Articles Tagged with Heart Disease

The Icy Origins of Heart Attacks

Winter was coming and it hit hard, destroying the preserved food and even leaving the trees and bushes empty. All that was left was an animal here and there. But even this was getting rare and hunting was not as easy as before. Mankind’s difficulties were not over as soon as expected.


The ice age was one of those points in human history that changed everything. Not getting enough vitamins resulted in people’s blood vessel walls developing tiny cracks. Eventually, bleeding started everywhere in their bodies. Scurvy, known today as the sailor’s disease, became one of the biggest threats to our distant ancestors.

When everything else fails, though, one can count on evolution. Moreover, our incredible system of body cells came up with an idea to stop the bleeding. It introduced lipoprotein(a) (Lp(a)) and used it to repair the cracks in the blood vessel walls. Unfortunately this led to a dangerous narrowing of the width of those walls, thus making it harder to keep the blood flowing.

Especially in the heavily used blood vessels near the heart, this led to problems. The absence of micronutrients and the pressure from the ever-pumping organ caused minute cracks in the blood vessel walls, resulting in their being repaired using Lp(a). Over time, the blood vessel walls became blocked, the blood flow stopped, and a heart attack occurred. An organic process, designed to save humanity, turned into one of its greatest threats.

Inside the artery wall weakened by vitamin deficiency the Lp(a) particle fulfills two distinct repair functions: First, the sticky protein apo(a) lines up with the defective collagen molecules to prevent further damage and blood leakage to the outside. Secondly, the LDL-part of the Lp(a) molecule is needed for another ‘repair mechanism’: it supplies cholesterol and other fats for the synthesis of new cells.
Inside the artery wall weakened by vitamin deficiency the Lp(a) particle fulfills two distinct repair functions: First, the sticky protein apo(a) lines up with the defective collagen molecules to prevent further damage and blood leakage to the outside. Secondly, the LDL-part of the Lp(a) molecule is needed for another ‘repair mechanism’: it supplies cholesterol and other fats for the synthesis of new cells.

The new understanding regarding the development of heart disease that you can read on this website provides both the scientific proof for the facts described above and the solution to it.

End of heart disease now possible – New study proves atherosclerosis is early form of scurvy

Scientists at the Dr. Rath Research Institute in California have published a groundbreaking study in the American Journal of Cardiovascular Disease proving that heart disease is an early form of the vitamin C deficiency disease scurvy. Building on a discovery made by Dr. Matthias Rath in the early 1990s, this publication deals a major blow to the cholesterol theory of heart disease and the pharmaceutical industry’s associated $30 billion annual sales in patented cholesterol-lowering statin drugs.

In his initial discovery, Dr. Rath had revealed that coronary heart disease occurs exactly for the same reason that clinical (early) scurvy does – a deficiency of vitamin C in the cells composing the artery wall. Humans, unlike animals, develop heart disease because their bodies cannot produce vitamin C. The average human diet provides enough vitamin C to prevent scurvy, but not enough to guarantee stable artery walls. As a consequence of vitamin C deficiency, millions of tiny cracks and lesions develop in the artery walls. Subsequently, cholesterol, lipoproteins and other blood risk factors enter the damaged artery walls to repair these lesions.

Of all these risk factors, by far the most important is a molecule known as Lipoprotein(a). Primarily found in humans and sub-human primates, Lipoprotein(a) functions as a repair molecule compensating for the structural impairment of the vascular wall. In general, animals that produce vitamin C in their bodies do not produce Lipoprotein(a).

In human beings, in the case of a chronic deficiency of vitamin C, the arterial repair process becomes continuous. Over the course of many years atherosclerotic deposits develop, eventually leading to heart attacks and strokes.

In this latest research, transgenic mice were used that mimic human metabolism with regard to two distinct genetic features: an inability to produce vitamin C, and the ability to produce Lipoprotein(a). When given a diet containing an insufficient amount of vitamin C, the mice were found to deposit Lipoprotein(a) in their vascular walls and develop atherosclerosis. The degree to which they developed heart disease was found to be inversely related to their intake of vitamin C. Mice with the highest intake of vitamin C had the lowest depositions of Lipoprotein(a) in their arteries and the least atherosclerotic lesion development.

With the publication of this study, we strongly believe that the abolition of heart disease as a cause of human mortality is now possible.

Online access:
Study Authors: John Cha, Aleksandra Niedzwiecki, Matthias Rath
Contact: Paul Anthony Taylor


Our Study Proves That Heart Disease Is Linked To Vitamin C Deficiency

Heart attacks and strokes have consistently remained the leading causes of death. Atherosclerosis, the underlying cause of these diseases, results in 17 million deaths worldwide each year. Yet, high blood cholesterol levels, a fatty diet and obesity have been blamed as the causes of heart disease. However, cutting down dietary fat and the artificial reduction of blood cholesterol with cholesterol-reducing medicines have not been successful in addressing this issue. Atherosclerotic plaques occur primarily in the coronary arteries rather than in the entire 60,000-mile-long vascular system. The absence of plaque in the veins, and the fact that animals do not suffer from atherosclerosis while humans do, cannot be explained by conventional medicine and the cholesterol theory of heart disease.

Studies conducted at our Research Institute now enable a new understanding of the cause of heart attack and stroke: They are the result of a structural weakness of the artery wall, which is primarily caused by a deficiency of vitamin C and other micronutrients in our diet.
Studies conducted at our Research Institute now enable a new understanding of the cause of heart attack and stroke: They are the result of a structural weakness of the artery wall, which is primarily caused by a deficiency of vitamin C and other micronutrients in our diet.

In 1990, Dr. Rath and the late two-time Nobel Laureate Dr. Linus Pauling published1 the revolutionary concept that a chronic insufficiency of vitamin C damages blood vessel walls. This damage triggers a biological “repair” process in which cholesterol-carrying lipoproteins deposit in the artery walls like a biological form of mortar. With time, this “repair” process can lead to a buildup of atherosclerotic plaque. The most effective “repair” molecule is a large, sticky substance known as lipoprotein (a) [Lp(a)]. Dr. Rath observed an inverse relationship between the internal production of lipoprotein (a) and vitamin C, which he described as the scurvy-heart disease connection. Humans, unlike most animals, do not produce vitamin C in their bodies. Due to its unique structure, Lp(a) can act as a surrogate for vitamin C and protect the integrity of the blood vessels during times of vitamin C deficiency and the development of scurvy.

However, whilst the significant role of Lp(a) in cardiovascular disease has been recognized, there are no effective pharmaceutical drugs that can lower it. Doctors believe that Lp(a) levels are part of our genetic makeup and focus instead only on artificial reduction of the cholesterol-carrying LDL (“bad” cholesterol).

Researchers at the Dr. Rath Research Institute have developed a unique animal model {Gulo-/-; Lp(a)+} with two characteristics of human metabolism: a lack of the specific gene (Gulo-/-) necessary for vitamin C production and an ability to produce human Lp(a). This animal model can replicate a unique event in human evolution some 40 million years ago, when humans lost the ability to make their own vitamin C and the Lp(a) gene emerged.

Our study with this animal model showed that a complete absence of dietary vitamin C intake results in a significant increase in serum Lp(a) levels. Moreover, this is accompanied by increased accumulation of Lp(a) in the arteries at the site of highest mechanical stress near the heart, leading to the appearance of plaques. On the other hand, supplementation of vitamin C effectively decreased the deposition of Lp(a) along the artery walls and consequently decreased Lp(a) blood levels. This confirms that Lp(a) can function as a repair molecule accumulating at the sites of blood vessel wall damage (insufficient collagen production) during vitamin C deficiency. The study has been published in the April, 2015 issue of the American Journal of Cardiovascular Disease2.

This unique mouse model allows the mimicking of the human metabolism in its critical aspects: a lack of vitamin C production and the uniqueness of Lp(a) synthesis. Our study thus confirms the connection between vitamin C deficiency, Lp(a) accumulation and atherosclerosis. Moreover, our results showed that supplementing with vitamin C effectively reduced levels of Lp(a) and other associated risk factors that are most common in heart attacks and strokes.


1 M. Rath, L. Pauling, Proc. Nati. Acad. Sci. USA Vol. 87, pp. 6204-6207, 1990
2 J. Cha, A. Niedzwiecki, M. Rath; Am J Cardiovasc Dis 2015;5(1):53-62

bodyxq Heart: Interactive Education

With the launch of our free bodyxq apps for Apple iOS and Android, we are putting at your fingertips the world’s first truly interactive health education program that enables you to travel inside the organs of the body and explore their functions.


With the help of this innovative apps, people of all ages can easily see and understand the functions of the human heart – and zoom in on them right down to the level of the billions of cells from which all of the body’s organs are built. You can also modify important factors, such as micronutrient deficiency, and watch how they contribute to the development of cardiovascular diseases such as arteriosclerosis, high blood pressure, heart failure and irregular heartbeat. Through using the interactive features on bodyxq, you will easily see how diseases originate at the cellular level and learn about important factors that keep the cells healthy and functioning optimally.

Education about the root cause of disease will allow millions of people to take action to help prevent diseases and improve their health. They can now actively participate in essential decision-taking affecting their own health. bodyxq is making basic health doable for everyone.

Download our Free Apps

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Call to End Heart Disease


In April 1992 Dr. Matthias Rath and two-time Nobel Laureate Dr. Linus Pauling issued their historic “Call for an International Effort to Abolish Heart Disease.” The basis of this Call was the scientific discovery that the primary cause of cardiovascular disease is not elevated blood levels of cholesterol, but a long-term deficiency of vitamins and other micronutrients in our diet.The Call aimed at encouraging the international scientific and medical community to launch a global research effort to confirm this new understanding – with the goal of saving millions of lives!

Because micronutrients are not patentable, there was essentially no interest from established medical institutions to respond to this Call. In April 2015, almost a quarter of a century later, Dr. Rath and his research team finally confirmed the new understanding about the cellular origin of cardiovascular disease in a series of breathtaking experiments.

The scientific confirmation of the new concept of cardiovascular disease was first presented to the public at a symposium in the Dutch city of Maastricht on April 22, 2015. Based on the new scientific evidence available now, the attendees at the symposium supported the “Rath-Pauling Manifesto” – thereby renewing the call to scientists, doctors, health authorities and people worldwide to engage in a vigorous international effort to render heart attacks, strokes and other forms of cardiovascular disease largely unknown in future generations.

Please pass this “Rath-Pauling Manifesto” on to your friends and colleagues. Ask them to support this international effort to “End Heart Disease” with their signatures and their commitment not to rest until this goal is achieved.

Below you will find the original call from 1992.


A Call for an International Effort to Abolish Heart Disease

Heart disease, stroke, and other forms of cardiovascular disease now kill millions of people every year and cause millions more to be disabled. There now exists the opportunity to reduce greatly this toll of death and disability by the optimum dietary supplementation with vitamins and other essential nutrients.

During recent years we and our associates have made two remarkable discoveries. One is that the primary cause of heart disease is the insufficient intake of ascorbate (vitamin C)1,2, an insufficiency from which nearly every person on earth suffers. Ascorbate deficiency leads to weakness of the walls of the arteries and to lesions in stressed regions that initiate the atherosclerotic process.

The other discovery is that the atherosclerotic plaques are not composed of LDL (low-density lipoprotein), but are instead composed of a related lipoprotein3,4, rather which, than cholesterol, is the major risk factor for heart disease.

Moreover, certain essential nutrients, especially the amino acid L-lysine, can block the depositions of this lipoprotein and even reduce existing plaques. We have concluded that the optimum supplementation of ascorbate and many other nutrients could largely prevent heart disease and stroke and be useful in treating existing disease. Published clinical and epidemiological data support this conclusion5,6.

The goal is now in sight: the abolition of heart disease as the cause of disability and mortality for the present generation and future generations.

With millions of lives each year at stake, no time should be lost!

We call upon our colleagues in science and medicine to join in a vigorous international effort to investigate the role of vitamin C and other nutrients in controlling heart disease.

We call upon the national and international health authorities and other health institutions to support this effort with political and financial measures.

We call upon every human being to encourage physicians and medical institutions to take an active part in this process.