HDL Cholesterol Is Dignified Cholesterol

Majid Ali, M.D.

HDL cholesterol is dignified cholesterol. LDL cholesterol is naked cholesterol. With these simple words I begin to explain the fundamental difference between what the men of money call “good” cholesterol and “bad” cholesterol. I consider HDL cholesterol dignified because it wears its protein gown elegantly and behaves in dignified and healing ways. I designate LDL cholesterol naked because it lives in rags and readily becomes naked—it is easily oxidized, insulted, roiled, and hurtful, so to speak. I discuss this subject at length in a companion article on the lipid molecular ecosystems in nature, and include brief text from that later in this article.

There Is Only One Cholesterol.

Cholesterol has one molecular formula and one three-dimensional structure. Whether traveling adorned by its protein-gown or un-gowned, it is the same cholesterol. Gowned cholesterol is a guardian angel of cell membranes and facilitates cellular cross-talk. Un-gowned cholesterol is easily insulted—readily oxidized, losing its electron energy in technical language—and strikes back with its lacerating (oxidizing) spears. So the real issue is the availability of protein gowns, which are manufactured in the liver. The problem begins when a liver loaded with pollutants and drug poisons fails to produce the necessary gowns for cholesterol. Every cholesterol molecular is identical. The availability of protein gowns determines how a cholesterol molecule acts. I offer detailed information on this subject in my 90-minute DVD entitled “Cholesterol” available at http://www.majidali.com.

The Liver Makes the Cholesterol Gowns

I anticipate the reader’s question: What organ of the body makes the cholesterol gowns and why do some people have more of them and others have less. The answer: the liver makes nearly all protein gowns for cholesterol. The healthier the liver, the more the production of cholesterol gowns.

The trio of toxicities of foods, environments, and thoughts pollute, poison, and pervert the liver’s ability to make proteins, among them the proteins that serve as gowns for cholesterol. The real culprits is the sordid story of statin drugs are drug tzars. They control doctors to push drugs and control the media to keep the focus away from the issues of liver and the health of its guardian angel, the bowel.

Dignified Cholesterol Prefers Peaceful Company

Natural un-rancid (unoxidized) cholesterol likes the company of un-rancid fats, untangled proteins, and un-sticky sugars. The naked LDL cholesterol, by contrast, surrounds itself by other oxidizing and hurtful substances. This explains why the more HDL one has the more peaceful his endo cells lining one’s blood vessels are. The more oxidized and hurtful LDL cholesterol there is, the more the tissue injury.

Lipoproteins Adorn Cholesterol

A clear knowledge of these basic scientific facts of molecular biology of cholesterol allows everyone to see through the deceptions and distortions of cholesterol monsters, the money men of medicine who keep on their payrolls some medical professors who write editorials and set cholesterol standards. So begins the story of what I consider to be the biggest fraud in American medicine.

No Drugs for Liver Health

Cholesterol cannot flow through the body without being bound to its carrier proteins, that transport it back and forth between the liver, gallbladder, and various cell populations of the body. The liver overloaded with toxins cannot produce enough of the needed proteins, hence the naked and vulnerable proteins. This is the real story of “good” cholesterol” and “bad” cholesterol. Next time you hear it, be amused and pretend that you are most grateful for receiving knowledge about good and bad cholesterol.

There are no drugs—hence no profits—for coaxing the liver to produce enough protein gowns for cholesterol. Profits are in drugs. Cholesterol monsters know how to use TV and newspapers like The New York Times to drown commonsense. Doctors dare not defy the cholesterol standards of the standard-setters—they have children to feed—and people are too frightened to think for themselves.

Evolution’s intelligent Design

Evolution not only created protein gowns for cholesterol but also for cell membranes. This further thickens the plot of the LDL and HDL cholesterol stories. Drs. Brown and Goldstein discovered that cells contain specific receptors for LDL, and that there is a correlation between LDL binding and control of the enzyme that limits cholesterol production in the liver. So,the number of LDL receptors of a cell varies with its requirements for cholesterol. Specifically, cells protect themselves against excess of cholesterol by reducing the number of their LDL receptors and vice versa. A natural consequence of reduced numbers of LDL receptors is decreased cellular uptake of LDL cholesterol and hence, a corresponding rise in blood cholesterol levels. As valuable as these insights into the cholesterol homeostasis are, it is recognized that they do not explain how raised blood cholesterol levels cause vascuclar plaques formation.

The oxygen-starved cells are quickly overloaded with toxins and get covered with cellular grease (see my article The Grease and Detergent Model of Disease for details). This makes memebrane receptors for LDL dysfunctional. The enthusiasts of the cholesterol-plaque-plumbing model of heart disease blissfully ignore all such considerations. What sells statin drugs and coronary procedures is the sordid story of “good” cholesterol” and “bad” cholesterol. There are no drugs—hence no profits—for de-greasing cell membranes and restoring their receptor functions. Profits are in drugs. Cholesterol monsters know how to use medical professors and news media to distort truth. What people need is the knowledge of evolution’s intelligent design and how we can preserve that design with healthful foods, environments, and thoughts. So the fundamental dichotomy between the profitability needs of cholesterol monsters and people seeking healthy hearts.

Cholesterol In Lipid Redox Ecosystem

Below is text from a paper which my colleague, Omar Ali, M.D. and I published in Journal of Integrative Medicine in 1997 to present our view of molecular-ecology of cholesterol:

“Lipids in plasma membranes are essential for membrane fluidity, surface potentials, surface ligand activity, and transport functions. To serve these diverse functions, lipids exist in blood and plasma membranes not as discrete molecular species—as it might seem from the conventional description of the lipid chemistry—but as dynamic “lipid redox ecosystems” in which external pro-oxidant influences are vigorously counterbalanced by antioxidant defenses that exist within the lipid particles. For example, LDL is a large lipoprotein complex that includes the following: cholesterol moieties, apolipoprotein B, neutral and polar lipids including polyunsaturated fatty acids and phospholipids, and lipophilic antioxidant species that include beta carotene and vitamin E. Lipoprotein (a) {Lp [a]} is structurally similar to LDL but is distinguished from it by the presence in it of a highly glycosylated protein designated apoliprotein(a). Lp(a) is considered atherogenic because it is taken up by foam cells, however elevated levels are associated with IHD (ischemic heart disease) in most but not all reports. It binds to apolipoprotein B (apo-B)-containing lipoproteins and proteoglycans.”

In our 1997 article, we addressed the subject of oxidative modification of LDL cholesterol with the following words: “In the past, it has been assumed “that the oxidative modification of LDL occurs primarily in the arterial intima, in microdomains sequestered from antioxidants in plasma.” It has been further assumed that if oxidized LDL were to be generated in the circulating blood, it would be swept up within minutes by the liver168. Hence, all research in atherogenesis has been exclusively directed to investigation of atherogenic changes in vascular wall. It is important to note that these assumptions were made without benefit of direct microscopic observations of the oxidant phenomena in the circulating blood. Those assumptions are clearly not warranted in view of our morphologic observations of oxidative coagulopathy and AA oxidopathy documented in this report. Furthermore, the mechanisms of oxidation of LDL are deemed “unknown.” Here again the fundamental phenomenon of spontaneity of oxidation in the blood ecosystem has been ignored. Our observations also challenge that viewpoint as well as the cholesterol hypothesis of IHD, thus clearing the way for a wholly novel view of pathogenesis of atherogenesis and ischemic coronary artery disease. The clinical implications of this view, as we show in Part-II of this article, are vastly different from those of the prevailing cholesterol theory. “

*Cholesterol rate-limiting enzyme is called HMG CoA (3-hydroxy-3-methyglutaryl coenzyme A) reductase.


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