The Urine Test That Finally Gave Me Answers: 5 OAT Markers Every Chronic Illness Warrior Should Know
I spent years collecting “normal” lab results while feeling anything but normal.
Normal thyroid. Normal CBC. Normal metabolic panel. Normal, normal, normal and yet I was exhausted in a way sleep couldn’t touch, anxious without a clear reason, and carrying a brain fog so thick that some days it felt like thinking through wet cement. Every doctor I saw had a different theory. Nobody had a unifying answer.
Then I ran the Mosaic Diagnostics Organic Acids Test a 76-marker urine analysis that measures what conventional blood panels don’t even look for and the picture changed completely. Markers were flagged that explained my neuroinflammation, disrupted gut bacteria, impaired mitochondrial function, and a nutrient depletion pattern that had been silently undermining my health for years.
One of those markers told me my brain was, quite literally, on fire.
This is not a post about scary lab results for the sake of drama. It’s a post about knowledge the kind of specific, actionable metabolic knowledge that can change the trajectory of your health when everything else has come back “fine.” Below are the five OAT markers that have taught me the most, explained in plain language, with the science behind why each one matters.
You can view a real Mosaic Diagnostics OAT sample report here to see exactly how these markers appear in context and how the full 76-marker panel is organized.
First: What Makes the OAT Different From Standard Lab Testing?
Most routine lab panels are designed to detect disease that’s already fully expressed. They’re looking for things like dangerously low thyroid hormones, anemia severe enough to show up in red blood cell counts, or blood sugar elevated enough to confirm diabetes. What they’re generally not designed to do is detect the functional imbalances and subclinical disruptions that precede those disease states the early-warning biochemistry of a body under stress.
The Organic Acids Test operates in that space. It measures compounds that your body produces as metabolic byproducts and excretes through urine byproducts that reflect, in remarkable detail, what’s happening in your gut microbiome, your mitochondria, your neurotransmitter pathways, and your vitamin and mineral status at a cellular level.
When Clostridia bacteria overgrow in your colon, they produce specific compounds that show up in your urine. When your mitochondria are running inefficiently, the backup metabolites appear in your urine. When certain fungi are proliferating in your gut, their waste products including oxalates get absorbed into circulation and excreted through your kidneys. The OAT catches all of it.
That’s what makes it such a high-yield test for people who’ve been chasing answers. It doesn’t just describe what you have it gives you mechanistic clues about why you feel the way you do.
If you’re ready to get that level of data on your own body, order the Organic Acids Test through My Labs for Life here and start seeing the full picture.
OAT Marker #1: Quinolinic Acid When Your Immune System Turns Against Your Brain
There is a molecule your own immune system can produce that is classified as a brain neurotoxin. Most people have never heard of it. It’s called quinolinic acid, and when it showed up dramatically elevated on my OAT, my practitioner used the words “your brain is on fire” and meant it biochemically.
Here’s the pathway: tryptophan, the amino acid you get from protein-rich foods, follows several metabolic routes in the body. One of those routes the kynurenine pathway normally ends with the production of NAD+, a vital energy molecule every cell needs to function. Quinolinic acid (QA) is an intermediate step along that route, and under healthy conditions, an enzyme called QPRT converts it quickly into NAD+ and moves the process along.
The problem starts when that conversion gets blocked. And two major drivers of that blockage are systemic inflammation and toxic burden particularly exposure to phthalates, the endocrine-disrupting chemicals found in plastics, food packaging, personal care products, and vinyl materials. When phthalates inhibit QPRT, quinolinic acid backs up in the system and accumulates.
And elevated quinolinic acid doesn’t just sit there passively. It’s a potent NMDA receptor agonist meaning it overstimulates receptors on brain neurons and drives an excessive influx of calcium into those cells. This calcium flooding triggers a cascade of damage: oxidative stress, mitochondrial dysfunction, free radical formation, and in sufficient concentrations neuronal death. Research has also shown that QA can compromise the structural integrity of the blood-brain barrier, the tight-junction protection that separates circulating blood from delicate brain tissue.
The macrophages and microglia your brain’s own immune cells are the primary producers of quinolinic acid during neuroinflammatory states. This means the very cells meant to protect your brain can, under the wrong conditions, produce a compound that damages it.
For people experiencing unexplained anxiety, cognitive decline, depression, emotional dysregulation, or the kind of neurological heaviness that feels bigger than ordinary stress, elevated quinolinic acid is a pattern worth ruling in or out. The OAT measures it directly. Most standard panels don’t.
OAT Marker #2: 4-Cresol The Gut Bacteria Marker That Explains Dopamine Problems
If quinolinic acid is the marker I find most alarming, 4-cresol is the one I find most clarifying and I mean that as a genuine compliment to the test.
4-cresol is a metabolite produced specifically by pathogenic Clostridium species in the gut most notably Clostridium difficile and related strains. These bacteria aren’t part of a healthy microbiome. They’re opportunistic pathogens that proliferate when beneficial bacteria are depleted, often after antibiotic use, high-sugar diets, immune stress, or chronic dysbiosis.
The compound they produce, 4-cresol, has one documented primary mechanism of harm: it inhibits dopamine beta-hydroxylase (DBH), the enzyme responsible for converting dopamine into norepinephrine. When DBH gets blocked, dopamine builds up in neurons and nerve endings faster than it can be converted. That excess dopamine doesn’t just sit still it gets oxidized into reactive quinones that are directly toxic to neural tissue, and the downstream deficiency of norepinephrine creates its own problems: poor concentration, mood dysregulation, fatigue, emotional blunting, and impaired stress response.
What I love about this marker and why I’d run this test just for 4-cresol alone is how clearly it explains things. If 4-cresol is elevated and homovanillic acid (HVA, the downstream dopamine metabolite) is also elevated on the same report, you have a complete picture: gut bacteria are producing a compound that’s jamming your dopamine conversion pathway. That’s not a hypothesis. It’s metabolic evidence.
About 15% of OATs show 4-cresol as the primary positive Clostridium marker. It’s less common than its companion marker HPHPA, but equally significant in terms of neurological impact. And because treatment targeted antimicrobials followed by probiotic restoration is relatively well-defined, it’s a highly actionable finding.
This is a prime example of the OAT’s strength: not just flagging that something is wrong, but pointing to a specific mechanism with a specific origin and a specific treatment path.
OAT Marker #3: HPHPA The More Common Clostridia Signal, and Why It Matters
While 4-cresol is the more specific Clostridium marker, HPHPA 3-(3-hydroxyphenyl)-3-hydroxypropionic acid is the one that shows up most frequently in positive tests. Roughly 80% of OATs with elevated Clostridium markers show HPHPA as the primary finding, making it one of the most common actionable abnormalities on the test.
Like 4-cresol, HPHPA is a Clostridium metabolite that inhibits dopamine beta-hydroxylase. The mechanism is the same: dopamine backs up, toxic dopamine quinones form, norepinephrine drops, and both the central nervous system and the sympathetic nervous system are affected. What distinguishes HPHPA clinically is its potency in children with severe gut Clostridium overgrowth, HPHPA concentrations in urine can sometimes exceed even the major norepinephrine metabolite VMA by a factor of a thousand on a molar basis. It can, in extreme cases, be the dominant organic acid in the entire urine sample.
Dr. William Shaw’s foundational research, which identified HPHPA in the urine of patients with autism and schizophrenia at dramatically elevated concentrations compared to controls, opened an entirely new window into gut-brain dysbiosis. Subsequent research from laboratories around the world has replicated those findings consistently high HPHPA and 4-cresol are a recurring biochemical signature in populations with significant neurological and behavioral disruption.
For adults without autism who are simply dealing with unexplained mood issues, anxiety, cognitive difficulties, or treatment-resistant depression, elevated HPHPA is worth taking seriously. The gut’s impact on brain chemistry is not a metaphor or a wellness trend. In the case of HPHPA and the dopamine pathway, it is a documented molecular mechanism.
OAT Marker #4: Oxalates The Sneaky Systemic Disruptor Hidden in “Healthy” Foods
This is the marker that surprises people the most including people who eat an extremely clean, plant-rich diet. In some cases, especially those people.
Oxalic acid (and its ionic form, oxalates) is an organic acid that enters your body from three primary sources: your diet, fungal organisms in your gut, and your own metabolism. On the OAT, oxalate markers appear alongside yeast and fungal markers and the relationship between the two is important to understand.
Certain fungal species, particularly Aspergillus and Candida, use glyoxalate as an intermediate in their own energy production pathways. As a byproduct, they produce oxalates. When someone has significant gut fungal overgrowth, oxalate production often rises proportionally. This means that elevated yeast markers and elevated oxalates on the same OAT report are frequently telling the same story: a fungal population that has grown beyond what a healthy microbiome would permit.
But here’s the part that catches people off guard: many of the highest-oxalate foods are things people commonly consider health foods. Spinach. Almonds. Beets. Swiss chard. Dark chocolate. Nut-heavy ketogenic and paleo diets can drive significant dietary oxalate loads. People who’ve adopted green smoothies as a daily ritual are often consuming large amounts of raw spinach one of the most oxalate-dense foods in existence.
When oxalate burden gets too high, the systemic effects are far-reaching. Oxalates bind to calcium and iron, forming crystals that can deposit in soft tissue kidneys (the classic kidney stone), joints, muscles, and in some cases the vulvar tissue (a recognized contributor to vulvodynia). Oxalate-bound calcium gets pulled from circulation, creating downstream calcium and magnesium imbalances. Oxalates have been associated with chronic muscle pain, fibromyalgia-like presentations, fatigue, and impaired mitochondrial enzyme function.
The OAT is currently the most practical clinical tool for assessing oxalate status in functional medicine practice. It also helps distinguish whether the oxalate burden is coming primarily from diet, from active fungal overgrowth, or from a metabolic issue a distinction that completely changes the treatment approach.
If you’ve been eating “clean” for years and still feel terrible, this marker is worth a close look.
OAT Marker #5 (The Hidden Gem): Elevated Pyruvate + Lactic Acid Your Body’s Secret B1 Signal
This is the one I want to make sure doesn’t get skipped, because it’s the marker that most often gets overlooked even by experienced practitioners and the downstream implications are significant.
On the OAT, there’s a section measuring pyruvic acid and lactic acid as part of the mitochondrial metabolic profile. When both markers are elevated simultaneously, it creates a pattern with a very specific biochemical meaning: the pyruvate dehydrogenase complex (PDH) is not functioning efficiently.
PDH is the enzymatic gateway between glycolysis (breaking down glucose) and the Krebs cycle (generating cellular energy). Every time your body converts pyruvate into acetyl-CoA to enter the energy-production cycle, PDH is the enzyme making that conversion happen. And PDH requires thiamine vitamin B1 as an essential cofactor. Without adequate thiamine, PDH slows down. Pyruvate backs up. Lactic acid accumulates. And your cells increasingly rely on inefficient anaerobic metabolism to produce energy.
This is what functional thiamine deficiency looks like at the biochemical level and here’s the important nuance: it can show up on the OAT before a standard serum thiamine test ever flags anything. Blood levels of thiamine can appear in the normal reference range while the cells are functionally depleted, particularly in people with high carbohydrate intake (which burns through thiamine rapidly), regular alcohol use (which aggressively depletes B1), or high coffee and tea consumption (tannins impair B1 absorption).
The symptoms of subclinical thiamine deficiency are broad, vague, and commonly attributed to other things: persistent fatigue that doesn’t resolve with rest, heart palpitations, tingling or numbness in the hands and feet, poor memory, difficulty concentrating, anxiety, and feeling disproportionately exhausted after carbohydrate-heavy meals. Because these symptoms overlap with dozens of other conditions, B1 deficiency frequently goes unrecognized and untreated.
An additional marker on the OAT 3-methyl-2-oxovaleric acid can add further weight to the thiamine deficiency picture when elevated alongside pyruvate and lactic acid. Together, these markers make a functional argument for B1 repletion that a standard vitamin panel would likely miss entirely.
This is why I consider the OAT indispensable for anyone dealing with chronic, unexplained symptoms. The patterns it reveals aren’t exotic rarities. They’re common, clinically significant findings that point toward real, correctable imbalances if you know how to read them.
Connecting the Dots: Why These Five Markers Often Appear Together
One of the things I’ve come to appreciate most about the OAT is how its markers interact. These five don’t always show up in isolation.
High quinolinic acid frequently coexists with markers of systemic toxic burden and immune activation the same conditions that also deplete B vitamins and stress mitochondrial function. Elevated HPHPA or 4-cresol from Clostridia overgrowth often correlates with elevated oxalates, because a dysbiotic gut that permits pathogenic bacterial growth typically also has an impaired environment for controlling fungal populations. Mitochondrial inefficiency from B1 deficiency creates further oxidative stress, which can drive the kynurenine pathway further toward quinolinic acid production.
In other words, these markers don’t exist in isolation inside your body, and they don’t exist in isolation on the test. They build on each other. They tell an interconnected story about a system under compound stress and the OAT gives you the ability to read that story in a way that no single conventional test can.
This gut-to-brain-and-back dynamic is exactly the territory that Healthy Gut Healthy Brain was built to explore. Every article, resource, and recommendation on this site is grounded in the understanding that your gut and brain are not separate systems operating independently they are deeply, biochemically linked, and what disrupts one disrupts the other. The OAT is one of the clearest windows into that connection available to us right now.
What Happens After You Run the Test?
Getting the OAT back is just the beginning. The real value is in knowing what to do with the results.
Elevated quinolinic acid calls for investigating and reducing toxic burden, particularly phthalate exposure, while supporting the kynurenine pathway with targeted nutrients and anti-inflammatory strategies. Elevated 4-cresol and HPHPA point toward an antimicrobial protocol targeting pathogenic Clostridium, followed by robust probiotic restoration and a diet that doesn’t feed the overgrowth. Elevated oxalates may require a temporary low-oxalate diet combined with antifungal treatment if fungal markers are simultaneously elevated. The elevated pyruvate/lactic acid B1 pattern typically calls for thiamine supplementation and the response is often faster and more noticeable than people expect.
None of this is one-size-fits-all, and none of it should be self-directed without qualified support. But having the data puts you in a completely different position than operating on guesses and process-of-elimination. You can prioritize. You can track. You can retest and see whether the interventions are moving the markers.
That feedback loop test, treat, retest is how functional medicine actually works. And the OAT is one of the best tools available for creating it.
Who Should Consider Running the Organic Acids Test?
This test tends to be highest-yield for people dealing with any of the following:
Neurological and mood-related symptoms: chronic anxiety, depression, brain fog, poor memory, cognitive fatigue, emotional dysregulation, or mood instability that hasn’t responded fully to standard approaches.
Energy and mitochondrial issues: persistent fatigue that rest doesn’t resolve, post-exertional malaise, or exhaustion disproportionate to activity level.
Gut-related symptoms: bloating, irregular digestion, food sensitivities, history of antibiotic use, or a suspicion that gut health is affecting other systems.
Pain and inflammation: unexplained muscle aches, joint pain, chronic widespread pain, or inflammatory conditions without a clear root cause.
Autoimmune and complex chronic illness: conditions where gut dysbiosis, toxic burden, and nutrient depletion are likely contributing factors.
Children and adults on the autism spectrum, where Clostridium overgrowth, dopamine pathway disruption, and oxalate burden are documented and commonly undertreated metabolic contributors.
If you’ve been told your labs are normal while you continue to feel far from it, the OAT is often the test that finally starts filling in the blanks. It’s not a replacement for comprehensive clinical care, but it adds a layer of specificity and actionability that most conventional workups simply don’t provide.
How to Order and What to Expect
The Mosaic Diagnostics OAT is collected entirely at home. After ordering, a kit arrives with collection materials and instructions. You collect the first morning urine of the day concentrated after an overnight fast and ship the sample back to the lab. Results are typically returned within two weeks.
The 76-marker report is thorough, and the marker categories are organized clearly enough that even a first-time reader can begin to see the patterns. That said, working with a practitioner experienced in OAT interpretation will help you extract the most value from the results particularly when multiple markers interact, as they often do.
The sample OAT report from Mosaic Diagnostics is worth reviewing before you order if you want to familiarize yourself with the format and understand what you’ll be looking at.
Your symptoms have a biochemical story. The OAT helps you read it.
About Healthy Gut Healthy Brain
Healthy Gut Healthy Brain exists because the path to feeling well doesn’t start with a prescription it starts with understanding. The gut-brain axis is one of the most researched and most underutilized frameworks in modern health, and this site is dedicated to making that science accessible, personal, and actionable. From functional testing deep-dives like this one, to practical protocols for reducing neuroinflammation, rebalancing the microbiome, and supporting the nutrients your brain and gut need most everything here is designed to help you maintain optimal health from the gut to the brain and back again. You deserve to understand your own biology. That’s what we’re here for.
These statements are for educational purposes and are not intended to diagnose, treat, cure, or prevent any disease. Always work with a qualified healthcare practitioner to interpret lab results and guide treatment decisions.
References
- Guillemin GJ. “Quinolinic acid, the inescapable neurotoxin.” The FEBS Journal. 2012;279(8):1356–1365. doi:10.1111/j.1742-4658.2012.08485.x Landmark review establishing quinolinic acid as a brain endogenous excitotoxin produced by macrophages and activated microglia during neuroinflammation, acting via NMDA receptor agonism and disruption of the blood-brain barrier.
- Mosaic Diagnostics. “How the Organic Acids Test Provides Insights into Toxic Exposures.” MosaicDX.com, 2024. https://mosaicdx.com/resource/how-the-organic-acids-test-provides-insights-into-toxic-exposures/ Describes the mechanism by which environmental phthalates inhibit the enzyme converting quinolinic acid to nicotinamide, causing QA accumulation and downstream neuroinflammation.
- Shaw W. “Increased urinary excretion of a 3-(3-hydroxyphenyl)-3-hydroxypropionic acid (HPHPA), an abnormal phenylalanine metabolite of Clostridia spp. in the gastrointestinal tract, in urine samples from patients with autism and schizophrenia.” Nutritional Neuroscience. 2010;13(3):135–143. doi:10.1179/147683010X12611460763968 Foundational paper identifying HPHPA and 4-cresol as Clostridium metabolites significantly elevated in urine samples from patients with autism and schizophrenia.
- Shaw W. “Inhibition of Beta-oxidation Pathway of Fatty Acids and Dopamine-Beta-Hydroxylase by Phenyl Derivatives of Short-Chain Fatty Acids from Gastrointestinal Clostridia Bacteria is a Major Cause of Autism.” Published via Mosaic Diagnostics / PubMed. PMID: 37363147. Details the mechanism by which HPHPA and 4-cresol inhibit dopamine beta-hydroxylase, leading to dopamine accumulation, norepinephrine deficiency, and toxic dopamine quinone production in the brain.
- Passmore IJ, Letertre MPM, Preston MD, et al. “Clostridioides difficile infection increases circulating p-cresol levels and dysregulates brain dopamine metabolism: linking gut-brain axis to autism and other neurologic disorders.” bioRxiv (preprint). 2021. doi:10.1101/2021.10.22.465382 Demonstrates that C. difficile infection drives elevated circulating p-cresol (4-cresol), inhibits dopamine beta-hydroxylase, and disrupts dopaminergic signaling in brain regions relevant to neurodevelopmental disorders.
- Pascucci T, Colamartino M, Fiori E, Sacco R, Coviello A, Ventura R, et al. “P-cresol Alters Brain Dopamine Metabolism and Exacerbates Autism-Like Behaviors in the BTBR Mouse.” Brain Sciences. 2020;10(4):233. doi:10.3390/brainsci10040233 Animal model study confirming that 4-cresol exposure directly alters brain dopamine metabolism and amplifies autism-like behavioral phenotypes.
- Mosaic Diagnostics. “Guide to Oxalate Test Results.” MosaicDX.com, 2024. https://mosaicdx.com/resource/oxalates-great-plains-laboratory/ Clinical overview explaining how Candida and Aspergillus species produce oxalates via glyoxalate pathway intermediates, and how proportional vs. disproportional oxalate elevations on the OAT guide clinical interpretation.
- Mosaic Diagnostics. “Oxalate Control.” MosaicDX Clinical Reference Document. https://mosaicdx.com/wp-content/uploads/2023/02/GPL_Oxalate-Control.pdf Reviews the three primary sources of urinary oxalates (diet, fungal overgrowth, and human metabolism), the correlation between elevated arabinose and high oxalates, and management strategies including calcium-magnesium citrate supplementation.
- HealthMatters.io. “Oxalic Acid Organic Acids Test (OAT) Biomarker Explanation.” https://healthmatters.io/understand-blood-test-results/oxalic Summarizes the clinical significance of elevated urinary oxalates on the OAT, including associations with kidney stones, fibromyalgia, vulvodynia, autism, muscle pain, and cardiac abnormalities.
- MedLink Neurology. “Thiamine (B1) Deficiency.” Updated 2025. https://www.medlink.com/articles/thiamine-deficiency Comprehensive neurological reference establishing that impaired pyruvate dehydrogenase activity from thiamine deficiency leads to elevated pyruvate and lactate, noting that subclinical thiamine deficiency presents with vague symptoms including fatigue, irritability, headache, and lethargy long before overt neurological signs appear.
- Donnino M. “Effect of Thiamine on Pyruvate Dehydrogenase Activity in Septic Shock.” NIH Grant K02-HL107447-01A1. NIH-funded research establishing thiamine as an essential cofactor for the pyruvate dehydrogenase complex, confirming that thiamine deficiency causes anaerobic metabolism predominance and lactic acidosis, and that thiamine administration can rapidly reverse this biochemical pattern.
- Mosaic Diagnostics. “Organic Acids Test (OAT) 101: Essential Information for the Practitioner New to the OAT.” MosaicDX.com, 2025. https://mosaicdx.com/resource/organic-acids-test-oat-101-essential-information-for-the-practitioner-new-to-the-oat/ Practitioner-facing primer covering OAT marker categories, pattern recognition for Clostridium (4-cresol, HPHPA, HVA correlation), the kynurenine pathway and quinolinic acid as a neuroinflammation marker, and clinical treatment considerations for bacterial overgrowth.