Four other facts about calcium in your arteries that I find fascinating:
Statins accelerate calcium build-up in arteries and on heart valves1
You can see considerable calcium deposits in the arteries of mummies from Egypt and other parts of the world
Warfarin (commonly used in treating atrial fibrillation, or AF – an abnormal heart rhythm) accelerates calcium build-up in arteries, due to its action as a vitamin K antagonist2
There is some reasonably strong evidence that vitamin K supplementation may slow, or possibly even reverse, calcium build-up in arteries
At the risk of going too far off-piste here, in vitamin K supplementation, as with many things to do with vitamins, the mainstream researchers have determinedly tested the wrong form. There are three forms of the vitamin (and probably more, but let’s go with three for now): K1, 2 and 3. K1 is often called phylloquinone, which is the one most tested while K3, often called menaquinone, has never been properly tested as a way of preventing or reversing calcification. ‘Overall, the available observational population-based evidence, based on dietary intake measures, suggests menaquinone [K3] intake may be more likely to protect against vascular calcification than phylloquinone intake. Yet currently, the only intervention studies have examined the effect of phylloquinone…’3
So, observational studies show that K3 is almost certainly the only K vitamin that provides protection but, with wearisome inevitability, it has not been studied in any clinical trial. Only K1 has been used. And this, I am afraid, is typical of mainstream medicine’s approach to vitamins. Start by failing to clearly define the ‘normal’ range of a vitamin – see especially vitamins D and B12, then give a very low dose of the wrong form of the vitamin and then claim that vitamins have no benefits whatsoever – on anything. Do I detect the dead hand of the pharmaceutical industry here?
Once you have done this you can move on to claim that vitamins are dangerous and damaging to health and then, to the sound of distant cheers from all pharmaceutical companies everywhere, ban them. Why? ‘Everyone need drugs. Everyone.’
Here is a clue about vitamins. ‘Vit’ is short for vital, as in vital for health. As in, if you don’t get a sufficient amount in your diet, you will die. As in … well, you get the idea. (Processed foods are often stuffed with synthetic vitamins, the natural ones having been destroyed in the manufacturing process. Oh well.) But more on vitamins later. Let’s get back to the main subject: atherosclerosis.
Atherosclerotic plaques are the underlying cause of heart attacks and strokes. They start life as fatty streaks in the middle sections, or media, of the artery walls and grow into plaques. This process starts early. When I say early, I mean early, as it is possible to see thickenings or fatty streaks in the arteries of foetuses within the womb.
The most dangerous phase of plaque development would seem to be the vulnerable plaque which, if it ruptures, can cause a complete blockage in an artery. This can happen in arteries throughout the body but most commonly affects the coronary arteries, which supply blood to the heart, or the carotid arteries, which supply blood to the brain.
Notes
1. https://www.ncbi.nlm.nih.gov/pubmed/25769003
2. https://www.ncbi.nlm.nih.gov/pubmed/26714212
3. http://advances.nutrition.org/content/3/2/158.long
HEART ATTACKS
The heart is supplied with blood by several different coronary arteries, which branch off at regular intervals. Let’s say there are four of them – not quite right, but it will do (some people have coronary arteries that others do not possess). The naming system is complex.
All the coronary arteries supply blood to different sections of the heart. The left anterior descending (LAD) artery, for example, supplies blood to the left ventricle that does the heavy lifting of pumping blood out of the aorta at high pressure. The LAD is, therefore, the most ‘mission critical’ artery in the heart although, obviously, they are all pretty important.
Classically, when you have a heart attack, one of the coronary arteries will suddenly get blocked by a blood clot. This usually happens when a vulnerable plaque ruptures. This, in turn, drastically reduces the blood supply and the area of the heart supplied by that artery can infarct, which is why heart attacks are often called myocardial infarctions (MIs) by the medical profession.
Most textbooks define an infarct as ‘death’ or ‘necrosis’ of heart muscle. However, this is simply wrong. It is true that a certain amount of heart muscle affected will die, and the remnants of dead cells will then be cleared away. But, assuming that you survive the MI, a repair process kicks into action to convert heart muscle cells (myocytes) into scar tissue. To repeat, infarction does not represent heart muscle death. Yes, some cells die, but most of them simply stop contracting in a desperate attempt to save energy. These cells are then converted into scar tissue, which requires very little oxygen to survive.
This is a tightly controlled process, ensuring that the basic structure of the heart remains intact. If this did not happen, an infarcted area of the heart would simply disintegrate, which would be instantly fatal. The infarction process was well described in the paper ‘Infarct scar – a dynamic tissue’:
Following MI, with loss of necrotic cardiac myocytes [dead heart muscle cells], a reparative process is quickly initiated to rebuild infarcted myocardium [rebuilding the area of heart damaged by sudden blood loss] and maintain structural integrity of the ventricle. A series of cellular responses are called into play driven largely by cell-cell signalling that serves to regulate tissue repair. Initially, inflammatory cells are attracted to and invade the site of injury … new blood vessels are formed (angiogenesis), and fibroblast-like cells appear and replicate. This early inflammatory phase of healing with resultant granulation tissue formation is followed by a fibrogenic phase that eventuates in scar tissue – a rebuilding of infarcted myocardium.1
Apologies for the jargon, but I thought it was worthy of full inclusion as I want you to know that we are most certainly not looking at a simple, passive process in MI. The infarcted area does not die. Instead it is reconstructed into scar tissue, but obviously this area of the heart cannot pump afterwards as it will be made of passive scar tissue, rather than healthy, contracting heart muscle cells (myocytes).
Sometimes, after an obstructive blood clot, the heart muscle does not infarct when the blood supply is lost. Instead, the affected area of heart muscle simply stops beating and enters a state known as hibernation. Just like in a hibernating bear, everything is still turning over, but at a very low rate. So, the myocytes are still alive but no longer contracting in order