugs lowering cholesterol and modulating other plasma risk factors have become a predominant therapeutic approach in the prevention of cardiovascular disease.



A new scientific rationale about the initiation of atherosclerosis and cardiovascular disease has been proposed. It can be summarized as follows: cardiovascular disease is primarily caused by chronic deficiencies of vitamins and other essential nutrients with defined biochemical properties, such as coenzymes, cellular energy carriers, and antioxidants. Chronic depletion of these essential nutrients in endothelial and vascular smooth muscle cells impairs their physiological function.


For example, chronic ascorbate deficiency, similar to early scurvy, leads to morphological impairment of the vascular wall and endothelial microlesions, histological hallmarks of early atherosclerosis. Consequently, atherosclerotic plaques develop as the result of an overcompensating repair mechanism comprising deposition of systemic plasma factors as well local cellular responses in the vascular wall. This repair mechanism is primarily exacerbated at sites of hemodynamic stress, explaining the predominantly local development of atherosclerotic plaques in coronary arteries and myocardial infarction as the most frequent clinical manifestation of cardiovascular disease.


Animal studies have confirmed this scientific rationale resulting in patents for the combination of ascorbate with other essential nutrients in the prevention and treatment of cardiovascular disease. Based on this patented technology, we have developed a nutritional supplement program, which was tested in this study in patients with coronary heart disease.


Aims and materials

The aim of this study was to determine the effect of a defined nutritional supplement program on the natural progression of coronary artery disease. This nutritional supplement program was composed of vitamins, amino acids, minerals, and trace elements, including a combination of essential nutrients patented for use in the prevention and reversal of cardiovascular disease.


The following daily dosages of nutritional supplements were taken for a period of one year: Vitamins: Vitamin C 2700 mg, Vitamin E(d-Alpha-Tocopherol) 600 IU, Vitamin A (as Beta-Carotene) 7,500 IU, Vitamin B-1 (Thiamine) 30 mg, Vitamin B-2 (Riboflavin) 30 mg, Vitamin B-3 (as Niacin and Niacinamide) 195 mg, Vitamin B-5 (Pantothenate) 180 mg, Vitamin B-6 (Pyridoxine) 45 mg, Vitamin B-12 (Cyanocobalamin) 90 mcg, Vitamin D (Cholecalciferol) 600 IU. Minerals: Calcium 150 mg, Magnesium 180 mg, Potassium 90 mg, Phosphate 60 mg, Zinc 30 mg, Manganese 6 mg, Copper 1500 mcg, Selenium 90 mcg, Chromium 45 mcg, Molybdenum 18 mcg. Amino acids: L-Proline 450 mg, L-Lysine 450 mg, L-Carnitine 150 mg, L-Arginine 150 mg, L-Cysteine 150 mg. Coenzymes and other nutrients: Folic Acid 390 mcg, Biotin 300 mcg, Inositol 150 mg, Coenzyme Q-10 30 mg, Pycnogenol 30 mg, and Citrus Bioflavonoids 450 mg. Further information at:



The study was designed as a prospective intervention before-after trial over a 12 month period and included 55 outpatients age 44-67 with various stages of coronary heart disease. Changes in the progression of coronary artery calcification before and during the nutritional supplement intervention were determined by Ultrafast Computed Tomography (Ultrafast CT).



The natural progression rate of coronary artery calcification before the intervention averaged 44% per year. The progression of coronary artery calcification decreased on average 15% over the course of one year of nutritional supplementation.


In a subgroup of patients with early stages of coronary artery disease, a statistically significant decrease occurred, and no further progression of coronary calcification was observed. In individual cases, reversal and complete disappearance of previously existing coronary calcifications were documented.



This is the first clinical study documenting the effectiveness of a defined nutritional supplement program in halting early forms of coronary artery disease within one year. The nutritional supplement program tested here should be considered an effective and safe approach to prevention and adjunct therapy of cardiovascular disease.