Establishing Accurate Cardiovascular Risk

Thanks to everyone that made it to my Cardiovascular health seminar on June 19th. This was part of our wellness workshops that we do every other tuesday at our clinic. As promised I've posted the information from the talk here. It was a bit bio-chemistry heavy, so even if you were at the class, it isn't a bad idea to go through the information again in case it didn't all stick the first time.

None of this information came directly from me, and rather is sourced from a lot of people that I really respect, including Chris Masterjohn, Chris Kresser, and the authors of dozens of published medical studies.

Basically our talk covered the real causes of cardiovascular disease. We have, as a culture, hanged our blame for cardiovascular disease on Cholesterol since a number of studies were incorrectly interpreted, or outright misrepresented to show that higher cholesterol levels cause heart attack and artherosclerosis.

Initial studies into artherosclerosis used rabbit models and found that injected cholesterol did not cause any artherosclerosis, but feeding rabbits cholesterol did cause artherosclerosis. What this means is that it is the introduction into the blood stream from the digestive system that becomes the crucial factor to creating the artherosclerotic plaques. This factor is something called a lipoprotein. These are the vehicles that carry cholesterol through the blood. The last L in HDL and LDL refers to this lipoprotein.

It works like this: cholesterol is fat soluble, which means it cannot be dissolved in blood (which is water based). In order to move through the blood it needs to be carried in a lipoprotein. A lipoprotein is the vessel that delivers cholesterol to the cells, brain and areas of the body that need it. Coincidentally it's also how fat soluble vitamins are carried through the blood.

We have this idea that cholesterol is bad in any quantities and the lower we can get our number the better. But in fact cholesterol is a vital part of proper body function, and does multiple important things including: sex hormone synthesis, stress hormone synthesis, cell membrane integrity, proper brain function, proper eye function, nerve conduction, development, bile creation, fat soluble vitamin absorption, and several studies are finding that adequate cholesterol levels have a protective effect against mental and emotional disorders.

If the cholesterol isn't the problem, what is? The lipoproteins that carry the cholesterol through the body are capable of oxidizing (or becoming denatured, or molecularly malformed). This oxidation creates a molecule that can penetrate through the inner most layer of the arteries, and once embedded in the arterial walls, can attract immune cells to cause inflammation, the result being the formation of an artherosclerotic plaque. If the LDL is not oxidized, studies indicate that even if they do penetrate into the vessel wall they will not attract the immune cells that ultimately result in an artherosclerotic plaque.

The body tries to protect against the oxidation of these Lipoproteins by packaging them with antioxidants when they are created. When the liver packages cholesterol and sends it out into the blood stream it includes Vitamin E and Coenzyme Q10, both of which are powerful antioxidants and protect the lipoproteins from oxidation. One reason that LDL is associated more highly with artherosclerosis than HDL is that the LDL cholesterol is packaged with less vitamin E than HDL. This extra Vitamin E is able to protect the HDL from oxidation more so that the HDL cholesterol isn't likely to penetrate into the vessel lining and cause the aggregation of immune cells.

The real fallacy of the current cholesterol testing is the thought that it is the total amount of cholesterol in the blood that causes the problem. What we're finding out is that it isn't the amount of cholesterol as much as it is the number of lipoproteins. The more LDL lipoproteins in the blood the more capacity for oxidative damage. It's like carpooling. If there are 400 people on the highway with you and they're all in their own individual cars, there are a lot of cars, and probably some snarled traffic. If on the other hand that same number of people are all carpooling and rather than 400 cars there are 9 buses, 15 vans and 10 cars, then there are only 34 vehicles rather than 400. Much less traffic, much less road rage. The same thing goes for cholesterol. If your LDL cholesterol is 100 and your particle size is very small, then you have a lot of vehicles on the road and more chances for oxidation. On the other hand if you have a lot of large fluffy particles (everybody's carpooling) then your chances of these LDLs oxidizing is much less. Another way to think of it is imagine you are in a room with balloons (LDL particles) all over the floor. You put on spiked shoes, are blindfolded and have to walk across the room trying not to step on and pop any balloons (you are now oxidative damage). The same amount of air has to be used to fill the balloons in the room, but you can use as many or as few balloons as you like. You would choose to fill only a few balloons really full, then you will have less chances of stepping on a balloon. If you fill a lot of balloons only partially full then you are more likely to step on a balloon with every step, you'll have more popping. So the ideal with LDL is to have fewer particles, that are large, rather than lots that are small. In fact this particle size is much more important than the total amount of LDL cholesterol these lipoproteins carry.

Another factor to consider is what makes up the lipoproteins. If the problems start when these LDL particles oxidize, then the question becomes: can we make them more stable and keep them from oxidizing? The answer fortunately is, yes. Lipoproteins are made from polyunsaturated fatty acids. These are inherently unstable fats, so we want to make sure we get them from good sources and don't over consume them. The industrial seed oils typically used in America for cooking are actually already oxidized because of the heat needed to extract them. Using only cold pressed, or extra virgin oils reduces the pre-oxidation of these fats so that when they are used to construct the Lipoprotein membranes they are already much more stable.

The last factor to consider is the antioxidant capacity of both our lipoproteins and our blood. Our antioxidant capacity is a relative thing. We begin with our background level of inflammation. This is a result of the amount of stress, injury, toxins, our metabolic rate and unhealthy nutritional ingredients. Then that background inflammation is measured against our antioxidant level (a function of the antioxidants we take in and the antioxidants that our bodies manufacture (like glutathione, superoxide dismutase and coenzyme Q10). We may be more than covering our inflammation with our antioxidant level if we are eating a healthy and nutrient rich diet, or we may be coming in way under par if we are frequenting fast food and consuming junk food. The more our antioxidant deficit the more these Lipoproteins will oxidize and lead to artherosclerosis and heart disease. 

We also need to protect our endothelium. Remember the oxidized LDL need to actually penetrate into our endothelium in order to initiate the formation of arthersclerotic plaques. We can prevent this by improving the integrity of our endothelium. How do we do this? Something called shear stress. Shear stress is a term in physics referring to stress occurring parallel to a surface, or in terms of fluid dynamics in a laminar flow to the walls. In blood vessels we see that the areas with the greatest shear stress have the least incidence of artherosclerosis and the areas with the least have the greatest incidence of artherosclerosis. Shear stress causes the endothelial cells to get busy protecting the vessel walls by improving collagen synthesis, organizing cells in a more protective formation, causing dilation of the vessel and increasing the blood flow through the region. We can increase our shear stress in our vessels simply enough, by getting some exercise. (And we can help this proces along by making sure we are getting adequate vitamin C in our diets as Vitamin C is an important cofactor in the formation of collagen)


So, are there tests that can give us a true evaluation of our true cardiovascular risk? Yes, here are the tests that I recommended and in fact we can order these tests directly through our office. 


LDL particle size
This can be measured by various labs, the testing methods include the VAP (vertical auto profile), the NMR (nuclear magnetic resonance) and a few types of electrophoresis testing. These tests are inexpensive and are often covered by insurance.

Apo B/A1
This tests the actual number of particles. Apo B refers to apolipoprotein B which is a protein found on the surface of LDL particles. There is only one of these proteins per particle so looking at the count of Apo B will tell you how many LDL you have in the blood, or how many cars on the road. The Apo A1 tells you how many HDL you have, as there is one and only one Apo A1per HDL particle. Recent studies seem to indicate that it is the ratio of the two that indicates most reliably the cardiovascular risk.

HsCRP
The High Sensitivity C-Reactive Protein is an indicator of the amount of inflammation in the blood. This is a useful marker as it will indicate the tendency for the LDL particles to oxidize, and as we know it is the oxidized particles that really pose the most risk in terms of cardiovascular risk.

Just to recap:
1. Get accurate testing...see above.

2. Reduce the chances of oxidation: ensure adequate antioxidant capacity by reducing your oxidative risk (stress, food and environmental toxins, general physical damage, metabolic activity-ie excessive calories, industrial seed oils, unhealthy omega 3:6 ratio) and increasing your antioxidant activity (eats your fresh greens and fruits, grass fed meats, organ meats, and eliminate nutrient poor and calorie dense foods)

3. Improve endothelial integrity: get moving!

Thanks for reading, and thanks all those who made it to this seminar!
Kieran

PS: here's a letter you can bring to your doctor requesting more accurate testing:

Establishing Accurate Cardiovascular Risk 

The typical measures used to evaluate a person’s risk of experiencing a heart attack or stroke, or other disease risk associated with Atherosclerosis are the LDL (low density lipoprotein), HDL (high density lipoprotein), VLDL (very low density lipoprotein), particle size (the smaller, denser the LDL the worse), the total cholesterol (the added together LDL and HDL), blood pressure, and triglycerides. 

While these measures are valuable, newer research is showing that there are other measures that more accurately indicate cardiovascular risk. 

Apo B/A1

Apo B-Apolipoprotein B is a measure of the artherogenic particles (particles that cause artherosclerosis found in LDL and VLDL cholesterol). The best measure of this test uses it as a ratio measured against apolipoprotein A-1 (a protein found in HDL cholesterol), an ideal ratio yields a lower number. In the medical journal “Nutrition, Metabolism, and Cardiovascular Disease” Schianca et al established 0.9 as the upper safe ratio for males, and 0.8 for females. A clear cut off is difficult to establish and many would argue that the idea of a clear number at which absolute health risk is established is a result of flawed logic and rather the relative risk of CV event increases with an increased Apob/ApoA-1 ratio and needs to be weighed with other signs of risk such as those below.

HsCRP

High Sensitivity C reactive protein is a marker of inflammation. 2 concurrent readings 2 weeks apart should be done for best accuracy. A HsCRP less than 2 mg/L demonstrates the lowest risk factor. 

LDL particle size

Established through Vertical Auto Profile, Electrophoresis, or Nuclear Magnetic Resonance, this identifies patients as either pattern A or B in regards to their LDL particle size. Our understanding of lipid metabolism would indicate that the smaller, denser particles have spent more time in circulation and would therefore have accumulated more oxidative damage, resulting in more artherogenic capacity. 

Conclusion

The problem with current cholesterol testing is that it fails to measure the ability of that cholesterol to cause damage. Cholesterol is an essential part of a healthy functioning body. The amount of cholesterol in the body isn’t the issue as much as the ability of that cholesterol to oxidize. The likelihood of the cholesterol to oxidize is a function of the anti-oxidative capacity of the body, and the overall level of inflammation in the body. Drugs to reduce total cholesterol fail to fully address this issue. This end is better served by ensuring the body has adequate anti-oxidative capacity through healthy diet, relaxation, and in some people supplementation. CoQ10 and Alpha Lipoic Acid are 2 potent antioxidants that assist in the fat soluble tissue. Amino acid supplementation can also help by promoting the production of glutathione, the body’s antioxidant powerhouse. N-acetyl Cysteine is a great start for this. Lastly, milk thistle increases the generation of glutathione by optimizing liver function. 

Kieran Jones L.Ac. Advanced Wellness and Rehabilitation