Cholesterol Is Only A Secondary Risk Factor

Worldwide, hundreds of millions of people have elevated blood levels of cholesterol, triglycerides, LDL (low-density lipoproteins), lipoprotein (a) and other risk factors. Contrary to what the pharmaceutical companies selling cholesterol-lowering drugs want to make you believe – there is nothing wrong with cholesterol levels of 220 or 240. Cholesterol is, at best, a “secondary” risk factor because the primary risk factor determining your cardiovascular status is the weakness and instability of your blood vessel walls. Elevated blood levels of cholesterol and other blood risk factors are not the cause of cardiovascular diseases but are the consequence of developing the disease.

Conventional medicine is limited to treating the symptoms of secondary risk factors. Drugs blocking the synthesis of cholesterol and other lipid-lowering agents are now being prescribed to millions of people These drugs are known to cause cancer and have other severe side effects. You should avoid them whenever you can.

Again, the reasons for elevated cholesterol levels are only partially understood by conventional medicine. Inherited disorders (genetic risk) and a high-fat diet (dietary risk) are the two main reasons given in the textbooks of medicine. The most important reason is completely missing: a chronic deficiency of vitamins and other essential nutrients.


Modern Cellular Health provides a new understanding of the factors causing high blood levels of cholesterol and other secondary risk factors, as well as their natural prevention. Cholesterol, triglycerides, low-density lipoproteins (LDL), lipoprotein (a) and other metabolic products are ideal repair factors, and their blood levels increase in response to a weakening of the artery walls. A chronic weakness of the blood vessel walls increases the demand for production of these repair molecules in the liver. An increased production of cholesterol and other repair factors in the liver increases the levels of these molecules in the bloodstream and, over time, renders them risk factors for cardiovascular disease.Thus, the primary measure for lowering cholesterol and other secondary risk factors in the bloodstream is to stabilize the artery walls and thereby lower the metabolic demand for increased production of these risk factors inside the body itself.

Therefore, it is not surprising that vitamins and other nutrients help in stabilizing the artery walls, and also, in parallel, helping to decrease blood levels of cholesterol and other risk factors naturally.

My recommendations for people concerned with elevated cholesterol and other secondary risk factors. Lowering cholesterol without first stabilizing the artery walls is an insufficient and ill-fated cardiovascular therapy. Start as early as possible to increase the stability of your artery walls with essential nutrients to normalize blood levels of cholesterol and other risk factors.

Lipoprotein (a) A Secondary Risk Factor

On the following pages, I would like to describe in more detail lipoprotein(a), a secondary risk factor that is particularly important. The main function of lipoprotein(a) is very useful; it fulfills a variety of repair functions, such as, during wound healing. However, if the artery wall is destabilized by a long-term vitamin deficiency, lipoprotein(a) turns into a risk factor ten times more dangerous than cholesterol. Let’s have a closer look at how lipoprotein(a) molecules differ from other fat molecules.

Cholesterol and triglycerides do not swim in the blood like fat swim in soup. Thousands of cholesterol molecules are packed together with other fat molecules in tiny round globules called lipoproteins. Millions of these fat-transporting vehicles circulate in our body at any given time. The best known among these lipoproteins are high-density lipoproteins (HDL, or “good cholesterol”) and low-density lipoproteins (LDL, or “bad cholesterol”).


LDL-Cholesterol. Most cholesterol molecules in the blood are transported in millions of LDL particles. By carrying cholesterol and other fat molecules to our body cells, LDL is a very useful transport vehicle to supply nutrients to these cells. LDL has been named the “bad cholesterol” because, until recently, researchers believed that LDL was primarily responsible for the fatty deposits in the artery walls. This theory is now out of date.

Ten Times More Dangerous Than Cholesterol

Lipoprotein(a) is an LDL particle with an additional adhesive protein surrounding it. This biological adhesive tape is named apoprotein(a), or brief, apo(a). The letter (a) could, in fact, stand for “adhesive.” The adhesive apo(a) makes the lipoprotein(a) fat globule one of the stickiest particles in our body. Together with my colleagues at Hamburg University, I conducted the most comprehensive studies on lipoprotein(a) in the artery wall. These studies showed that the atherosclerotic lesions in human arteries are largely composed of lipoprotein(a) rather than LDL molecules. Moreover, the size of the atherosclerotic lesions paralleled the amount of lipoprotein(a) particles deposited in the arteries. In the meantime, these findings have been confirmed in a series of further clinical studies.

Lipoprotein(a) blood levels vary greatly between one individual and another. What do we know about the factors influencing the lipoprotein(a) levels in your blood? Lipoprotein(a) levels are primarily determined by inheritance. Special diets do not influence lipoprotein(a) blood levels. Moreover, none of the presently available lipid-lowering prescription drugs lower lipoprotein(a) blood concentrations. The only substances that have thus far been shown to lower lipoprotein(a) levels are vitamins. Professor Carlson showed that two to four grams of vitamin B3 (nicotinic acid) a day could lower lipoprotein(a) levels up to 36%. Because high levels of nicotinic acid can cause skin rash, you are well advised to increase the daily intake of nicotinic acid slowly.

Our own research showed that vitamin C alone or in combination with lower dosages of nicotinic acid may also have a lowering effect on the production of lipoproteins and thereby on decreasing lipoprotein blood levels. Together with the “Teflon” agents lysine and proline, these two vitamins can considerably reduce the cardiovascular risk associated with lipoprotein(a) levels.

Lipoprotein(a) is a particularly interesting molecule because of its inverse relationship to vitamin C. The following discovery triggered my interest in vitamin research: lipoprotein(a) molecules are primarily found in humans and a few animal species unable to produce vitamin C. In contrast, animals able to produce optimum amounts of vitamin C do not need lipoprotein(a) in any significant amount. Lipoprotein(a) molecules apparently compensate for many properties of vitamin C such as wound healing and blood vessel repair. In 1990 I published the details of this important discovery in the Proceedings of the National Academy of Sciences and invited Linus Pauling as co-author for this publication.

Source: Dr. Rath – research article on

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