Hormonal
Activation of the kynurenine pathway via IDO/TDO enzymes during inflammation promotes immune tolerance and prevents hyperinflammation by depleting tryptophan and producing kynurenine, which activates the aryl hydrocarbon receptor (AhR) to drive regulatory T cell differentiation.
This paper highlights that the body's natural response to stress (inflammation) involves shifting tryptophan metabolism to protect against excessive immune damage. While not a direct supplement protocol, it suggests that maintaining healthy tryptophan metabolism and understanding the balance of immune response is crucial for aging. Future therapies might target this pathway, but currently, no specific dose is recommended for general use.
Activation of tryptophan (Trp) metabolism along the kynurenine (Kyn) pathway prevents hyperinflammation and induces long-term immune tolerance.
Why this rating
The paper is a mini-review citing multiple animal models and observational human studies, but lacks direct clinical trial data on intervention outcomes.
Source
Tryptophan Metabolism in Inflammaging: From Biomarker to Therapeutic Target
Freek J. H. Sorgdrager et al. · Frontiers in Immunology · 2019
DOI 10.3389/fimmu.2019.02565
More from this paper
- The kynurenine/tryptophan (Kyn/Trp) ratio in blood serves as a robust biomarker for the rate of physiological aging (inflammaging) and predicts age-related diseases and mortality.Good
- Targeting tryptophan metabolism, specifically by inhibiting TDO or boosting de novo NAD+ synthesis, may extend lifespan and improve metabolic health in animal models.Moderate
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