Inflammation is tissue defense and repair: heat, swelling, immune mediators, and a change in local blood flow. Acute, localized inflammation can clear injury. Chronic, systemic inflammation is a different process. It tracks low cellular energy, leaky vessels, excess estrogen, PUFA, and gut endotoxin, and it sits under aging, fibrosis, and many degenerative diseases.[1][2]

Why chronic inflammation is not "defense"

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Before birth, injuries heal with less scarring. Two differences matter: high CO2, which limits lactate, and the absence of stored n-3 and n-6 polyunsaturated fats. In adulthood those fats accumulate. Prostaglandins and related agents rise. Cells shift toward lactic acid instead of carbon dioxide. Chronic systemic inflammation becomes the central factor in degenerative disease.[1] A pooled analysis of 160,309 people across 54 prospective studies found each three-fold rise in baseline C-reactive protein predicted about 55% higher non-vascular mortality (RR 1.55) and a similarly elevated risk of vascular mortality and ischaemic stroke, tracking chronic low-grade inflammation across a wide range of degenerative outcomes rather than any single disease.[3]

Cellular energy metabolism is the basis for maintaining the barrier functions. Energy depletion causes the endothelial cells lining blood vessels to become excessively permeable.

— Ray Peat[4]

Low energy opens barriers. Open barriers let endotoxin and inflammatory signals spread. Estrogen increases lipid peroxidation, free fatty acids, prostaglandins, and NF-κB-driven cytokines. Serotonin, histamine, and nitric oxide join the same field. See Tissue leakiness, Estrogen, Endotoxin, Serotonin.

One protective set

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The same supports that restore oxidation lower chronic inflammation. Thyroid raises energy and barrier tone. Progesterone opposes unopposed estrogen. Gelatin and glycine, niacinamide, saturated fats, and vitamin E appear together in the leakiness essay as anti-inflammatory and barrier-protective.[5]

Antioxidants, thyroid hormone, progesterone, and antiinflammatory agents, including glycine or gelatin, niacin, and saturated fats, can prevent, and in many cases reverse, these degenerative inflammatory processes.

— Ray Peat[6]

Aspirin blocks cyclooxygenase and cuts prostaglandin excess; its useful range is wider than a single enzyme story. Coffee and food energy support the same arc when the gut can handle them. Lower dietary PUFA and clear endotoxin so the fuel for inflammatory eicosanoids falls. See Aspirin, PUFA, Harm reduction.

Chronic inflammation is energy failure made public. Fix the field; do not only chase one cytokine.

See also

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References

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  1. ↑ 1.0 1.1 Ray Peat, Inflammation email Q&A, raypeatemails.com.
  2. ↑ Ray Peat, "Leakiness, aging, and cancer," raypeat.com.
  3. ↑ Emerging Risk Factors Collaboration, "C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis," Lancet 375, no. 9709 (2010): 132–140, https://pubmed.ncbi.nlm.nih.gov/20031199/.
  4. ↑ Leakiness, aging, and cancer, Ray Peat newsletter
  5. ↑ Ray Peat, "Antioxidants, thyroid, progesterone…," raypeat.com.
  6. ↑ Leakiness, aging, and cancer, Ray Peat newsletter