Is Inflammation the Real Cause of Heart Disease?

Written by David Roberts, MPH

New research points to chronic inflammation, not just cholesterol, as a major driver of heart disease — about a quarter of heart attack and stroke patients show none of the traditional risk factors. Sulforaphane and curcumin both target the inflammatory pathways involved.

Why Are Doctors Rethinking What Causes Heart Disease?

Cardiologists have long known something doesn't add up. About a quarter of people hospitalized for heart attacks and strokes don't have the traditional risk factors [1].

That means no high cholesterol, no high blood pressure, no smoking history, no diabetes.

A May 2026 cover story in Scientific American lays out the case that chronic, low-grade inflammation may be the missing piece [1].

Inflammation isn't a new idea in cardiology. What's changed is how central researchers now think it is — not just a side effect of heart disease, but a possible root cause [1].

Part of the evidence comes from drug trials. Researchers have tested inexpensive anti-inflammatory drugs, including colchicine, to see whether reducing inflammation cuts cardiovascular risk on its own [1].

Early results have been promising enough to shift how some cardiologists think about risk assessment — not replacing cholesterol as a factor, but adding inflammation as a second, independent one [1].

What Is Chronic Inflammation, and How Does It Damage Arteries?

Inflammation is the body's normal response to injury or infection. The problem starts when it doesn't turn off.

When inflammation becomes chronic, immune cells keep attacking blood vessel walls long after any real threat is gone [2][5].

This ongoing activity contributes to plaque buildup, arterial stiffening, and endothelial dysfunction — all of which raise heart attack and stroke risk [5].

Oxidative stress feeds this cycle directly. Unstable molecules called free radicals accumulate and further activate the inflammatory signaling that keeps arteries under attack [2].

Immune cells called macrophages play a central role. They absorb excess cholesterol in artery walls and can become foam cells — a key building block of arterial plaque [5].

The more inflamed the surrounding tissue, the more this process accelerates, which is part of why researchers now view inflammation and cholesterol as interconnected, not competing, explanations [1][5].

Can Sulforaphane Help Calm Chronic Inflammation?

Yes. Sulforaphane, a compound found in broccoli sprouts, activates the body's own antioxidant defense system [2].

That activation suppresses NF-κB, the signaling pathway responsible for producing many of the inflammatory proteins involved in artery damage [2].

In animal studies, sulforaphane reduced myocardial hypertrophy, fibrosis, and inflammation in heart tissue [3].

Human data backs this up. In a 12-week clinical trial, sulforaphane supplementation reduced a key inflammatory marker by 40%, cut total cholesterol by 12%, and lowered LDL cholesterol by 24% [4].

What Role Does Curcumin Play in Vascular Health?

Curcumin, the primary active compound in turmeric, works through a similar pathway — inhibiting NF-κB signaling in blood vessel walls [5][6].

Research shows curcumin reduces oxidative stress in endothelial cells, the thin layer of tissue lining every blood vessel [6].

That matters because endothelial dysfunction is one of the earliest measurable changes in developing atherosclerosis [6].

Clinical trials on curcumin have found improvements in vascular health markers, particularly in people already at elevated cardiovascular risk [6].

Curcumin has one well-documented limitation: on its own, it's poorly absorbed by the body. Most of an oral dose is metabolized before it ever reaches the bloodstream [5].

This absorption problem is why researchers studying curcumin's cardiovascular effects often note that formulation and delivery method affect how much of a dose reaches blood vessel tissue [5][6].

How Do Sulforaphane and Curcumin Compare on Inflammatory Markers?

Sulforaphane's data here comes from a single 12-week human trial — a real signal, not yet large-scale replication.

Curcumin's vascular findings are similarly early-stage compared to established cardiovascular drugs.

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