Inflammation: The Common Thread Behind Nearly Every Chronic Disease

When most people hear "inflammation," they think of a swollen ankle or a sore throat. That kind of inflammation—acute inflammation—is your body doing its job. White blood cells rush to the scene, fight off whatever's wrong, and the swelling goes down. Problem solved.

But there's another kind of inflammation. The kind that doesn't announce itself. The kind that lingers for months or years without any obvious symptoms. And according to a growing body of research, this chronic, low-grade inflammation may be the underlying driver behind most of the diseases that kill us.

A recent editorial published in the journal Cells by Chavda, Feehan, and Apostolopoulos (November 2024) pulled together findings from 12 separate studies to make a compelling case: addressing inflammation at its root could be the key to preventing and treating a staggering number of chronic conditions.

Here's what they found—and what it means for you.

The List of Diseases Is Longer Than You Think

The editorial connects chronic inflammation to a list of conditions that covers nearly every major organ system:

• Cardiovascular disease—inflammation damages blood vessel walls and promotes plaque buildup
• Type 2 diabetes—inflammatory cytokines interfere with insulin signaling
• Cancer—chronic inflammation creates an environment where tumors can grow and evade the immune system
• COPD and respiratory disease—persistent lung inflammation destroys tissue over time
• Autoimmune conditions (lupus, rheumatoid arthritis, ulcerative colitis)—the immune system's inflammatory response turns against the body itself
• Neurodegenerative disorders including Alzheimer's—neuroinflammation damages neurons
• Gastrointestinal disorders including Crohn's disease
• Allergies, skin conditions, and joint problems

That's not a short list. And the editorial argues these aren't coincidental associations—inflammation is a mechanistic driver in each case.

What's Actually Driving the Inflammation?

The research points to a set of factors that most of us encounter every day:

Aging. As we get older, our immune systems undergo what researchers call "immune senescence." Mitochondria become less efficient, free radicals accumulate, and the immune system shifts toward a chronically activated state. This is sometimes called "inflammaging"—and it happens to everyone to some degree.

Diet. The quality of what you eat directly shapes your inflammatory profile. Diets high in processed foods, refined sugars, and unhealthy fats promote inflammation. The gut microbiota—trillions of microorganisms in your digestive tract—responds to your diet and can either dampen or amplify inflammatory signaling throughout your body.

Obesity. One of the 12 studies reviewed found that in 203 obese patients, a metric called the platelet/high-density lipoprotein ratio (PHR) served as a reliable marker of inflammation—and correlated directly with Type 2 diabetes markers. Fat tissue, especially visceral fat around organs, is metabolically active and produces inflammatory cytokines continuously.

Smoking. Another study examined heated tobacco products versus traditional cigarettes. While heated products induced fewer pro-inflammatory cytokines, they still increased immunosuppressive markers like IL-10, IL-35, and TGF-β. The takeaway: there's no "safe" form of tobacco when it comes to inflammation.

Sedentary behavior, chronic stress, and poor sleep round out the list. Each independently contributes to elevated inflammatory markers—and in combination, they compound each other.

The Science: What's Happening at the Cellular Level

Several of the reviewed studies shed light on the specific molecular pathways involved:

The NLRP3 inflammasome and Alzheimer's. Researchers found that inhibiting the NLRP3 inflammasome—a protein complex that triggers inflammatory responses—reduced neuroinflammation and improved cognitive function in Alzheimer's disease models. This suggests that brain inflammation isn't just a byproduct of the disease but an active contributor to its progression.

Gut barrier breakdown and Crohn's disease. A study on phospholipase C-β3 (PLC-β3) showed that reduced activity of this enzyme disrupted Wnt/β-catenin signaling in the intestinal lining, leading to severe inflammation. The gut barrier is only one cell layer thick—when it breaks down, bacterial components leak into the bloodstream and trigger systemic immune responses.

Red blood cell fragility. In a study of over 9,000 healthy participants, mild systemic inflammation (measured by high-sensitivity CRP) was linked to increased red blood cell fragility. Even "healthy" people with slightly elevated inflammation markers showed measurable biological effects.

The oral-systemic connection. One study found that non-surgical periodontal treatment—essentially treating gum disease—significantly reduced inflammatory biomarkers and disease activity in women with rheumatoid arthritis. Inflammation in one part of the body can fuel inflammation elsewhere.

Where Treatment Is Heading

The editorial highlights several promising therapeutic strategies:

• Targeted biologics: Monoclonal antibodies like infliximab, etanercept, and adalimumab that specifically target TNF-α (a key inflammatory cytokine) are already showing efficacy in lupus, rheumatoid arthritis, and ulcerative colitis.
• Repurposed drugs: Metformin, widely used for diabetes, has been shown to downregulate pro-inflammatory markers including IL-1β, IL-6, TNF-α, and COX-2—with potential applications in cancer prevention.
• JAK-STAT pathway inhibitors: These target a specific inflammatory signaling cascade and are being explored for chronic inflammatory conditions.
• Nutritional interventions: Dietary polyphenols and bioactive compounds show anti-inflammatory properties. Microbiome modulation through probiotics and prebiotics could reduce dependence on traditional anti-inflammatory drugs.
• NADH supplementation: In a COPD study, NADH improved antioxidant defenses and reduced pro-inflammatory markers (TNF-α, IL-17, IFN-γ) in cigarette smoke-exposed lung tissue.

The Monitoring Problem—and Why It Matters

Here's what struck us most about this research: the evidence that chronic inflammation drives disease is overwhelming and growing stronger every year. But for most people, there's still no practical way to know whether they're inflamed.

Unless your doctor specifically orders a high-sensitivity CRP blood test—which most don't unless you're already showing symptoms—you have no visibility into your own inflammatory status. And even when inflammation is measured, it's typically a single snapshot, not ongoing monitoring.

That's why we're building Sensa. Our at-home kit lets anyone order a simple saliva-based vial, spit into it, and see their inflammation level within minutes through a chemical reaction—no needles, no lab visits, no waiting days for results. Because if the research is telling us that inflammation is the upstream driver of most chronic disease, then giving people a way to monitor it at home isn't just convenient—it could be genuinely life-changing.

What You Can Do Right Now

While the science of anti-inflammatory therapeutics advances, the most effective interventions are also the most accessible:

1. Move daily. Regular physical activity has potent, well-documented anti-inflammatory effects. Even 30 minutes of moderate movement matters.
2. Eat whole foods. Prioritize vegetables, fruits, whole grains, fatty fish, nuts, and olive oil. The Mediterranean diet has the strongest evidence base for reducing inflammatory markers.
3. Manage your weight. Visceral fat is one of the strongest drivers of chronic inflammation. Even modest weight loss can significantly reduce inflammatory cytokine levels.
4. Sleep 7–9 hours. Sleep deprivation reliably increases CRP and IL-6. Good sleep is anti-inflammatory medicine.
5. Reduce stress. Chronic psychological stress keeps your immune system in a pro-inflammatory state. Meditation, deep breathing, and regular breaks aren't luxuries—they're health interventions.
6. Don't ignore your oral health. As the periodontal study showed, gum disease doesn't stay in your mouth—it contributes to systemic inflammation.

The more we learn about inflammation, the clearer the picture becomes: it's not just a response to disease—it's often the cause. And the earlier you can see it, the more you can do about it.

Source: Chavda VP, Feehan J, Apostolopoulos V. "Inflammation: The Cause of All Diseases." Cells. 2024;13(22):1906. Published November 18, 2024. PMC11592557.