Functional Cardiology – part 3

Three Possible Responses

There are three possible responses that occur when vascular endothelium (the blood vessel cell lining) is damaged. Remember that the real problem behind Cardiovascular Disease (CVD) – which we will revisit and break down in detail later in this primer – starts in the endothelium (the lining of the arteries) as Endothelial Disease (ED).

Where there may be hundreds of possible ways to damage the endothelial tissue via toxins, biotoxins (living organisms like virus, bacteria, mold, parasites…), nutritional factors, etc. there are only a few possible responses of the endothelium and its underlining structures: a local inflammatory response, an oxidative stress response, or an autoimmune reaction. Don’t be too confused by the names, but all three possible responses include inflammation, which is the more damaging aspect of each response.

Understand that your vessels, like every tissue, normally maintain a fine balance between injury and repair. It’s like a teeter-totter that tips gently back and forth; vessels are damaged by endless assaults and then healed by a collection of innate physiologic responses that viewed as a whole, over time, we call health. If an individual has the unfortunate event of continual and prolonged damage, the repair can actually bring about problems that we shall soon see. For now, let’s review the three responses of the endothelium.

The first possible response is acute, local inflammation. Again, there are literally hundreds of possible causes, but let’s use an example of vascular injury from high Homocysteine levels. Homocysteine is a toxic byproduct of protein catabolism that is an intermediate metabolite; which means it is supposed to be converted to another nontoxic substance and under normal circumstances it should never accumulate to levels that would injure the body.

Homocysteine is highly corrosive to endothelial tissue and sets up a series of events that increase inflammation under the cell lining; it also damages the kidneys as well increasing what is known as the Renin-Angiotensin-Aldosterone-System (RAAS). This RAAS response does several things, including increasing Sympathetic nervous system activity (which increases blood pressure, increasing anxiety, decreasing detoxification…), increases water retention, increases cortisol release from the adrenal glands, increases vasoconstriction, which all work together in your body’s attempt to solve the problem of toxic exposure. However, prolonged injury, as in chronically elevated Homocysteine levels, will lead to ED and CVD.

The second possible response of the vessel is a reaction to oxidative stress, which is an increased production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) – free radicals that can cause severe cellular damage. As I stated, all three reactions cause inflammation and several chemical changes including a down-regulation of the nitric oxide system. Epithelial nitric oxide production is extremely protective to the cell; decreased production of nitric oxide will cycle-up the inflammation in and under the endothelial cell layer.

The third response is the most common and is therefore the most common cause of ALL heart problems – Autoimmune Endothelial Disease (AED) is a new term we’ll use for an autoimmune reaction occurring in the endothelial tissue. If you’ve read my book, “Help, My Body is Killing Me…” you will be up to snuff on what an autoimmune disorder is, but I’ll review:

An autoimmune disease is a normal reaction of your immune system to a foreign invader that it either cannot kill or isn’t killable. Normally your immune system ‘turns on’ to an enemy attack (bacteria, virus…) and kills it. Should your initial immune response not be sufficient to kill the antigen (that which it ‘turned on’ against) it will gradually increase in intensity.

The initial ‘killer response’ is from the Th1 side of your immune response, which might be described as the SWAT team that does one thing and does it well: kill things. Should the Th1 response NOT be able to kill the pathogen, it will suppress, thus allowing the Th2 response to fire. The Th2 response is primarily responsible for making antibodies that ‘tag’ the antigen so the Th1 killer cells can find and destroy the enemy.

The above is a brief summary of a normal immune response. What can go wrong is if the immune response erroneously turns on against something it shouldn’t have – such as a heavy metal toxicity, an environmental poison, or some other non-living substance the patient was exposed to. Secondly, the immune system can turn on against something that just doesn’t die so easily. Common biotoxins (living organisms that can attack the body) that infiltrate endothelial tissue include: H. Pylori, Coxsackie virus, Chlamydia Pneumonia, Lyme, Cytomegalovirus, Gingivitis, Candida, Strep and Staph. All these little buggers can burrow into the endothelial cells and create an immune response. Since they have a way to go intra-cellular (hide inside the cell), the Th1 response has a difficult time finding them.

Over time, a ramped-up immune response does two things:

1. It destroys endothelial tissue (both receptors and entire cells) due to collateral damage in its attempts to kill the antigen, and
2. It starts to mistake self-tissue for the enemy and begins direct destruction.

A continual, low-grade immune response as seen in AED is very inflammatory and vasoconstrictive. We’ll go into more detail about this and give a various examples to ‘drive it home’.

Remember, this is a Heart Primer BUT this exact same process can/does occur in the vessels in the brain which causes TIAs and Strokes!

Schedule a time to speak with Dr. Conners HERE