A patient presents with elevated inflammatory markers, CRP, LDH, ferritin, ESR, and the immediate response is to suppress. Anti-inflammatory agents are introduced. Supplements are layered. In some cases, corticosteroids are used early and aggressively.
From a conventional standpoint, this makes sense. Inflammation is associated with disease progression, tissue damage, and symptom burden.
Clinically, however, this approach is often incomplete and at times, it may be counterproductive.
The Assumption: Inflammation is Harmful
Inflammation has become a generalized target in oncology and integrative care alike. It is often viewed as something to reduce, control, or eliminate.
But inflammation is not inherently pathological.
It is required for:
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Antigen recognition
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Immune cell activation
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Cytokine signaling
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Tumor targeting
Without it, the immune system does not engage.
Inflammation, in its appropriate form, is the initiating signal that allows the immune system to recognize and respond to abnormal tissue. Antigen-presenting cells rely on inflammatory cues to process and display tumor antigens, T cells require cytokine signaling to activate and proliferate, and cytotoxic function depends on a coordinated inflammatory environment to execute tumor cell killing.
In the absence of this signaling, immune cells may be present but remain functionally inactive, unable to distinguish malignant cells from normal tissue or generate a sustained response.
Clinically, this may be why overly suppressing inflammation can be counterproductive; it does not simply reduce “damage,” it can remove the very signals required for immune engagement, surveillance, and effective therapeutic response.
What is Often Missed: Not all Inflammation is the same
In practice, inflammation exists in different functional states:
1. Acute, functional inflammation
This is necessary. It reflects active immune engagement and signaling. It is often transient and associated with immune activation. As with many other lab markers, repeat, ongoing testing is the key to evaluate a “good” spike in inflammation vs. a continual rising trend.
2. Chronic, dysregulated inflammation
This is the pattern most commonly associated with cancer progression. It is persistent, low-grade, and driven by cytokines, metabolic dysfunction, and microenvironmental stress.
Chronic inflammation driven by the terrain and/or disease will often continue to rise with ongoing lab testing.
3. Immune-paralyzed states
This is less recognized. In these patients, inflammatory markers may be low or only mildly elevated, but the immune system is not effectively responding. These patients may fail to mount meaningful responses to therapy.
The clinical mistake is treating all three states the same.
Biomarkers: Beyond High or Low
Inflammatory markers are frequently interpreted in isolation.
That approach is insufficient.
CRP
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Elevated CRP is not inherently negative
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Persistent, non-resolving elevation is more concerning than transient increases
Ferritin
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Acts as both an iron storage marker and an inflammatory protein
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Disproportionate elevation often reflects chronic immune activation
ESR
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Slower-moving marker
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Useful in trend comparison, particularly when discordant with CRP
LDH
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Often overlooked
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Reflects tumor burden, tissue turnover, and metabolic stress
The clinical value lies in patterns and trends—not single values.
Where Integrative Care Missteps
In an effort to support patients, inflammation is often suppressed indiscriminately.
This includes:
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High-dose curcumin, Omega 3, boswellia….others.
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Broad antioxidant use
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NSAIDs or steroid reliance
These interventions may reduce inflammatory markers.
They may also reduce immune signaling.
This becomes particularly relevant during active immunotherapy or immune-based treatments.
Clinical Reality
Some of the most challenging patients are those with:
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Low or minimally elevated CRP and other inflammatory markers
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Lymphopenia
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Poor response to therapy
In these cases, the issue may not be excess inflammation.
It is insufficient or ineffective immune activation.
Suppressing inflammation further in this group may worsen outcomes.
My Opinion and Strategic Position
The goal is not to eliminate inflammation. It is to differentiate the type, trends and timing of the inflammatory response. This may require some restraint for a few months.
Inflammation can be viewed as a valuable ‘tool’.
References:
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Mantovani A, Allavena P, Sica A, Balkwill F. Cancer-related inflammation. Nature. 2008;454:436–444.
Medzhitov R. Origin and physiological roles of inflammation. Nature. 2008;454:428–435.
Chen DS, Mellman I. Oncology Meets Immunology: The Cancer-Immunity Cycle. Immunity. 2013;39(1):1–10.
Sanmamed MF, Chen L. A Paradigm Shift in Cancer Immunotherapy: From Enhancement to Normalization. Cell. 2018;175(2):313–326.
Binnewies M, Roberts EW, Kersten K, et al. Understanding the tumor immune microenvironment (TIME) for effective therapy. Nature Medicine. 2018;24:541–550.
Chang CH, Qiu J, O’Sullivan D, et al. Metabolic Competition in the Tumor Microenvironment Is a Driver of Cancer Progression. Cell. 2015;162(6):1229–1241.
Leone RD, Powell JD. Metabolism of immune cells in cancer. Nature Reviews Cancer. 2020;20:516–531.
Buck MD, Sowell RT, Kaech SM, Pearce EL. Metabolic Instruction of Immunity. Cell. 2017;169(4):570–586.
Ferrucci L, Fabbri E. Inflammaging: chronic inflammation in aging, cardiovascular disease, and frailty. Nature Reviews Cardiology. 2018;15:505–522.