|Cellular Medicine in Heart Disease|
Why Cholesterol Is Not the Cause of Heart Disease
As a result of Dr. Rath’s discovery of the vitamin C-scurvy-heart disease connection, we now understand the role of cholesterol in heart disease. High blood cholesterol can lead to cardiovascular deposits only when combined with the loss of the integrity and functional weakness of the blood vessel wall, which triggers the need for its biological repair. This is why some animals, such as bears, do not massively die of heart attacks despite the fact that every 100 ml of their blood contains about 600 mg/dl of cholesterol. They produce vitamin C in their bodies, which ensures optimum collagen production and the stability of their arteries, so they do not worry about cholesterol. Dr. Rath’s groundbreaking discovery is detailed in his book Why Animals Don’t Get Heart Attacks, But People Do!
Cardiovascular Research at the Dr. Rath Research Institute
Our research in the area of cardiovascular disease focuses on health-beneficial effects of vitamins and essential nutrients in various aspects of cardiovascular disease, its initiation, and stepwise progression.
Among various projects, we have been investigating the role of nutrients in controlling abnormal migration and the growth of smooth muscle cells in the arterial wall, a hallmark of atheroma development and growth. We are also studying how nutrient synergy can be applied to curb inflammation leading to arterial wall cell damage and blood leukocyte recruitment. We have shown that nutrient synergy is more effective than individual antioxidants in decreasing oxidative stress associated with endothelial and smooth muscle cell damage, lipid and lipoprotein oxidation and their intra-arterial wall accumulation.
A significant part of our efforts has been concentrated on applying nutrient synergy in controlling pathological aspects of the remodeling of the extracellular matrix in the arterial wall. Such pathology leads to lost integrity and weakening of arterial wall structure, impaired arterial contractility, lipoprotein retention and oxidation, pathological behavior of arterial wall resident cells, increased plaque instability and the risk of its rupture.
Our other research areas include the aspects of sex hormone imbalance in the development of cardiovascular disease, as well as the cardiovascular aspects of impaired glucose metabolism (diabetes mellitus). Our research findings have contributed to a better understanding of nutrient synergy in controlling uterine smooth muscle tissue contractility (important in preventing miscarriage) and in autoimmune mechanism-mediated impairment of bronchial smooth muscle tissue contractility (asthma).
Studies in Heart Disease