Right now we’ll go over blood vessel inflammation since it’s prevalent in most diseases of the first world. First I’ll cover briefly what happens when an unstable plaque ruptures. We’ll cover the the two main competing theories on how plaque is formed the Response to Retention and the Response to Injury hypothesis, the RRH and RTIH respectively. From there I’ll explain what an LDL particle actually is (the so called bad cholesterol), and the role of antioxidants. So let’s continue shall we?

Just like kids throughout the ages being reckless and unstable so too are these young whippersnappers. The real deadly fallout from this disease occurs in the younger, more vulnerable and unstable plaque. When the protective cap, as thin as a cobweb, ruptures-look out. These young unstable plaques look more like a zit or whitehead pimple bulging into the lumen of the artery. If the cap (the pimple) ruptures the toxic, atherogenic, immune cell, oxLDL lipid pool is released into the circulation causing platelets to adhere together forming an intraluminal thrombus-a blood clot. Technically a platelet plug forms from the gruel which acts as a stimulus for the hemostatic mechanism (figure 3 see previous blog). If the plug is sufficiently large blood flow to myocardial cells is impeded and either unstable angina, a heart attack, or sudden death occurs. Recent evidence suggests that sudden death and a certain type of heart attack called NSTEMI occur not from the formation of a thrombus, but from plaque rupture and the subsequent downstream bathing of the cardiac muscle in toxic atheromatous chemicals.[1] This picture suggests a scenario more like an acute poisoning of cardiac tissue.


This is an unusual fact. Nearly all laboratory animals with atherosclerosis never have heart attacks and in the wild, meat eating predators don’t develop atherosclerosis. Zoo animals that have atherosclerosis do not go on to have heart attacks. It seems that the heart attack is almost uniquely human even though many animals may have atherosclerosis. For example the baboon can develop arterial plaques but they never rupture, same with the fluffy rabbit. Then again the baboon doesn’t have to deal with the stress of a Friday morning deadline choking down a handful of Bugles in an effort to raise his blood sugar from 25 mg/dl to normal, while multitasking his screaming boss, the phone, printer, copier and pizza delivery guy. Nor does the humble rabbit smoke old, cancerous cigars and drink diet Fresca all day long while hiding from the sun. Is it our stress that adds the final blow or is it our particularly awful diet and lifestyle? Nobody knows for sure but both are disastrous.


The main difference between the RRH and the most accepted theory called the RESPONSE TO INJURY HYPOTHESIS (RTIH, see below) is the role and oxidation of LDL at the initial site of injury. In the RRH did the small LDL particle become trapped in the endothelium first due to its small size and then was oxidized or did the LDL particle become oxidized first while in the bloodstream (or on the surface of the endothelium) which made it easier for it to stick to the endothelium and insert under the endothelial surface?

At this point, after setting down this article, you are now engrossed in a re-run of The Flying Nun because you couldn’t care less and I don’t blame you. It might seem to be irrelevant tripe served best by hooded monk-like academics, but it’s the key to understanding how we can treat this problem. Literally, the fates of millions ride on what the truth is.

Here’s the key:

#1. If LDL needs to be oxidized first before it can do any damage then the treatment for this problem involves antioxidants.

#2. If unoxidized, native LDL can easily stick to and burrow under the endothelial surface then BIG Pharma has a better chance of justifying the use of statins because reductions in LDL number would have an impact on endothelial damage.

Even if #2 is correct, if it’s small dense LDL (sdLDL) that’s causing all the problems then the best strategy is to simply change your diet away from high-carb which promotes pattern B. Pattern B is the one which predominates with sdLDL. The above version, the Response to Retention Hypothesis, states that cholesterol (in the form of regular, old, LDL, not oxLDL) becomes trapped in the sugary, proteoglycan matrix of the subendothelium by an infiltrative process mainly and accelerated at endothelial injury sites. In other words LDL cholesterol itself is bad and if there is enough LDL in the blood it will tend to accumulate within arteries without much coaxing. From there it oxidizes to initiate the immune response. This is referred to as the “Response to Retention” hypothesis. After LDL penetrates the endothelium where it is retained, it then becomes oxidized and only then does it initiate the inflammatory response.

Once LDL is oxidized (oxLDL) it acts as a powerful stimulus on the immune/inflammatory system. This then heralds the true start of the immune response. Macrophages are attracted to the oxidized LDL particles. In an effort to protect the area they engulf the oxLDL thus forming foam cells which act as a further inducement for inflammation through the release of chemical cytokines (messenger molecules) from the foam cell. Eventually this becomes an atheroma (plaque) with a fibrous cap.


But is this a true description? Many physicians believe the Response to Retention Hypothesis because this is what their statin drug rep tells them to be the case. It rather conveniently leaves out oxidation as a primary mover in the initiation of atherosclerosis. Therefore, prescribing statins to lower the amount of LDL makes sense. It’s the best thing to do. It is seen as a numbers game. Accordingly, the most successful treatments result in the greatest reductions in a patient’s serum LDL cholesterol which is supposed to translate into a reduction in cardiovascular (CV) events and all-cause mortality.

It is an elegant theory but so are the canals of Mars. There are several clinical facts that completely deflate this theory. Lamentably, there is no linear correlation between LDL and CVD risk if you were to plot these two on a graph. As mentioned earlier the simple fact that half the patients with therapeutic levels of LDL still have heart attacks exposes the theory’s inaccuracy. Furthermore, studies reveal that statins do not decrease all-cause mortality. In fact, it depends on the study population: graphing all-cause mortality and LDL concentration is inversely associated with women meaning that the higher the cholesterol the lower all-cause mortality, and sometimes it takes on a U shape with men. The U shape means that there is a magic “low point” for total cholesterol (or LDL) below which all-cause mortality increases and above which the same thing occurs. The LDL low point’s range extends much higher than the recommended safe levels of LDL (higher than 100 mg/dl). More proof comes from other trials where reductions in LDL do not show a typical dose-response curve. In other words you get the same percent risk reduction for CVD whether you decrease LDL a tiny amount (10%) or by a huge margin (40%). Scientists know that when this occurs something else is producing the outcomes since no linear correlation between LDL and CVD risk reduction can be seen. This finding contradicts what the theory predicts: each incremental decrease in LDL corresponds to a similar decrease in CVD risk in a linear fashion.

This theory is incomplete or just plain wrong. Further proof lies in the fact that unfortunately, even those with perfect LDL levels of 70 mg/dl still have heart attacks. Major cardiac events still occur in nearly 20% of those whose LDL level is considered optimal (70 mg/dl). I like the example of Dick Cheney who had at least three heart attacks while taking high-dose statins. Looked at differently,about half of those with high LDL have perfectly good tickers as cardiologist and noted author Dr Sinatra mentioned in an interview for Life Extension Magazine 2013. These findings mean that there is something else going on that has nothing to do with LDL levels.

Conversely, some studies show an inverse relationship even for men such as the Framingham Followup Study which showed a decrease in CV events as LDL levels increased over time. It showed that elderly patients with higher cholesterol levels have less heart attacks, lower all-cause mortality and live longer than those with lower levels of cholesterol. The positive findings some statin studies have demonstrated in select patient populations shows that they have more to do with their pleotropic properties. The medical establishment coined the term pleiotropic and then misspelled it, when describing the anti-inflammatory, aspirin-like, properties of some statins.

The above theory is a flawed description of atheroma formation. It wrongly states that native LDL cholesterol can insert under the endothelium on its own in an unoxidized state. LDL itself is viewed as a dangerous molecule that can cause atherosclerosis but there has never been good quality evidence in 70 years to support this theory. As you spit your custard pie across the room in disgusted disbelief I’ll remind you to read any number of excellent books on this subject which make a mockery of this theory using the drug company’s own studies for ammo. The best is Anthony Colpo’s The Great Cholesterol Con.

There is a better, more complete explanation which we will explore next.



Figure 7 LDL particle[2]

Before we go any further let me explain what LDL really is (See figure 7). Cholesterol is a waxy material which is insoluble in water (or blood plasma). When it leaves the liver it is packaged it into a sphere of special fats and protein so that it can be soluble in plasma. This package is made up of a core of cholesterol and triglycerides, and a special outer skin of fats called a phospholipid membrane which, due to the way the fats were altered by giving them a charged or polar end, makes them soluble in water. The membrane is made from whatever fats you prefer to eat either monosaturated, polyunsaturated, or saturated fat. If you follow your doctor’s advice and cook with the heart smart, cheap seed oils like the supposed healthy canola oil or Wesson vegetable oil, your LDL will have a membrane of Ω6PUFA phospholipids. Lastly, a lipoprotein carrier (Apo B) is embedded within the skin much like Antarctica seen floating in the sea on an Earth globe. This lipoprotein particle is what we refer to when we talk of blood cholesterol.

The astute reader might notice that lipid (fat) is insoluble in water. Just watch what olive oil does when you pour a small amount into a saucepan full of water. It beads up and stays on top as little globules. Therefore, when scientists refer to lipids in the blood-no such thing exists. It’s a misnomer at the very least. There are no blood lipids only lipoproteins that carry lipids.

As Chris Masterjohn puts it:

In 1933, the famous proponent of the cholesterol-fed rabbit model Nikolai Anitschkov declared that atherosclerosis had been shown to be of an “infiltrative” character rather than a “degenerative” [degenerative in this sense means oxidative] character and was driven by lipids [lipoproteins] rather than by inflammation [oxidation]. He did not deny inflammation was involved, but believed that it was secondary to lipid infiltration [this is essentially the response to retention theory]. Many opponents continue to claim that the root cause driving heart disease has nothing to do with lipids and everything to do with inflammation and that it is degenerative rather than infiltrative in character.

As we will see below, these are all correct! Atherosclerosis is largely driven by the degeneration of lipids which infiltrate the blood vessel and thereby cause inflammation. Inflammation from other sources [lifestyle]may accelerate the process or further the degeneration of the atherosclerotic plaques once they are formed, but the initiating factor for fatty plaques appears to be the degeneration of lipids [the oxidation of fatty acids contained in the LDL particle]— especially the degeneration of polyunsaturated fatty acids (PUFA).” [3] [Emphasis mine]


In other words if degeneration drives the process then it’s the oxidation of polyunsaturated fatty acids (PUFA) on the outer coat of the LDL particle not simple, unchanged LDL cholesterol, which is the main contributing factor in atherogenesis.

This is a better description of what really happens at the cellular level. It’s one of the most important concepts in the entire debate. I have been warning you throughout this book how dangerous the omega 6 PUFA’s are because they generate inflammatory mediators and they easily oxidize. Saturated fats do not oxidize very easily. That’s why you don’t have to refrigerate coconut oil. You simply put it back on the shelf in the cupboard at room temperature because it will not turn rancid (oxidize). If you follow the AHA advice and consume omega 6 PUFA, your LDL particle will be made up of those same fatty acids. You then put your LDL at greater risk for oxidation which drives the entire atherosclerotic process. This is the exact opposite of what you want to do. Here is a perfect example of how I would have easily advanced my heart disease if I had listened to the “authorities.” Omega 6PUFA are what we call vegetable oils like corn, safflower, sunflower, peanut, canola and soy. Surprisingly, these are the same oils that the American Heart Association (AHA) still recommends for consumers as “heart smart” fats. Yes, no kidding.

Now that we know that oxLDL is a dangerous player in this game we’ll discuss the next theory, the most complete and accurate, that clearly explains the role of injured endothelium as the most fundamental process in atherosclerosis.


It is vitally important to understand that the most easily oxidized form of LDL is the polyunsaturated form. This particle is made when the patient eats a diet rich in Ω6PUFA, the heart smart oils. Consumption of saturated fat and monosaturated fat like olive oil makes for a particle much less capable of being oxidized and this is one of the most important points I will make in this book.

LDL particles rich in polyunsaturated fatty acids are more readily oxidized than are LDL particles enriched in saturated fatty acids or monounsaturated fatty acids.[4]

Once oxidized their potential to act as potent inflammatory agents is well known. While initial interest with oxLDL stemmed from its ability to induce foam cells formation (the beginnings of plaque), it is now viewed as a potent activator of the inflammatory pathway and as a key factor promoting atherosclerosis by different mechanisms….Accordingly, although LDL-C level is an accepted predictor of CHD [accepted by those invested in statin stock], other factors that influence LDL phenotype such as particle size and oxidative transformation, have a profound effect on their atherogenicity.

Either way once LDL is trapped within the intima both processes endothelial dysfunction, and further oxidation of LDL are driven by oxidation and free radical formation because the endothelium becomes its own machinery for the generation of tremendous amounts of ROS’s [reactive oxygen species].[5] [Emphasis mine]

I will take umbrage with the statement in the first paragraph “although LDL-C is an accepted predictor of CHD.” It is NOT a good predictor of CHD, never was, never will be (see the graph below provided by Dr Barry Sears which I will post within the next two blogs-it’s a few pages further down).


In reference to oxLDL we therefore have a powerful tool in the prevention of atherosclerosis which includes the dietary restriction of the HEART SMART, inflammatory seed oils-omega 6 PUFA-while replacing them with monosaturated EVOO, omega 3PUFA, and saturated FA like butter and coconut oil. Statins may reduce the number of particles but the intelligent use of potent antioxidants and dietary discretion will prevent the oxidation of LDL in the first place rendering it harmless. Furthermore antioxidants interrupt numerous redox reactions that occur in other high risk areas including the endothelium in all of your blood vessels not just your heart’s vessels, while decreasing brain inflammation to name just two important areas. Furthermore, enriching your body with antioxidants, especially in the form of living polyphenols from fruits and vegetables, decreases your overall chances of dying. According to Dr. Richard Cutler, the former director of the National Institute of Aging:

“The amount of antioxidants in your system is directly proportional to how long you live.”

Our antioxidant status is what we need to remember: we can change our disease status for the better and even cure heart disease. I did it with a lot less information at my disposal than you have. If I can do it stumbling in the dark then it ought to be a breeze for you by simply following my principles that successfully worked for me. One thing I know for sure. Heart disease is only deadly when we follow our cardiologist’s dietary recommendations and take their prescription drugs while doing nothing as far as real dietary change and lifestyle are concerned.


[1] ( 06/07/2014

[2] 12/18/2011

[3] Chris Masterjohn High Cholesterol And Heart Disease — Myth or Truth? The Response-to-Injury Rabbit Never Developed Atherosclerosis — Why Not?August 23, 2008
( 12/14/2011

[4] Daniel Steinberg. Low Density Lipoprotein Oxidation and Its Pathobiological Significance. (

[5] Patrick Mathieu; Philippe Pibarot; Jean-Pierre Després Metabolic Syndrome: The Danger Signal in Atherosclerosis Month: 9 Year: 2006 12/18/2011

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Category: Inflammation, PREVENTIVE MEDICINE

About the Author ()

Dr. Christopher Rasmussen (aka Reality Renegade) is the author of his upcoming book, "InflaNATION: Industrial Diners & A Doc In The Box." By deliberately avoiding harmful industrial foods and the Commercial Sick Care System with its Pills and Procedures paradigm, Dr Rasmussen cured himself of a deadly disease-which became the reason for writing this book. In the book, he provides the facts you must know and the solutions to regain your health, maintain wellness, and outlive your parents' generation in an extraordinarily toxic world.

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