The Longevity Podcast: Optimizing HealthSpan & MindSpan

Atherosclerosis, Unmasked

• Dung Trinh

Share episode

Send us a text

We trace the life cycle of atherosclerosis from quiet plaque buildup to sudden artery-closing clots that cause heart attacks, strokes, bowel infarction, and limb ischemia. We share clear warning signs, risk checks, imaging options, lifestyle moves, and modern therapies that change outcomes.

• why plaque forms and why it ruptures
• how one mechanism drives four major diseases
• cardiac, brain, gut, and leg warning signs
• transient ischaemic attack as an urgent red flag
• physical clues including pulses, bruits, and ABI
• key labs LDL, HDL, triglycerides, HbA1c, hsCRP, Lp(a)
• imaging with coronary calcium scoring and carotid ultrasound
• prevention through smoking cessation, diet, and weight control
• medications statins, ezetimibe, bempedoic acid, PCSK9 inhibitors
• antiplatelet risks and benefits
• when and how procedures restore blood flow
• the role of ultra-processed foods in rising risk

If you experience chest pain, stroke-like symptoms, severe abdominal pain after meals, or leg pain at rest with cold toes, contact a doctor immediately


This podcast is created by Ai for educational and entertainment purposes only and does not constitute professional medical or health advice. Please talk to your healthcare team for medical advice.

Never miss an episode—subscribe on your favorite podcast app!

SPEAKER_00:

You know, if you're looking for the uh the single biggest driver of modern mortality, the one chronic condition that quietly defines how long and how well we live well, you've found it.

SPEAKER_02:

It really is. It's the root of the problem for so many things that seem disconnected. We're talking heart attacks, strokes.

SPEAKER_00:

And today we are diving deep into that root, atherosclerosis. The silent, simmering disease that is, without a doubt, the number one cause of death and disability across the industrialized world.

SPEAKER_02:

It's a systemic issue and understanding the um the core mechanics of how it starts is really the first step toward managing your own health long term.

SPEAKER_00:

Absolutely. And to guide us through this, we've got some truly authoritative sources today, straight from Harvard Health. The materials reviewed by Dr. Christopher P. Cannon, who's the editor-in-chief of the Harvard Heart Letter.

SPEAKER_02:

So we're getting the definitive roadmap here.

SPEAKER_00:

We are. Okay, so let's unpack this. Our mission is to strip away the complex jargon and really understand the story of atherosclerosis. What is it exactly? Why does it strike in so many different parts of the body?

SPEAKER_02:

And what new tools do we have right now to prevent it and to treat it?

SPEAKER_00:

Exactly. We want you to walk away from this understanding the invisible forces at play inside your own circulatory system.

SPEAKER_02:

Okay, so to start at the very beginning, let's just define the term. Atherosclerosis is fundamentally this chronic, slow process of plaque building up inside the walls of your artery.

SPEAKER_00:

Your body's plumbing.

SPEAKER_02:

Your body's plumbing, yeah. The critical pipes carrying oxygen-rich blood everywhere it needs to go. Plaque is the gunk that builds up on the inside of those pipes day after day, year after year.

SPEAKER_00:

And when we say plaque, this isn't just some kind of you know generic sludge. What are the main ingredients in this highly dangerous cocktail?

SPEAKER_02:

Well, the primary ingredient is cholesterol, specifically the kind that comes from low density lipoproteins, the dreaded LDL cholesterol.

SPEAKER_00:

The bad one.

SPEAKER_02:

The bad one. But it's not just fat. These claques are actually complex mixtures. They include smooth muscle cells, fibrous tissue, and often calcium. It gets hard and sticky.

SPEAKER_00:

And it narrows the artery.

SPEAKER_02:

It narrows the artery, choking off blood supply to essential organs. We're talking the heart, the brain, even your digestive system.

SPEAKER_00:

Aaron Powell Okay, so that narrowing, that sort of chronic starvation of tissue, that's bad enough. It causes long-term issues. But that's usually not the sudden catastrophic event, right?

SPEAKER_02:

No, not at all. The narrowing is the slow-moving chronic phase. The real risk is the acute crisis.

SPEAKER_00:

And this work gets, I think, really interesting. The source material makes it so clear that this plaque, it's not just sitting there. It's not a static obstruction.

SPEAKER_02:

It's a ticking volatile time bomb. That is the crucial insight.

SPEAKER_00:

So what's the trigger?

SPEAKER_02:

The most dangerous step in the whole process is when that fatty fibrous plaque ruptures or cracks. Think of it like breaking open a volval capsule inside the artery wall.

SPEAKER_00:

And the body's response.

SPEAKER_02:

The body panics. It activates its emergency response, the clotting cascade, right there at the site of the damage.

SPEAKER_00:

Which is designed to stop bleeding. But in this case, it forms a blood clot, a thrombus, inside the artery itself.

SPEAKER_02:

Precisely. And while the plaque may have only narrowed the pipe by, say, 70%, that thrombus that forms can completely block the remaining 30% in a matter of minutes.

SPEAKER_00:

Total blockage. And that means the organ supplied by that artery suddenly starves for blood and oxygen.

SPEAKER_02:

That's it. That rapid tissue death or severe injury, whether it's in the heart causing a heart attack or in the brain causing a stroke, it's fundamentally the same mechanism.

SPEAKER_00:

It's just about the location of the ruptured plaque.

SPEAKER_02:

It's staggering, really. One underlying pathology can manifest in such a huge range of massive health problems. The sheer scope of diseases coming from atherosclerosis is immense.

SPEAKER_00:

So let's break down those four primary disease pathways, the material outlines. Let's start with the one everyone thinks of the heart.

SPEAKER_02:

Right. Coronary artery disease, or CAD. This is when the arteries feeding the heart muscle itself get narrowed. At first, it leads to chest pain or angina, especially when you exert yourself. But if that plaque ruptures and fully blocks one of those coronary arteries, that's a heart attack.

SPEAKER_00:

Okay. Then we shift dramatically to the brain. We hear about different kinds of strokes, but atherosclerosis is the villain behind the most common kind.

SPEAKER_02:

It is. About 75% of strokes in industrialized countries are what we call thrombotic strokes. And again, it's the exact same pattern. A thrombus forms inside a brain artery that was already damaged and narrowed by plaque.

SPEAKER_00:

Cutting off that vital blood supply.

SPEAKER_02:

And that rapid oxygen loss causes the specific neurological damage that we define as a stroke.

SPEAKER_00:

What's truly counterintuitive to me is the link to the digestive system. Most people just don't think about clogged arteries causing stomach pain.

SPEAKER_02:

It's a huge, often missed piece of the puzzle. When the arteries that supply your intestines narrow, it creates pain because your digestive system needs a massive surge of blood to process a meal.

SPEAKER_00:

So if the flow is restricted.

SPEAKER_02:

The symptoms are very particular, a dull or cramping pain that usually starts 15 to 30 minutes after you finish eating.

SPEAKER_00:

And if that blockage is sudden and total?

SPEAKER_02:

Then you're looking at a bowel infarction, which is as severe as it sounds. The source material calls it effectively a heart attack, but in your intestines. Severe pain, vomiting. It's a crisis.

SPEAKER_00:

Finally, let's go to the legs, the furthest extent of the circulatory system. This is where the condition causes peripheral artery disease, or PA.

SPEAKER_02:

Right, and PA is often misunderstood. People just dismiss it as getting old, but it's severe atherosclerosis. It's usually narrowing the major arteries of the legs, like the femoral and popocheal arteries.

SPEAKER_00:

And the main symptom.

SPEAKER_02:

The Hallmark symptom is something called intermittent claudication. It's a crampy, painful feeling in your calf or thigh muscles that starts when you walk or exercise, but, and this is key, it eases immediately when you rest.

SPEAKER_00:

So we have this silent process happening for decades, and its impact is felt across every major organ system, which explains why it's so hard to catch, because it often flies completely under the radar.

SPEAKER_02:

That's right. This disease can be developing for years with no noticeable symptoms at all. It's only when the blood supply drops to a critical level that the body starts sending out distress signals.

SPEAKER_00:

Okay, so let's break down those signals. What does it actually feel like when the heart is screaming for more oxygen?

SPEAKER_02:

For the heart, you know, beyond that classic chest pain or angina, the body can react with a whole cluster of serious symptoms. We're talking shortness of breath, unusual sweating, a sudden wave of nausea, feeling dizzy or lightheaded, even palpitations.

SPEAKER_00:

Aaron Powell All signs the heart muscle is under severe duress.

SPEAKER_02:

Exactly. Due to not getting enough blood.

SPEAKER_00:

And when the brain is the organ being choked off, the symptoms become neurological.

SPEAKER_02:

They do. You see sudden functional deficits, dizziness or confusion, weakness or even paralysis that strikes one side of the body, sudden severe numbness.

SPEAKER_00:

Vision problems, too, right?

SPEAKER_02:

Yes, visual disturbances, even abrupt loss of vision, or problems with coordination difficulty, walking, staggering, slurred speech.

SPEAKER_00:

And the source material highlights a critical warning sign that you absolutely cannot ignore, even if it goes away on its own.

SPEAKER_02:

That would be the transient ischemic attack or TIA. This is when those exact stroke-like symptoms appear, the slurred speech, the numbness, but then they disappear completely within an hour or so.

SPEAKER_00:

It's temporary. The physical damage is temporary, but the event itself is an enormous warning sign. It means a clot formed and luckily dissolved, but that unstable underlying plaque is still there. It's a five-alarm fire.

SPEAKER_01:

Let's go back to those unusual abdominal symptoms. What kind of pain are we listening for?

SPEAKER_00:

It's described as dull or cramping, and the timing is the key. 15 to 30 minutes after eating, usually in the middle of the abdomen. If it's severe, acute pain with vomiting or swelling, you have to think about that sudden blockage, the bowel infarction.

SPEAKER_02:

And in the legs, what does it look like when it goes beyond just cramping when you walk?

SPEAKER_00:

If the narrowing gets really extreme, the pain will start happening even at rest, often at night, and you'll see visible signs of tissue starvation. The feet and toes get cold, the skin might look pale or even bluish, and you often see hair loss on the legs because the follicles aren't getting enough circulation.

SPEAKER_02:

Those are all major alarm bells.

SPEAKER_00:

Profoundly reduced blood flow. That gives us a really clear picture. But the good news is we have sophisticated ways of detecting this long before a crisis hits. So let's pivot to how doctors look for this and how you can identify your own personal risk profile.

SPEAKER_02:

It always starts with a thorough medical review. Doctors were looking for family history. Did a parent or sibling have heart disease at a young age, a history of high cholesterol, and then of course the lifestyle factors smoking, diet, exercise.

SPEAKER_00:

Aaron Powell And the physical exam itself goes much deeper than just the standard vitals.

SPEAKER_02:

Oh, absolutely. Beyond blood pressure and heart rate, doctors are manually checking pulses in your neck, wrists, groin, and feet to assess the strength of the blood flow. But crucially, they use a stethoscope to listen for uh brutes.

SPEAKER_00:

Brutes, okay, that's a term we don't hear every day. What does that sound actually signify?

SPEAKER_02:

Think back to our plumbing analogy. Brutes are the rough, whooshing sound of turbulent blood flow. It's like a hiss. It's the sound of blood trying to rush past a serious obstruction in the artery.

SPEAKER_00:

So if a doctor hears that, it's a major red flag.

SPEAKER_02:

It's a key clinical sign that plaque is causing major interference. They also compare the blood pressure in your legs to the pressure in your arms.

SPEAKER_00:

And that comparison brings us to a really powerful, simple diagnostic tool, the ankle brachial index or ABI.

SPEAKER_02:

The ABI is fantastic. It's non-invasive and it gives you a hard number. It's just the ratio of the blood pressure at your ankle to the pressure at your elbow. In a healthy person, the pressure should be about the same or even a little higher in the angle.

SPEAKER_00:

So if that ratio is off.

SPEAKER_02:

If the pressure in your ankle is significantly lower than your arm, specifically an ABI of 0.9 or lower, it's a clear, quantifiable sign of impaired circulation. It means the plumbing below the waist is clogged.

SPEAKER_00:

Beyond the physical exam, blood markers give us a huge snapshot of what's brewing silently. What are the key things to track on our annual blood work?

SPEAKER_02:

Well, the standard lipid panel is first total LDL and HDL cholesterol plus triglycerides. We also tracked fasting blood sugar and HBA1C for diabetes risk, which is a massive accelerant for atherosclerosis.

SPEAKER_00:

But the source material also highlights a few more specific tests.

SPEAKER_02:

It does. Things you might want to ask your doctor about, like HSCRP, which is a marker for general inflammation in your body, and another one is LPA or lipoprotein. It's a particularly sticky, fatty particle that's independently linked to a higher risk of heart attack.

SPEAKER_00:

Okay, so we have the history, the physical findings, the blood markers. If those start to look concerning, the next step is to get a visual confirmation.

SPEAKER_02:

That's where imaging comes in. The calcium score test is a CT scan of the heart that measures calcium buildup in the coronary arteries. Calcium is a definitive sign of long-term atherosclerosis. For the brain, a carotid ultrasound can look for plaque in the arteries supplying the head.

SPEAKER_00:

This all brings us to the proactive side. So what does this mean for controlling this condition? Let's start with prevention, because the material really stresses that its progression can be delayed and even halted.

SPEAKER_02:

Prevention starts and ends with lifestyle. It sounds obvious, but the most essential step is simple. Avoid smoking entirely, or if you do smoke, you must quit. Smoking just directly damages the arterial lining and accelerates everything.

SPEAKER_00:

And then we move to diet and weight, which seems so directly linked to the ingredients in that arterial gunk.

SPEAKER_02:

It is. Maintaining a healthy weight is vital, especially avoiding fat around the waist. Diet-wise, the focus should be on fruits and vegetables and a strict avoidance of saturated and trans fats.

SPEAKER_00:

What about cooking oils?

SPEAKER_02:

The recommendation is clear. Stick to monounsaturated oils like olive oil and polyunsaturated oils, like sunflower or canola. And your protein should mostly come from fish and plant sources like soy, beans, and legumes.

SPEAKER_00:

The source also provides some really actionable timelines for checkups, which I find incredibly useful.

SPEAKER_02:

They do. If you have no existing problems, get your cholesterol checked every five years starting at age 20, blood pressure checked every two years. And if you're overweight or have high blood pressure, start getting fasting blood sugar checked every few years starting at age 45.

SPEAKER_00:

The goal is to catch the risk factors while there's still just risk factors.

SPEAKER_02:

Before they become advanced plaque.

SPEAKER_00:

Exactly. If lifestyle isn't quite enough, that's when medicine comes in. And treatment, the material confirms, can effectively slow or halt the worsening of the disease. The cornerstone is lowering that dangerous LDL cholesterol.

SPEAKER_02:

And that means statins. Drugs like a torvostatin or symvostatin, they're the workhorses. Their mechanism is ingenious. They block the H and G CoA reductase enzyme, which is basically the control switch for cholesterol production in the liver.

SPEAKER_00:

Aaron Ross Powell So the liver just produces less cholesterol.

SPEAKER_02:

Simple as that.

SPEAKER_00:

But what's fascinating is that science has moved beyond just statins. We now have treatments that attack the problem from completely different angles.

SPEAKER_02:

That's what's so promising. We have non-statin drugs with varied mechanisms. For example, isidema works in your gut. It blocks cholesterol absorption from food. Then there's bempadoic acid, which tells the liver to make less cholesterol, but through a different pathway than statins.

SPEAKER_00:

And finally, the most advanced class. The PCS-Canine inhibitors.

SPEAKER_02:

Yes, the PCS-Canine inhibitors. These are revolutionary. They dramatically increase the number of LDL receptors on the surface of your liver cells. Think of those receptors as little vacuum cleaners.

SPEAKER_00:

More vacuums, more cleaning.

SPEAKER_02:

More vacuums means the liver can grab that circulating bad cholesterol out of the bloodstream much, much faster. It's incredibly effective.

SPEAKER_00:

Beyond cholesterol, we also have to think about the risk of the clod, that acute trigger.

SPEAKER_02:

Right, which brings in anti-clotting medications like aspirin and other antiplatelet drugs. These reduce the likelihood of a thrombus forming, but there's a vital warning here. Because they inhibit clotting, they increase the risk of bleeding. So that requires a very careful medical assessment.

SPEAKER_00:

And finally, for the most severe cases where an organ is already compromised, we have the physical interventions.

SPEAKER_02:

These are procedures to immediately restore blood flow. For the heart, we have angioplasty, often with a stent to keep the artery open, or bypass surgery. The same techniques are used for blocked abdominal or leg arteries.

SPEAKER_00:

And for the brain.

SPEAKER_02:

If the critical carotid arteries are dangerously narrowed, a procedure can be done to physically clear or open that artery to prevent a stroke.

SPEAKER_00:

That really brings together the entire life cycle of this condition, from the molecules to the high-tech solutions.

SPEAKER_02:

The key takeaway is that while there is no cure, the prognosis is better than ever. People are living significantly longer with better quality of life because we can delay the beginning and worsening of the disease, even for those with a strong genetic predisposition.

SPEAKER_00:

So, what does this all mean for you? The disease operates silently for years, but when those distress signals finally appear, that crampy leg pain, chest discomfort, sudden vision loss, you have to act.

SPEAKER_02:

The instruction is immediate. If you experience these symptoms, contact a doctor immediately. Waiting even a few hours when symptoms are acute is what turns a manageable chronic problem into a life-threatening crisis.

SPEAKER_00:

And this leads us to a final thought for you to consider, pulled directly from the recent research accompanying our source material. The dramatic rise in atherosclerosis over the last century perfectly aligns with a dramatic shift in our global diet.

SPEAKER_02:

Specifically ultra processed foods.

SPEAKER_00:

Exactly. And given that these foods have recently been linked directly to claque buildup in neck arteries, what does that imply for the future prevalence of this chronic disease in rapidly industrializing nations that are just now enthusiastically adopting this same Western dietary model?

SPEAKER_02:

Something to chew on.