The Missing Link in Heart Disease: Inflammation, Not Just Plaque

Join Dr. James Odell for Season 2 of the Science of Self-Healing Podcast! He's the medical and executive director for BRMI, as well as a practicing naturopathic doctor for over 35 years, and he's here to share with you his extensive knowledge of medicine from a different perspective.

The Bioregulatory Medicine Institute

The Science of Self-Healing Podcast

For decades, heart disease has been framed as a problem of clogged arteries and cholesterol numbers. But what if that story is incomplete?

In this episode of The Science of Self-Healing, we explore the missing link in cardiovascular disease: chronic inflammation. Far beyond a simple plumbing issue, the heart is an immune-responsive organ—constantly shaped by stress, environmental toxicants, infections, and the invisible pressures of modern life.

You’ll discover how chronic stress rewires immune signaling, why air pollution and heavy metals quietly inflame the cardiovascular system, and how infections can leave lasting inflammatory scars on heart tissue long after symptoms fade. I’ll discuss the biology behind endothelial dysfunction, arrhythmias, heart failure, and plaque instability—and why inflammation is now recognized as the common thread connecting them all.

This episode also explores what the science says about restoring healthier cardiac terrain: key inflammatory biomarkers to watch, the role of omega-3s and anti-inflammatory fats, the overlooked importance of thiamine and mitochondrial support, and lifestyle practices that activate the heart’s natural anti-inflammatory pathways.

If you’ve ever felt that conventional heart health advice doesn’t tell the whole story, this conversation offers a new lens—one that shifts the focus from symptom suppression to understanding why the heart becomes vulnerable in the first place.

Because heart disease isn’t just about plaque. It’s about inflammation, environment, and terrain.

Transcript: The Missing Link in Heart Disease: Inflammation, Not Just Plaque

Hello, everyone, and welcome to the Science of Self-Healing podcast. For health and wellness knowledge from a different perspective. Produced by the Bioregulatory Medicine Institute, also known as BRMI. We are your source for unparalleled information about how you can naturally support your body's ability to regulate, adapt, regenerate, and self-heal. I'm your host, Dr. James Odell, the medical and executive director for BRMI, as well as a practicing naturopathic doctor for over 35 years. And remember, this podcast is for informational purposes only and is not intended to be a substitute for the direct care of a qualified health professional who oversees and provides unique and individual care. The information here is to broaden our different perspectives and should not be construed as medical advice or treatment. Let's get started.

Understanding Inflammation: Your Body's Double-Edged Sword

Hello everyone, and welcome to another episode of The Science of Self-Healing. I'm so glad you're here today because we're diving into a topic that affects virtually all of us—how everyday factors like stress, environmental toxins, and infections can fundamentally change the landscape of our hearts and blood vessels.

Now, I want to start with a concept that might surprise you: your heart isn't just a mechanical pump. It's actually an immune-responsive organ that's constantly communicating with your environment. And today, we're going to explore how that communication can go awry—and more importantly, what we can do about it.

Let's begin with inflammation itself. You've probably heard this word thrown around a lot, but what does it actually mean for your heart?

Think of inflammation as your body's emergency response team. When you cut your finger or catch a cold, inflammation is what mobilizes immune cells to the site, increases blood flow to bring in resources, and promotes healing. It's actually a beautiful, adaptive process that's designed to protect you.

The problem starts when this emergency response never shuts off. When inflammation becomes persistent, dysregulated, or excessive, it's like having emergency sirens blaring 24/7—it transforms from a healing process into a destructive one.

In your cardiovascular system—that's your heart and all your blood vessels—chronic low-grade inflammation is now recognized as the underlying driver of nearly every major heart condition. We're talking about atherosclerosis, which is the hardening and narrowing of your arteries, hypertension or high blood pressure, scarring of the heart muscle called myocardial fibrosis, heart failure, irregular heartbeats or arrhythmias, and even blood clots that can lead to strokes.

Here's something fascinating: we used to think of atherosclerosis as simply a plumbing problem—you know, like pipes getting clogged with fat. But we now understand it's actually an immune-mediated inflammatory process. What happens is that the inner lining of your blood vessels, called the endothelium, gets injured. This triggers a cascade of events: immune cells called monocytes get recruited to the site, they transform into macrophages—think of these as cellular vacuum cleaners—and they start releasing chemical messengers called cytokines. Meanwhile, the smooth muscle cells in your vessel walls start multiplying. It's a whole inflammatory cascade.

And similar processes happen right within your heart muscle itself, leading to structural changes—we call this remodeling—and impaired ability of the heart to contract effectively.

Your Heart's Hidden Immune System

Now, let me share something that might challenge what you learned in biology class: your heart is not immunologically inert. In other words, it's not just sitting there passively pumping blood.

The cells that make up your heart—the cardiomyocytes that do the actual contracting, the endothelial cells that line your blood vessels, fibroblasts that provide structural support, and even immune cells that live right there in the tissue—all of these participate in immune signaling.

Under inflammatory conditions, these cells start producing cytokines, which are chemical messengers that tell other cells what to do, chemokines that attract more immune cells, and reactive oxygen species—essentially these are damaging molecules that create oxidative stress. Together, these molecules alter the very architecture of your heart tissue and change how electrical signals travel through your heart.

Over time, this inflammatory signaling literally reshapes your heart's structure. It thickens the walls, stiffens the chambers so they can't fill properly, and disrupts the conduction pathways that coordinate your heartbeat. Imagine trying to conduct an orchestra when the musicians keep changing positions and the acoustics of the hall keep shifting—that's what's happening in an inflamed heart.

The Biology of Stress: More Than Just "In Your Head"

Alright, let's talk about stress. And I want to start by saying this: stress is not just in your head. It's not "all emotional," and it's definitely not something you should just ignore or push through.

Chronic psychological stress activates two major systems in your body. The first is the hypothalamic-pituitary-adrenal axis—let's just call it the HPA axis for short. The second is your sympathetic nervous system, which is essentially your body's gas pedal. When these systems fire up, they flood your body with stress hormones: cortisol, adrenaline, and noradrenaline.

Now, in short bursts, these hormones are incredibly adaptive. They're what help you run from danger or perform under pressure. But here's the problem: chronic activation—when these systems are running all the time—leads to immune dysregulation and inflammation.

What happens is your cells can develop something called cortisol resistance. Normally, cortisol has anti-inflammatory effects, but when your cells stop responding to it properly, those anti-inflammatory effects diminish. Meanwhile, pro-inflammatory cytokines—the chemical messengers that promote inflammation—start to dominate.

At the same time, this sympathetic overdrive increases your heart rate, raises your blood pressure, and makes your heart muscle demand more oxygen—all while it's already dealing with inflammation. It's like forcing an injured athlete to keep running a marathon.

Research has shown that chronic stress increases circulating levels of several inflammatory markers. Let me mention a few: C-reactive protein, or CRP, interleukin-6, which we abbreviate as IL-6, and tumor necrosis factor-α, or TNF-α for short.

These cytokines aren't just markers—they're active participants. They contribute directly to endothelial dysfunction, which means the inner lining of your blood vessels stops working properly. They destabilize the plaques in your arteries, making them more likely to rupture and cause a heart attack. And they contribute to that remodeling of heart muscle we talked about earlier.

But wait, there's more. Stress also changes which immune cells are traveling through your bloodstream and where they go. It promotes a shift toward pro-inflammatory phenotypes—basically, it trains your immune cells to be more inflammatory—and these cells then infiltrate your heart and blood vessel tissue.

The Autonomic Nervous System: Your Body's Balancing Act

Now, let's talk about something called autonomic balance. Your autonomic nervous system has two branches: the sympathetic system, which is your accelerator, and the parasympathetic or vagal system, which is your brake.

Stress skews this balance toward sympathetic dominance—your foot is always on the gas—while suppressing parasympathetic or vagal tone. This is a big problem because vagal activity actually has anti-inflammatory effects. When you have reduced vagal activity, you lose those anti-inflammatory signals, and you also impair something called heart rate variability.

Heart rate variability is the natural variation in time between heartbeats, and it's actually a good thing—it shows your heart can adapt. Low heart rate variability is strongly associated with increased cardiovascular mortality. So when stress suppresses your vagal tone, it creates an electrophysiological environment—an electrical environment in your heart—that's prone to arrhythmias and sudden cardiac events.

Environmental Toxicants: The Invisible Threat

Let's shift gears now and talk about something you might not immediately connect to heart health: air pollution.

Air pollution represents one of the most pervasive and underestimated cardiovascular risk factors. We're particularly concerned about fine particulate matter, which scientists call PM2.5 because the particles are 2.5 micrometers or smaller—that's about 30 times smaller than the width of a human hair.

These tiny particles are so small they penetrate deep into your lungs and actually enter your systemic circulation—they get into your bloodstream. Once there, they trigger oxidative stress and immune activation. These particles stimulate those macrophage cells we talked about earlier, as well as endothelial cells, to release inflammatory mediators that accelerate atherosclerosis and impair how your heart muscle functions.

Repeated exposure leads to chronic vascular inflammation, increased arterial stiffness—your blood vessels literally become less flexible—and something called microvascular dysfunction within the heart, which means the tiny blood vessels that feed your heart muscle don't work properly.

Over time, this inflammatory burden contributes to ischemia, which is inadequate blood flow, hypertension, and heart failure—and this can happen even in individuals without traditional risk factors like high cholesterol or family history.

Heavy Metals: Silent Saboteurs

Now let's talk about heavy metals—substances like lead, mercury, cadmium, and arsenic. These exert cardiotoxic effects, meaning they're literally toxic to your heart, by disrupting mitochondrial function and something we call redox balance.

Let me explain mitochondria for a moment. These are the powerhouses of your cells—they produce ATP, which is essentially cellular energy. Mitochondria are particularly vulnerable to damage because they have high oxidative activity and limited repair capacity. It's like they're working at full throttle all the time with minimal maintenance crew.

When heavy metals induce mitochondrial dysfunction, several things happen: ATP production goes down, so your cells have less energy; reactive oxygen species increase, creating more oxidative damage; and inflammatory pathways get activated.

This metabolic stress impairs the ability of cardiomyocytes—your heart muscle cells—to contract effectively. It also promotes fibrosis, which is basically scarring of the tissue. Over time, this gradually reduces cardiac efficiency and resilience. Your heart has to work harder to do the same job.

Emerging Concerns: Microplastics and Endocrine Disruptors

We're also learning about newer threats. Emerging research has identified microplastics and endocrine-disrupting chemicals as contributors to cardiovascular inflammation.

These compounds interfere with hormone signaling—they essentially act as hormone imposters in your body. They disrupt calcium homeostasis, which is critical for heart muscle contraction, and they interfere with immune regulation.

In cardiac tissue, they may promote oxidative injury, endothelial inflammation, and abnormal coagulation—meaning your blood's clotting system doesn't work properly. These are subtle changes, but they alter cardiac terrain over decades. They're playing the long game with your heart health.

Infections: Direct and Lasting Impact

Now let's talk about infections, which remain a direct and potent cause of cardiac inflammation.

Viral myocarditis occurs when viruses directly infect cardiomyocytes or trigger immune-mediated injury. Basically, either the virus damages the heart cells directly, or your immune system's response to the virus causes collateral damage. The resulting inflammation can be transient—it comes and goes—or it can progress to chronic cardiomyopathy, which is a disease of the heart muscle.

Bacterial infections such as endocarditis inflame the heart valves and surrounding tissue. This leads to structural damage, embolic events where pieces break off and travel through the bloodstream, and systemic immune activation. Even when the acute infection is resolved and you feel better, residual inflammation may persist, predisposing your heart to long-term dysfunction.

Here's something really interesting: beyond acute illness, chronic low-grade infections can perpetuate systemic inflammation. Persistent immune activation places continuous stress on cardiovascular tissues.

Scientists have actually identified molecular remnants of bacteria and viruses within atherosclerotic plaques—those buildups in your arteries. This suggests that infectious burden contributes to plaque instability and acute coronary events like heart attacks.

In some cases, infections can even initiate autoimmune responses in which your immune system mistakenly targets cardiac tissue. This phenomenon highlights the delicate balance between immune defense and self-tolerance—your immune system's ability to distinguish between invaders and your own tissue. It underscores how infections can permanently alter cardiac terrain even after the pathogens themselves are cleared from your body.

The Convergence: How It All Comes Together

So here's the big picture: stress, toxicants, and infections converge on shared biological pathways that amplify inflammation.

One of the most important is endothelial dysfunction. Inflammation impairs the production of nitric oxide by your endothelium—that inner lining of blood vessels. Nitric oxide is crucial because it promotes vasodilation, meaning it helps your blood vessels relax and widen. When you don't have enough, your vessels can't dilate properly, and you're more prone to thrombosis, which is clot formation. Endothelial dysfunction is a unifying feature of hypertension, atherosclerosis, and heart failure.

The reality is that traditional cardiovascular risk models—the tools doctors use to predict your risk—often underestimate the contributions of inflammatory factors. We focus heavily on cholesterol, blood pressure, smoking, and family history. But incorporating inflammatory biomarkers, environmental exposure histories, and stress assessments may significantly improve early detection and prevention.

A Path Forward: Addressing the Inflammatory Heart

So what do we do about all this? Addressing the inflammatory heart requires a multifaceted approach. We need to think about reducing environmental exposures, managing chronic stress, supporting immune regulation, targeting oxidative stress, and treating underlying infections.

Measuring Inflammation: Key Biomarkers for Heart Disease

Let me tell you about some key biomarkers of inflammation—these are measurable indicators in your blood that can tell us what's going on.

First, we look at elevated levels of C-reactive protein, or CRP. This is a systemic inflammatory marker that's associated with cardiovascular disease, autoimmune disorders, and chronic inflammation in general.

We also measure increased concentrations of pro-inflammatory cytokines. Remember those chemical messengers we talked about? These include tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). When these are elevated, it indicates ongoing inflammatory processes.

A higher erythrocyte sedimentation rate—ESR for short—and increased white blood cell count, or WBC, suggest higher immune activation. Basically, these tell us your immune system is working overtime.

There are other inflammatory markers we can measure too: serum amyloid A, fibrinogen, procalcitonin, and lipid peroxidation products with names like F1-isoprostanes and malondialdehyde. These tongue-twisters are all associated with chronic inflammation and oxidative stress.

Natural Anti-Inflammatory Support

Now let’s talk about what you can actually do. Research shows that omega-3 polyunsaturated fatty acids are among the most effective natural agents for reducing degenerative inflammation. As our understanding has evolved—particularly the recognition that vascular inflammation underlies coronary artery disease—fish and fish-oil supplementation has been endorsed by the American Heart Association for cardiovascular prevention.

Just as important, however, is what not to consume. Pro-inflammatory seed oils can counteract these benefits, making it essential to reduce “bad” oils while intentionally increasing high-quality, anti-inflammatory fats. In short: avoid inflammatory oils, and prioritize the right ones.

Let me explain how these good oils work. The active ingredients in fish oil are eicosapentaenoic acid—EPA—and docosahexaenoic acid—DHA. These enhance the conversion of an enzyme called COX to prostaglandin E3.

Now, prostaglandin E3 is a natural anti-inflammatory agent. It competitively inhibits the effects of arachidonic acid conversion to prostaglandin E2, which is a highly inflammatory substance. Think of it like this: prostaglandin E3 and prostaglandin E2 are competing for the same parking spots in your cells. When E3 takes the spot, the inflammatory E2 can't park there.

Prostaglandin E3 also inhibits the synthesis of TNF-α and IL-1β—those inflammatory cytokines we mentioned earlier. Additionally, EPA and DHA can inhibit something called the 5-LOX pathway, which converts arachidonic acid to inflammatory substances called leukotrienes, also through competitive inhibition.

Another powerful natural anti-inflammatory is curcumin, which comes from Curcuma longa, a flowering plant of the ginger family that you probably know as turmeric. This has been used for centuries in both Ayurvedic and Chinese medicines as an anti-inflammatory agent, a treatment for digestive disorders, and to enhance wound healing.

Several clinical trials have demonstrated curcumin's antioxidant, anti-inflammatory, and antineoplastic effects—that last one means it may help prevent abnormal cell growth. Curcumin is known to inhibit inflammation by suppressing NF-κB, which is a master regulator of inflammation. It restricts various activators of NF-κB as well as stemming its expression, essentially turning down the volume on inflammatory signaling.

We also have proteolytic enzymes—these are enzymes that break down proteins. Examples include serrapeptase, bromelain, and nattokinase. These target inflammatory processes through three primary mechanisms.

First, they scavenge reactive oxygen species, or ROS. The enzymes neutralize these damaging molecules, thereby reducing oxidative stress and inhibiting the activation of inflammatory cytokines at the transcription level—basically stopping them before they're even made.

Second, they directly degrade circulating inflammatory cytokines. These proteolytic enzymes break down pro-inflammatory cytokines that are already floating around in your bloodstream, leading to reduced systemic inflammation.

Third, they prevent cytokine release by degrading receptors involved in exocytosis. That's the process cells use to secrete substances. By degrading these receptors, the enzymes inhibit cytokine secretion and the downstream inflammatory signaling that follows.

Now, I want to highlight something particularly exciting about nattokinase. Recent research has shown that nattokinase has potent fibrinolytic activity—that means it can break down fibrin, which is the protein that forms the mesh-like structure of blood clots. But here's what's really interesting: studies suggest that at fairly high therapeutic doses, nattokinase may actually help clean out arterial deposits over time.

We're talking about taking it consistently for about a year or longer. What appears to happen is that nattokinase helps break down the fibrin that's often found within atherosclerotic plaques, potentially helping to reduce plaque burden and improve vascular health. This isn't an overnight fix—it's a gradual process of supporting your body's natural ability to clear vascular debris. But for people looking for natural approaches to supporting cardiovascular health, this is one of the most promising interventions we have. Of course, if you're on blood thinners or have bleeding disorders, you'd want to work closely with a healthcare provider before using nattokinase at these higher doses.

Coenzyme Q10, specifically ubiquinol, supplementation may also offer benefits, potentially improving symptom severity and reducing hospitalizations for people with heart conditions.

Now, let's talk about something that's often overlooked but absolutely critical: thiamine, also known as vitamin B1. I mentioned it briefly in the context of diuretics, but thiamine deficiency deserves much more attention because it's far more common than most people realize, and it has profound effects on heart health.

Thiamine is essential for cellular energy production. It's a cofactor for several enzymes involved in glucose metabolism and ATP production—remember, ATP is that cellular energy currency we talked about earlier. Your heart is one of the most metabolically active organs in your body, beating about 100,000 times per day, so it has enormous energy demands. When you don't have adequate thiamine, your heart literally doesn't have the fuel it needs to function properly.

Thiamine deficiency can lead to a condition called wet beriberi, which manifests as high-output cardiac failure. In this condition, the heart actually pumps more blood than normal, but the body's tissues can't use oxygen efficiently, leading to fluid accumulation, shortness of breath, and rapid heart rate. In severe cases, it can progress to cardiovascular collapse.

So why is thiamine deficiency so common? There are several reasons. First, our modern diet is often depleted of thiamine—refined grains and processed foods have had much of their thiamine removed. Second, alcohol interferes with thiamine absorption and increases its excretion, so anyone who drinks regularly is at higher risk. Third, certain medications deplete thiamine, particularly loop diuretics like furosemide, which are commonly prescribed for heart failure—creating a bit of a vicious cycle. Fourth, chronic illnesses, digestive disorders, and even high glucose levels can increase thiamine requirements or reduce absorption.

Here's what's concerning: studies have found that a significant percentage of people with congestive heart failure are thiamine deficient, yet it's not routinely tested or supplemented. Some signs that someone might be deficient include fatigue, muscle weakness, nerve problems like tingling or numbness, mental confusion, and of course, heart-related symptoms like shortness of breath and rapid heartbeat.

The good news is that thiamine supplementation is safe, inexpensive, and can make a dramatic difference. For people with heart failure, especially those on diuretics, thiamine supplementation isn't just helpful—it may be essential. Some studies have shown significant improvements in heart function and symptoms with thiamine repletion. This is one of those simple interventions that can have outsized benefits.

Other natural treatments to consider include amino acids such as taurine and L-carnitine, and the mineral magnesium, all of which may support heart health.

Lifestyle Interventions: The Power of the Parasympathetic

Beyond supplements, we have compelling evidence for lifestyle interventions. Relaxation therapies like Transcendental Meditation, yoga, and Tai Chi have emerged as promising methods to enhance quality of life for those with congestive heart failure, or CHF.

These practices work in part by enhancing parasympathetic tone—remember that's your body's brake system that has anti-inflammatory effects. Other anti-inflammatory therapies and lifestyle interventions that enhance parasympathetic tone include adequate sleep, regular physical activity, and meaningful social connection. These all play critical roles in restoring healthier cardiac terrain.

Conclusion: A New Paradigm for Heart Health

So let me bring this all together. The inflammatory heart represents a convergence of modern stressors, environmental burdens, and biological challenges. Stress, toxicants, and infections form an interconnected web that reshapes cardiac biology over time.

Understanding heart disease through the lens of inflammation and terrain shifts our focus from symptom suppression to systemic restoration. By addressing the upstream drivers of inflammation—the stress, the environmental exposures, the chronic infections—we move closer to preventing cardiovascular disease, not merely managing its late-stage consequences.

And there's so much more emerging research we need to explore in future episodes: the gut-heart axis and how your microbiome affects cardiovascular inflammation, mitochondrial support strategies beyond what we discussed today, the potential role of grounding or earthing in reducing inflammation, how electromagnetic field exposure might affect heart rate variability, and even post-viral cardiac inflammation that's getting increased attention lately.

The science of heart health is evolving rapidly, and we're discovering that the heart responds to far more than we once thought—from the air we breathe to the bacteria in our gut to how we manage daily stress.

Well, that is all for today's podcast. I hope this has given you a new lens through which to view heart health—not just as a matter of cholesterol numbers, but as a complex interplay of inflammation, environment, and terrain.

Tune in in two weeks for another episode of The Science of Self-Healing.

Till then, be well.

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This article is for informational purposes only and is not intended to be a substitute for the direct care of a qualified health practitioner who oversees and provides unique and individualized care. The information provided here is to broaden our different perspectives and should not be construed as medical advice, diagnosis, or treatment.