Below is the full podcast episode and a shortened blog summary. I encourage you to listen to the full podcast for depth and inspiration from my human (non-AI) voice. It’s also available on your favorite podcast apps here (Apple, Spotify, etc.). 

Heart Disease in “Healthy” People?

In my clinic, I’m seeing more and more individuals—often in their 30s to 50s—diagnosed with heart disease. They don’t smoke, eat reasonably well, are active, and many are at normal weight with decent cholesterol numbers and other labs. Yet they show up with abnormal plaque scores or even full-blown heart attacks.

This isn’t just anecdotal anymore. A study from Cedars Sinai showed a 30% rise in heart attack deaths in the 25–44 age group—a trend that worsened after the COVID pandemic.

So what’s going on?

The Sinking Ship Analogy

Imagine heart disease like a sinking ship. Traditional risk factors like high cholesterol or high blood pressure are obvious leaks. But what if your ship is sinking from damage in less visible areas—like emotional stress, subtle biological imbalances, or immune dysfunction?

In this post (and podcast episode), I’ll walk you through overlooked risks I commonly see in younger patients with “surprise” heart disease—and how to spot and reduce them.

Case Study: Susan’s Surprise Plaque

Susan, 46, had no family history of early heart disease. She didn’t smoke, had no major risk factors, and was a healthy runner with a busy life as a tech exec and mom. Yet her heart scan showed plaque—something we should not see in someone her age.

Her labs were normal. Her lifestyle seemed ideal. But beneath the surface were powerful emotional and physiological triggers that helped us uncover her real risk.

Science Background: Why the Tunnel Walls Matter

We tend to focus on cholesterol particles (lipoproteins) in the blood because these are easily measured. But these are like boats floating through a tunnel—and we forget to look at the health of the tunnel walls, or what I call the endothelial cell lining (ECL).

Here’s how the system works:

  • Lipoproteins: Boats carrying cholesterol through the bloodstream.

  • ECL (Endothelial Cell Lining): Inner wall of the artery, like the tunnel surface.

  • Immune Cells: The repair crew that responds when the tunnel wall is damaged.

Even if your boats (cholesterol) are normal, a damaged or inflamed tunnel wall can spark plaque buildup and inflammation. An overzealous repair crew (your immune system) is often the culprit behind ECL damage.

The Concept of Arterial Flammability 🔥

I use the term “arterial flammability” to describe how vulnerable your arteries are to inflammation. If your ECL is “dry brush in a drought,” all it takes is a small spark, like the hidden or overlooked risks we’ll discuss, to start a fire.

Let’s explore the hidden sparks that make arteries more flammable. The podcast episode goes into more detail on each of these risks.

1. Genetic Vulnerability 🧬

Some people inherit fragile or inflammation-prone ECLs. While your parents may have lived into old age without heart disease, their lifestyles might have been less stressful (or at least less digitally stimulating), and more active. Modern habits can amplify genetic risk, even if your cholesterol is normal.

Key protective molecules like nitric oxide (NO) and KLF proteins (Kruppel-like Factor) help maintain healthy arteries. If your body makes less of these due to genes or lifestyle, your tunnel walls are more likely to be flammable.

 2. The Role of Variability 📉

We often obsess over averages—blood pressure, glucose, cholesterol—but it’s swings and fluctuations that can quietly cause damage.

a. Blood Pressure Variability (BPV)

Even with normal average blood pressure, wide swings in systolic BP are risky. A 2024 study in the British Journal of Cardiology found that BPV alone increased the risk of heart attacks and strokes.

If your systolic BP fluctuates more than 10–13 mmHg in older adults (or 7–10 mmHg in younger people), that’s cause for concern.

b. Glucose Variability

Even without diabetes, large glucose spikes and dips create oxidative stress and inflammation in the arteries. Tools like continuous glucose monitors (CGMs) can help reveal hidden patterns.

In Susan’s case, her average glucose was normal—but CGM revealed big swings, especially from chronic stress, overexercise, poor sleep, and often undernutrition.

c. Heart Rate Variability (HRV)

Low HRV reflects chronic stress and poor parasympathetic tone, and is associated with higher heart disease risk. It’s one of the most underappreciated metrics and is easily tracked with many wearables. Refer to an older blog post on HRV here.

 3. Aerobic Deconditioning 🏃‍♀️

Many patients are missing aerobic fitness despite doing “some” exercise. This isn’t about running marathons—it’s about keeping daily steps >6,000–7,000, maintaining good VO₂ max, and being able to climb stairs without feeling wiped out.

Low nitric oxide from sedentary living increases arterial flammability. Even light walking helps, but brisk, moderate-intensity activity is the sweet spot for getting a steady dose of nitric oxide.

Susan was extremely fit but overtrained. Running helped her cope with emotional stress, but overexercise without recovery can also increase arterial strain. Read my prior post on aerobic exercise here and on VO2 max here.

4. Emotional Risk Factors

A. Hurry (Schedule) Sickness

Many patients, especially high-functioning ones, suffer from a constant sense of being behind—rushing from task to task, even during downtime. I call this Schedule Sickness.

This chronic mental pacing keeps the sympathetic nervous system in overdrive, lowers nitric oxide, and fuels vascular inflammation. Multiple studies link perceived time pressure to higher blood pressure and heart risk.

B. Perfectionism

Not healthy ambition—but toxic perfectionism. The kind that tells you you’re not enough unless everything is flawless.

This creates:

  • Constant cortisol elevation

  • Poor sleep

  • Self-critical thought loops

And ultimately, it damages your blood vessels. In one study, 56% of suicide victims showed signs of external pressure to be perfect when friends and family of the victims were interviewed. It’s a silent, chronic stressor many never recognize until disease shows up.

5. External Triggers: Microplastics & COVID

  • Microplastics: Early research suggests they may harm endothelial cells through inflammation and oxidative stress. Avoid heating food or drinks in plastic containers when possible.

  • COVID: Even mild COVID infections can increase heart disease risk for up to 3 years. Repeated infections may further inflame arteries, especially when combined with emotional and metabolic stress.

What Labs Can—and Can’t—Tell You

Markers like hsCRP and myeloperoxidase (MPO) can suggest inflammation but aren’t always reliable. You can have normal labs and still be at risk which is often the case in my patients with surprise heart disease.

That’s why it’s crucial to look at patterns, not just numbers—especially variability and emotional health.

Final Thoughts

If this all sounds overwhelming, remember: you don’t need to chase every metric. Just increasing your aerobic fitness, managing your emotional stress, and improving recovery can positively impact many of these variables at once.

Susan, despite her athleticism, had missed the emotional piece. Like many patients, she defaulted to working harder and exercising more—easier than facing emotional discomfort.

But your inner voice, your schedule, and your expectations may be your most overlooked risk factors for chronic disease.