Inflammation Is Not Our Enemy (Science Proof No. 3)
Written by: Sven Altorfer
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Time to read 8 min
Inflammation is an active protective program – when injuries occur, the body deliberately activates immune cells and messenger substances to limit dangers and initiate repair.
The resolution of inflammation is itself an active process: signaling molecules such as resolvins, protectins, maresins, and lipoxins end the reaction in an orderly manner, rather than simply letting it fade away.
The CANTOS study demonstrated in over 10,000 heart attack patients: targeted inhibition of IL-1β reduced cardiovascular events by approximately 15% – independent of blood lipid levels, supporting the causal role of chronic inflammation in atherosclerosis.
Excessive anti-inflammatory action comes at a price: under canakinumab, more fatal infections occurred – the body needs not as little inflammation as possible, but the right inflammation at the right time.
Why our body needs fire – and why it must go out again.
Fire is something peculiar. When used correctly, it provides warmth, protects, and enables change. When it gets out of control, that same fire can destroy.
With inflammation it is remarkably similar.
Today we often talk about inflammation as if it were fundamentally something bad. Yet biologically, life without inflammatory reactions would hardly be possible.
Inflammation is initially a protective program.
Why do we need inflammation?
Imagine we cut our finger. Within a short time, the tissue changes: the area can become red, warm, swollen, and tender.
This is not a mistake by the body. It is the visible result of a highly coordinated biological program.
Blood vessels change. Immune cells are activated. Chemical messengers are released. Damaged tissue and potential pathogens are recognized.
The body simultaneously attempts to limit dangers, eliminate damaged structures, and initiate repair.
Acute inflammatory reactions are therefore an essential part of immune defense and wound healing.[3]
The real art begins after that
For a long time, inflammation was often described as if it simply faded away once the trigger disappeared.
Today we know that the resolution of inflammation – the so-called resolution – is itself an active and highly coordinated biological process.[2]
Immune cells change their tasks. Cell debris is cleared. Repair processes take over. The body's own signaling molecules help end the inflammatory reaction in an orderly manner.
These signaling substances include so-called Specialized Pro-Resolving Mediators (SPMs) such as resolvins, protectins, maresins, and lipoxins.
The body needs not just a start signal for inflammation. It also needs stop signals.
What happens when the fire doesn't go out?
Problems arise when inflammatory activity is not completely ended or when new inflammatory stimuli keep appearing.
Then chronic or low-grade systemic inflammatory activity can develop. It doesn't have to look like acute inflammation: no obvious redness, no severe swelling, no clearly localized pain.
Chronic systemic inflammatory processes are linked in research to numerous diseases across the lifespan, including cardiovascular disease, diabetes, chronic kidney disease, and certain neurodegenerative and autoimmune diseases.[3]
The biology is complex: inflammation can be a cause, amplifier, consequence – or part of a self-reinforcing cycle, depending on the situation.
THE STUDY: CANTOS
One of the most important studies on the question of whether inflammation itself can be part of a disease process was the CANTOS study.
10,061 people who had previously suffered a heart attack and had persistently elevated hsCRP levels of at least 2 mg/L were randomly treated with placebo or different doses of canakinumab.[1]
Canakinumab is a monoclonal antibody that specifically inhibits the inflammatory messenger interleukin-1β (IL-1β). Importantly: the medication does not primarily lower blood lipids.
10,061
Participants
3.7 years
median follow-up
IL-1β
specifically inhibited
0.85
Hazard ratio at 150 mg
≈15%
relative risk reduction
none
Reduction in lipid levels
What was examined?
The central question was: can targeted inhibition of an inflammatory pathway reduce further cardiovascular events – independent of cholesterol reduction?
The primary endpoint consisted of non-fatal heart attack, non-fatal stroke, or cardiovascular death.
What was observed?
At the 150 mg dose of canakinumab, the hazard ratio for the primary endpoint was 0.85 compared to placebo. This corresponds to approximately 15 percent relative risk reduction.[1]
At the same time, lipid levels were not reduced. This provided strong evidence that a specifically targeted inflammatory pathway itself can contribute to atherosclerotic disease activity.[1]
But then comes the other half of the story
If inflammation can be problematic, a simple conclusion sounds tempting: then one should suppress inflammation as much as possible.
CANTOS shows why that is too simplistic. Under canakinumab, more fatal infections occurred than under placebo. Overall mortality was not significantly different.[1]
Biologically, this is understandable: the same inflammatory mechanisms that can be problematic with chronic dysregulation are simultaneously part of our defense against pathogens.
Our body doesn't need as little inflammation as possible. It needs the right inflammation – at the right time.
Start – control – resolve
1. START
An injury, infection, or other danger is recognized. Immune cells and inflammatory mediators are activated.
2. CONTROL
The body attempts to eliminate the trigger and limit damage spatially and temporally.
3. RESOLUTION
The reaction is actively ended. Cell debris is cleared, repair processes take over, and tissue returns as much as possible toward equilibrium.
What are resolvins and other SPMs?
Specialized Pro-Resolving Mediators are a group of the body's own signaling molecules involved in the orderly termination of inflammatory reactions.[2]
These include resolvins, protectins, maresins, and lipoxins. They do not simply act like a blanket "off-switch" for the immune system, but rather promote processes that belong to resolution – for example, clearing cell debris and returning to tissue stability.
Research on these signaling molecules is dynamic. Therapeutic applications are being investigated, but are not yet conclusively established depending on the indication.[2]
Acute and chronic inflammation are not the same
An acute inflammation following injury or infection can be exactly what our body needs.
A persistent low-grade inflammatory activity over months or years is biologically something different.
The fire itself is not the problem. The problem is the lack of regulation.
Can you feel chronic inflammation?
Not necessarily.
Acute inflammation often produces typical signs such as pain, warmth, redness, or swelling. Chronic low-grade inflammatory processes can be much less noticeable.
But this does not mean that fatigue, malaise, or other nonspecific complaints are automatically due to "silent inflammation."
Markers such as CRP or hsCRP can provide additional medical information, but are not specific to a single cause and must always be interpreted in clinical context.
Why is CANTOS so important?
Observational studies had long shown that inflammatory markers are often elevated in people with cardiovascular disease.
CANTOS posed the stronger question: what happens when you specifically target an inflammatory pathway?
The fact that the 150 mg dose significantly reduced the rate of cardiovascular events, even though lipid levels were not reduced, strengthened the causal significance of the IL-1β inflammatory pathway in atherosclerosis.[1]
SCIENTIFIC CLASSIFICATION
What this study does not prove
CANTOS did not examine healthy people. Participants had already suffered a heart attack and had elevated hsCRP levels.
The study therefore does not prove that every person should attempt to lower inflammatory values with medication.
It also does not prove that inflammation is fundamentally "bad."
And it says nothing about whether dietary supplements, individual foods, or specific lifestyle interventions produce the same effect.
Science also means clearly stating what a study does not show.
What can we take from this?
Perhaps we should stop viewing inflammation as fundamentally an enemy.
It is part of a highly sophisticated protective system. It helps us respond to injuries and pathogens, mobilize immune cells, and initiate repair.
But just as important as the ability to start an inflammation is the ability to end it in an orderly manner.
Our body needs fire. But it also needs a mechanism to extinguish it.
That is precisely where one of the most fascinating insights of modern inflammation research lies.
Original studies & further reading
1. Ridker PM et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. New England Journal of Medicine. 2017;377(12):1119–1131. PMID: 28845751. DOI: 10.1056/NEJMoa1707914. Open PubMed
2. Fredman G, Serhan CN. Specialized pro-resolving mediators in vascular inflammation and atherosclerotic cardiovascular disease. Nature Reviews Cardiology. 2024;21(11):808–823. PMID: 38216693. DOI: 10.1038/s41569-023-00984-x. Open PubMed
3. Furman D et al. Chronic inflammation in the etiology of disease across the life span. Nature Medicine. 2019;25(12):1822–1832. PMID: 31806905. DOI: 10.1038/s41591-019-0675-0. Open PubMed
EDITORIAL NOTE
SCIENCE PROOF deliberately distinguishes between biological plausibility, clinical observations, and reliable efficacy evidence. This article is scientific information and not medical advice.
SCIENCE PROOF BY THE CHANGE
One study. One insight. Explained clearly.
Current research. Without exaggeration. Without promises of a cure. Simply sound Science.
Sven Altorfer
Sven Altorfer is Head of Research and Development at Swiss Health Nutrition AG. With his expertise in nutrition and bioactive substances, he advocates for natural health approaches to promote preventive measures and the body's self-healing powers.
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