Editor’s note: Wellness Word is an informational column which is not meant to replace a healthcare professional’s diagnosis, treatment or medication.
The cause of heart attacks – Part 1
Stop what you are doing for a sec and count to forty.
That’s about how long it will take for the next heart attack to happen in this country. This approximate rate will continue non-stop, every hour around the clock, 24 /7, for 365 days, and about every fifth one will result in death. That’s a lot of people.
What is particularly unfortunate, however, is the fact that nearly every single one could be prevented. Almost 800,000 heart attacks occur in a year, and, aside from fairly rare instances, most should never even happen.
Now pause again and think about this number: $20,000,000,000. That is the approximate worth of the cholesterol-lowering drug industry this year, and that many zeros equals a lot of pills. You might wonder why if high cholesterol causes plaque in arteries, and that causes heart attacks, how can there be that many heart attacks every year if so many people are taking those drugs?
The short answer is this: cholesterol-lowering drugs do not sufficiently treat the primary cause of heart attacks. Unless we use an approach that fully addresses the cause or causes of a disease, we should expect the disease to continue showing up regardless of how fancy and technologically advanced our band-aids get. Heart attacks are a primary example of this painfully accurate medical dictum.
Think about this issue from a different perspective.
If cholesterol, in and of itself, were the primary cause of cardiovascular disease, there should be no variable circumstances, but these two questions refute that. 1) Why do people get plaque build up in their arteries, but not in their veins? 2) Why don’t other animals in the wild, with similar or higher cholesterol levels than we have, get cardiovascular disease?
If you look at the answers to these questions in more detail, you will see they call into question the very foundation of the conventional, medication-based treatment approach currently in use, and begin to point towards the need for an additional explanation as to what is going on. More importantly, exploring these questions helps point towards a more effective solution to this most pressing of medical problems.
Blood samples for cholesterol levels are always taken out of veins and yet these very blood vessels don’t get plaque in them like the arteries do whose blockages lead to heart attacks.
Simple logic would suggest then that high cholesterol, in and of itself, cannot be the direct cause of plaque forming in a blood vessel, or it would form in veins just like it forms in arteries.
Animals in the wild, with similar or higher cholesterol levels don’t get cardiovascular disease. The cholesterol levels of brown bears in the wild vary during the year between about 250mg/dL and 425mg/dL.
In other words, most card-carrying cardiologists would prescribe them a fairly hefty dose of a statin at the low end, and at the high end, at least a few would walk them hand in paw, straight to the treadmill for a stress test. In fact, no brown bear in the wild has ever been found to have any plaque in their arteries at all.
Simple logic applied here would suggest that high cholesterol, in and of itself, cannot be the direct cause of plaque forming in arteries and heart attacks occurring from that.
So why is the number one therapeutic intervention for heart attack prevention a cholesterol lowering drug?
I am not suggesting that cholesterol has no role in plaque and heart attacks at all. Cholesterol is, of course, a primary ingredient of plaque. The bottom line is this: if, under average circumstances, cholesterol carrying molecules are going to enter into the walls of your arteries and lead to plaque growing there, the conditions in and around those arteries must have allowed for it.
When looked at this way, we can explain both of the above questions.
• Conditions in veins must be different in some way than they are in arteries, which allows for the cholesterol carrying molecules floating around in both vessels to lead to trouble in one, but not the other.
• Conditions in the arterial systems of bears must be different as well, leading to them being apparently resistant to the impact of cholesterol, regardless of how high it is.
The cause of heart attacks must then be considered multi-factorial, with perhaps an equally important aspect influencing resistance to them being the conditions in and around the blood vessels, and not just the level of cholesterol carrying particles in the system.
If we are to be as thorough as possible in our efforts to prevent heart attacks, we should not stop at lowering cholesterol. In fact, that should be a secondary focus, with the primary focus instead being the conditions which allow for it to become a problem.
Daniel Chong, is a licensed ND who can be reached at 503.893.4364/drdanielchong.com
