Overview and effective alternative approaches to atherosclerosis


What is it?

Atherosclerosis or arteriosclerotic vascular disease is a potentially serious condition that occurs when the blood vessels (arteries), that carry oxygen and nutrients from the heart to the rest of the body, become thick and stiff because of build-up of fats (triglycerides), cholesterol, calcium and other substances, found in the blood, on the artery walls (known as atheromatous plaques or atheroma), which can restrict blood flow to organs and tissues damaging them and stopping their proper functioning.



Figure A shows a normal artery with normal blood flow.

The inset image shows a cross-section of a normal artery.

Figure B shows an artery with plaque buildup.

The inset image shows a cross-section of an artery with plaque buildup.

These plaques are rich in macrophages, so they are usually weak and prone to rupture:

if they burst, it triggers a blood clot (thrombosis) on the plaque’s surface, that rapidly slow or stop the blood flow outright, leading to death of the tissues fed by the artery in approximately five minutes.

This catastrophic event is called “infarction”.
More cases can happen:

coronary-artery1. If the oxygen supply to the heart muscle, trought the coronary arteries (the main arteries which supply the heart), is reduced (coronary heart disease), a myocardial infarction (heart attack) can occur;

2. If the oxygen supply to the brain is interrupted (carotid artery disease), a stroke can occur;

3. If the oxygen supply to the extremities (e.g. legs) is reduced, gangrene can result (thromboembolism).


endothelial-disfunction1For this reason atherosclerosis, often considered a heart problem, can affect large or medium-sized arteries anywhere (the entire artery tree) in the body, but mainly affects the larger high-pressure vessels such as the coronary, renal, femoral, cerebral, and carotid arteries.

Therefore atherosclerosis is the cause of heart attacks, ictus and peripheral vascular disease (collectively known as “cardiovascular disease (CVD)”).


First step: Physical exam

The doctor may listen to arteries for an abnormal whooshing sound called a bruit. He can hear a bruit when placing a stethoscope over an affected artery. A bruit may indicate poor blood flow due to plaque buildup.
The doctor also may check to see if any pulses (for example, in the leg or foot) are weak or absent. A weak or absent pulse can be a sign of a blocked artery.

Next steps: Diagnostic Tests

Blood Tests: for check the levels of certain fats, cholesterol, sugar, and proteins in the blood.

ECG (Electrocardiogram)
: it detects and records the electrical activity and pathways of the heart. It also takes measurements of the heart rhythm.

Chest X Ray: it takes pictures of the organs and structures inside the chest, such as heart, lungs, and blood vessels.

Doppler ultrasound
: the doctor may use a special ultrasound device (Doppler ultrasound) to measure blood pressure at various points along the arm or leg. These measurements can help the doctor gauge the degree of any blockages, as well as the speed of blood flow in the arteries.

Ankle-Brachial Index: this test compares the blood pressure in the ankle
with the blood pressure in the arm to see how well the blood is flowing.
An abnormal difference may indicate peripheral vascular disease.

Echocardiogram: it uses sound waves to create a moving picture of the heart. The test provides information about the size and shape of the heart and how well the heart chambers and valves are working.

Computed Tomography Scan: a computed tomography (CT) scan creates computer-generated pictures of the heart, brain, or other areas of the body. The test can show hardening and narrowing of large arteries. A cardiac CT scan can show whether calcium has built up in the walls of the coronary (heart) arteries. This may be an early sign of CHD.

Stress Testing (exercise stress test): the patient exercises to make his heart work hard and beat fast while heart tests are done. A stress test can show possible signs and symptoms of CHD, such as:

– Abnormal changes in the heart rate or blood pressure
– Shortness of breath or chest pain (angina)
– Abnormal changes in the heart rhythm or heart’s electrical activity

Angiography: is a test which uses dye and special x rays to show the inside of arteries. This test can show whether plaque is blocking arteries and how severe the blockage is. A thin, flexible tube (called catheter) is put into a blood vessel in the arm, groin (upper thigh), or neck. Dye which can be seen on an x-ray picture is injected through the catheter into the arteries. By looking at the x-ray picture, the doctor can see the flow of blood through arteries.

Other Tests: other tests are being studied to see whether they can give a better view of plaque buildup in the arteries (e.g. magnetic resonance imaging (MRI) and positron emission tomography (PET)).

Ultrafast Computed Tomography

Dr. Rath doesn’t primarily look at risk factors circulating in the bloodstream, but he focuses directly on the key problem of the atherosclerosis: the atherosclerotic deposits inside the walls of the coronary arteries. He recommends just one exam to diagnose early atherosclerosis: Ultrafast Computed Tomography (Ultrafast CT).

The latter is the most precise diagnostic technique available today to detect coronary heart disease already in its early stages. It is very useful because allows to measure the size of the coronary deposits non-invasively (this diagnostic test measures the area and density of calcium deposits without the use of needles or radioactive dye).

Causes and Risk factors

Atherosclerosis is a chronic, slow and progressive disease that may start in childhood. In some people the disease progresses rapidly in their 30s. In others it doesn’t become dangerous until they reach their 50s or 60s, because it is a progressive silent process which remains asymptomatic for decades. Therefore Atherosclerosis is a complex process.
Conventional medicine doesn’t know exactly how it begins or what causes, but some theories have been proposed.
Many scientists believe plaque begins to form because the inner lining of the artery, called the endothelium (this thin layer of cells keeps the artery smooth and allows blood to flow easily), becomes damaged.
The possible risk factors of damage to the arterial wall are:

– High levels of cholesterol and triglycerides in the blood

– High Blood Pressure

– Smoking (greatly aggravates and speeds up the growth of atherosclerosis in the coronary arteries, the aorta and the arteries of the legs)

– High amounts of sugar in the blood due toinsulin resistance or diabetes

– Abdominal obesity (“spare tire”)

– Stress

– Not eating fruits and vegetables

– Excess alcohol intake (more than one drink for women, one or two drinks for men, per day)

– Not exercising regularly

– Genetics (people with a parent or sibling who has/had atherosclerosis and cardiovascular disease have a much higher risk of developing atherosclerosis than others)

Conventional medicine

Atherosclerosis is preventable and treatable.


Traditional doctors consider that lifestyle changes, such as following a healthy diet, exercising, quit smoking and managing stress, are often the best prevention for atherosclerosis.

Medical treatment

Doctors suggest various drugs to slow the effects of atherosclerosis (medical treatments often focus on alleviating symptoms and not on causes of desease):

Cholesterol medications: statins and fibrates are widely prescribed for lowering cholesterol (the “bad” cholesterol).

Anti-platelet medications: these medications, such as aspirin, are prescribed to reduce the likelihood that platelets will clump in narrowed arteries, form a blood clot and cause further blockage.

Beta blocker medications: they are commonly used for coronary artery disease. They lower the heart rate and blood pressure, reducing the demand on the heart.

Angiotensin-converting enzyme (ACE) inhibitors: they lower blood pressure by blocking the actions of some of the hormones which help regulate blood pressure and can also reduce the risk of recurrent heart attacks.

Calcium channel blockers: they lower blood pressure and are sometimes used to treat angina.

Water pills (diuretics): they lower blood pressure.

Surgical procedures (If the patient has severe symptoms or an artery blockage)

Angioplasty and stent placement: the doctor inserts a long, thin tube (catheter) into the blocked or narrowed part of the artery. A second catheter with a deflated balloon on its tip is then passed through the catheter to the narrowed area. The balloon is then inflated, compressing the deposits against artery walls. A mesh tube (stent) is usually left in the artery to help keep the artery open.

Endarterectomy: deposits are surgically removed from the walls of a narrowed artery. When this procedure is done on arteries in the neck (the carotid arteries), it’s called a carotid endarterectomy.

Thrombolytic therapy: when an artery is blocked by a blood clot, the doctor uses a clot-dissolving drug to break it apart.

Bypass surgery: the doctor creates a graft bypass using a vessel (vein) from another part of the body or a tube made of synthetic fabric. This allows blood to flow around the blocked or narrowed artery.

Cellular medicine: the true cause of atherosclerosis

Luckily Dr. Matthias Rath has replied to this question. Thanks to his scientific research, Dr. Rath and his team have discovered that the exact cause of atherosclerosis is the deficiency of vitamin C and other specific essential nutrients in the cells composing the artery wall.

Humans, unlike animals, develop cardiovascular disease because their bodies can’t produce vitamin C. Diet provides enough vitamin C to prevent scurvy, but not enough to guarantee stable artery walls. As a consequence millions of tiny cracks and lesions develop in the artery walls.

Subsequently cholesterol, lipoproteins, fibrinogen and other substances, found in the blood, enter into the damaged artery walls to repair these lesions. Of all these substances (risk factors), 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 which produce vitamin C in their bodies don’t produce Lipoprotein(a).

The repair process continues, if the human body has a long-term micronutrients deficiency and therefore, over the course of many years, atherosclerotic deposits develop.

For these reason the intake of particular micronutrients is very important.

One of these particular micronutrients is the amino acid lysine (called an essential amino acid, because, similar to vitamin C, it can’t be produced in the human body).

The latter, together with another amino acid, proline, is the main component of collagen.

These two amino acids comprise about 25% of all amino acids in the collagen molecule. A deficiency of lysine and proline can also trigger blood vessel wall weakness and instability.

Research and clinical studies conducted by Dr. Rath confirm that the most important function of vitamin C in preventing heart attacks and strokes is its ability to increase the production of collagen, elastin, and other reinforcement molecules in the body.

Key micronutrients to Prevent and treat atherosclerosis

Vitamin C: provides protection and the natural healing of the artery wall and reversal of plaques.
Vitamin E: provides antioxidant protection.
Vitamin D: optimizes calcium metabolism and the reversal of calcium deposits in the artery wall.
Folic acid: provides a protective function against increased homocysteine levels together with vitamin B6, vitamin B12 and biotin.
Biotin: provides a protective function against increased homocysteine levels together with vitamin B6, vitamin B12 and folic acid.
Copper: supports stability of the artery wall with the improved cross-linking of collagen molecules.
Proline: supports collagen production, stability of the artery wall and reversal of plaques.
Lysine: supports collagen production, stability of the artery wall and reversal of plaques.
Chondroitin sulfate and N-acetyl-glucosamine: support the stability of the artery wall as a “cement” for connective tissue.
Pycnogenol: acts as a biocatalyst for improved vitamin C function and improved stability of the artery wall.

Scientific research and clinical studies have already proven that vitamin C, vitamin B3 (niacin), vitamin B5 (pantothenic acid), vitamin E, carnitine, lysine and proline lower high blood levels of cholesterol and other secondary risk factors.


Clinical confirmation of nutrient synergy in atherosclerosis patients

Aim of the Study

The objective of this study was to determine the effect of a defined nutritional supplement program and specific nutrient synergy on the natural progression of coronary artery disease in 55 patients (50 men and 5 women) between the ages of 44-67 with coronary artery disease as documented by Ultrafast Computed Tomography.

Study Design

The study focused directly on the key problem – the atherosclerotic deposit inside the walls of the coronary arteries. For this study, Ultrafast Computed Tomography (UCT) was used. UCT is a modern technique that allows the measurement of the size of coronary deposits non-invasively. The computer automatically calculates a deposit’s size by determining the Coronary Artery Scan (CAS) score.

The higher the CAS score, the more calcium has accumulated, which indicates more advanced coronary heart disease. Changes in the size of the coronary artery calcifications in each patient were measured over an average period of one year without vitamin supplementation followed by one year with the vitamin program. In this way, the heart scans of the same person was compared before and after the vitamin program. This study design had the advantage of the patients serving as their own controls.

Study Results

During the course of the 12-month nutritional supplement program, the fast growth of coronary deposits was slowed during the first six months of the study and essentially stopped during the second six months. After one year of using the specific supplement program, the coronary deposits entirely disappeared, indicating on a natural healing process of the artery wall.

For the first time in medical history, the reversal of atherosclerotic deposits without bypass surgery, angioplasty, and medication was documented. The results of this remarkable discovery were published in the Journal of Applied Nutrition in 1996.

Abstract PDF Journal of Applied Nutrition. 1996;48(3):68–78


Study about cholesterol

Aim of the Study

Cellular Health opens up the possibility of the effective prevention and control of lipid metabolism disorders through the targeted use of nutrients synergy, such as specific vitamins, minerals, and amino acids.

These micronutrients help strengthen the artery walls, thus reducing the need for elevated production in the liver of triglycerides, cholesterol, lipoprotein(a), and other risk factors that are used as “repair” factors for weak arterial walls. Thus, the primary measure for lowering cholesterol and other secondary risk factors in the bloodstream is to stabilize the artery walls, thereby decreasing the metabolic demand for the excess production of these risk factors in the liver.

The nutrient synergy program tested in the study had a unique dual action. This program not only controlled the blood cholesterol and other lipid levels, but it also nourished and improved the condition of the blood vessel walls.
Following are the interim results of two clinical pilot studies in patients with elevated cholesterol and lipoprotein(a) plasma levels who have been following a nutrient synergy program for three months.

Study Design

Fourteen patients, between the ages of 34-68 and suffering from fat metabolism disorders, were the participants in this study. They took daily dosages of specific cellular nutrients for three months. At the same time, they continued to take their usual prescription medications. To obtain interim results, blood tests were obtained at the beginning of the study and following twelve weeks of vitamin treatment.

Interim Study Results

At the beginning of the study, the average blood lipoprotein(a) level of patients was 71 mg/dl, and the average total cholesterol level was 293 mg/dl. After three months on the vitamin program, the average level of lp(a) decreased by 13%.

Cholesterol-data-study-pilot-1Total cholesterol in all patients decreased by 14%, LDL decreased by 10%, triglycerides decreased by 22% and homocysteine decreased by 3%. HDL (good cholesterol) increased in this time period by 8%.

It is important to note the decrease of lp(a) levels since there is no successful conventional treatment available to lower this significant blood risk factor for heart disease. Lipoprotein(a) is a tenfold greater risk factor for heart disease than cholesterol or LDL cholesterol.

Dr Rath Research Institute – Clinical Study – Cholesterol

Studies demonstrating the effectiveness of single micro nutrients and special combination of micro nutrients

Hypothesis: lipoprotein(a) is a surrogate for ascorbate.
Rath M, Pauling L.
Proc Natl Acad Sci U S A. 1990 Aug;87(16):6204-7.

Plant-Derived Micronutrients Suppress Monocyte Adhesion to Cultured Human Aortic Endothelial Cell Layer by Modulating Its Extracellular Matrix Composition
Ivanov, Vadim PhD; Ivanova, Svetlana MD; Kalinovsky, Tatiana MS; Niedzwiecki, Aleksandra PhD; Rath, Matthias MD
Journal of Cardiovascular Pharmacology

Evolution of angiotensin II-mediated atherosclerosis in ApoE KO mice
John Cha, Vadim Ivanov, Svetlana Ivanova, Tatiana Kalinovsky, Matthias Rath, Aleksandra Niedzwiecki
Spandidos Publications

Nutrient supplementation modulates angiotensin II-mediated atherosclerosis in ApoE KO mice.
Ivanov V, Cha J, Ivanova S, Kalinovsky T, Rath M, Niedzwiecki A.
Mol Med Rep. 2010 May-Jun;3(3):417-25. doi: 10.3892/mmr_00000274.

Anti-atherogenic effects of a mixture of ascorbic acid, lysine, proline, arginine, cysteine, and green tea phenolics in human aortic smooth muscle cells.
Ivanov V, Roomi MW, Kalinovsky T, Niedzwiecki A, Rath M.
J Cardiovasc Pharmacol. 2007 Mar;49(3):140-5

Extracellular matrix-mediated control of aortic smooth muscle cell growth and migration by a combination of ascorbic acid, lysine, proline, and catechins
Ivanov V, Ivanova S, Roomi MW, Kalinovsky T, Niedzwiecki A, Rath M.
J Cardiovasc Pharmacol. 2007 Nov;50(5):541-7.

Enhancement of Cardio-Protective Effects and Attenuation of Adverse Effects of Female Sex Hormones on Cultured Human Vascular Smooth Muscle Cells by a Combination of Ascorbic Acid, Lysine, Proline, Arginine, Cysteine, and Epigallocatechin Gallate
Vadim Ivanov, MD, PhD, Svetlana Ivanova, MD, Waheed Roomi, PhD, Tatiana Kalinovsky, MS, RN* Aleksandra Niedzwiecki, PhD, Matthias Rath, MD

Bioflavonoids effectively inhibit smooth muscle cell-mediated contraction of collagen matrix induced by angiotensin II.
Ivanov V, Roomi MW, Kalinovsky T, Niedzwiecki A, Rath M.
J Cardiovasc Pharmacol. 2005 Nov;46(5):570-6.

Anti-atherogenic effects of a mixture of ascorbic acid, lysine, proline, arginine, cysteine, and green tea phenolics in human aortic smooth muscle cells.
Ivanov V, Roomi MW, Kalinovsky T, Niedzwiecki A, Rath M.
J Cardiovasc Pharmacol. 2007 Mar;49(3):140-5.

Detection and quantification of lipoprotein(a) in the arterial wall of 107 coronary bypass patients.
Rath M, Niendorf A, Reblin T, Dietel M, Krebber HJ, Beisiegel U.
Arteriosclerosis. 1989 Sep-Oct;9(5):579-92.

Morphological detection and quantification of lipoprotein(a) deposition in atheromatous lesions of human aorta and coronary arteries.
Niendorf A, Rath M, Wolf K, Peters S, Arps H, Beisiegel U, Dietel M.
Virchows Arch A Pathol Anat Histopathol. 1990;417(2):105-11.

Lipoprotein(a) in the arterial wall.
Beisiegel U, Niendorf A, Wolf K, Reblin T, Rath M.
Eur Heart J. 1990 Aug;11 Suppl E:174-83.

Antiatherosclerotic effect of probucol in WHHL rabbits: are there plasma parameters to evaluate this effect?
Finckh B, Niendorf A, Rath M, Beisiegel U.
Eur J Clin Pharmacol. 1991;40 Suppl 1:S77-80.

Hypoascorbemia induces atherosclerosis and vascular deposition of lipoprotein(a) in transgenic mice.
Cha J, Niedzwiecki A, Rath M.
Am J Cardiovasc Dis. 2015 Mar 20;5(1):53-62. eCollection 2015.

Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig.
M Rath and L Pauling
Proc Natl Acad Sci U S A. 1990 Dec; 87(23): 9388–9390.