Cholesterol and Heart Disease

Functions of cholesterol. Hedgehog is a gene important for embryos. By Spevvy at Wikimedia.

Sometimes we need to think outside of the box” when it comes to finding answers to many of our health questions. The case of cholesterol, heart disease, and the medications used to combat it illustrates this principle very strongly.

Comment onStudy: Boosting Good Cholesterol With Niacin Did Not Cut Heart Risks” on All Things Considered 27 May 2011.  It appears there are multiple causes for cardiovascular disorders.  There is strong theoretical work that suggests cholesterol is a response by normal cells to an assault on cell membranes. So people who continue to claim that high cholesterol is a cause for cardiovascular disease are misinforming the public, and putting research on the wrong track. We need to use our understanding of basic chemistry to study what may be the cause of disease. By recognizing multiple causes of high LDL (low density lipids, a type of cholesterol), we can treat it in multiple ways, like diet, exercise, taking niacin and calcium supplements, and getting rid of toxins.

Updated: 2 Sept 2014


A study of Niaspan showed that it did raise “good cholesterol” (HDL, High Density Lipids), but it did not lower the rate of heart attacks. Patients on Niaspan were more likely to have a stroke than those on placebo.  NIH halted a big study of this drug early as a result.  NPR reporter Scott Hensley tells us that even though earlier observational studies (not experimental) show that high levels of HDL in people have been associated with “a lower risk of heart attack,” this does not mean that HDL helps to get rid of a cause of a heart attack. Based upon the assumption of causation, the HDL hypothesis states that raising HDL cholesterol should lower the risk of heart disease (it is hard to avoid thinking that “risk” does not mean “cause” in this hypothesis). More than 3400 patients were studied and all were also taking cholesterol-lowering drugs to control LDL (Low Density Lipids).  However, the FDA wants more studies, and does not recommend that patients stop taking niacin.

A Need for More Information

This is just one more study showing that there are probably multiple causes of cardiovascular disease. It may even be possible that by attempting to control cholesterol levels, doctors are completely missing the likely culprit on which they should be concentrating their efforts. The reason may lie in that there is no experimental study showing that high LDL directly causes heart disease, stroke or high blood pressure, when all other possible causes are fully controlled.  The problem may lie in that they may not be able to imagine what else may need to be controlled.  This is not the first time scientists have been accused of lacking an imagination. Reliance on “observational” studies (studies that use associations to “test” for “risks”) imply cause and effect, when only correlation has been demonstrated.

The problem with Niaspan may stem from its chemistry and the action of niacin on different parts of the body and different tissues.  The biggest problem with pharmaceutical companies lies in the fact that they are more concerned with the action of a drug on one particular tissue, ignoring its effects on other tissues in the body. This may be the root of the difficulty with Niaspan.

Cholesterol, Calcium & Toxins

Basic Chemistry

Cholesterol molecule

The scientists might look more closely at the chemistry of the drugs that use niacin (e.g. Niaspan), a vitamin which helps to raise HDL in the blood, but at high levels it might hamper the ability of the brain to regulate blood pressure at its BP center in the medulla (because niacin reduces the amount of calcium that can cross blood capillaries into the tissues everywhere, see below), thus counteracting the effects of niacin at the local capillary level.

In order to understand how niacin might affect calcium flow we need to get at differences in how these nutrients get to the cells that need them.  Both nutrients can passively diffuse across cell membranes without using any energy, and thus their rate of diffusion is determined by ion content of the extracellular fluids. Active transport, however, can ignore this ion content and transport some nutrients much faster.  Absorption across the gut epithelium is different from secretion from blood vessels in the tissues, since absorption will involve pharmaceutical or mega dose levels of niacin or calcium when taken in supplements or drugs, but secretion from blood vessels will occur at lower “physiological” concentrations.

Cholesterol crystals (blue) in an articular joint’s synovial fluid. From Wikimedia.

If we limit our thinking to only the absorption end of the trail, niacin and calcium at the mega dose level in drugs (Niaspan) or supplements both appear to be absorbed by passive diffusion (Roe 1989). Thus, one would think there should be no difference on niacin’s activity whether or not calcium is present.  However, at physiological levels there is a difference in mode of transport (Roek 1989). Physiological levels would occur at the other end of the trail when niacin and calcium have reached blood vessels supplying the needy tissues and are secreted.  Niacin at these levels is actively transported by binding to plasma proteins which are secreted from blood vessels faster than calcium which secretes by passive diffusion (Roek 1989). For more on calcium see my post Coffee and Prostate Cancer.

Toxic Damage?

Calcium Supplements, by Kham Tran at Wikimedia

So instead of the ratio of HDL to LDL, maybe the ratio of niacin to calcium should be examined.  In order to balance out the active transport of niacin and the passive diffusion of calcium, everyone who takes niacin should also increase their calcium intake.  However, as I mentioned elsewhere (see my posting Calcium Supplements), there may be enough damage in the body by toxins to prevent the uptake of calcium by all the cells anywhere it is needed.  Furthermore, gut epithelial absorptive cells may be damaged by toxins, as well, preventing calcium from even getting the chance for distribution to needy cells. Since few scientists even consider controlling their test subjects by screening for the presence of toxins or for toxic damage to blood vessels, they are missing the chance of actually finding a cause of these cardiovascular problems.

This problem demands thinking outside of the box. Ravnskov (2002) raised the questions about the assumptions scientists were making about cholesterol. For some reason, it has largely been ignored by scientists.  All beginning college biology courses discuss cholesterol and students learn that it is a necessary ingredient for protecting blood vessels, produced by the liver when needed, and used by all cells. Many scientists, including Ravnskov, have shown evidence that high levels of homocysteine in the blood are a bigger threat than cholesterol for heart disease.  Furthermore, the body will make more LDL cholesterol if you try to remove it by diet or drug because it is so important to the body to stiffen the cell membranes when they are in danger.

It may also be true that all three conditions, high blood pressure, heart attack, and stroke have the same cause, as yet untested. We cannot assume from association studies that high levels of LDL cholesterol cause these disorders, although extremely high amounts of LDL seem to make it difficult for major arteries to maintain a healthy level of elasticity, making a poor condition worse. Instead of trying to counteract a normal and healthy response by the body to a threat, the researchers might try to find the threat.  It was assumed that if the HDL was raised, then the LDL won’t cause as much harm, but studies have shown that even though an optimum ratio of LDL to HDL is associated with healthy cardiovascular systems, it is harder to figure out how to replicate the optimum ratio in a patient who has the wrong ratio.

Complications of persistent high blood pressure, from Mikael Häggström.

Something else must be causing the problem with high blood pressure–something that causes the body to stiffen cell membranes, especially in arteries, which then causes blood pressure to rise.  Scientists may be ignoring the possibility of a toxin precisely because they assume that all toxins get into the blood and simple tests will show its presence there, or all serious toxins will have immediate and serious effects on the body, readily apparent to everyone.  That is only the case if they all agree on the symptoms of damage by toxins, and that they regularly check for their presence, which they don’t do now.  Again, most agreed-upon effects depend upon examination of blood and blood organs (e.g. liver, spleen, bone marrow).  If the cause is a toxin that can get into the body through normal routes that bypass blood vessels (lungs, gingiva, eyes) it might actually be damaging blood vessels, causing the body to raise the levels of LDL.  By damaging blood vessels, it never gets into the blood organs, making it nearly impossible for the usual tests of toxicity to work.

For a related post on cholesterol see On Finding Cholesterol in Egyptian Mummies and on Adolescent Blood Pressure and Obesity. Also see discussion of transport of ions, and toxins within the body, that can affect the transport of calcium in Toxins.

Other relevant posts:

Nutrition Reviews
Adolescent Blood Pressure and Obesity
Calcium Supplements
On Finding Cholesterol in Egyptian Mummies
Treating Sleep Disordered Breathing in Kids


Functions of cholesterol. Hedgehog is a gene important for embryos. By Spevvy at Wikimedia.
Cholesterol molecule
Cholesterol crystals (blue) in an articular joint’s synovial fluid. From Wikimedia.
Calcium Supplements, by Kham Tran at Wikimedia.
Complications of persistent high blood pressure, from Mikael Häggström, at Wikimedia.


Häggström, M. (2014). Medical gallery of Mikael Häggström 2014. Wikiversity Journal of Medicine 1 (2). DOI:10.15347/wjm/2014.008. ISSN 20018762

Ravnskov, U.  (2002).  The cholesterol myths: Exposing the fallacy that saturated fat and cholesterol cause heart disease.  Winona Lake, Indiana: New Trends Pub. Inc. 320 pp.

Roek, D. A. (1989). A comparison of drug-nutrient and nutrient-nutrient interactions. In: Bodwell, C. E. & Erdman, J. W., eds. Handbook on drug and nutrient interactions. 3rd ed. New York, N.Y.: Marcel Dekker Inc.  Pp. 365-377. (There is an earlier edition, 1988, published by CRC Press in Google Books where you can read some of this chapter 15, with the same page numbers.)

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