Kynurenine is a central metabolite in the tryptophan degradation pathway, known as the kynurenine pathway, which plays a vital role in neurotransmitter balance, immune regulation, mitochondrial energy production, and oxidative stress control. It sits at a critical metabolic crossroads—linking the amino acid tryptophan with the synthesis of nicotinamide adenine dinucleotide (NAD+), a molecule essential for cellular energy and redox balance.
On the Neurotransmitter XL panel, kynurenine helps reveal whether tryptophan is being converted primarily into serotonin and melatonin (supporting mood and sleep) or diverted into stress- and inflammation-related pathways that generate neuroactive metabolites like quinolinic acid and kynurenic acid. Imbalances in kynurenine metabolism are often associated with chronic stress, immune activation, depression, fatigue, and mitochondrial dysfunction.
In healthy physiology, approximately 95% of tryptophan is metabolized via the kynurenine pathway, and only a small portion goes toward serotonin synthesis. However, under stress or inflammation, this balance shifts dramatically. Cytokines (especially interferon-γ) activate the enzyme indoleamine 2,3-dioxygenase (IDO), which accelerates the conversion of tryptophan into kynurenine.
While this response supports immune regulation and helps modulate inflammation, chronic activation can have unintended effects:
Reduced serotonin and melatonin production, leading to mood and sleep disturbances.
Accumulation of neurotoxic metabolites such as quinolinic acid, which can overstimulate NMDA receptors.
Reduced NAD+ synthesis, impairing mitochondrial function and energy metabolism.
Oxidative and nitrosative stress, damaging neurons and cellular membranes.
Thus, kynurenine serves as a sensitive marker of systemic stress, immune activation, and neurotransmitter depletion.
The kynurenine pathway begins when tryptophan is broken down by one of two enzymes:
Indoleamine 2,3-dioxygenase (IDO) – activated by inflammatory cytokines.
Tryptophan 2,3-dioxygenase (TDO) – stimulated by cortisol and stress hormones.
Once tryptophan enters this pathway, it is converted into kynurenine, which can then branch into several key routes:
Kynurenic acid – neuroprotective and anti-inflammatory.
3-hydroxykynurenine and quinolinic acid – neurotoxic, pro-oxidative metabolites.
Nicotinamide adenine dinucleotide (NAD+) – the final product, essential for cellular energy and mitochondrial function.
This biochemical flexibility allows the body to adapt to stress and immune challenges, but chronic overactivation can tip the balance toward neurotoxicity and energy deficits.
Kynurenine and its metabolites influence multiple systems:
Neurotransmission: Modulates glutamate receptor activity (via kynurenic and quinolinic acids).
Immune regulation: Controls T-cell function and inflammatory responses.
Energy metabolism: Serves as a precursor for NAD+, critical for mitochondrial ATP production.
Stress adaptation: Reflects the body’s metabolic shift under chronic psychological or inflammatory stress.
Prolonged activation of the hypothalamic-pituitary-adrenal (HPA) axis stimulates TDO, increasing kynurenine synthesis. Over time, this leads to serotonin depletion and increased production of downstream metabolites that can impair energy and mood regulation.
Cytokines such as interferon-γ, TNF-α, and IL-6 activate IDO, diverting tryptophan into the kynurenine pathway. Elevated neopterin on the panel typically accompanies high kynurenine, indicating inflammation-driven pathway activation.
Several nutrients are required to maintain healthy kynurenine metabolism and prevent harmful metabolite buildup:
Vitamin B6 – for conversion into kynurenic acid (protective pathway).
Niacin (B3) – for NAD+ synthesis and feedback regulation.
Magnesium and zinc – cofactors for enzymatic balance.
Deficiencies can lead to accumulation of intermediate metabolites such as quinolinic acid, contributing to neuroinflammation.
When mitochondrial NAD+ synthesis is impaired, the kynurenine pathway can become congested, leading to a rise in quinolinic acid and oxidative stress. Low NAD+ levels indicate reduced conversion efficiency and compromised energy metabolism.
Gut bacteria influence tryptophan availability and can modulate kynurenine levels. Dysbiosis or intestinal inflammation increases IDO activity and can accelerate tryptophan degradation.
Because the kynurenine pathway links neurotransmission, inflammation, and mitochondrial energy, elevated levels can manifest as:
Fatigue and low energy
Low mood, anxiety, or irritability
Sleep disruption or non-restorative sleep
Cognitive fog or poor concentration
Muscle aches or slow recovery from exercise
Sensitivity to stress or sensory overload
When the balance between kynurenic (protective) and quinolinic (toxic) metabolites shifts unfavorably, neurotoxic stress may increase, contributing to depressive and anxiety symptoms.
| Related Marker | Interpretation Insight |
|---|---|
| Tryptophan | Low tryptophan with high kynurenine suggests stress- or inflammation-driven diversion. |
| Serotonin | Decrease indicates that tryptophan metabolism is being redirected away from serotonin synthesis. |
| Quinolinic Acid | High levels point to oxidative stress and potential neurotoxicity. |
| NAD+ | Low levels reflect impaired conversion of quinolinic acid to NAD+, indicating mitochondrial strain. |
| Neopterin | Elevated levels confirm immune activation (interferon-γ–mediated) driving IDO activity. |
| SAM / SAH Ratio | Low methylation capacity can further impair neurotransmitter synthesis and detoxification. |
Together, these markers help identify whether elevated kynurenine is due to inflammation, chronic stress, cofactor depletion, or mitochondrial dysfunction.
Less commonly, decreased kynurenine may indicate limited tryptophan availability, low IDO/TDO activity, or nutrient deficiencies preventing pathway activation. This can occur in cases of severe protein restriction, malnutrition, or poor enzyme function, often accompanied by low NAD+ and serotonin.
Chronic dysregulation of the kynurenine pathway contributes to a range of physiological and neurological effects, including:
Depression, anxiety, and mood instability
Burnout and chronic fatigue
Neuroinflammation and mitochondrial dysfunction
Reduced stress resilience and poor recovery
Immune dysregulation and oxidative stress
Because kynurenine sits at the interface between the nervous, immune, and energy systems, its interpretation provides valuable insight into overall metabolic resilience.
Practice mindfulness, breathwork, or yoga to reduce cortisol and cytokine activity.
Include anti-inflammatory nutrients such as omega-3 fatty acids, curcumin, and resveratrol.
Address chronic infections or autoimmune activity that elevate interferon-γ and IDO.
Ensure sufficient vitamin B6, B3, magnesium, and zinc to maintain balanced kynurenine metabolism.
Support NAD+ regeneration through niacin, nicotinamide riboside, or nicotinamide mononucleotide (NMN) under guidance.
Maintain redox balance with CoQ10, alpha-lipoic acid, and antioxidants.
Engage in moderate aerobic exercise, which promotes kynurenine aminotransferase (KAT) activity, converting kynurenine into neuroprotective kynurenic acid.
Address dysbiosis with probiotics, prebiotics, and a fiber-rich, anti-inflammatory diet.
Limit alcohol, processed foods, and toxins that disrupt the intestinal barrier.
Kynurenine is a pivotal biomarker linking tryptophan metabolism, stress physiology, and immune activation. Elevated levels indicate a metabolic shift toward inflammation and oxidative stress—often at the expense of serotonin and NAD+ synthesis. On the Neurotransmitter XL panel, interpreting kynurenine alongside tryptophan, serotonin, quinolinic acid, NAD+, and neopterin provides a comprehensive view of how chronic stress and inflammation are impacting mood, energy, and cellular health.
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A low kynurenine level on the Neurotransmitter XL panel suggests that the tryptophan-to-kynurenine conversion pathway—known as the kynurenine pathway—is underactive or blocked. Because kynurenine serves as the central metabolite connecting tryptophan, serotonin, and NAD+ (cellular energy metabolism), low levels may indicate that tryptophan is not being effectively utilized for downstream biochemical processes. This can point to issues such as nutrient cofactor deficiencies, low enzyme activity, mitochondrial inefficiency, or overall suppression of immune and stress-related pathways.
While elevated kynurenine is often linked with chronic stress and inflammation, low kynurenine may reflect a different kind of imbalance—one where the body lacks the metabolic resources or enzymatic function to convert tryptophan into its essential derivatives.
Under normal conditions, roughly 95% of dietary tryptophan is metabolized through the kynurenine pathway. The first and rate-limiting step is catalyzed by either indoleamine 2,3-dioxygenase (IDO)—which is activated by inflammation—or tryptophan 2,3-dioxygenase (TDO)—which is stimulated by cortisol and stress hormones. These enzymes transform tryptophan into kynurenine, which is then further metabolized into a range of key compounds:
Kynurenic acid – a neuroprotective, anti-inflammatory metabolite.
3-hydroxykynurenine and quinolinic acid – energy- and redox-linked intermediates that also influence neurotransmission.
NAD+ – a vital coenzyme for mitochondrial energy production and redox balance.
When kynurenine levels are low, this entire pathway slows down, potentially reducing NAD+ synthesis and impairing mitochondrial energy metabolism.
If tryptophan levels are already low due to poor dietary intake, malabsorption, or excessive serotonin synthesis, there may not be enough substrate available to produce kynurenine. This can lead to both low serotonin and low NAD+, resulting in fatigue, low mood, and sleep difficulties.
Low kynurenine can result from decreased activity of IDO (immune-related enzyme) or TDO (stress-activated enzyme). This may occur in:
Low cortisol output (e.g., adrenal fatigue or HPA-axis suppression).
Blunted immune response or immune exhaustion.
Certain genetic polymorphisms that reduce enzyme efficiency.
Without proper enzyme activation, tryptophan may accumulate or remain unconverted, resulting in a metabolic bottleneck.
The kynurenine pathway depends on several essential nutrients and cofactors. Deficiencies can disrupt enzymatic conversion and lead to low kynurenine:
Vitamin B6 – needed for conversion of kynurenine to kynurenic acid (protective branch).
Niacin (B3) – regulates NAD+ synthesis and provides feedback control within the pathway.
Iron, zinc, and magnesium – required for enzyme function and redox reactions.
When these nutrients are lacking, conversion slows and the entire pathway underperforms.
Mitochondria rely on NAD+—derived from the kynurenine pathway—for energy production. When mitochondrial function is compromised (due to oxidative stress, toxin exposure, or nutrient depletion), feedback inhibition can reduce kynurenine synthesis, resulting in both low kynurenine and low NAD+ levels.
Since IDO activity increases in response to immune stimulation (via interferon-γ), very low kynurenine can also suggest a lack of immune activation. This is not always beneficial—it may indicate immune suppression, chronic viral load, or inadequate cytokine signaling, which prevents the body from adapting metabolically to stress or infection.
Aggressively suppressing cortisol or inflammation (e.g., through chronic use of high-dose antioxidants or anti-inflammatory medications) can inadvertently reduce TDO and IDO activity, slowing the tryptophan-to-kynurenine conversion.
Low kynurenine levels can contribute to a combination of mood, energy, and immune symptoms, such as:
Chronic fatigue or low stamina
Low mood or emotional flatness
Sleep disturbances (due to low melatonin synthesis)
Reduced stress tolerance or apathy
Cognitive fog and low motivation
Weak immune response or frequent infections
Because kynurenine is a precursor for NAD+ and neuroactive metabolites, persistently low levels can contribute to mitochondrial energy depletion, neurotransmitter imbalance, and loss of resilience under stress.
| Related Marker | Interpretation Insight |
|---|---|
| Tryptophan | Low tryptophan alongside low kynurenine suggests precursor deficiency; normal tryptophan with low kynurenine indicates reduced enzyme activity. |
| Serotonin | If serotonin is high while kynurenine is low, more tryptophan is being shunted toward serotonin rather than energy metabolism. |
| NAD+ | Low NAD+ often accompanies low kynurenine due to reduced substrate flow. |
| Neopterin | Low or normal neopterin indicates low immune activation and reduced IDO stimulation. |
| Vitamin B6 / B3 Markers (Cystathionine, Nicotinamide) | Abnormalities indicate cofactor insufficiency slowing pathway efficiency. |
By analyzing kynurenine together with these markers, clinicians can pinpoint whether the low levels are due to nutrient insufficiency, low enzyme activity, mitochondrial dysfunction, or immune suppression.
Chronically low kynurenine can lead to:
Reduced NAD+ synthesis and ATP production, impairing mitochondrial energy generation.
Neurotransmitter imbalances, with excessive serotonin relative to energy metabolism.
Decreased neuroprotective metabolites (kynurenic acid), increasing vulnerability to oxidative stress.
Poor immune regulation, reducing resilience against infections and chronic inflammation.
Fatigue and burnout, due to reduced redox and methylation capacity.
Over time, this imbalance can contribute to energy depletion, mood disorders, immune weakness, and slower recovery from stress.
Replete cofactors essential for kynurenine metabolism: vitamin B6, niacin (B3), iron, magnesium, and zinc.
Ensure adequate dietary tryptophan intake from sources such as turkey, fish, tofu, and eggs.
Include NAD+ precursors like niacinamide, nicotinamide riboside (NR), or NMN.
Support mitochondrial health with CoQ10, alpha-lipoic acid, and carnitine.
Avoid chronic cortisol suppression; maintain healthy adrenal rhythm through sleep, moderate exercise, and relaxation.
Support immune integrity with omega-3 fatty acids, vitamin D, and probiotics.
Moderate physical activity and endurance training can enhance kynurenine aminotransferase (KAT) activity, promoting neuroprotective kynurenic acid production.
Limit excessive alcohol, caffeine, or toxin exposure that interferes with enzyme function.
Low kynurenine levels reflect an underactive tryptophan metabolism—often signaling insufficient enzyme activity, nutrient cofactors, or mitochondrial capacity. Because the kynurenine pathway is crucial for both neurotransmitter regulation and NAD+ energy synthesis, its suppression can contribute to fatigue, low mood, poor stress tolerance, and immune weakness.
Interpreting kynurenine alongside tryptophan, serotonin, NAD+, and neopterin on the Neurotransmitter XL panel helps clarify whether the imbalance stems from nutritional deficits, low enzyme activation, or metabolic sluggishness.
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Yes, you can. When entering values for the biomarker, you will see an "Edit Range" button. Click this button, and you'll have the option to enter a custom range.
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Optimal Result:
1 - 2.7 µmol/g Crea.