A Harvard Health Letter (2019) publication says it’s indeed possible. It’s a great article, although I don’t agree with every view this article said about arterial plaque. 

Here’s one quote:

Making plaque disappear is not possible… 

I do agree with this. While you can’t make arterial plaque disappear entirely, “you can shrink it, you can stabilize it,” says Dr. Christopher Cannon, cardiologist and Harvard Medical School professor who was featured in the Harvard Health Letter. 

The key is lowering LDL. 

Now, here’s one part I disagree with the Harvard Health Letter. Here’s why. Half of the people who had a heart attack have normal LDL values, so how can lowering LDL be the key? The actual role of LDL (or “bad” cholesterol, as what some people will say) is debatable. 

How do you get the cholesterol out of the plaque? By lowering levels of cholesterol in the blood…

The Harvard Health Letter states that LDL cholesterol levels encourage the formation and growth of plaque.

However, if you look at people with genetically high cholesterol levels (like people with familial hypercholesterolemia), their levels are in the hundreds or more. They usually see no problems until they develop another cardiovascular (CV) risk factor, like smoking, having an inflammatory disease, or having insulin resistance.


The Danger of Arterial Plaque

Don’t get me wrong. When LDL cholesterol leaks through the artery wall and gets stuck, it can form harmful plaque. And this plaque puts us at risk for heart attack and stroke. 

Heart attack is the most common cause of death (especially in the US), while stroke is the most common cause of long-term disability. I haven’t even mentioned kidney disease, eye disease, and other conditions. That’s why plaque is a significant issue.

Development of Atherosclerotic Plaque

The Development of Atherosclerotic Plaque. Source: Rumberger JA. Cardiac CT With The Experts At Princeton Longevity Center.

While exceptionally high LDL cholesterol in the blood can be a risk factor, it’s not as critical as most folks would think. 

Unfortunately, our current culture in primary care medicine doesn’t recognize that fact. The physicians making up our medical community, the medical standards committees, the patients—none of them realize the importance of preventing plaque.

And that’s what our upcoming book, “PREVENTION MYTHS: Why a Stress Test Cannot Predict your Heart Attack—and the Tests that Can” is all about. It will tell you how to detect, measure, manage, and prevent plaque.

How Does Arterial Plaque Form?

I agree with Dr. Cannon and Harvard Health that plaque forms when LDL cholesterol gets stuck inside the artery wall. However, I think Dr. Cannon and Harvard Health skipped some critical parts. 

For example, how does cholesterol get into the walls of the artery? 

The Intima Layer

Plaque growth starts when there’s an injury in the inner lining of the artery wall. That endothelial, single-cell layer is what we will call the “intima.”

Layers of the Artery

Layers of the Artery. Source: American Stroke Association. Atherosclerosis and Stroke.

What could damage the intima?

One is high glucose, which causes about 80% of intima damage. This is an important fact as over half of Americans have prediabetes (Karlamangla, 2016). 

Sometimes, people can control their glucose level but at the cost of having high insulin. So, even with relatively low glucose, having high insulin levels can be a significant risk as well (Di Pino, 2019). 

We have an opportunity here for prevention. If we can prevent damage to the intima, we can prevent plaque. If we can prevent plaque, then we prevent all other diseases caused by plaque.

How do we prevent damage to the intima? 

For at least 80% of the time, the answer is by controlling glucose and insulin levels. Otherwise, maintaining intima health requires other interventions, like not smoking, controlling lipoprotein(a), and minimizing inflammatory diseases and other inflammation sources.

The Media Layer

Once LDL cholesterol has passed through the intima layer, it can be stuck between the intima and media layers. The media is the muscle cell lining of the artery wall. It keeps the arteries structurally intact. 

In the intima-media space, if more LDL particles get lodged, they can grow into a plaque. The body senses these deposits as “foreign matter.” It would then send white blood cells to the area.

Plaque In the Intima-Media Space

Plaque In the Intima-Media Space. Source: Aguiar-Souto, P. & González-Juanatey, José. Chronic Stable Angina: Pathophysiology and Clinical Manifestations.

Now, this is one important piece many people miss. As you see, CV events are not only about LDL cholesterol or plaque. There’s also inflammation that brings forth the most danger. 

But what is CV inflammation?

Cardiovascular Inflammation 

As I mentioned earlier, the body sometimes sets up an inflammatory reaction to the plaque in the artery walls

This is a dangerous situation. Immune cells (such as neutrophils and macrophages) can release enzymes to digest that plaque. In addition, they also release cytokines, chemicals that will attract other immune cells into the area.

So when a person has a heart attack or stroke, it’s not the plaque or LDL cholesterol itself that causes the event. It’s the inflammatory components from the white blood cells—the enzymes digesting the plaque and the cytokines further driving inflammation within the area of the plaque.

It’s sometimes easier to visualize this by looking at simple examples of inflammation. I did this video showing inflammation of the skin due to chemicals or psoriasis.


When Tim Russert, former host of “Meet the Press,” died of a sudden heart attack in 2008, the lining of his arteries demonstrated inflammation. The inside of Russert’s arteries were described as like the face of a teenager with acne.

Let me cover another subtle yet essential item—9p21. For those of you that have read or heard Brad Bale and Amy Doneen’s book “Beat the Heart Attack Gene,” they called 9p21 as the heart attack gene. This 9p21 gene increases the probability of muscle cells in the media layer to form a cap over the plaque.

Here’s part of the problem: We want a stable cap, but that’s not what you get if there’s inflammation. 

Inflammation turns fatty deposits into soft plaque beneath the cap, which is dangerous. If that cap breaks up, “hot” plaque could leak into the bloodstream and form a clot. That clot can get stuck in the heart (causing a heart attack) or in the brain (causing a stroke).

Clot Formed From Hot Plaque Could Cause Heart Attack or Stroke

Clot formed from hot plaque.

Prediabetes and CV Inflammation

Now we know the danger of CV inflammation. But what causes CV inflammation? 

At least 75% of CV inflammation is caused by type 2 diabetes and its predecessor, prediabetes. (Note that these conditions also damage the intima prior to plaque formation.) For simplicity’s sake, we also call prediabetes insulin resistance and metabolic syndrome.


Here’s the bad news. According to the CDC, 84% of prediabetes patients have no clue they have the problem (CDC, 2020). Ironically, prediabetes can be easily diagnosed with simple tests, like the oral glucose tolerance test (OGTT) with insulin survey.


How Does Arterial Plaque Shrink? 

We have been talking about plaque formation for now. But how does the shrinkage of arterial plaque happen?

According to Feig at al. (2016), these are the possible mechanisms by how plaque shrinks at the microscopic level:

  • There’s decreased retention of atherogenic apolipoprotein B within the arterial wall. Apolipoprotein B is the major protein component of VLDL, IDL, and LDL. (More on these terms in the “What are Lipoproteins?” section.) Because VLDL, IDL, and LDL are atherogenic (they form fatty plaques), the level of apolipoprotein B indicates the atherogenic potential of these lipoproteins.
  • Cholesterol and other toxic lipids flow out from plaques.
  • Foam cells (immune cells filled with cholesterol) are removed from plaque.
  • Phagocytes (healthy immune cells) remove dead tissue debris and other components of the plaque.

The Cholesterol Myth

If we’re going to deal with plaque reversal, we need to dispel the cholesterol myth—that cholesterol is the bad guy. 

I do agree with Dr. Cannon and Harvard Health that LDL is not as bad as we make it out to be. In reality, we need cholesterol to make different things, like vitamin D, hormones, bile, and cell membranes. 

Anyway, if cholesterol is indeed a bad guy, cutting it out of the diet wouldn’t work. Why? That’s because the liver produces 75% of the body’s cholesterol. When cells need more cholesterol, the liver just sends cholesterol to these cells through LDL particles. 

I have mentioned LDLs many times already. Before we describe what is an LDL, let’s talk about its bigger family—the lipoproteins.


Lipoproteins are complex particles (Feingold, 2016). They contain lipids (“lipo” means fat) and proteins. They have 2 parts:

  • a central hydrophobic (“water-hating”) core. Non-polar fatty substances stay in this core (e.g., cholesterol esters, triglycerides, other lipids).
  • a hydrophilic (“water-loving”) surface. This is where polar substances (like proteins) are found.

This is what a lipoprotein looks like:


Lipoprotein. Source: Feingold KR, Grunfeld C. Introduction to Lipids and Lipoproteins.

Types of Lipoproteins

According to Feingold (2016), lipoproteins are classified based on their size, lipid composition, and apolipoproteins. 

For this part, we’ll cover 5 classes. In order of decreasing size and increasing density, they are chylomicrons, VLDL (very-low-density lipoproteins), IDL (intermediate-density lipoprotein), LDL (low-density lipoprotein), and HDL (high-density lipoprotein).

Chylomicrons vs VLDL vs IDL vs IDL vs LDL vs HDL

Chylomicrons vs VLDL vs IDL vs IDL vs LDL vs HDL. Source: Source: Feingold KR, Grunfeld C. Introduction to Lipids and Lipoproteins.

Chylomicrons are large triglyceride-rich particles made by the intestine. (Most fats in our diet are triglycerides.) Chylomicrons carry triglycerides and cholesterol from what we eat, then carry them to the liver and body tissues. Note that the higher the fat content of our meal, the larger the chylomicron size.

VLDLs are smaller and denser than chylomicrons. They are also triglyceride-rich, and they are produced by the liver. Once muscles and adipose tissues remove triglycerides from VLDLs, these particles now become cholesterol-enriched IDLs. Chylomicron remnants, VLDL, and IDL are collectively called remnant cholesterol.

LDLs come from VLDL and IDL particles. They are more enriched in cholesterol. People usually call LDLs “bad cholesterol.” That’s because they carry cholesterol from the liver to the arteries, contributing to fatty buildups. However, note that the term “bad cholesterol” is a misnomer. 

Finally, the HDLs which are usually dubbed as the “good cholesterol.” Like in LDL, that term is also a misnomer. The role of HDL is the opposite of that of LDL. HDLs carry cholesterol away from arteries and back to the liver. 

The Importance of Lipoproteins

Lipoproteins are designed to take fats and break them into tiny particles. If the body doesn’t have these lipoproteins, fats could coalesce to form emboli (plural for “embolus”). These emboli can be lodged and stop circulation, which may cause a heart attack or a stroke like clots. 

The Role of HDL Cholesterol in Plaque Reversal

Until recently, we called HDL the “good cholesterol.” Many still call HDL by that name, but it’s also a misnomer. Recent information shows that calling HDL the “good cholesterol” (and LDL the “bad cholesterol”) is overly simplistic in terms of what is really happening.

Likewise, the concept of reverse cholesterol transport is excessively simplistic. Reverse cholesterol transport is the theory that HDL brings cholesterol back from the body to the liver to be digested, burned, or metabolized (Feig, 2016). 

Nowadays, many are saying it’s time to stop calling HDL the “good cholesterol” (Ward, 2018) Like Robert Rosenson, MD at Mount Sinai who said: 

HDL can be a good, bad, or neutral particle.

… and Matthew Budoff, MD at LA Biomedical Research Institute, who said: 

It is the number of HDL particles and not the cholesterol content that is important.

Budoff, however, is not yet ready to give up on the term “good cholesterol.” His point is that: 

For 95% of people, it is good. 

Plus, the concept is easier for many to understand.

Even though the reality is far more complicated than “good” and “bad” cholesterol, it’s valid to look at the positive impact of HDL on plaque and plaque reversal. There’s just too much scientific evidence to deny the role of HDL in plaque reversal (Feig, 2016).

What are the HDL-driven mechanisms for plaque stabilization and reversal? The mechanisms include:

  • Stimulation of reverse cholesterol transport from foam cells in the plaque.
  • Protection of the intima layer by activating the eNOS pathway. (eNOS is endothelial nitric oxide synthase, an enzyme that can synthesize nitric oxide, a gas that has several biological roles.)
  • Inhibition of LDL oxidation. 

Still, currently available clinical agents cannot stop most CV events. While HDL has been considered the “good cholesterol” for years, clinical intervention studies to causally link plasma HDL cholesterol levels to decreased progression or regression of atherosclerotic plaques are relatively few. 

That’s because of the lack of therapeutic agents that would selectively and potently raise HDL cholesterol. The negative results of these performed studies cast uncertainty on the role of HDL in atherosclerosis. 

It is becoming clearer, though, that HDL function rather than quantity is most crucial, and therefore, discovering agents that enhance the quality of HDL should be the goal.

LDL Cholesterol: The Old Standard Theories Vs. New Thoughts

Harvard Health (2019) says too much LDL cholesterol in the blood lodges within artery walls and forms plaques. That’s why people (and even most standard-bearers in medicine) still call it the “bad cholesterol.” Same with HDL being called the “good cholesterol” for carrying cholesterol away from the arteries.

Again, I don’t agree 100% with this statement. This is an old theory. I will tell you there are a lot of reasons they think of that, but it’s complicated. The explanation is more than that. 

Suppose someone died from a heart attack or stroke. When you open the artery during an autopsy, most of the plaque will be oxidized LDL. Do you know what else we can find there? Remnants of inflammation, like cytokines, and inflammatory biomarkers like TNF alpha, myeloperoxidase, and Lp-PLA2.


Let me just say that LDL particles are the ones you’ll find oxidized as plaque. However, such plaque isn’t harmful… until it gets inflamed. 

As mentioned in the “Cardiovascular Inflammation” section, CV inflammation (usually from prediabetes) produces these soft plaques. As discussed in the “How Does Arterial Plaque Form?” section, the body’s immune system attacks plaque, leaving fluid and inflammatory cells. In short, it’s inflammation that makes plaque unstable. 

How We Reversed Arterial Plaque—True Stories

According to Dr. Cannon (Harvard Health, 2019): 

If we have a 30% blockage in the artery from soft plaque, the goal is to try to suck out the cholesterol from the inside so the plaque shrivels down to 15% and leaves nothing inside it.

That’s a great goal. (And the CIMT or carotid intima-media thickness test is one excellent screening technique that can demonstrate this.) 

Are there true-life examples of people actually reversing plaque? 

Yes. I’ll cover 3 stories of significant plaque reversal: mine, John Lorscheider’s, and Gerry Kurth’s.  You’ll see that there are patterns.

How Did I Reverse My Arterial Plaque

Despite a disciplined lifestyle, I still had arterial plaques in my mid-50s. Those plaques were due to significant prediabetes. My prediabetes was, in turn, due to significant genetic and epigenetic challenges.

In the most popular video on our YouTube channel, I told my own story. I reversed my arterial age by roughly 20 years in just 18 months!

How did I do it? 

The pattern was the same I see over and over with my patients. I tried many things. 

But I started making significant permanent changes when I began restricting carbs. I went down to a variable amount between 50 and 100 grams of carbs per day. That resulted in a decrease in hunger. I was able to lose about 10 pounds, going from 165 lbs to 155.

I added some supplements, such as niacin. I added omega-3 supplements to the frequent salmon in my diet. 

I also made a few medication changes. 

For instance, I switched blood pressure meds. I switched from an ARB (Losartan) to an ACE inhibitor (Ramipril). There is debate over this issue, but most scientific evidence indicates that ACE inhibitors are better than ARBs at decreasing CV inflammation. (And anyone with high blood pressure or plaque is at high risk for CV inflammation.) 

Either way, the ACE inhibitors and ARBS are related classes. Both are better at CV inflammation management than other standard blood pressure drug classes, such as diuretics, beta-blockers, and calcium channel blockers.

I’d be amiss if I didn’t admit this—I’d always been a statin hater. I still am. It’s my opinion that most statin prescriptions cause more harm than benefit. 

So, to summarize, my pattern was similar to others. I discovered I had prediabetes. So I restricted my carbs. (This decreased my appetite.). I lost significant weight (10 pounds). I added some supplements and changed med prescriptions to the right statin and ACE inhibitors.

Here’s the main article where I covered the story of how I reversed 20 years of arterial plaque.


And here’s the follow-up article.


I’m 63 now, and my arterial age is still 53. I have gained back a lot of weight but am still staying low on carbs. My waist remains at 32 inches. I’ve been doing a lot of resistance training because I’m approaching my mid-60s. Once we reach our mid-60s, muscle mass loss becomes one of the most significant risk factors for heart attack and stroke (Volpi, 2004).

How Did John Reverse His Arterial Plaque 

John Lorscheider reversed his calcium score by 59%. 

John followed a similar pattern that I’ve described before. He discovered he had type 2 diabetes. His blood sugar hit 290 on a Kraft insulin survey, so he restricted his carbs. John lost 40 pounds; he did not appear heavy when we last met. 

Moreover, he added some supplements and made adjustments to his prescriptions. His blood pressure dropped so much when he lost the weight, we had to take him off his BP meds. Since he had plaque, he decided to stay on a statin; he switched to low-dose rosuvastatin.


How Did Gerry Reverse His Arterial Plaque

Gerry followed the familiar pattern. He discovered he had type 2 diabetes, so he restricted his carbs. He lost weight, added some supplements, and made adjustments in his prescriptions. He took ACE inhibitors and low-dose statins.

Gerry’s nickname is Quanticus; he loves to quantify things. You can see that as he tells his story. He provides detail in his history that very few patients or doctors can provide.


The Calcium Score Paradox

Patients will often come to see me because they had a positive calcium score. They forget that soft plaques don’t show up on a calcium score—calcium score is only indicative of stable, hardened, calcified plaque. And it’s the soft plaque which we should be worried about. 

Then why do we look at a calcium score

Because we can see that there is a correlation between calcified plaque and CV risk. If you’ve got a lot of calcium, you have a much higher risk of heart attack and stroke.

But if calcium indicates plaque is stable, why does a higher calcium score usually mean a higher risk?

In a patient with an incomplete plaque history, higher calcium scores usually mean higher risk. A higher calcium score means the arteries have already been through several cycles of laying down plaques, inflaming those plaques, and calcifying and stabilizing those plaques.

I have plenty of patients who’ve been through that cycle. They’ve come out the other end. They feel great. They feel fine. They’re very comfortable with where they need to be and knowing that their plaques are now stable.

Why does that become an issue? 

Patients often come to see me really worried. “Oh Doc, I had a calcium score; it was over a thousand. I’m going to die.” However, there are certain obstacles we must get over (and here’s where that hump is). 

We discover that they have undiagnosed prediabetes. We should get them a better lifestyle, supplement, and medication regimen. We advise them to lose weight. We get the carbs out of their diet. If we get all these things under control, then they can start stabilizing their plaque.

What happens to their calcium score? 

Well, they go back and repeat the calcium score. They can’t help it. I tell them not to do that, but they do it anyway. Instead of dropping, the calcium score often sees an increase. They were expecting to do a victory lap. They struggle to remember what I’ve warned them. “Look, once you calcify that soft plaque, you’re going to stabilize it.”

Expect such a situation. It occurs regularly with my patients. Don’t panic if you get an increase in your calcium score. You may have some decrease. But calcium, once it’s in there, usually doesn’t entirely go away.

At this point, the best goal is not to get rid of plaque and calcium completely. Your goal must be to stabilize plaque. And stable plaques do not cause a heart attack or stroke.

Can You Reverse Hardened Arteries?

“I have plaque in my arteries. I want to reverse it. What do I do next?”


Note that arterial plaque is very common. It increases with age. 

From the images below, it’s clear that 40% of women and 75% of men have a positive calcium score by age 55. That means they’ve already had CV inflammation and soft plaques. Calcified plaque is stable. That means they have stable plaque in their arteries.

Calcium Score Distribution in Men

Typical steps for plaque reversal include significant weight loss and first-time statin use. You see these in the above 3 examples: John, Gerry, and me.

Can you reverse hardened arteries?

It’s not practical for most people to reverse hardened plaque as seen in a calcium scan, much less eradicate it. It would be like eliminating scars on the skin. Reversing soft plaque and inflammation, though, is a possibility. Soft plaque is much more likely to be reversed than calcified plaque.

However, everyone should expect that they can stabilize their plaque. And that’s almost as good. Stable, calcified plaque doesn’t create the risk of heart attack and stroke with soft plaque. That was demonstrated in the Honda study.


How to Reduce Arterial Plaque 

Here’s the critical difference between Harvard Health’s position and mine. They say the key is lowering levels of cholesterol in the blood. I would say stop the injury to the intima, that recurring inflammation, that recurring glucose and insulin spikes.

Statins Can Help

Statin prescriptions are not as simple as most doctors think. Most doctors look at age and LDL levels. They don’t look at plaque, CV inflammation, or glucose levels. Gain, note that half the people having heart attacks have normal LDL values. So it doesn’t take significant logic to realize that something else is going on.

I rarely prescribe Lipitor (atorvastatin), yet most doctors go straight to it. Here’s why I don’t. The goal for statins in most of my patients is not to decrease cholesterol (except for a few of my familial hypercholesterolemia patients nervous about their higher LDL levels).

The actual goal here is to decrease CV inflammation. We want to get that liquid and those inflammatory immune cells out of the plaque. And once that has happened, we want to safeguard against its return.

Even if you’re a statin hater, you can’t change the wealth of objective scientific evidence showing that statins help. Despite that statement, I still think most statin prescriptions do more harm than good. 

Lipitor lowers LDL, as most statins do. However, Lipitor has less impact on inflammation than other statins. To make things worse, it increases insulin resistance. It worsens the root cause—prediabetes or insulin resistance—in the vast majority of cases.

Be aware that Lipitor is not the only statin that worsens prediabetes. All of them, with one exception, increase diabetes risk. That exception is Livalo (pitavastatin). The manufacturer knows this and currently priced Livalo far higher than most statins.

High-dose statins create a much greater risk for insulin resistance than a low dose. And low-dose statins work very well for decreasing inflammation. So, most of my patients are on Livalo (pitavastatin) or low-dose Crestor (rosuvastatin).

Crestor in doses of 5mg/day or less has an excellent preventive effect on CV inflammation. But it doesn’t drive prediabetes. We often spread the doses to twice per week. Even weekly doses of Crestor have shown a positive impact on people that just didn’t tolerate statins.

Consider Supplements & Other Medications

Many people are comfortable taking supplements but not medications. 

Take red yeast rice as an example. It is a favorite of many folks. It is a supplement that was the precursor of statins. Like statins, it blocks HMG CoA reductase, the liver enzyme that promotes cholesterol production. People who prefer red yeast rice assume this supplement can provide the benefits without the risk of statins.


I can see the logic of preferring red yeast rice. But I think this makes more sense for those taking high-dose statins for the wrong reasons. You should know that you can get benefits with less risk with just a low dose of the right statin.

Other supplements for plaque reversal include vitamin D3, niacin, berberine, bergamot, and cinnamon. Vitamin D3 can support immune function. Niacin improves LDL, HDL, triglycerides, and Lp(a). Bergamot is also an HMG CoA reductase inhibitor, like statins and red yeast rice.


Harvard Health finishes its article by saying that ezetimibe (Zetia) can inhibit cholesterol absorption in the digestive tract. Do I agree? Yes. But again, we’re not highly focused on cholesterol. Recent information, though, indicates that ezetimibe in combination with statins has a significant impact on CV inflammation (O’Riordan 2019).

We also use ACE inhibitors when possible for blood pressure management. That’s because ACE inhibitors have a positive multiplicative effect on CV inflammation, especially when combined with statins.

Monitor and Control Your Glucose Metabolism

With prediabetes and diabetes occupying a central role in terms of plaque reversal, you should know what is your blood glucose level and how you metabolize carbs. 

You may also need to monitor excessive body fats. We used to think fat was inert, harmless energy storage tissue. But research over the past decade has shown that it is anything but true. Excess body fat causes a lot of problems. It causes insulin resistance, which causes high glucose, high insulin, and early heart attacks, deaths, and strokes.

My recommendations here: Control your glucose metabolism. Measure your blood sugar levels. Make sure you know what you have.

I’ve heard this once, and I’ve heard it a thousand times. “Doc, I know you look at glucose, but my doc has been looking at this for years. I’ve been watching him, and I don’t have prediabetes or diabetes.” 

Here’s the thing. Until you’ve had a Kraft insulin survey, or at least an OGTT with insulin response, you won’t know that. Alternatively, you can do glucose tolerance tests at home or use a fingerstick glucometer.


You can also use a continuous blood glucose monitor, like Freestyle Libre or Dexcom G6. However, both devices require a prescription. Insurance companies don’t pay for these unless you have documented serious diabetes, so doctors rarely understand why you might want to try these. (Contact us if you’d like to get a prescription for these devices.)


Manage Your BMI Realistically

Even if you think you’re as muscular as Arnold Schwarzenegger, you should target a BMI in the low 20s. At one point, his BMI was as high as 30, even though he had very little fat. 

Many men think their high BMI is because of a lot of muscle. When Arnold had that increased BMI and low fat, he was Mr. Universe. If you look like Mr. Universe, maybe you really do have the Schwarzenegger effect. 

Keep Your Muscle Mass High 

Loss of muscle mass is a big killer, especially beyond age 65.

By the time we reach age 65 (and after age), there’s a lot of science that would suggest that our major risk factor is the loss of muscle mass. As you might imagine, that correlates with increasing insulin resistance. Insulin resistance, in turn, drives plaque formation and CV inflammation. And it’s inflammation and the things associated with it that can kill us.

Sleep Is Critical

Get at least 7.5 hours of good sleep. If you’re having problems with this, focus on:

  • Sleep hygiene;
  • Exercise (HIIT and resistance training especially);
  • Not using pills. (Even OTC sleeping aids are associated with falls in the night, and long-term inability to sleep.)

Take Care of Your Oral Health 

Did your gums ever bleed when you went to the dentist? Chances are you have a problem. 

If your gums bleed when you go to the dentist, you should get checked for arterial plaque and prediabetes. Around half (47%) of adults 30 years and older have periodontitis (Eke, 2012). The most common cause of periodontitis is prediabetes.


Explore Autophagy and Intermittent Fasting

Many haven’t heard of the term “autophagy.” But breaking it down into two components helps—“auto” means “self,” and “phagy” means “to eat.” 

Think of autophagy on a cellular level. Parts of the cell are dissolved, digested, and used for new cell parts’ energy and components. In short, autophagy is recycling at a cellular level.


Multiple articles, journals, studies, and scientists have described the role of autophagy in health. (de Cabo, 2019; Sun, 2018). They’ve researched biomarkers such as MTOR, IGF-1, and other biomarkers that are a part of this picture. 

Scientists are now on a search for supplements that stimulate autophagy. Candidates include resveratrol, berberine, and even black market forms of rapamycin (Easter 2019)

Is rapamycin a “fountain of youth” pill that can reverse plaque?

This happens all the time. There is a search for a magic pill. A candidate is found, but it has dangerous side effects. Still, there will be plenty of risk-takers that will try it. 

Rapamycin is one of those drugs. It is supposed to be a “fountain of youth” pill. A veritable fountain of youth would be worth the significant risks. But the major mechanism for rapamycin is simply to stimulate autophagy.


Again, there is a better, safer, faster, and cheaper way in terms of lifestyle—fasting is the ultimate stimulus for autophagy. 

Long considered a fringe activity, intermittent fasting became mainstream with a science review article in the New England Journal article on December 26, 2019 (de Cabo, 2019). 

In this article, the authors re-analyzed old data used to support caloric restriction. They found much of the benefit due to recurrent fasting episodes. They showed that the time has come for physicians and other medical professionals to understand and use intermittent fasting and other fasting types for their patients.


The Verdict

There is too much scientific evidence to deny that arterial plaque can be reversed. Yet many prominent cardiologists deny it.


You don’t have to spend time over arcane academic or scientific articles, though. Just go to our videos. If you’d like a more well-known name, how about Harvard Health? There are multiple Harvard Health Letters describing plaque reversal on a very understandable level.

I’d debate a few of the finer points with Harvard Health authors, though. But we agree that certain people have reversed their arterial plaque. We also agree that the stabilization of arterial plaque is a far more practical goal for most of us.

My name is Ford Brewer. My team and I work to prevent heart attack, stroke, cancer, and dementia. Our goal is to help you understand how to prevent major killers and disablers. Most of them are driven by the process of cardiovascular inflammation. 

If you want to know more about the science of preventive medicine or you have questions about certain aspects of your health, check out our webinars, membership programs, and online courses

If you’d like to learn about the basics of heart attack & stroke prevention for free, complete this form, and get access to our CV inflammation course. If you’re interested in other ways of how we can help you, check out our services page


Aguiar-Souto, P. & González-Juanatey, José. Chronic Stable Angina: Pathophysiology and Clinical Manifestations. Revista Espanola de Cardiologia Suplementos. 2010;11-21. doi: 10.1016/S1131-3587(10)02003-0. 

American Stroke Association. Atherosclerosis and Stroke. American Stroke Association website. https://www.stroke.org/en/about-stroke/stroke-risk-factors/understanding-risky-conditions/atherosclerosis-and-stroke. Last reviewed December 5, 2018. Accessed November 15, 2020.

Brewer F. Cardiovascular Inflammation and Plaque Formation. PrevMed website. https://prevmedhealth.com/cardiovascular-inflammation-and-plaque-formation. Accessed November 10, 2020.

Brewer F. Does Niacin Work? The Great Niacin Debate. PrevMed website. https://prevmedhealth.com/does-niacin-work-the-great-niacin-debate. Accessed November 13, 2020.

Brewer F. How to Test for Cardiovascular Inflammation. PrevMed website. https://prevmedhealth.com/how-to-test-for-cardiovascular-inflammation. Accessed November 13, 2020.

Brewer F. More Important Than LDL? The Triglyceride/HDL Ratio. PrevMed website. https://prevmedhealth.com/more-important-than-ldl-the-triglyceride-hdl-ratio. Accessed November 10, 2020.

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