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Did you know…

Validated biomarkers of oxidative stress, the “rust” of biological ageing, have existed in research laboratories for decades. None of them appears in the standard clinical panel. F2-isoprostanes are considered the most reliable in-vivo marker of lipid peroxidation. 8-hydroxy-2-deoxyguanosine (8-OHdG) measures DNA oxidative damage. Malondialdehyde has been studied for lipid peroxidation for half a century. And each of them, in disease-progression studies, correlates with the trajectory of cardiovascular disease, diabetes, and neurodegeneration.

The claim, in the reference of oxidative stress research

The 2025 review in Frontiers in Molecular Biosciences summarizes the consensus:

“Clinically validated biomarkers of oxidative stress, such as F2-isoprostanes (which indicate lipid peroxidation), 8-OHdG (which indicates DNA damage), and the activities of redox enzymes like superoxide dismutase (SOD) and glutathione peroxidase (GPx), show strong correlations with disease progression and end-organ complications.”

Frontiers in Molecular Biosciences, 2025

The technical status:

“F2-isoprostanes better reflect oxidative stress because this marker is more specific and is not influenced by dietary intake. F2-isoprostanes are frequently viewed as the most reliable biomarkers for monitoring oxidative stress in vivo.”

Why they are not in the clinical panel

None of these assays is technically difficult. Mass spectrometry for F2-isoprostanes has been standardized since the 1990s. ELISA kits for 8-OHdG have been commercially available for two decades. The obstacle is not analytical. It is that the clinical framework does not measure the underlying process. Ordinary medicine measures organ damage after it has happened (troponin after infarct, creatinine after kidney injury). It does not measure the upstream oxidative burden that would flag the injury before it happens.

What the ordinary panel does contain

Ferritin is a routine measurement. It rises with iron stores, but it also rises as an acute-phase reactant with inflammation and with oxidative stress. A high ferritin without iron overload is a hint of oxidative burden.

High-sensitivity CRP is routine. It captures systemic inflammation, which is upstream of and downstream of oxidative stress in most chronic conditions.

Both are proxies. Neither is a direct measurement. Both are routinely available. Between them and the validated oxidative-stress biomarkers sits a technical gap the medical system has chosen not to close.


This entry is a companion to fiches on antioxidant biology and to the broader argument on what routine care does not measure.

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