Cholesterol

The fundamental and direct answer to your question is: The disease atherosclerosis results in at least one arterial plaque in an artery, but it almost always results in multiple arterial plaques in multiple arteries. Oxidized vLDL (very Low-Density Lipoprotein) and LDL cholesterols are what cause a plaque to form in the first place, and as time passes, additional cholesterol and other lipids (triglycerides, fats and fat derivatives) accumulate within the cells that make up the arterial walls thus narrowing, or "clogging," the arteries.

In the beginning, an arterial plaque is caused when a sufficient number of oxidized vLDL and LDL cholesterol particles embed themselves in the same general area of an arterial wall and cause a cascade of events, starting with an immune response to the artery's injury. In the vast majority of people who have atherosclerosis, a newly-formed plaque evolves over four or more decades; gradually accumulating dead macrophages (a type of white blood cell that is part of the immune system), lipids, calcified layers, and layers of fibrotic material. In persons with the disease hypercholesterolaemia, who suffer from exceptionally high cholesterol levels, plaques develop and thicken at a much greater rate.

The primary layman's term for atherosclerosis is "hardening of the arteries" since the arteries gradually become stiff, rough and misshapen rather than pliable, smooth and straight or gently curved.

I thought that it was important for you to know that what clogs an artery is not only made of cholesterol, therefore what follows is some selected additional information on arterial plaques: The constituents of a mature arterial plaque may not even be half cholesterol. Some of the additional constituents were mentioned earlier, but a more complete and specific list includes phospholipids, dead and living smooth muscle cells (that make up part of an arterial wall), a large specialized protein that is part of every vLDL and LDL cholesterol particle, blood platelets, fibrin and red and white blood cells snared in the cross-linked fibrin net. In general, the more of the lumen that is blocked, the lower the fraction of cholesterol contained in the arterial plaque. Also, the ratio of cholesterol to the other materials contained in a plaque varies from one plaque to another, even in the same person, and from person to person. Another reason for the variance is that different amounts of oxidized cholesterol become embedded in an arterial wall before the cascade of events occurs that ultimately results in formation of an arterial plaque.

I want to make it clear that I am not a medical doctor, and more importantly, I have not even played one on TV. But, I truly did earn a Ph.D. in chemical kinetics. Knowledge is not the most important thing gained from obtaining a Ph.D. What is, is learning what questions must be answered in order to solve or understand the problem at hand. With respect to atherosclerosis, the most important ultimate question is: What can one do to minimize their risk of developing an arterial plaque in the first place? The answer to this question can probably only be answered completely after the answer to other questions are known. A lot of the risk factors for developing atherosclerosis are known; perhaps all of them. Therefore, it is logical that we begin looking for how to prevent, or at least how to slow the progression of, atherosclerosis by eliminating as many risk factors as possible. It appears that things can only go downhill once a plaque has formed, however the human body does have an amazing ability to heal itself, hence it is my opinion that it is possible to prevent, and even reverse, atherosclerosis in most people provided that the disease has not progressed too far.

I believe that the three most important facts yet known about atherosclerosis are: 1) Only vLDL and LDL cholesterol particles become stuck to and then embedded in arterial walls. 2) Only oxidized cholesterol molecules are found in the arterial walls; and 3) when the density of oxidized cholesterol in an arterial wall reaches some magic number, the eventual result is a very damaging immune response. These three facts lead to the four most important preliminary questions, the answers to which must be known in order to answer the ultimate question: 1) Do only vLDL- and LDL cholesterol particles containing oxidized cholesterol penetrate and embed in an arterial wall? Or 2) Is the cholesterol in the particles oxidized after they penetrate and embed in an arterial wall, or do both 1) and 2) occur? 3) Can powerful antioxidants such as vitamin C, lipoic acid, eugenol, natural mixed tocopherols (d,α-, d,β- and d,λ-tocopherols), or other natural and safe antioxidants chemically reduce some forms of oxidized cholesterol back to cholesterol?

For the time being, I take 1000 mg of vitamin C and 200 mg of lipoic acid twice a day for their well-known powerful antioxidant and radical scavenger abilities. Since I am not any reader's doctor, I am not recommending that anyone take these two supplements, and there is one Warning! Anyone taking any medication, including insulin, for high blood sugar, it is very important that he or she does not take lipoic acid without speaking to his or her doctor first. I do recommend that the reader never consume any food that contains "partially-hydrogenated [name of oil]" since all of those modified oils contain trans fats, which are known to raise the LDL cholesterol of almost everyone. One should also never heat olive oil and other oils that contain a high percentage of unsaturated oils above approximately 350 ˚F because doing so will convert some of the [naturally-occuring] cis double bonds to transdouble bonds. This means that one should not stir fry with olive oil and other "delicate" oils. Lastly, I strongly recommend that cooks do not heat oils to the point that they smoke. Any oil that is smoking is being oxidized and is hot enough to form trans double bonds. Use fat, not oil, if a pan needs to be that hot. Coconut fat, palm kernel fat, and beef tallow are much healthier alternatives to oils that are heated to the smoking point.

Those taking statins (and many other medications) should avoid grapefruit as it changes the rate certain drugs are absorbed into the bloodstream. With several cholesterol lowering drugs like simvastatin, for example, grapefruit juice can boost the level of statin to potentially dangerous levels. However, if you are not taking a statin to lower cholesterol, eating red grapefruit has been shown in a small 2006 study to lower cholesterol.

What Was The Study?

A research study was conducted in 2006 among "patients suffering from Coronary Atherosclerosis," and the results were published in the Journal of Agricultural and Food Chemistry. Though it was a small study of just 57 people, all had undergone coronary bypass surgery and had been unsuccessful trying to lower cholesterol with prescription medicine. The research study participants ate a low-calorie, low-fat diet for 30 days, and were split into three equal sized groups: one group ate a red grapefruit daily, one group had white grapefruit daily, and the diet of the third group was not supplemented with grapefruit.

What Did The Study Prove?

The study showed that eating red grapefruit lowered both total cholesterol, LDL (bad) cholesterol and triglycerides. The study results are well explained by WebMD's Grapefruit May Improve Cholesterol article. The author explains, "The red grapefruit group improved their cholesterol most, followed by the white grapefruit group. They ended up with notably lower total cholesterol and LDL ("bad" cholesterol) than the comparison group." In all, the group that ate red grapefruit also showed the most improvement as red grapefruit also lowered triglycerides; triglyceride levels did not change for the white grapefruit or control group.

Why Does Grapefruit Lower Cholesterol?

It is hypothesized that it is the anti-oxidants and overall chemical makeup of red grapefruit that help lower cholesterol. According to the published study, "It was found that red grapefruit has a higher content of bioactive compounds and a higher antioxidant potential than blond grapefruit." The study goes on to say, "In conclusion, fresh red grapefruit contains higher quantities of bioactive compounds and has significantly higher antioxidant potential than blond grapefruit. Diet supplemented with fresh red grapefruit positively influences serum lipid levels of all fractions, especially serum triglycerides and also serum antioxidant activity."

Can Everyone Lower Cholesterol By Eating Grapefruit?

No! While this study shows that red grapefruit can lower total cholesterol, LDL (bad) cholesterol, and triglycerides, it can be DANGEROUS to eat grapefruit while taking just one of many prescription medicines - especially cholesterol-lowering statin medication. As I reported in The Danger of Grapefruit and High Cholesterol, if you take Zocor (simvastatin), Lipitor (atorvastatin) and Pravachol (pravastatin) you should not eat grapefruit or drink grapefruit juice because grapefruit juice increases the level of statin in the blood, to a potentially dangerous level. If you take a statin - or many other prescription medications - be sure to talk with your doctor before consuming grapefruit.

Conclusion

For those not on prescription medications of any sort, red grapefruit has been shown in a small study to lower total cholesterol, LDL (bad) cholesterol and triglycerides. But if you take any prescription medication - especially statins to lower cholesterol - you should avoid grapefruit and grapefruit juice, or at least discuss with your doctor.