When the body experiences immune stress – due to  physiological or psychological stress – the enzyme IDO (indoleamine 2,3-dioxygenase) is upregulated. This enzyme converts tryptophan into kynurenine (KYN), diverting it away from protective microbial metabolites like IPA and towards the stress-associated kynurenine pathway.

Although the kynurenine pathway is regulated by host enzymes, its activation is closely shaped by the state of the gut microbiota. A balanced microbiota, rich in fiber-fermenting species, produces SCFAs and other beneficial metabolites that suppress inflammatory signaling and downregulate IDO. In contrast, when imbalanced,this regulatory control is weakened, increasing immune stress and raising kynurenine production. Thus, the microbiota doesn’t just shape its own metabolic output; it also helps regulate the body’s inflammatory tryptophan metabolism.

Importantly, IDO1 not only channels tryptophan into the kynurenine pathway – it also acts as a modulator of microbial ecology. By depleting tryptophan locally, IDO1 limits the availability of this key amino acid to gut microbes. This immune-driven restriction of nutrients can suppress microbial proliferation, reduce the output of beneficial indole metabolites, and shift the microbial ecosystem in ways that reinforce imbalance. 
 
In this way, kynurenine production is primarily host-driven but is also influenced by – and in turn influences – the gut microbiota. Elevated KYN reflects a shift toward immune-associated metabolism, shaped by a disrupted dialogue between the immune system and the microbial ecosystem.  

What does kynurenine reflect?

Kynurenine is a sensitive signal of the immune response. Elevated KYN levels in blood have been linked to contexts of persistent immune activation, metabolic stress, and aging. 

Importantly, KYN levels and ratios (e.g., KYN/TRP) are used in research and clinical contexts to track immune tone and systemic stress.   

When tryptophan shifts toward (excessive) kynurenine
Factors that increase KYN production: 
 

• Immune stress and activation 
• Psychological or oxidative stress 
• Infections 
• Low fiber intake  
• Microbial imbalance  
• Insufficient nutrient intake (e.g., niacin, zinc)

This shift can reduce the availability of tryptophan for serotonin or microbial pathways (like the production of IPA) and increase production of downstream metabolites such as quinolinic acid (QA), which can be stress-associated or overstimulating in excess. 

Why we measure KYN in our Gut Health Test

Kynurenine is not inherently “bad” – in fact, it plays important roles in immune regulation and NAD+ production. But persistently elevated levels reflect a body under immune strain. When combined with other markers like IPA and TRP, KYN helps reveal: 
 

• Whether tryptophan metabolism is skewed toward immune stress. 
• The balance between host-driven and microbial-driven pathways. 
• Early shifts in immune or metabolic function, even before imbalances are outwardly noticeable.

This test is not meant to be diagnostic. Instead, it offers a snapshot of your tryptophan metabolism and how it may reflect your immune and gut health status – providing a tool for lifestyle feedback and improvement tracking.

Quick summary

• KYN is a host-derived metabolite that rises with immune stress and also plays a role in immune regulation and redox balance. 
• High KYN levels reflect immune activation and a shift away from microbial tryptophan metabolism. 
• KYN is useful for detecting low-grade inflammation and stress-related metabolic strain.