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INTRODUCTION to CHOLESTEROL and STATINS by Burton Linne
Here are three compositions: Origin that I wrote; Mike Ciell’s in depth review of the entire theory of both the propaganda campaign against cholesterol and the Pauling/Rath discoveries that my Plaque Wash & Rejuvenation System© applies in actual practice; and Uffe Kravnskov’s personal dealing with the statin drugs from a clinical physician’s perspective.

This webpage constitutes a full tutorial on the issue of cholesterol and plaque. Heavy reading. Upon understanding it you will be changed permanently for the good. This material destroys all justification for the statin drug industry, proves the U.S. National Institutes for Health (NIH) are supporting outright lies, and that the entire mainstream medical population are pushing suicide pills as if a legitimate positive therapy for a disease now proven not to exist. Plaque in your blood vessels is a biological necessity to avoid quick demise by bleeding to death. Accumulative layers of it is an unintended consequence that always kills you unless you intervene as disclosed by Matthias Rath, MD in 1990.

I suggest you use the 28 or 29 sheets of paper needed to print this page out on hard copy because staring at this back lit screen for the time needed to get all this, will fatigue you and may harm your eyesight.

Anti-Cholesterol Theory Origin by Burton Linne
The entire anti-cholesterol movement is built on 1950’s autopsies of killed American soldiers in the Korean War. The army pathologists noticed that young American men had hardening of the arteries. This is an old man’s disease, not teenagers.

I wore the uniforms you see in this picture. Analysis of the white, somewhat stiff fatty substance that had partially filled their arteries near the heart was identified as cholesterol. Based on that observation alone, the entire theory was born that hardening of the arteries, atherosclerotic occlusive cardiovascular disease, is caused by an excess of cholesterol.

60+ years of research and millions of dollars later, there still is no validation of the anti-cholesterol theory of heart disease. Ask exactly how this soft, gooey fat molecule manages to stick to the slick inside of a constantly wiggling, twisting pipe with fast moving thick fluid (blood) rushing by at least once every second, and you get a blank stare. Nobody can answer the question. There is no answer. The premise is false. Cholesterol does NOT stick to the artery. It sticks to Lp(a).

How Plaque is Created & Removed—Technical Explanation by Chemist/Pharmacist Mike Ciell RPh and
Cholesterol by MD and PhD Uffe Ravnskov

One Pharmacist’s View Of Coronary Heart Disease: Comparing The Lipid Theory With The Unified Theory
By Mike Ciell, R.Ph.Tampa, FL August 24, 2004 www.ourhealthcoop.com

EXECUTIVE SUMMARY
Conventional wisdom argues that cholesterol, an oily substance produced in the body, is the enemy and must be managed to prevent coronary heart disease. Fighting cholesterol is inherent in the “Lipid Theory” of heart disease. Alternatively, Linus Pauling, two-time Nobel laureate and Ph.D. and Matthias Rath, M.D., created the “Unified Theory” of heart disease, identifying vitamin C, L-lysine, and L-proline as critical nutritional agents that could both improve blood vessel function (flow) and reduce cholesterol plaques (blockages). Some researchers have said that vitamin C is the equivalent of “nature’s perfect statin.”

Cholesterol drawing:Most animals produce vitamin C endogenously (within their bodies) and never demonstrate signs of Cardiovascular disease. Humans, alternatively, must rely on dietary ascorbate to maintain health, and when insufficient supplies of ascorbate are present, humans suffer from a variety of chronic diseases, including coronary heart disease.

Pauling’s and Rath’s research provides evidence that cholesterol plaques are actually the body’s back-up mechanism for repairing damaged blood vessels, and that. if you provide the body with enough free-circulating vitamin C, along with L-lysine and L-proline, the body’s primary mechanism for making vascular repairs can be employed and cholesterol numbers can ultimately fix themselves.

Coronary Heart Disease — The Leading Cause Of Death In America Today
Coronary heart disease CHD, the most common form of Cardiovascular disease, is the leading cause of death in America. Over 13 million Americans suffer from CHD, which results in more than one million heart attacks per year, of which more than one half will be fatal. These statistics are in sharp contrast with the cardiac health of Americans at the beginning of the 20th century.

Heart Disease Used To Be Relatively Rare
In 1900 heart attacks were almost nonexistent, and most cases of heart disease that did occur were usually the result of an infectious disease (rheumatic fever for example) or congenital heart defects. In the ensuing decades, this once rare condition steadily rose in frequency to become the leading cause of death in America

The big question: What has caused this problem?
Social changes since 1900 are certainly in play, including:
Widespread use of cigarettes after WWI;
a huge increase in refined sugar use;
sedentary suburban lifestyles; packaged,
chemical-laden food replacing fresh, raw choices

Ask any reasonably-educated person with heart disease what the problem is and you’re likely to hear things like, “I have to watch my diet, get more exercise, stop smoking and so forth.” Good starting points, but, as I cover in this article, there’s more.

Korean War Autopsy Connection
It was during the Korean War that doctors thought they had discovered the “real” cause of heart disease. Autopsies on young soldiers killed in action showed well-developed atheromas (arteriosclerotic plaques) in their coronary and carotid arteries. Additionally, fatty streaks of the intima of their arteries, arterioles, and heart muscle existed.

While similar fatty streaks were observed in dead Korean and Chinese soldiers, the well-developed atheromas found in American soldiers were conspicuously absent. Analysis of the plaques found showed it was a saturated fat (palmitic acid). The atheromas also contained quite a lot of a familiar waxy substance—better known as cholesterol.

The Lipid Theory Of Cardiovascular Disease
Thus, out of the battlefields of Korea was born The Lipid Theory of Cardiovascular Disease. For almost 60 years, this “lipid theory” has been central to medical explanations of and treatment for Cardiovascular disease. Simply put, the Lipid Theory posits that a diet high in cholesterol and saturated fat will cause gooey substances (cholesterols) to be deposited in the blood vessels, clogging them up. Clogged blood vessels clearly restrict blood flow to the heart, ultimately causing angina. Eventually a piece or clot will break loose, causing a TIA (angina or a mini stroke), a stroke or a full-blown heart attack. Conventional thinking has centered on removing causative agents— cholesterol and bad fats to stop coronary heart disease.

For decades we have used diet and drugs to attempt to reach ever-lowering “cholesterol levels” recommended by the American Heart Association. Tragically, statistics show that heart disease continues to be on the rise, claiming ever more lives.1

A Plumber’s Take On “Plugs” In The System
So what’s wrong with the Lipid Theory? Any plumber looking at the Lipid Theory model would say, “It simply doesn’t make sense.”

Let’s start by thinking about “sludge” in a plumbing system. Sludge tends to plug up the smallest pipes in the system first—not the largest.

Lipoprotein(a) image:Likewise, if the system is Cardiovascular, you would expect sludge (plaques) to build up first in the capillaries and arterioles, long before appearing in the carotid and coronary arteries. The first blockages, similarly, you would expect to occur way downstream of the pump, not in close proximity to the heart, where the pressure is the greatest.

Yet, this is not the way cholesterol plugs up arteries. It’s the exact reverse. So a plumber’s take would be that something else is happening.

The Myth About “Good” and “Evil” (Fats)
When autopsied plaques have been analyzed, they are found to contain cholesterol, but of a very particular type. The offending cholesterol is a highly-oxidized variety of LDL cholesterol attached to a specific protein (Apo A). The whole complex is called Lipoprotein A or Lp(a); more on Lp(a) further in this article.

The fats found inside these plaques, as it turned out, were unsaturated fats (not the supposedly evil saturated fats). Fatty streaks in the intima of the arteries are saturated fat, but this appears to be quite normal, since it is the same in many animals.

Avoiding saturated fat, using “healthy” polyunsaturated oils, and building a diet on a base of carbohydrates (grains, breads, and starchy veggies) has been drummed into us by well-meaning authorities, including luminaries such as: the USDA, the American Heart Association, and the American Diabetes Association.

Yet, it is a basic physiological fact that all carbohydrates are metabolized to glucose. If glucose is not used for fuel, it is automatically converted to and stored as saturated fat (only a small part-about 100 grams - will actually ever be stored as glycogen).

Telling people to avoid eating saturated fat while simultaneously telling them to eat food that will be converted into saturated fat — fails a basic logic test. Fat, I will argue, is not the real problem.

Animal Models, A Genetic Mutation, & Modern Diets
It helps at this point to explain some genetic history. Only a few animals (the higher apes, the guinea pig, and a species of fruit bat) ever show coronary heart disease. Heart disease, however, appears only when these animals are fed a diet that is lacking in adequate amounts of vitamin C.

Zookeepers learned the connection between vitamin C and heart health a long time ago. When their gorillas were fed a diet of early versions of processed “gorilla-chow,” instead of a diet rich in vitamin C from fresh fruits and vegetables, they got sick and developed heart disease.

In contrast, bears — whose cholesterol levels can be three times as high as man’s and whose heart rates slow way down during hibernation, remarkably never show any atherosclerosis.

So what’s going on in bears and other animals that is missing in humans, apes, guinea pigs and some fruit bats?

Endogenous Production of Ascorbate and a Genetic Mutation
Other animals produce vitamin C endogenously (which means most animals manufacture ascorbate inside their bodies), and this production of vitamin C is essential to maintaining health, including maintaining healthy arteries.

For example, a 150-pound goat has a typical blood concentration of ascorbate equivalent to taking 13,000 mg (13 grams) of vitamin C per day. And, ascorbate concentrations rise much higher in times of stress. Compare this abundance of vitamin C in a goat with the paltry 60mg recommended daily allowance for humans. Consider further the percentage of people who do not get enough vitamin C from their diets, and it’s no wonder that heart disease is so prevalent.2

Some millions of years ago, a genetic mutation occurred, causing humans to rely on their diets for vitamin C. This mutation was not life-threatening, however, because our early ancestors thrived in the tropics, where vitamin C was in ready supply in fresh fruits and vegetables.

Scurvy (and heart disease) became a real problem for ancestors who settled in other regions of the world, areas with less readily-available dietary ascorbate.

During the Ice Ages, however, many of our ancestors did indeed succumb to scurvy and heart disease, when plant-foods were not as plentiful.3

Ancestors who were able to survive possessed a valuable genetic mutation, whereby damaged (leaky) blood vessels could be patched by a back-up mechanism, an animal food component called cholesterol. Modern humans inherited this ability to use cholesterol to make repairs, which, in other animals, are made through an abundance of freely-circulating vitamin C.

Cholesterol Carriers Mechanisms Of Moving Cholesterol In The Body
Now let’s talk about cholesterols.LDL has been called the bad or “lethal” cholesterol, while HDL is considered the “healthy” cholesterol. I’m afraid this is nothing but nonsense. There is no good or bad cholesterol. LDL, HDL are just two different types of cholesterol carriers.

When it comes to how cholesterol moves in the body, I believe it was Dr. Andrew Saul who used the analogy of a bus line, which is an apt one. Since cholesterol is an oily substance that travels through a watery bloodstream, it must be carried (similar to passengers and cargo on a bus) to various destinations in the body.

The HDL Bus Line
The HDL cholesterol molecule has a higher protein-to-lipid ratio (contains more protein than lipid material). Protein is denser than lipid, hence the name “high density lipoprotein” The HDL “bus line” thus carries a single “bag” of this dense cholesterol as cargo in each of its buses. In this way, the HDL cholesterol gets a ride straight to the liver and is eliminated as bile acids via the gall bladder and intestines.4

The LDL Bus Line
The LDL cholesterol molecule, in contrast, has more lipid or oil content, thus a lower protein-to-lipid ratio, and hence the name “low-density lipoprotein.” The LDL bus line in contrast, carries two bags of cholesterol as cargo.

The LDL bus line transports cholesterol to a variety of sites in the body, where it is used to repair and/or protect tissues or to be used in the synthesis of many vital compounds.

LDL cholesterol’s role is so important that nature lets the LDL bus line transport twice the number of cholesterol “passengers” as the HDL bus line does. LDL cholesterol is thus taken to important destinations in the body such as:

• Skin, where cholesterol reacts with sunlight to produce the “best kind” of Vitamin D (think healthy bones),
• Sex hormones (the estrogens, testosterone, and progesterone) and their “precursor” molecules (DHEA, DHEA-S and pregnenolone, as well as adrenal stress hormones like cortisol),
• Nerve cells so they are well-insulated and don’t short circuit,
• Scar tissue to repair tissue injuries,
• Cell walls to waterproof us so we don’t melt in the rain or when we take a bath, and
• Blood vessels for vital Cardiovascular repairs, as well!

The body was designed pretty exquisitely, and clearly cholesterol’s real mission is to save our lives, not to kill us.Cholesterol Readings Health, The Highs and Lows
Now, without looking at specific numbers (like we medical professionals love to do), let’s consider three cases and determine what a person’s cholesterol readings suggest about health:

1. High LDL - A relatively high LDL reading may indicate that the body needs to repair a lot of things and transport cholesterol to areas of stress or disrepair. 2. Low HDL - A low HDL reading may mean the body needs to hold on to cholesterol to both make repairs and to synthesize molecules that are scarce. 3. Lower LDL High HDL — A lower LDL and high HDL reading is likely to indicate the body’s systems are pretty well maintained. With no need for a lot of cholesterol, excess cholesterol is regularly eliminated.

As a goal, we want to strive for the third case, with a high percentage of the total cholesterol being of the HDL variety. In mathematical terms, total cholesterol over HDL should be less than 3.5.

However, when we artificially lower our cholesterol through pharmacological inhibitors (like statindrugs), we really cannot infer anything about our state of health with regards to cholesterol levels.

With drugs, we can make less cholesterol available to block our blood vessels, but at the same time, we will make less cholesterol available to perform vital functions (like converting sunlight to vitamin D, insulating nerve cells, healing scars, etc.).

Total cholesterol, as it turns out, has never been an indicator of who is more likely to suffer a heart attack. In fact, Dr. William Castelli, director of the prestigious Framingham Study, said:

The more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower peoples’ serum cholesterol…we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories, weighed the least and were the most physically active.5,6

The ongoing Framingham population study also found that there was virtually no difference in coronary heart disease events for individuals with cholesterol levels between 205 mg/dl and 294 mg/dl - where the vast majority of the U.S. population lands.

Even for those with extremely high cholesterol levels, up to almost 1200 mg/dl, the difference in CHD events compared to those in the normal range was trivial. Now that being said, please do not take this as carte blanche to consume as much saturated fat and calories as you want.

Castelli’s comments were made decades ago, when much of our livestock was still grass-fed and the adding of hormones and growth enhancers (both of which become concentrated in animal fat) was just beginning.

Diets high in domestic animal fat and partially hydrogenated poly-unsaturates (metabolic poisons) have their own set of health risks. As an aside, this is my main concern with Dr. Atkins’ dietary guidelines. Without emphasis on the quality of fats and proteins and balancing complex carbohydrates into the equation, we may be trading short-term health benefits for long term health risks.

Anyway, because cholesterol supports so many essential physiological processes, it doesn’t make a lot of sense to pharmacologically inhibit cholesterol production to get our numbers right. In fact, in study after study, the group with the lowest cholesterol levels had the highest mortality (death due to all causes).

I find the mortality rates for those with the lowest cholesterol readings particularly troubling. I believe it’s far better to help our bodies make necessary repairs and let the numbers fix themselves. Nature ultimately does not waste energy, so when less cholesterol is needed, less cholesterol will be produced.

Linus Pauling’s Unified Theory Of Cardiovascular Disease — Making Repairs Naturally
A lot of people have heard that Linus Pauling had some theory about vitamin C and heart disease treatment. It’s true and it’s called the “Unified Theory of Human Cardiovascular Disease,” which posits that ascorbate deficiency is one of the primary causes of Cardiovascular disease.

Using data gleaned from literally hundreds of published research papers by world-class scientists (MDs and PhDs), Pauling and his research partner, Matthias Rath MD described the link between Cardiovascular disease and vitamin C.

In their Unified Theory of Human Cardiovascular Disease, genetic differences, in species which are susceptible to CVD, are taken into account. The Unified Theory explains how the human body precisely regulates blood concentrations of cholesterol and provides compelling evidence that, with proper nutrition (and not drugs) Cardiovascular disease can be prevented and even reversed.

The Common Ground And Differences Of The Two Theories
Both the Lipid Theory and the Unified Theory agree that atherosclerotic plaques are deposited in response to injury of the blood vessel wall. Drs. Brown and Goldstein were awarded the Nobel Prize in Medicine in 1985 for this discovery.

Pauling and Rath, however, had a different concept of cause and effect, proposing that the genetic weakness of certain species (that do not produce ascorbate endogenously) must be addressed nutritionally, to promote healthy blood vessels.

While Pauling and Rath saw cholesterol as clearly correlated with Cardiovascular disease, they did not consider cholesterol as the enemy.

The Lipid Theory, on the other hand, argues that cholesterol is the enemy. Consequently, those who embrace the Lipid Theory emphasize: Decreasing the amount of cholesterol and lipids (patch material) in the body through diet and drugs, and making the blood itself less sticky (by means of blood thinners such as Coumadin, Plavix, aspirin, etc.), to ensure adequate blood flow and prevent heart attacks. To help put these theories into context better, let’s turn to one of my favorite topics: biochemistry.

The Biochemistry Of It All
Biochemistry is literally the chemistry of life, and, as a pharmacist, this is one of my specialties. Biochemistry helps us understand the structure and function of cellular components, including proteins carbohydrates, lipids, nucleic acids, and other biomolecules as well as enzyme -mediated reactions.

When I’m researching something new, I like to understand what is going on at a molecular level. To make the case for the Unified Theory, it’s valuable first to understand the roles of lipoprotein A, collagen, and vitamin C.

Lipoprotein A or Lp(a)
Lipoprotein A, otherwise known as Lp(a), is another special cholesterol carrier (bus line) found only in species that do not produce their own ascorbate (Vitamin C). Like LDL, the Lp(a) bus carries two bags of cholesterol, which are covered with a protein coat called apo(a). This coat allows cholesterol to move through the watery bloodstream. However, unlike LDL, Lp(a)’s protein coat is very sticky — think of the “a” as meaning adhesive.

In a non-ascorbate producing animal, the amount of Lp(a) is inversely proportional to the amount of circulating ascorbate. That means that higher vitamin C concentrations lead to less production of the sticky Lp(a) particles.

Under stress and when insufficient vitamin C is in circulation, the ability to produce Lp(a) allows the body to patch damaged blood vessels and prevent death by hemorrhage.

Thus, the sticky Lp(a) particle circulates through the vessels and adheres to spots where a blood vessel wall is damaged. Due to the Velcro-like surface of Lp(a), circulating LDL particles also will adhere where Lp(a) is busy patching damaged blood vessels, escalating the process of atherosclerosis formation.

Interesting Facts About Lp(a)
Lp(a) levels are influenced by genetics (inheritance) Diet does not influence Lp(a) levels 7 Cholesterol-lowering drugs have not been shown to lower Lp(a) levels. Both ascorbate (vitamin C) and niacin (vitamin B-3) have been shown to lower Lp(a) levels

Natural amino acids, L-lysine and L-proline, prevent the outer coat (apo-a) of a Lipoprotein A carrier from being sticky. These amino acids convert apo-a from a Velcro to a Teflon quality. L-lysine and L-proline also help remove plaque that is already present in blood vessels (by preferentially binding with receptors on Lp(a) and, thus, displacing Lp(a) cholesterol from artery walls).

Lp(a) is the single greatest risk factor predicting re-stenosis of blood vessels (the narrowing of blood vessels after widening in bypass surgery)

Collagen
Collagen is by far the most abundant protein in the body. While literally a fiber, collagen acts like a “glue,” which holds our cells together. Collagen is actually the body’s preferred repair substance, whether for closing wounds, healing blood vessels, or helping the skin remain wrinkle-free.8

The collagen fiber looks like a 3-strand rope. The rope consists of a strand of L-glycine molecules, a strand of L-proline molecules, and a strand of L-lysine molecules. These strands of amino acid chains are twisted around each other in a helical fashion and, in fact, do look like a rope.

When an injury occurs and the collagen fiber breaks, the frayed ends dangle just as if a rope were cut. If adequate ascorbate is present, the amino acids at the broken ends are hydroxylated. That means the end molecules of L-glycine, lysine and proline are chemically changed to L-hydroxyglycine, L-hydroxylysine and L-hydroxyproline. This allows them to be spliced back together (much like a sailor splicing a rope together). This simple chemical change also explains why vitamin C has the ability, not only to repair the damage, but also to start breaking up existing plaques, as will soon become apparent.

Of all the amino acids, L-glycine is the simplest one chemically and, in general, is always in ample supply in the body. L-proline and L-lysine, the other two amino acids in the collagen fiber, however, are not always in ample supply, and the body benefits from supplementation to ensure good collagen synthesis. [proline is made from protein; but lysine must be provided from food]

Vitamin C —Ascorbate or Ascorbic Acid[ascorbic acid is NOT vitamin C]
By now, you may have surmised that vitamin C is the linchpin of the Unified Theory. Vitamin C, or rather the lack of sufficient ascorbate, has implications in practically every chronic disease — osteoporosis, diabetes, arthritis, cancer, macular degeneration, allergies, and chronic or re-occurring infections are just a few examples.

Unfortunately, most people, including doctors, think of vitamin C as the substance that prevents scurvy. A small daily dose of 60 mg is sufficient to prevent scurvy, and conventional wisdom has been that additional vitamin C will just create expensive urine.

Pauling and Rath, however, hypothesized that most humans suffer from chronic, sub-acute scurvy and CVD is merely one of the symptoms of the underlying disease. Have your gums ever bled when you flossed your teeth? Have you ever had a nosebleed for no apparent reason? Have you ever had a wound that was slow to heal? If so, you may have (had) a deficiency in ascorbate in your system.

When a person develops a chronic condition (which adds stress to the body and further depletes already inadequate ascorbate stores), many tell-tale symptoms of scurvy often appear. The correct diagnosis is typically missed and scurvy sequelae are instead called symptoms of some chronic disease (i.e., poor wound healing in diabetics, hemorrhages in diseases like Crohn’s and ulcerative colitis, etc.).

Some salient facts about vitamin C and Cardiovascular disease
During the 1950’s, a brilliant Canadian physician, Dr. G. C. Willis, demonstrated that vitamin C was indeed related to cholesterol metabolism. A deficiency in ascorbate caused increased cholesterol synthesis (production). Feeding animals increased amounts of cholesterol reduced their vitamin C levels, and, conversely, vitamin C supplementation decreased cholesterol levels. Dr. Willis also showed that vitamin C could reverse atherosclerosis in guinea pigs, a species that does not produce ascorbate endogenously. 9,10,11,12,13

In 1971, British physician, Dr. Constance Spittle, demonstrated that patients with existing CVD exhibited a transitory rise in blood cholesterol when given vitamin C therapy, while patients with no CVD showed the reverse, namely, lower blood cholesterol levels. Spittle’s explanation: the vitamin C therapy was actually healing the vessel walls, thus releasing the cholesterol from the existing plaques. By the way, this research was published in the prestigious British medical journal, The Lancet.14

Finally, in 1985, when Mevacor (the first statin drug) was the hot new pharmaceutical, Dr. H. J. Harwood, Jr. showed that vitamin C was in fact “nature’s perfect statin.” Low vitamin C levels trigger the enzyme HMG-CoA Reductase to increase its activity and catalyze the synthesis of more cholesterol to ensure an adequate supply of patch material. Alternatively, high vitamin C levels were shown to inhibit the enzyme activity and cause cholesterol levels to fall.15

Dr. Harwood’s research shows a fundamental difference between drugs and nutrients: drugs can only inhibit or accelerate a biochemical process whereas nutriceuticals allow the body to modulate (i.e. up regulate or down regulate) enzymatic activity based on the body’s current physiological needs.

There is another very important difference in the mechanism of action of the statins compared with that of vitamin C. The statins, by their mechanism of inhibition of HMG-CoA reductase, also inhibit the production of enzyme CoQ-10. Vitamin C on the other hand actually increases the production of this important enzyme. CoQ-10, which incidentally is transported in the bloodstream by lipoproteins also, is thought to be the first antioxidant depleted when LDL is subjected to oxidation thus furthering the plaque forming process. The importance of this is illustrated by the fact that in 1989 the pharmaceutical giantMerck received a US patent permitting them to add CoQ-10 to their statins Mevacor and Zocor. However, to date, they have seen no financial need to do so. 16

Pauling’s Final Pieces of the Puzzle — L-lysine & L-proline
Pauling repeated many of the experiments previously cited, and he found that vitamin C did in fact help reverse some of the plaque in heart disease (remember, vitamin C chemically changes the end amino acid residues). However, there were still blockages in the blood vessels of the experimental animals.

Remembering that plaques formed only in the damaged areas of the vessels — and that damaged collagen looked like a frayed 3 strand rope— he theorized there would be bonding sites (receptors) on the Lp(a) that would be specific to the amino acid fragments of collagen (glycine, lysine, and proline). Being ubiquitous in the body, Pauling ruled L-glycine out, reasoning that Lp(a) would not stick anywhere there is a glycine moiety (glycine particle).

L-Lysine Binds with Lp(a) Receptors
Pauling then turned his attention to L-lysine, hypothesizing that lysine receptors on the Lp(a) may account for why Lp(a) sticks exclusively to the damaged collagen fibers.

To understand what Pauling was up to with lysine, it’s useful to imagine the way the body uses antihistamines. An antihistamine binds to histamine receptors (steals their parking places if you will) and thus preventing allergens from attaching and causing an allergic response.

Similarly, Pauling added L-lysine to the vitamin C he gave his test animals. Sure enough, the Lp(a) became way less sticky and more of the plaques were removed. The L-lysine essentially acts as a male end of a plug to the female receptors in Lp(a). This is how Lp(a) attaches to the broken strands — just like a plug in a wall socket. When there is extra L-lysine circulating in the bloodstream, the L-lysine plugs into and seals Lp(a)’s sockets, thus creating a smooth, inert Lp(a) particle, which can no longer adhere to the body. It is exactly like a parent putting a childproof plug into an empty outlet — no other plugs or little fingers are able to attach.

While the extra lysine is sealing the sockets on L(p)a, remember that vitamin C has changed the plug itself. By converting the end amino acids to hydroxyaminos, it essentially replaced the standard plug with a European type plug. Now there is no way at all for the L(p)a to make the connection.

In chemistry we say different reactants (here vitamin C and L(p)a) have different affinities to the same substrate (the dangling amino acids of the broken collagen fiber). The reactant with the greatest affinity will preferentially bind to the substrate and displace reactants already bound but having a weaker affinity to the substrate (in this case, the good guys have the greatest affinity and the bad guys fall off).

For all of these reasons, one can readily see that the combination of L-lysine and vitamin C is indeed a very powerful plaque-buster. The combination is, in fact, so powerful that Pauling and Rath were awarded a U.S. patent for a solution containing ascorbate and L-lysine to remove plaques from donor organs prior to transplant surgery.17

You see, once a transplanted organ is in place, blood must quickly perfuse through the new organ or areas of tissue will necrose (die). Bathing transplanted organs in their vitamin C-lysine solution prior to implantation quickly removed any plaques in the major vessels and greatly enhanced transplantation outcomes. Pretty impressive for vitamin C and a lowly amino acid, don’t you think?

L-Proline binds with Additional Lp(a) Receptors
Encouraged by their results with L-lysine, Pauling and Rath began to look at L-proline. L-proline is a unique amino acid, with a five-member ring structure, which contains the amine portion of the molecule (it’s the only imino amino acid).

The biochemical significance of this is that L-proline prefers to be in oil rather than water. L-proline is thus lipophilic as opposed to the hydrophilic L-lysine.

Since Lp(a) is a combination of a water-loving protein (apo a) and the oily cholesterol, Pauling and Rath hypothesized that lipophilic proline would block any receptors that might exist on the oily portion of Lp(a). When they added L-proline to their vitamin C-lysine solution, the effects were astonishing. Blockages completely cleared.

By having extra L-proline in the bloodstream (in addition to the supplemented L-lysine and vitamin C) all of the receptor sites on the L(p)a are sealed and the molecule does ,in essence, become Teflon coated.

With sufficient supply, vitamin C preferentially binds to and hydroxylates (chemically alters) dangling lysine and proline ends (in areas where the artery was damaged). After hydroxylation, the lysine and proline strands in vessel walls no longer fit the Lp(a)’s receptor sites, and some of the Lp(a) particles (or plaque patches) start to strip away from the vessel walls. The experiments of Willis and Spittle previously cited confirm this process.

Some Final Thoughts
The conundrum of causation versus correlation;it’s an age-old question and is an important question when it comes to Cardiovascular disease.Think about a child who has seen a number of house fires. He correctly observes that firemen are always present at house fires and concludes, erroneously, that firemen must cause these fires. The child does not yet understand that the firemen are actually there to save the day.

It’s the same thing with the Lipid Theory, where cholesterol is seen as an evil cause of Cardiovascular disease, simply because it is highly correlated with the disease.

With the Unified Theory, we instead view cholesterol, homocysteine, C-reactive protein, and Lp(a) for what they really are: the body’s dire attempt to save itself. These so-called “bad guys” are really just markers of malnutrition and proliferate when the body is under stress.

Treating the symptoms of nutritional deficiency withdrugs becomes nothing more than an experiment, where we get to observe the toxic effects on a malnourished body. Unfortunately, it has now become standard to treat side effects with other drugs. And, in my profession, this is called polypharmacy.

As a first-year pharmacy student, I was told over and over again: Never practice polypharmacy! Instead, we were taught to replace the offending therapy to get rid of unwelcome or dangerous side effects. Not so today, where prescriptions are layered on top of one another.

As a cautionary note, while polypharmacy is generally considered a bad professional practice, I am not advocating that anyone reading this article drop their prescriptions (there may be some extenuatuing circumstances - i.e., an allergy or intolerance to an alternative therapy). I am advocating for informed discussions with medical practitioners, as well as the addition of a nutritional approach to supplement conventional approaches.

Meanwhile, I often have wondered what it would be like if first-year medical, nursing, and pharmacy students were introduced to the Unified Theory? I’m not naïve enough to expect this any time soon, but part of writing this paper was about documenting good science that merits more attention by mainstream medicine.

I find it practically criminal that, despite overwhelming scientific evidence, the Center for the Study of Alternative and Complementary Medicine of the NIH has not done one clinical trial to test Pauling’s and Rath’s work. The Center is funded by tax dollars, so you would think that an incredibly affordable solution to the number one cause of death in this country would get some attention, but, alas, not so far.

Meanwhile, I feel privileged to get information on the Unified Theory in front of so many people through Our Health Co-op. May my article be read widely and contribute not only to better awareness, but also to making the case for formal clinical trial research someday!

Until then, here’s to your health and to our community!
Mike Ciell, Registered Pharmacist

An Interview with Uffe Ravnskov, MD, PhD

When did you begin to suspect that the cholesterol theory of atherosclerosis might be wrong? What led you to this conclusion? Before then, had you believed in the cholesterol theory? Was this part of your training?

I have never thought that it was true. I heard about it for the first time in 1962 shortly after getting my MD. My biochemical knowledge was still intact at that time and I knew that cholesterol was one of the most important molecules in your body, indispensable for the building of your cells and for producing stress and sex hormones as well as vitamin D.

The idea that cholesterol in the blood should kill us if its concentration is a little higher than normal, as they wrote in the Framingham paper, seemed to me just as silly as to claim that yellow fingers cause lung cancer.

Would you tell my readers about your training, publications, university appointments, other professional activities?

The first seven years as a doctor I worked in different medical departments in Denmark and Sweden. In 1968 I started my academic career at the Department of Nephrology, University Hospital in Lund, where I got my PhD. After a few years I organized a research team to investigate the association between hydrocarbon exposure and glomerulonephritis

Unfortunately I caught one of my coworkers in producing a fraudulent paper. It was unfortunate, because it is risky to be a whistleblower in the academic world. Instead of excluding the fraudulent researcher it was my research that was questioned. The resistance against my research from my superiors became intolerable, and I therefore decided to go into private practice.

Nevertheless I succeeded in publishing the main part of my research in major medical journals after having left the department. I have summarized my findings and conclusions on the web as well.

In the late eighties the cholesterol campaign was started in Sweden. I was very surprised because I couldn’t recall anything in the scientific literature in support of it. I started reading it systematically, and I soon realized that I was right.

Since then I have published about eighty papers and letter, and also books, translated into five languages, where I present my arguments and criticism.

How has your work been received by your colleagues; by healthcare professionals and consumers around the world?

In the beginning nobody took notice. To ignore criticism is the most effective way to maintain a false idea. My first book was published in Sweden in 1991 with a Finnish edition shortly afterwards. The Swedish one made no impact whatsoever, and the Finnish one was put on fire in a television show.

Ridicule and slander have been used as well, as a means to muffle me

After I had aired my warnings against statin treatment in Dutch television, for instance, Dutch researchers described me in a following show as a crackpot who had been kicked from the universities of Copenhagen and Lund. The directors of the show offered my critics a possibility to discuss the issue with me on television, but all of them declined. On his blog, Michael Eades has described how one of them later on belittled me in a scientific paper.

But I have also realized that I am not alone.

Seven years ago I started THINCS, The International Network of Cholesterol Skeptics (www.thincs.org ), which by now includes about eighty doctors, professors and other researchers from all over the world, who share my skepticism, and I have received two international awards for my contributions.

Also encouraging is the hundreds of emails that I receive every year from patients, who have regained their health after having stopped their cholesterol-lowering treatment.

Your work seems to validate what many integrative health care professionals have been saying for decades. How does the alternative community respond to you?

There is a much more open attitude from these people.

If the cholesterol hypothesis is an error, does this mean that all of its therapies – low cholesterol diet, cholesterol lowering natural therapies and medications — are wrong?

Absolutely. This kind of treatment is meaningless, costly, and has transformed millions of healthy people into patients.

Specifically, what are your views on statins?

Their benefit is trivial, and has been seen only in male patients who already have heart disease.

Worse is that their many adverse effects are ignored or cleverly belittled by the trial directors. Independent researchers have found many more and in much higher numbers. If they are true it means that today millions of previously healthy people probably consider their weak and painful muscles, their bad memory, their sexual failure, and their cancer to be a consequence of increasing age, and so do their doctors.

The risk of cancer is most alarming. Both animal experiments, epidemiological studies and several of the statin trials have shown that low cholesterol predisposes to cancer.

The widespread use of statin treatment probably explains why the decrease of the smoking habit that has been going on in many countries hasn’t been followed by a decrease of cancer mortality. We should have seen a decrease because smoking predispose not only to bronchial cancer, but to all kinds of cancer.

Drug companies market vigorously the highest, strongest doses of statins. Lipitor is pushed at the highest dosage, 80 mg. This dosage is the most powerful for lowering cholesterol and LDL, but it also causes more adverse effects and costs more than lower doses. What are your thoughts about this?

The outcome from these trials is a further demonstration that the small benefit from statin treatment has nothing to do with cholesterol.

For instance, although cholesterol plummeted and remained at about 50 percent below the initial value during the whole SEAS trial, it did not change mortality, but it increased the number of cancer with statistical significance.

Even worse was the result of the ENHANCE trial, where atherosclerosis in patients with familial hypercholesterolemia progressed the most among those whose cholesterol was lowered the most.

If statins can be helpful in reducing the incidence of heart attacks, who should take them?

In my view, nobody.

When I was practicing, I used to describe the benefit in this way: Considering your age and your previous heart attack, your chance to be alive in five years is about 90 percent. You can increase that chance to 92 percent if you take a statin pill every day, but then you may also expose yourself to its many adverse effects.

From the data I have seen, statins have not produced a reduction in overall cardiac deaths. Do you have any idea of why this is?

You are right. Heart mortality in Sweden is going downwards, but the reduction started already in the 1960’s. The cause is most probably that treatment of acute myocardial infarction has improved, because the mortality curve has not changed after the introduction of the statins.

The reason may be that their small benefit is counteracted by an increasing frequency of heart failure.

As you know, the statins block not only the synthesis of cholesterol, but also of other vital molecules, for instance coenzyme Q10, and muscle cells, including those of the heart, can’t function properly without Q10.

Do you think mainstream medicine will ever relinquish its view that elevated cholesterol causes heart disease, and that statins are the magic bullet?

I hope so. The failures of the most recent statin trials have been commented on by several journalists in the major U.S. newspapers. In Sweden a revolution is going on. Here, a general practitioner treated her own obesity successfully by eating a low-carbohydrate diet with a high content of animal fat. When she advised her obese and diabetic patients to do the same, she was reported to the National Board of Health and Welfare for malpractice.

After a two-year-long investigation she was acquitted, as her treatment was considered to be in accord with scientific evidence.

At the same time, the Board dismissed two experts, who had been appointed for updating the dietary recommendations for diabetics, because it came up that they were sponsored by the food industry. Instead the Board has asked independent researchers to review the scientific literature.

The subject has gained general attention due to a number of radio and television shows, where critical experts including myself have discussed the issue with representatives of the official view.

Most important, thousands of patients have experienced themselves that by doing the opposite as recommended by the current guidelines they have regained their health!

The effect has been that the sales of butter, cream, and full-fat milk are increasing in Sweden after many years of decline, and a recent poll showed that a majority of Swedish people today think that the best way of losing weight is by a low-carbohydrate, fat-rich diet.

Further progress was achieved this spring. Several times, colleagues of mine and also I, have asked the Swedish Food Administration for the scientific basis of their warnings against saturated fat. We have been met with the argument that there are thousands of such studies, or by referrals to the WHO guidelines or the Nordic Nutrition Recommendations.

As the main argument in the latter two — that saturated fat raises cholesterol — we were not satisfied with their answer, and finally the Food Administration published a list with 72 studies that they claimed were in support of their view on saturated fat, and twelve that were not.

We scrutinized the lists and found that only two of the 72 studies supported their standpoint; eleven studies did not concern saturated fat at all, and the unsupportive list was incomplete, to put it mildly.

We published a short report with our comments to these lists in the Swedish medical journal Dagens Medicin. A response from the Food Administration appeared seven weeks later in which they pointed out that their recommendations were directed to healthy people, not to patients. They maintained that they were based on solid scientific evidence, without mentioning anything about saturated fat, and without answering our critical comments.

But this is not all. Earlier this year Sachdeva et al reported that the mean cholesterol in 137,000 patients with acute myocardial infarction was lower than normal.

As usual, the authors didn’t understand their own findings, but concluded that cholesterol should be lowered even more. A few months later Al-Mallah et al. came up with the same result and conclusion, although they also reported that three years later, mortality was twice as high among those who had been admitted with the lowest cholesterol.

These results created a fierce debate in one of the major Swedish newspapers. It was opened by ninety-one-year old Lars Werkö, the ‘Grand Old Man’ in Swedish medical science, retired professor in internal medicine and former head of The Swedish Council on Technology Assessment in Health Care, together with Tore Scherstén, retired professor in surgery and former secretary of the Swedish Medical Research Council.

“Now it is time to sack the cholesterol hypothesis and to investigate the reason of this scientific breakdown” they wrote.

They also criticized American researchers in AHA and NHLBI and their followers for sloppy and fraudulent science.

They were of course attacked by two professors and representatives of the current view, but none of them came up with any substantial evidence, only with personalities.

Are there other risk factors that should be followed? Such as: C-reactive protein, fibrinogen, homocysteine, lipoprotein A… Any other factors?

Such analyses may be helpful for doctors to put the right diagnosis in patients with a disease of unknown origin.

But to check healthy people’s blood to find deviations from normal is the freeway to unnecessary medication.

Are there other alternative therapies besides statins that people might consider?

There is no reason for healthy people to take drugs, or anything else to prevent heart disease, as long as we do not know the very cause.

Don’t forget that people who die from a myocardial infarction have on average lived just as long as other people. In my talks I used to ask people, who put the same question to me, if they know a better way of dying?

What diet do you recommend people follow?

I do not give medical advice to people I haven’t seen and examined myself, and as I am retired, it means that I give no advice at all except to my family and nearest friends. I inform people by writing and lecturing. Then they have to decide themselves what to do.

In 20 years, do you expect changes in how we view heart disease, its causes and treatments?

I am confident that we will see a change in the next few years. There is a growing skepticism among medical scientists. What is happening in Sweden these days may hopefully inspire researchers in other countries to air their skepticism openly.

Recently, experts selected by WHO and FAO published a new report . Here the authors concluded that there was no satisfactory or reliable evidence to support the idea that saturated fat causes heart disease, or diabetes or obesity.

A revolutionary change of direction, you may say. However, they did not change their recommendations!

Together with Kilmer McCully, the discoverer of the association between homocysteine and atherosclerosis, I have presented another hypothesis (You can read that paper in its entirety at this link.)

We think this hypothesis is much more likely because we are able to explain the many observations that do not fit with the present one.

Finally, I assume that much of what I have mentioned here may seem incredible, but all the facts, including references to the scientific literature, are available in my new book “Fat And Cholesterol Are GOOD For You!”

About Uffe Ravnskov, MD, PhD:

Dr. Ravnskov graduated from the University of Copenhagen with an M.D in 1961.

1961-1967: Various appointments at surgical, roentgenological, neurological, pediatric and medical departments in Denmark and Sweden.

1968-1979: Various appointments at the Department of Nephrology, and the Department of Clinical Chemistry, University Hospital, Lund, Sweden.

1979-2000: A private practitioner and independent researcher, specializing in internal medicine and nephrology. Honored with the Skrabanek Award 1998, and author of: The Cholesterol Myths.

Burton Linne | www.cureheartdisease.us | cureheartdisease.us@gmail.com | Sacramento, California USA | December 2009