If you ever bring up the subject of heart disease at a (doctor’s) cocktail party-and you are not in the basement rec room playing naked twister-someone will probably walk up to you toting a martini with a 2 inch cigarette ash floating in it and tell you what wonderful drugs the statins are. She might say something like this squinting through pig snappers for eyes with breath not unlike canned salmon: “The revolutionary use of these miracle drugs has significantly dropped the death rate from heart attacks over the last few decades.” It’s true that cardiovascular mortality has decreased. According to Anthony Colpo in his book The Great Cholesterol Con the age adjusted death rate from heart disease was the highest around 1950. If you had a heart attack in the 1950’s you stood a better chance of dying than you do now-that’s called the death rate. It’s the percentage of a population that has a heart attack that go on to die from it. Death rates from heart disease have steadily dropped over the decades and they continue to drop. However, as Colpo clearly shows the true decline in deaths started occurring a decade before the war on saturated fat and cholesterol even began. Furthermore, as you can plainly see our drunkard’s comments are inaccurate. Statins are not responsible for this amazing trend either because the downward trend started thirty years before statins were introduced. This is an important point to remember because some Elites like to throw it about as proof that statins are powerful, life-saving drugs. I’ll return to this in a moment.
For all of you growing up in the classic music era, it was in 1966 that we were listening to Monday Monday by the Mama’s and the Papa’s, Wild Thing (The Troggs), Summer in the City (The Lovin’ Spoonful) and of course Donovan’s psychedelic Sunshine Superman. It was also in 1966 that the surgeon general issued the famous warning that is still on cigarette packages telling of all the nasty things tobacco can do to you. There is another term I want you to understand. It’s called incidence. The incidence is the number of new cases of something like a disease for example in a population usually per 100,000 people. So for example you might say that the incidence rate for disease X is 100. Meaning that for every 100,000 people there are 100 NEW cases of disease X per year. Not only were more people surviving heart attacks but the actual number of new cases started declining as well. Most experts consider the reason for the decline in the incidence (number of new cases in a population) of heart disease  to be due to that historic warning label. One thing is for sure. Americans will listen to authority figures especially when it comes to their health. Once people understood that cigarettes were bad for them many stopped smoking. The number of new cases of heart disease/heart attacks decreased because less people were smoking and smoking causes heart disease. Unfortunately the drop in incidence was short lived. While men quit smoking en masse, others picked up the habit in recent years such as women but not to the same extent. There were other more sinister factors that were about to take a huge toll on American health-a big change in diet and lifestyle as you’ll see.
INTERVENTION AND EMERGENCY MEDICINE
The decrease in death rate from heart attacks has been attributed to intervention-emergency treatment. Emergency medicine and cardiac care has gotten much slicker at saving lives over the last 60 years which should be obvious. How about looking at the last 10-20 years since statins have been in use? If the decline in mortality was due to the use of statins (it wasn’t until 1987 that the first statin was introduced) the incidence (new cases) itself would have decreased which is not what we see. Furthermore, the age-adjusted incidence of atherosclerotic heart disease has remained the same and may even be increasing  in spite of the huge decreases seen in smoking a known risk factor whose combustion products are coronary artery (endothelial) toxins.
ATHEROSCLEROSIS IS ON ITS WAY UP
Dr Eades the author of the bestselling book Protein Power, showed us a study on his website. The results were published in the Archives of Internal Medicine from the Mayo Clinic pathology department which has recently seen a reverse trend in atherosclerosis: increasing numbers of patients at autopsy showing significant atherosclerosis as of 1997-2004, thus reversing a 40 year downward trend.
In other words this and other studies are revealing that the incidence of heart disease appears to be increasing in spite of ubiquitous statin use. This is precisely the opposite of what you would expect when 25% of all middle age men are on a statin. What could be driving this increase in incidence?
THE GOOD, THE BAD AND THE UGLY
Let me first quickly give you a tutorial on “bad” cholesterol. Bad cholesterol is not really bad but it helps to sell pills to consumers who don’t have a science background. Bad cholesterol is LDL cholesterol, the good one is HDL and there is IDL and VLDL as well. The first letter of each acronym is (starting with LDL), low, high, intermediate and very low. OK so far? The VLDL is your triglycerides (TG) essentially and we can clearly call them ugly because, as you’ll see, they are a real danger to your health. In fact, the TG/HDL ratio is a much stronger predictor of future cardiac events like a heart attack than the poor, lonely LDL ever was. This will all make sense when you understand the relationship between diet and the TG/HDL ratio.
THE FLUFFY AND THE DENSE
I explain in great detail how heart disease develops in a chapter that you have never seen yet on inflammation and atherosclerosis. In it I explain that it’s only when LDL becomes oxidized (oxLDL) that it becomes dangerous and causes endothelial damage (inflammation) which leads to atherosclerosis (heart disease). Just to confuse things further there are at least two types of LDL. There is the large, fluffy particle and the small, dense particle forms. Only the small form can easily oxidize and become dangerous to your health. The large form is harmless to your endothelium. The endothelium is a tiny one-cell layer lining the inside of your arteries. Those cells are the “brains” of your blood vessels. They allow arteries to remain flexible, to change diameter, to allow immune cells into and out of the blood vessel to surrounding tissues like when you step on a thorn. The first question everyone should ask is what things or habits in our lifestyle promote the oxidation of LDL and what can be done to stop this process. It is NOT how much LDL you have in your blood but rather how much oxLDL you have. OxLDL can directly cause endothelial injury and inflammation. When I say InflaNATION much of that term refers to endothelial inflammation. The other 2 main forms of inflammation that I discuss are in the brain and in the belly as visceral fat which I will teach you about in separate blogs.
THE OX(LDL) CART
Periodically you’ll hear me mention the ox cart I rode to my own execution i.e., my heart attack. There is a related ox cart that makes atherosclerosis so deadly. It’s the oxidized LDL (oxLDL) cart. It is ridiculously naïve to think that only one component-cholesterol-is the sole cause of heart disease. I further acknowledge that the oxLDL particle is only one of dozens of risk factors that contribute to endothelial damage. However, it’s a big one because oxLDL can both initiate and sustain endothelial injury. Furthermore, its presence is critically needed at all stages of atherosclerosis from the very beginning all the way to initiating a heart attack. How one oxidizes LDL has everything to do with food, drink, body fat, disease states, medications and exercise. In other words your LIFESTYLE will help determine how much LDL you oxidize in your body. Regular native LDL, the unoxidized form, is harmless regardless of how much is in your blood. Those “authorities” who know the role of oxidized LDL are still in favor of using toxic, statin drugs to lower cholesterol. They shape the argument like this: in general since a small percentage of a person’s LDL is oxidized it would be prudent to lower one’s total LDL thus lowering the amount of oxidized particles in your body.
But why not simply reduce the potential to oxidize LDL in the first place? If you live a pro-inflammatory lifestyle you will have or be creating heart disease-period-because that type of lifestyle helps to generate the small, dense particle and it drives the free radical oxidization of said LDL. Those free radicals directly injure your endothelium too. Conversely if you change said lifestyle as I did, you will not develop heart disease, it will progress at a slower pace or you will be reversing it over time. It’s not LDL per se that can cause endothelial damage so why lower it? It’s oxLDL that causes all of the mischief. That of course is related to how you live your life.
Oxidized LDL (oxLDL) has been shown to play an important role in the pathogenesis of atherosclerosis….that oxLDL had a higher sensitivity for coronary artery disease than did LDL cholesterol and the total-to-HDL cholesterol ratio…(And) thathigher levels of oxLDL were related to a higher triglyceride-to-HDL… ratio and higher levels of CRP.
As a typical American you are living a pro-inflammatory lifestyle which usually predicts that your routine CRP screening test will most likely be pretty high and that’s not a good thing. That is to say that there is a positive association between CRP (a marker for inflammation) and the oxidation of LDL: the higher the CRP the more inflammation and oxidation of LDL. Furthermore, a high TG/HDL ratio also predicts a high level of circulating oxLDL since that ratio, when elevated, is associated with the small, dense, LDL particle type which is the most easily oxidized. OxLDL is an important mechanism by which inflammation promotes atherosclerosis. OxLDL has been found to inhibit key acute inflammatory (acute repair) responses in the arterial wall leading to the production of a chronic, smoldering, low-level inflammatory reaction which is the perfect milieu for the development of arterial plaque. Riding the oxLDL cart or not my friend is all up to you.
 Michael R.Eades. The blog of Michael R Eades, MD. Unsettling news for statinators.
 Anthony Colpo The Great Cholesterol Con. Second Edition. LuLu.com. 2006 p 7.
 Eades. IBID.
 Paul Holvoet et al Arterioscler Thromb Vasc Biol. 2003;23:1444-1448; (original citations: Goldstein JL, Brown MS. Molecular medicine: the cholesterol quartet. Science. 2001;292:1310–1312. Mertens A, Holvoet P. Oxidized LDL and HDL: antagonists in atherothrombosis. FASEB J. 2001;15:2073–2084. Ross R. Cell biology of atherosclerosis. Annu Rev Physiol. 1995;57:791–804.)