It can. But you haven’t heard this. Why not? Because there are two competing models of atherosclerosis. The old model describes arteries as so many mechanical tubes that have no way to protect themselves from the inevitable clogging that comes from the consumption of cholesterol and saturated fat. The other, new model sees arteries as living dynamic tissue that, in the context of a healthy diet, is capable of growth, repair, and rising to the challenge of rigorous exercise.
Atherosclerosis is not a “buildup” of fat in your arteries.
You might have heard that fatty foods causes arterial fat deposits just like kitchen grease you rinse down the drain, which, over time, builds up to clog the pipe. When you have a clogged pipe you simply bust through the clog with a plumbing snake or Draino. It would make sense to treat your body this way were your arteries anything like the plumbing under your sink.
But your arteries are nothing like the plumbing under your sink, and using the term “blocked arteries” can be very misleading. Why is that? Because once you’ve got this misleading image of clogged plumbing in your mind, the router-router treatment (surgery, whether angioplasty or stenting) can seem like a valuable intervention to a prevent heart attacks or strokes. In reality, atherosclerosis is not simply a buildup of debris that can be scooped out. Atherosclerosis is the result of scar tissue formation within the wall of an artery. And so attempting to remove plaque, by way of surgical intervention risks damaging the weakened underlying tissue.
Before a patient undergoes angioplasty or stent placement, he is warned of potential complications of the procedure. Those complications include heart attack, stroke, and death. When will those complications occur? When the surgeon manipulates a damaged artery so that the integrity of the repair is compromised. In extreme cases, the risk of surgery is less than the risk of death from atherosclerosis. But in my opinion those cases are few and far between because most people with atherosclerosis can get better results without resorting to interventions that create permanent anatomical changes to the structure of your arteries.
Your body can recover from arterial damage by making two distinct types of accommodations.
First, it may bypass the damaged and narrowed artery by expanding existing collateral arteries supplying the same tissue, kind of like widening a highway to accommodate increased traffic into the city center. We see evidence of this occurring all the time when we do angiograms. Smoking or unhealthy eating makes it harder for your body to do this.
The second process is one in which the body actually heals the damaged section of artery. You’ve seen something very similar if you’ve ever gotten a deep cut in your skin down to the fat. First, a messy scab forms and, over time, typically 6 months or so, the skin around the injury grows inward to close the gap. Smoking and bad diet disrupt these processes as well.
Atherosclerotic plaque forms not from cholesterol build up but from arterial damage.
Sometimes I wish there were scientific validity to the cholesterol building up inside the pipe model; it’s so much easier to explain to people. In reality, however, the body is more complicated.
Plaques form inside arteries in locations where the artery was, at some point in the past, acutely damaged by deposits of highly irritating pro-inflammatory fats that splatter on the insides of your arteries. These splattered fats annoy the arterial lining cells that they’ve landed on. To remove these caustic chemicals, the defiled cells release a cascade of inflammatory signals that communicate their need for help. Specialized cells then arrive to remove the offending fats and get the inflammation in your arteries under control.
Time is of the essence here and the process is very delicately balanced because, if repairs are not made before a micro-hemorrhage tears the collagen supporting your artery, a deadly blood clot may form. (Pages 192-198 of Deep Nutrition gives a play-by-play pictorial of this process.)
You’ve probably heard of stable and unstable plaque in the context of discussions of atherosclerosis.
When the body is allowed to repair damaged arterial walls uninterrupted, it can produce a stable plaque, constructed of a robust coat of protein surrounding an ever-shrinking fatty core. This serves as a long-term fix until such time that the body can replace the patch with healthy arterial tissue.
In the context of a bad diet and/or smoking, this process is continually disrupted forcing the body to make due with suboptimal solutions. And so it cobbles together a tenuously thin protein coat surrounding the fatty core of the plaque. Much like an emergency repair made to a breached hull of a ship in high seas, this coating is a temporary fix only, and unlikely to last very long.
Stable plaques are not a threat to your health. But here’s the problem: Using the the tools currently available for diagnosing atherosclerosis in clinical practice, angiograms and carotid ultrasounds, there’s no way to tell if a plaque is stable or unstable. Therefore, since the cardiologists who I trust don’t recommend stenting a stable plaque, I’m not enamored with the idea of stenting on the basis of an angiogram alone.
The modern American diet is wrecking your heart.
The combination of excessive carb and vegetable oil intake creates the perfect chemical assault on your arteries. The time to take heart health seriously is now, before you are feeling any symptoms. To find how exactly how, read chapters Eight and Nine in Deep Nutrition. (Now available at a discount price on Amazon.com)
The five things you need to know about atherosclerosis: