Quinolinic acid is a key intermediate in the kynurenine pathway, the primary route by which the amino acid tryptophan is metabolized into nicotinamide adenine dinucleotide (NAD+)—a molecule essential for cellular energy, mitochondrial function, and redox balance. Although it plays an important physiological role as a precursor for NAD+ synthesis, quinolinic acid can become neurotoxic when produced in excess, contributing to oxidative stress, inflammation, and excitatory neurochemical imbalances.
On the Neurotransmitter XL panel, quinolinic acid serves as a sensitive biomarker of chronic stress, immune activation, mitochondrial dysfunction, and neuroinflammation. When tryptophan metabolism is shifted toward the kynurenine pathway—typically by inflammation or cortisol—quinolinic acid levels may rise. This metabolite’s dual nature makes it both vital and potentially harmful: necessary for energy metabolism but detrimental when uncontrolled.
Under normal conditions, quinolinic acid is produced in small, regulated amounts as part of the NAD+ biosynthetic process. The final enzymatic conversion of quinolinic acid into NAD+ requires quinolinate phosphoribosyltransferase (QPRT), an enzyme dependent on adequate magnesium, niacin, and mitochondrial integrity.
In balanced metabolism, this pathway supports:
NAD+ synthesis for mitochondrial ATP production.
Cellular repair and redox control.
Energy-demanding processes such as DNA maintenance, neurotransmitter regulation, and detoxification.
However, when inflammation, oxidative stress, or nutrient deficiencies impair QPRT or downstream conversion, quinolinic acid can accumulate, triggering neurotoxic and pro-oxidative effects.
Quinolinic acid sits at a crucial intersection between inflammation, mitochondrial energy metabolism, and nervous system health. Elevated or imbalanced levels offer key diagnostic clues about the body’s internal stress and immune state. Specifically, it helps identify whether:
The kynurenine pathway is overactivated by inflammatory cytokines (e.g., interferon-γ).
Mitochondrial conversion to NAD+ is impaired, leading to toxic buildup.
Chronic stress or infection has shifted tryptophan away from serotonin toward stress metabolism.
Cofactor deficiencies (B3, magnesium, or zinc) are slowing NAD+ synthesis.
When interpreted alongside tryptophan, kynurenine, NAD+, neopterin, and serotonin, quinolinic acid offers one of the most complete pictures of how stress and inflammation affect both the brain and body energy systems.
Quinolinic acid rises through a convergence of stress-related and inflammatory processes that activate the enzymes indoleamine 2,3-dioxygenase (IDO) and kynurenine monooxygenase (KMO)—driving tryptophan metabolism down a pro-oxidative path.
Cytokines such as interferon-γ, TNF-α, and IL-6 upregulate IDO and KMO.
Activated immune cells (especially macrophages and microglia in the brain) produce quinolinic acid as part of the inflammatory response.
Elevated neopterin levels often accompany this pattern, confirming immune involvement.
When QPRT, the enzyme that converts quinolinic acid to NAD+, is impaired—often due to mitochondrial dysfunction, oxidative stress, or environmental toxin exposure (e.g., phthalates)—quinolinic acid accumulates.
This buildup reduces NAD+ availability, lowering ATP production and contributing to chronic fatigue, cognitive decline, and mood instability.
Conversion of quinolinic acid to NAD+ requires niacin (vitamin B3) and magnesium.
Deficiencies in vitamin B6, folate, or iron also slow related reactions in the kynurenine pathway, leading to partial blockages and excess quinolinic acid.
Quinolinic acid can generate reactive oxygen species (ROS) and nitric oxide (NO), amplifying oxidative stress.
This contributes to mitochondrial damage, enzyme inhibition, and impaired detoxification cycles.
Prolonged stress elevates cortisol and indirectly increases kynurenine and quinolinic acid through TDO activation.
This metabolic shift reduces serotonin synthesis while enhancing neurotoxic and energy-draining metabolites.
Excess quinolinic acid acts as an NMDA receptor agonist, overstimulating excitatory glutamate receptors in the central nervous system. This can result in:
Neuroinflammation and excitotoxicity (nerve cell overstimulation and oxidative damage).
Sleep disturbances and anxiety, due to excessive neural excitation.
Mood disorders such as depression, linked to serotonin depletion and increased inflammation.
Fatigue and cognitive slowing, caused by reduced NAD+ synthesis and mitochondrial impairment.
Chronic pain sensitivity, as quinolinic acid disrupts neuronal signaling and amplifies inflammatory pain pathways.
Over time, excessive quinolinic acid contributes to a “burnout” state—where both neurotransmitter balance and mitochondrial energy output are compromised.
Though less common, low quinolinic acid may indicate:
Low tryptophan availability (dietary deficiency or poor absorption).
Reduced IDO/TDO activity, often from low cortisol or immune suppression.
Impaired kynurenine pathway activation or low enzyme expression.
Inadequate stress or immune signaling leading to underactive metabolism.
In such cases, low quinolinic acid often parallels low NAD+, suggesting reduced mitochondrial output rather than inflammation.
| Related Marker | Interpretation Insight |
|---|---|
| Tryptophan | Low tryptophan with high quinolinic acid indicates chronic inflammation and excessive tryptophan diversion. |
| Kynurenine | Elevated kynurenine with high quinolinic acid suggests overactive IDO/KMO enzyme activity. |
| NAD+ | Low NAD+ alongside high quinolinic acid implies blocked conversion, possibly from cofactor deficiency or mitochondrial dysfunction. |
| Neopterin | Elevated levels confirm immune activation (interferon-γ–mediated). |
| Serotonin | Low serotonin combined with high quinolinic acid reflects tryptophan depletion and neurotransmitter imbalance. |
| Lactate / Pyruvate / Citrate | Abnormal levels indicate mitochondrial energy disruption secondary to oxidative stress. |
Together, these markers allow clinicians to determine whether quinolinic acid elevation results from inflammation, stress-driven enzymatic activation, nutrient depletion, or mitochondrial overload.
Persistent quinolinic acid elevation can contribute to:
Chronic fatigue and low energy (due to NAD+ depletion).
Cognitive fog, irritability, or mood swings.
Depressive symptoms and anxiety (linked to low serotonin and neurotoxicity).
Neurodegenerative stress from excitatory overactivation.
Sleep and circadian rhythm disturbances (from impaired melatonin balance).
Heightened oxidative and nitrosative stress, accelerating cellular aging.
Because of its broad systemic effects, quinolinic acid is a key marker of the biochemical interface between stress, inflammation, and energy metabolism.
Focus on anti-inflammatory nutrients such as curcumin, omega-3 fatty acids (DHA/EPA), resveratrol, and berberine.
Address underlying infections or immune triggers that elevate interferon-γ.
Support the gut barrier to reduce endotoxin-related immune activation.
Replete niacin (vitamin B3) and magnesium to support QPRT function and NAD+ synthesis.
Consider NAD+ precursors like nicotinamide riboside (NR) or NMN, under medical guidance.
Support mitochondrial health with CoQ10, alpha-lipoic acid, L-carnitine, and antioxidants.
Moderate exercise enhances kynurenine aminotransferase (KAT) activity, shifting metabolism toward kynurenic acid (neuroprotective) rather than quinolinic acid (neurotoxic).
Manage chronic stress to reduce cortisol and TDO stimulation.
Ensure sufficient vitamins B6, B12, folate, iron, and zinc, as deficiencies can slow safe tryptophan-to-NAD+ conversion.
Support GABA activity with calming botanicals such as valerian, passionflower, or magnesium glycinate to offset excitotoxic stress.
Quinolinic acid is a critical yet delicate metabolite—vital for NAD+ production but harmful in excess. Elevated levels indicate inflammatory activation of the kynurenine pathway, leading to neurotoxicity, oxidative stress, and mitochondrial dysfunction, while low levels may reflect suppressed metabolism or nutrient insufficiency.
On the Neurotransmitter XL panel, quinolinic acid—interpreted alongside tryptophan, kynurenine, NAD+, neopterin, and serotonin—provides a deep look into the body’s stress–inflammation–energy axis.
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A low quinolinic acid level on the Neurotransmitter XL panel suggests that the tryptophan–kynurenine–NAD+ pathway is underactive or insufficiently engaged. Because quinolinic acid is an essential intermediate in the body’s conversion of tryptophan to NAD+ (nicotinamide adenine dinucleotide)—a key cofactor for mitochondrial energy metabolism—low levels often reflect reduced cellular energy turnover, limited enzyme activity, or nutrient deficiencies required for proper conversion.
While elevated quinolinic acid is associated with inflammation and oxidative stress, low levels may indicate inadequate substrate availability or suppressed metabolic activity, resulting in impaired NAD+ synthesis and reduced mitochondrial performance. This can lead to fatigue, low stress tolerance, and poor recovery at the cellular level.
Quinolinic acid is produced in the kynurenine pathway, which metabolizes tryptophan through a series of enzymatic steps to ultimately generate NAD+, the molecule central to redox balance and energy metabolism.
The enzymes indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO) convert tryptophan into kynurenine.
Kynurenine then progresses through multiple enzymatic reactions—some of which depend on vitamin B6, niacin (B3), magnesium, zinc, and iron—to form quinolinic acid.
Finally, quinolinic acid is converted to NAD+ via quinolinate phosphoribosyltransferase (QPRT).
If any part of this chain is slowed, blocked, or starved of cofactors, quinolinic acid levels may fall below optimal ranges, indicating a downregulated or inefficient NAD+ synthesis pathway.
When upstream precursors like tryptophan or kynurenine are depleted, less substrate is available for quinolinic acid production. This is often seen in:
Low dietary protein intake
Malabsorption or gut inflammation reducing amino acid absorption
Stress-related depletion of tryptophan diverted to serotonin or immune pathways
Chronic undernutrition or restrictive diets
Low quinolinic acid can occur when IDO or TDO, the rate-limiting enzymes initiating the kynurenine pathway, are underactive. Causes include:
Low cortisol output (adrenal insufficiency or HPA-axis suppression)
Blunted immune activation or reduced interferon-γ signaling
Excess antioxidant or anti-inflammatory use, which may suppress normal immune enzyme function
This pattern reflects a body not mounting a typical stress or immune response—sometimes seen in burnout, chronic fatigue, or immune exhaustion.
The kynurenine-to-quinolinic acid pathway relies on several micronutrients to function efficiently:
Vitamin B6 – for enzymatic conversions along the pathway
Niacin (vitamin B3) – regulates NAD+ synthesis and pathway feedback
Iron and zinc – critical for enzyme activity
Magnesium – supports mitochondrial reactions and QPRT enzyme function
Deficiencies in these nutrients slow conversion rates, leading to low quinolinic acid and low NAD+.
Because quinolinic acid conversion to NAD+ occurs in the mitochondria, poor mitochondrial health can create feedback inhibition—reducing production even upstream. When ATP levels are low, the body may downregulate NAD+ synthesis to conserve resources, resulting in low quinolinic acid.
This pattern is common in chronic fatigue, low thyroid function, or metabolic slowdown.
An imbalanced gut microbiome can reduce the availability of tryptophan and its conversion through the kynurenine pathway. Certain bacteria metabolize tryptophan into indoles rather than kynurenine derivatives, lowering quinolinic acid output. Gut inflammation and dysbiosis may also suppress local IDO activity.
While high quinolinic acid is linked to inflammation, too little immune signaling can result in underactivation of the kynurenine pathway. This can occur when inflammation is excessively suppressed by:
Chronic use of corticosteroids or NSAIDs
High-dose antioxidant or anti-inflammatory supplements
Long-term immune-suppressive therapies
In such cases, the pathway remains inactive, and NAD+ synthesis slows.
Low quinolinic acid reflects reduced metabolic throughput rather than toxicity, but the downstream consequences can be equally significant. Common symptoms include:
Persistent fatigue or low energy
“Burned out” sensation or low stress resilience
Brain fog, slow cognition, and low motivation
Mood flatness or mild depression (linked to low NAD+ and serotonin balance)
Slow recovery after stress or exertion
Cold intolerance or sluggish metabolism
These symptoms often overlap with those of low NAD+ or impaired mitochondrial function.
| Related Marker | Interpretation Insight |
|---|---|
| Tryptophan | Low tryptophan with low quinolinic acid suggests precursor deficiency; normal tryptophan with low quinolinic acid points to low enzyme activity. |
| Kynurenine | Low kynurenine and quinolinic acid together indicate pathway underactivation. |
| NAD+ | Low NAD+ alongside low quinolinic acid implies inefficient energy metabolism or nutrient limitation. |
| Neopterin | Low or normal neopterin suggests reduced immune activation or cytokine signaling. |
| Serotonin | May be elevated relative to quinolinic acid if tryptophan is being preferentially converted toward serotonin rather than energy metabolism. |
Interpreting quinolinic acid in this context helps distinguish nutrient-related metabolic sluggishness from pathway overactivation due to inflammation.
Low quinolinic acid may reflect:
Underactive NAD+ production, leading to cellular energy deficits.
Mitochondrial slowdown, affecting metabolism, brain function, and recovery.
Low immune responsiveness, seen in chronic stress or immune exhaustion.
Reduced redox capacity, lowering resistance to oxidative damage.
Neurotransmitter imbalance, with serotonin favored over NAD+ synthesis.
Over time, this pattern can contribute to low vitality, mood dysregulation, and poor physical resilience.
Replenish niacin (B3), magnesium, vitamin B6, zinc, and iron.
Support mitochondrial metabolism with CoQ10, alpha-lipoic acid, L-carnitine, and ribose.
Consider NAD+ precursors such as nicotinamide riboside (NR) or NMN under medical guidance.
Ensure sufficient protein intake and amino acid balance.
Correct gut dysbiosis to improve tryptophan absorption and metabolism.
Manage chronic stress to maintain balanced IDO/TDO activity.
Avoid over-suppressing inflammation unless clinically necessary.
Support balanced immune activity with vitamin D, omega-3 fatty acids, and moderate physical activity.
Replenish antioxidants such as glutathione, vitamin C, and selenium.
Limit exposure to environmental toxins and heavy metals that inhibit mitochondrial enzymes.
Low quinolinic acid suggests a sluggish or underactive kynurenine pathway, often due to nutrient deficiency, mitochondrial inefficiency, or low enzyme activity rather than inflammation. This pattern typically points to impaired NAD+ synthesis, resulting in low energy, fatigue, and reduced resilience.
Interpreting quinolinic acid alongside tryptophan, kynurenine, NAD+, and neopterin on the Neurotransmitter XL panel helps clarify whether low levels stem from metabolic slowdown, poor nutrient availability, or suppressed immune signaling.
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I have been using Healthmatters.io since 2021. I travel all over the world and use different doctors and health facilities. This site has allowed me to consolidate all my various test results over 14 years in one place. And every doctor that I show this to has been impressed. Because with any health professional I talk to, I can pull up historical results in seconds. It is invaluable. Even going back to the same doctor, they usually do not have the historical results from their facility in a graph format. That has been very helpful.
Karin
Advanced Plan Member since 2020
What fantastic service and great, easy-to-follow layouts! I love your website; it makes it so helpful to see patterns in my health data. It's truly a pleasure to use. I only wish the NHS was as organized and quick as Healthmatters.io. You've set a new standard for health tracking!
Paul
Healthmatters Pro Member since 2024
As a PRO member and medical practitioner, Healthmatters.io has been an invaluable tool for tracking my clients' data. The layout is intuitive, making it easy to monitor trends and spot patterns over time. The ability to customize reports and charts helps me present information clearly to my clients, improving communication and outcomes. It's streamlined my workflow, saving me time and providing insights at a glance. Highly recommended for any practitioner looking for a comprehensive and user-friendly solution to track patient labs!
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3-OH-Kynurenine, Adrenaline, Betaine, Carnitine, Choline, Citrate, Citrulline, Creatinine enzyme. (Urine), Cystathionine (Vitamin B6), Dopamine, GABA, Glutamate, IDO-Activity, KMO-Activity, Kynurenic acid, Kynurenine, Lactate, Methylmalonic acid (Vitamin B12), NAD (Nicotinamide- Adenine- Dinucleotide), Neopterin, Nicotinamide, Nicotinic acid, Noradrenaline, Phenylalanine, Pyruvate, Quinolinic acid, S- Adenosylmethionine, SAM/SAH Ratio, Serotonin, Suberic acid, Trimethylamine, Trimethylamine N-Oxide, Tryptophan, Tyrosine
