How I Reversed 20 years of Arterial Plaque

Arterial plaque can be removed from artery walls, contrary to the widespread medical belief that it cannot be reversed, as evidenced by the speaker's own CINT imaging showing progression from artery age 73 in February 2015 to artery age 52 within two years of targeted intervention.

“today we're going to talk about removal of plaque from artery walls and uh, everybody knows you can't do that, right? Well, that's not right. Actually, I'm a poster boy for getting plaque out of my artery walls.”

In inflamed arteries, small dense LDL particles lose the ability to pass through the media layer after penetrating the intima layer, unlike in non-inflamed arteries where LDL passes straight through both layers, based on recent research by Brad Bale, Amy Donine, and David Vigorist.

“Normally LDL this uh the small dense LDL particles can go through this inima layer and then when they do they'll go straight on through the media layer. in uh arteries that have inflammation, they lose the ability to pass through this media layer. That's um research by the way that's only just a couple of months old. It was done by a mentor and friend Brad Bale uh along with Amy Donine and um David Vigorist.”

Flow studies such as angiograms and stress tests are inadequate for early intervention because they do not detect arterial disease until there is 50% occlusion, at which point blood flow is still minimally compromised, whereas plaque deposition and inflammation begin much earlier.

“so that's why flow studies like uh angogs and um stress tests are way too late. They don't really look at doing any kind of intervention and they're intervention or or surgery focused and they don't look at that until you get a uh 50% occlusion. As you can see, this is uh this with this kind of plaque, you still have very little occlusion.”

Inflamed plaque, not stable waxy plaque, causes heart attacks; when immune cells attack plaque and release enzymes, the resulting liquid plaque can breach the intima and contact blood, forming clots that occlude coronary arteries; over 90% of heart attacks result from clots derived from liquid plaque, not from stable plaque alone.

“This shows another thing, too. It shows inflamed plaque. What is inflammation of plaque? Inflammation of plaque is where your immune system attacks it. White cells go in or immune cells go in with antibodies. They release enzymes.”

The speaker switched from an ARB (angiotensin II receptor blocker) to the ACE inhibitor Ramipril for high blood pressure management; ACE inhibitors reduce inflammation and the process by which arteries lay down plaque in addition to lowering blood pressure, similar to statins in having effects beyond their primary indication.

“One was um Ramipril. I had high blood pressure. I was on an ARB. I switched to an ACE inhibitor. Uh we've mentioned that before. We'll mention that again in other videos. ACE inhibitors like statins do more than what they're prescribed for. ACE inhibitors are prescribed for high blood pressure. They actually decrease inflammation. That process that causes arteries to lay down plaque.”

Low-dose statin therapy (5 mg Crestor) reduces inflammation and plaque deposition without impairing glucose metabolism at lower doses, whereas higher statin doses carry increased risk of metabolic side effects; the speaker believes low-dose statin therapy was the most impactful intervention in achieving plaque reversal.

“Um I had been avoiding taking statins like most of my patients because of the side effects that I'd heard of. Uh I went ahead bit the bullet and took Crestor. Took a very low dose of Crestor um 5 milligrams. I could take a lower dose. Uh the lower doses impact inflammation. They don't impact diabetes at the lower doses.”

The speaker personally had genetic risk factors for cardiovascular disease including the 9p21 genetic variant (heart attack susceptibility gene on chromosome 9), the 4q25 variant (associated with atrial fibrillation and increased heart attack and stroke risk), and the ApoE3/3 genotype, in addition to high blood pressure and insulin resistance.

“I had some genetic challenges. I had 9p21. 9 stands for the number of the chromosome. You know, we got 23 chromosomes in there, 23 pairs. uh nine has a section on it uh called u p21 which has a lot of heart attack gene problems and in fact if you look at Brad and Amy's book beat the heart attack gene that's the one they're talking about 9P21 I also have 4q25 that one again on the fourth chromosome is really called an atrial fib gene”

Stable waxy plaque is relatively inert and does not directly cause heart attacks, whereas liquid plaque associated with inflammation is unstable and prone to rupture, leading to thrombosis and acute coronary events.

“This is what causes a heart attack. Not this. This is a waxy stable substance. This is a liquid.”

The 4q25 genetic variant, located on chromosome 4, is primarily associated with atrial fibrillation susceptibility, and current evidence suggests it also carries risk for myocardial infarction and stroke.

“I also have 4q25 that one again on the fourth chromosome is really called an atrial fib gene my mother has atrial fib I have atrial fib we um have some um predisposition for that with that genetics. It's not all just atrial fib though. Current evidence is beginning to indicate that it also has some risk associated with heart attack and stroke as well.”

Cracks in the intima layer of arterial walls can be detected via microalbumin creatinine ratio testing, and these cracks allow liquid plaque and inflammatory mediators to breach into the bloodstream and form intramural and luminal thrombi.

“This is plaque and the inima has a few cracks in it. We actually look at that when we're looking for um microban creatinine ratio. [clears throat and cough] That's one of our tests for inflammation. I'll talk about that in another video. But you see here this hot liquid plaque has leaked into the u bloodstream and this is a clot.”

The speaker mentions that plaque progression and risk can be visualized on ultrasound or imaging as a spectrum ranging from minimal plaque in healthy arteries to extensive plaque in disease, and the relationship between plaque burden and arterial flow obstruction is nonlinear (minimal flow impairment until deep levels of plaque are present).

“Let's look at it in terms of plaque progression. This end this end of the picture is a normal healthy artery with very little plaque. As you see it progressed, you get more and more plaque. One of the things you may notice is that the flow is not compromised until there is a way uh deep level of plaque here.”

Despite practicing exemplary preventive medicine including a plant-based diet, regular exercise, and following standard health recommendations throughout his career as an ER doctor and director of preventive medicine programs, the speaker still developed arterial plaque by age 57 with artery age 73, indicating that lifestyle measures alone are insufficient to prevent cardiovascular disease in genetically predisposed individuals.

“I'd always been the um the poster boy for good uh heart attack and stroke lifestyle. Uh nobody expected me to have that. Um I started off as an ER doc very early in my early 20s. Got very frustrated in seeing uh too many early heart attacks. Went to John's Hopkins to learn prevention and ended up running the program in prevention. I've uh taught a couple of the past presidents of the uh American College of Preventive Medicine... Good diet, good lifestyle, good exercise, all according plant-based diet, all according to the standard recommendations.”