The material contained within this presentation is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader’s discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility. Views expressed are those of the presenter and not necessarily those of Mosaic Diagnostics.
Webinar Q&A:
Q: I’m new at testing and trying to figure out which tests are important to start using in my practice. I was doing gut testing but seems like OAT is more comprehensive.
A: I always start with the OAT, and then complement it with a stool analysis is possible.
Q: Can you share the top two to three tests you use on patients initially?
A: I use the OAT, MycoTOX Profile, and Hair Heavy Metals. I will often add the IgG Food MAP too if possible. If there are a lot of gut symptoms too then a comprehensive digestive stool analysis is worthwhile as well.
Q: Do you recommend a biofilm disruptor prior to the Organic Acids Test?
A: No
Q: Does low pyroglutamic acid (on far left of scale) indicate adequate GSH?
A: Yes. The report indicates that low pyroglutamic has no known clinical significance, only high pyroglutamic.
Q: How do you treat a fatty acid metabolism problem?
A: A simple approach is L-carnitine supplementation. However, to go deeper, and this may be necessary for certain people, you need to determine what are the reasons behind the elevated fatty acid markers.
Q: How much elevated out of range could be considered as bad or negative?
A: For most markers, as I mentioned in my lecture, above the 2nd standard deviation line. There are exceptions such as high normal pyroglutamic in the view of known or suspected environmental chemical exposures that can indicate a worsening trend in glutathione status. The nuances within the OAT and the respective sections and certain markers become more obvious overtime and experience. A good example of this would be high normal HVA and low VMA, but an elevated HVA/VMA ratio. Even though the HVA and VMA are within their “normal” range, the ratio elevation indicates a developing block of the dopamine beta-hydroxylase or existing underactivity of this enzyme.
Q: If #7 is high and #21 is high, do you need to address dietary oxalates at all or is it more likely the candida?
A: Make this judgement based on the clinical picture of the individual. Not everyone needs to do the exact same thing for high oxalate. If they are symptomatic of oxalate, then a more aggressive program can be implemented. If you are picking up on high oxalate and they are not symptomatic and the arabinose is high too, then all they may need to do is treat the candida. If they are consuming high oxalate foods and the arabinose is high then addressing the candida and having them reduce high oxalate foods will usually take care of the elevated oxalate.
Q: In the first bacteria section, what markers are considered beneficial?
When do you order stool comprehensive test?
A: I feel a stool analysis is complementary to the OAT. The stool test will provide different and additional information. I always start with the OAT, but I have no problem doing a stool test as well.
Q: Is the OAT test still effective if a patient is on numerous psychiatric medications and supplements?
A: Yes, however, the medications may alter the neurotransmitter section, so you need to be aware of this.
Q: How do you conduct an OAT test on someone who is taking several medications/natural supplements?
A: I just have them do the test and make sure they follow the test instructions on what to avoid. Other than that, I personally do not have them stop medications or supplements.
Webinar Transcript
This is an automated AI transcript of the Webinar video seen above. For the most accurate account of Dr. Woeller’s presentation, please watch the webinar video on this page.
Hi everyone. Thank you for joining us today. I am Dr. Michelle Maddux. On behalf of Mosaic Diagnostics, I would like to welcome Dr. Julie Greenberg and am so thrilled to hear her OAT 101 fundamentals of the Organic Acids Test. Throughout the webinar, please put any questions that you have in the Q and A chat box. I’ll be compiling those and we’ll get to this as many as we possibly can, the last 10 or 15 minutes of our presentation. Thank you Dr. Green for being here today. And the floor is yours.
Thanks Michelle. And thanks to everyone for joining today. I’ll just give you a brief introduction. I’m Dr. Julie Greenberg. I’m a licensed naturopathic doctor in California, Oregon, and Washington. I’m also a registered herbalist through the American Herbalist Guild, and I specialize in dermatology at my clinic, the Center for Integrative and Naturopathic Dermatology. I also have a course education site at Root Cause Dermatology, and I hold degrees from Baier University, Stanford University, and Northwestern University.
All right, so we got some objectives for today for the next hour and a half. First of all, if you’re new to the OAT, I want to introduce you to the OAT. I want to show you the value of the OAT because it’s deep. I want to simplify analysis of the OAT. It is one of the more complicated functional medicine labs and I want to get you up and running using the OAT. Hopefully at the end of this hour and a half, you’ll feel competent enough to start using the OAT if this is new for you.
So my methodology — obviously I said I specialize in derm and I treat derm patients only. So eczema, psoriasis, acne, rosacea, and hair loss. These are all though, even though we think of them while it’s happening on the skin or the hair, what is she doing? They’re all inherently systemic inflammatory diseases. And therefore, in order to treat the root cause, I go to the gut, like probably most of you on here. And so I run an OAT and a stool test on every single patient. Everybody does at least one.
Sometimes I run additional tests. Some tests we’ll be talking about like mycotoxin, TOXDetect, heavy metals or hormone tests. At the end of this, I’m going to do a case study and show you how I use the OAT, and we’re going to look at some results for some other of these tests as well. So hopefully that will be helpful for you guys to see how do we translate like a theory of using the OAT with actually like a patient and helping them.
So why do I use an OAT on every single patient? Well, like I said, I also use a stool test. And stool tests are fantastic. I love them, but they aren’t perfect at showing every element. They’re pretty good at the bacterial elements and digestive markers, but they don’t show everything specifically. I feel like when it comes to fungal microbes, it’s not as good. And fungal organisms are a critical part of the puzzle, and you’re going to see that in this case study.
So I need to know about candida yeast as well as molds. Things like aspergillus and fusarium bacteria. So tests are great at bacteria for the ones that they test for, but they might not test for every bacteria. And so kind of getting a general overview of how much bacterial overgrowth is in a patient can be helpful from the OAT. Methylation and toxic exposure problems — I heavily rely on the OAT for this, and you’re going to see this in the case study. Nutritional markers are super, super helpful.
And then there’s areas of the OAT that I use less: things like mitochondrial function and neurotransmitters.
Okay, so it’s called the Organic Acids Test. So let’s start with organic acids. What are they?
So an organic acid is defined as an organic compound with acidic properties, that’s not particularly helpful, but most of them, if you go back to your biochem, they’re the COOH, carboxylic acids, also sul acids, alcohols and thiols. So names that you might recognize are like lactic acid, citric acid, oxalic acid, and uric acid.
And you know what happens is, within the body, we are breaking down products and our intestinal bacteria are breaking down products — amino acids, neurotransmitters, and intestinal bacteria action on our food breakdown. These degradation products, they go into the blood and then of course they go into the urine because what is urine after all, it’s just filtered blood. So these organic acid compounds are going into the urine and this OAT test is testing for these compounds.
All right, so the why is the OAT so complex? Well, there’s a lot going on in the OAT and where we’re gonna look at it. It’s not straightforward.
The nice thing about a stool test is like they’re actually testing for the organisms. So that’s pretty easy to understand. It’s like, oh, there’s H. pylori and the amount — that’s the end of that line. It’s H. pylori. As we said, these are testing metabolites. There’s a lot of biochemistry. So you’re not gonna see the organism, you’re gonna see metabolites and then you gotta figure out what to do with it. So it can feel a little overwhelming at first.
Years ago when I first looked at the OAT, I was overwhelmed and I was like kind of trying to figure it out and I was like, nope. I put it aside for a while and then I realized I was missing out on a big piece of the picture and helping my patients. So I came back and I dedicated to really learning and understanding the OAT. And what I’m hoping is that I can take all my knowledge and distill it down into this next hour and a half and make it really simple for you guys to get up and using so that you don’t feel overwhelmed. It really is worth learning, I promise you. It’s really powerful test and you will get it and sooner than you think, if you’re new to it — hopefully in about an hour and a half, you’re gonna feel pretty good about it.
Okay, so what’s the quick start to using the OAT? How are we gonna do this?
We’re gonna use some principles to keep it simple. First, we’re gonna grock it — and if you’ve never heard the term “grock,” it’s actually a Silicon Valley tech term, and it means to kind of grasp in the meaning of a lot of data, right? You don’t need to know each individual data point. It’s like, okay, what does this mess of data mean? And without needing to understand that minutia, we’re gonna get actionable data out of it. So we’re gonna grock it.
And you don’t even have to use every marker or even every section particularly to get started. We’re gonna chunk it. And what do I mean by chunk it? I mean, you don’t have to go through like each individual line item and the biochemistry of the OAT in order to use it. So you can analyze sections as a whole to get actionable data and you’re gonna see how to do that.
And then we’re gonna connect it. And that is pattern recognition. It’s gonna help us connect the dots between different sections and markers in different sections. Again, to get actionable data.
And what is underlined in all three sections? Actionable data. Because after all, right, you’re not taking a biochem exam at the end of this. No, we wanna use these functional medicine tests in order to figure out how to help patients and action on it. That’s what’s important. So that’s what we’re gonna focus on today.
So the actual OAT test has about, you know, 74 or maybe more individual lines and they’re split up into these sections. So what we’re gonna do today is we’re gonna go section by section and you’ll see very clearly we’re in different sections and we’re gonna kind of go through how do you analyze it and get meaning out of the values.
When we look at the actual lab results, you should know that there’s reference ranges. We’ll look at that and Mosaic splits it into four different reference range values. So it’s split up by gender, either male or female, and age either 13 years and under or over the age of 13. So there’s four different reference values depending on your patient.
And if you’ve never seen OAT representations, each line is gonna look like this. And just to make sure everyone understands what this is: so the 212, this number would be the value for your patient and this is the top of the reference range — 219.9. So this upper limit of normal for this right here is 219.9. Your patient came back at 212. Okay, what does that mean?
If this was down here in the orange box, this is the mean. And anything on either side of the orange, in the orange box is one standard deviation away from the mean plus or minus. If you’re still in between the bars, the lower limit and upper limit of normal, but you’re off the orange block, you are in two standard deviations away.
You can be outside the normal range like this patient, right? It’s the same marker, but this patient value is 3,894. So definitely high and over the upper limit of normal. So you’re gonna see an H for high. If it was the other way and below this lower limit you would see an L for low.
So just to make sure everyone’s on the same page as we start to go through it.
Related Tests and Panels
All right, so let’s do a quick little poll and we’re gonna ask the question: Are you currently using the OAT in your practice? And then Drew, whenever you feel like enough people have answered, you can go ahead and end the poll and show the results.
Okay, so we’ve got a 48, a 12, and a 48. Okay, good. So there’s actually a fair number of new people on here and that’s good because this is — I actually crafted this OAT 101 for both — someone who’s never used it before and someone who’s maybe using it and has been using it, you know, somewhat, but is still feeling a little bit overwhelmed by it. So everybody who answered, hopefully this presentation will help you.
Okay, and with that, let’s get started. So we’re gonna go into the first section you’re gonna see on the OAT, which is intestinal microbial overgrowth. And there’s two sections on here. There’s fungal and bacterial. And then again, at the end of this analysis, I’m gonna give you some tips and tricks and then we’re gonna look at a case study and then I’m gonna take questions at the end.
Okay? So this yeast and fungal marker section is for me personally, the one that is of most value that I use the most. I really love this section again, because as much as I love stool tests, they don’t do a great job with fungal organisms. And fungal organisms are underappreciated in terms of the impact they have on our patients and needing to address them to get them better.
So here we see it’s marker 1 to 9 and we can see, okay, there’s lots of things and again, these names don’t have meaning to most of us, but how do we translate it into meaning? So marker 7, arabinose — this is kind of the proxy for candida. And so we can see here immediately, even if you’ve never used an OAT, now that we understand what these boxes mean, you know, everything with an H — this is above the normal. So this person has 1, 2, 3, 4, 5, 6 high fungal markers — that’s high.
Sometimes I will only have number 7 be high and that’s enough for me to go treat because that’s a candida. But this person really is having a lot of fungal overgrowth. Okay?
So I always start with arabinose. For me, it’s kind of my main fungal marker. So I go down to 7, I see what’s happening with the candida — okay yes, this person is having candida overgrowth. What does the rest of this mean? Well, we’re gonna chunk it. So for me, markers 2, 4, and 5 — I know it says aspergillus here, but I still don’t include that. 2, 4, and 5 for me are really for aspergillus. And aspergillus is a mold. Mold is a multicellular fungal organism. Yeast like candida is a single-celled fungal organism.
So if any of these — 2, 4 and 5 — are high, then I’m starting to be concerned about aspergillus overgrowth. This person has two, so yep. And then marker 9, tricarballylic acid, is kind of more specific for fusarium mold. These patients also got overgrowth of fusarium mold. And then the other fungal markers are kind of non-specific. So marker 1, 3, 6, and 8 are kind of general. It could be the ones we’re seeing here. It could be other mold species — we don’t know.
But it is safe to say that whoever this patient is has a high fungal load and needs to be treated. So this talk is more about interpretation and not treatment. So you would treat with your appropriate antifungals, whether that’s herbs and stuff like that, or conventional pharmaceuticals. This person needs antifungal treatment.
Okay, let’s look at the bacterial marker section. So there’s kind of like two blocks to it. There’s these general bacterial markers and then there’s clostridia bacterial markers. I definitely use these and I like to cross-reference this with a stool test for more detail.
So the top section here from 10 to 14 — these are kind of just general bacterial overgrowth. And I know 14 says beneficial, but I don’t ignore this either because I’ve seen these high with like not-so-beneficial. And sometimes even the beneficial bacteria, when they get overgrown, they become — they act more pathogenic.
So if I’m seeing any highs in this area, I am concerned with bacterial overgrowth. And again, I’m gonna go back and look at my stool test. If you’re only using the OAT, certainly on the basis of these results, I would absolutely do antibacterial treatment.
And then the next section below at 15 to 18 are specifically clostridia bacterial markers. And clostridia is a genus. There’s good-guy clostridia and bad-guy clostridia, but these are really looking for more bad-guy clostridia. So you can see for example, 17 — 4-cresol — that’s a metabolite of C. diff (Clostridium difficile), not a good guy. You know, C. botulinum — these are not great clostridia strains. These are not like clostridia butyricum, you know, ones that we like.
So any highs here too are gonna tell you that you got some treatment to do here. And again, some stool tests do test for certain strains like C. diff, so you can cross-reference. And on the basis of this, I would definitely be treating this patient with antibacterials — whether that’s herbs like your berberine, your neem, your oregano or pharmaceuticals, whatever you’re trained in or you know, TCM, whatever you do.
Okay, the clostridia markers. So these — about 25% of OATs, about a quarter of them — seem to have an elevated clostridia marker. Most of the time it’s 16, this HPHPA. Maybe about 15% of the time it’s the 4-cresol with the C. diff. It’s less likely that you’re gonna get 15 or 18, but any of these, I’m paying attention to and wanting to treat down.
We’re gonna see this clostridia block come back in the neurotransmitter section. And so you can see how you can connect different parts of the OAT. So we’re gonna come back to these guys in a bit.
Okay, let’s look at the next section of the OAT, which is the oxalate metabolites. So we can see three here — glyceric, glycolic, and oxalic acid. What do these mean?
Well, these three can indicate a couple different things. One, they can indicate fungal overgrowth, and I usually see this oxalic acid high with candida overgrowth. And for this one, we’re actually gonna drop down into the biochemistry for just a minute. So we’re gonna do both with the OAT — we’re gonna stay high level and then for certain areas we’re gonna drop down and then we’re gonna come back out. So we’ll look at that in a minute.
Foods can elevate things like oxalic acid, and it’s not uncommon — about 80% of OATs will come back with high oxalic acid. I see a lot of candida on my OATs.
Okay, so we said fungal overgrowth is one thing you can be looking for. There can be hyperoxaluria, you know, sometimes genetic kind of SNP issues, but check in on consumption of high oxalate foods for your patients. Here’s a list of kind of more high-oxalate foods. So particularly if a patient is doing things like juicing celery or putting a ton of spinach in smoothies — if they’re really going hard on some of these foods — that can increase the oxalates and raise that oxalic acid marker for them.
And high oxalates can lead to mitochondrial dysfunction. So high oxalates can form crystals in the body. We see here a picture of calcium oxalate crystals in urine. And you see like these crystals have sharp edges.
So some symptoms in patients who have high oxalates could be muscle or joint pain where crystals are lodging in the muscle or joints, vulvodynia — that’s unexplained pain with urination — they can get into the bladder, headaches, kidney stones. If you have a patient with recurrent kidney stones, check on this oxalate marker. Even something like thiamin deficiency.
So there’s a lot going on with oxalates. Now I mentioned I often see oxalic acid or oxalates high with candida overgrowth. What’s going on there?
Well, you’re gonna see a couple different points where the microbes in our gut are affecting things in our body. And this is one.
So here we are in the Krebs cycle. So if you took biochemistry, this should look familiar, right? The Krebs cycle is for cellular respiration — the production of ATP and the mitochondria. And usually this is kind of going around.
Well, candida gets in there and it steals isocitrate from the Krebs cycle and it uses an enzyme called isocitrate lyase for its own purposes. And it kicks out this product and eventually oxalates. So when you have a lot of candida, it can be going through this and kicking out a lot of oxalic acid.
And we’re gonna see this in the case study. Usually when I clean up the candida, that oxalic acid number will come back down. And in the case study you’re gonna see initial labs, treatment, and retest. So we’ll see what happens with that.
Yeah, so that’s that little cycle pulled out by the candida that causes the high oxalates.
Okay, mitochondrial function. Now this is a pretty rich section. This is a section where I will say I’m not a heavy user of this section. Some people are, and this is 101, so we’re staying high level. But there are deep dives into this through Mosaic Edge. There’s a whole day OAT seminar coming up with Dr. Kurt Woeller, who’s excellent. He goes way into the biochemistry and more into this kind of stuff. So we’re gonna stay high level today with the mitochondrial stuff, but you can go much deeper in it if this is an area of interest for you.
High level — mitochondria, all of my patients remember the energy powerhouse of the cell. So they are primarily responsible for cellular energy, both in animals and plants. So in animals, cellular respiration is happening in the mitochondria — production of ATP. It’s the cellular energy for life, right? We have to be doing this. And even in plants, they’re involved in photosynthesis.
And what’s really cool is we think that our mitochondria came originally from specialized bacteria. And I just think it’s wild — the idea that we’ve incorporated bacteria into ourselves. So, you know, are we animals? Are we bacteria? I mean, maybe we’re both.
So the functions of the mitochondria, of course, are many. We talked about ATP production in that mitochondrial matrix, but our mitochondria are responsible for detoxification, central to steroid synthesis. A lot of people forget it turns cholesterol into pregnenolone. Pregnenolone is that kind of like mother steroid molecule that all the rest are made from. Even cortisol production starts here, and many other functions are going on in the mitochondria.
We all know how important mitochondrial function is, but one of the downsides of producing ATP — which again we have to — that’s life, that’s cellular energy — is that we know that free radicals are generated through the, each time we are creating ATP in the mitochondria. The radicals leak from the mitochondria. They form reactive oxygen species like superoxide anion and hydroxyl radicals.
And of course, the problem with free radicals is that it’s like an unstable atom, right? It’s only got one unpaired electron and it needs to stabilize itself to become a healthy atom. The danger is that it’s gonna go steal an electron from a healthy atom like our tissue or our DNA, and that causes DNA damage. Or antioxidants to the rescue — they’re gonna donate an electron, stabilize that free radical and prevent oxidative or DNA damage.
Okay, so we said the Krebs cycle is occurring here in the matrix of the mitochondria and it’s producing those reactive oxygen species. So mitochondria have special DNA — they have something called mtDNA or maternal DNA. And unfortunately, DNA throughout our body actually has pretty robust DNA damage repair mechanisms. Our DNA is damaged all the time, even just through replication, but it’s pretty good at fixing itself. Mitochondrial DNA is more susceptible to mutations because it doesn’t possess quite the robust DNA repair mechanisms. And there’s a high lipid content in mitochondria so they can start accumulating lipophilic toxins that can lead to mitochondrial dysfunction.
There are many diseases related to mitochondrial dysfunction that a lot of functional medicine doctors specialize in. For me, I use this section mostly if my patient has fatigue. Of course I’m checking in on things like iron and thyroid, but I want to check in on the health of their mitochondria and also with toxic things. But, you know, you might want to check in on the mitochondria of your patients for weakness, strokes, seizures, cardiomyopathy, arrhythmias, cognitive issues, diabetes, impairment of hearing, vision, growth, function of different organ systems.
As we said, the mitochondria are involved in life kind of all over the body. So how might we support mitochondria? Well of course we want to reduce exposures that are gonna damage it. Environmental toxins, pathogens in the gut, helping our patients figure out where they’re making poor lifestyle choices. Some medications can damage the mitochondria and excessive UV radiation. And we want to give mitochondrial support — maybe with antioxidants. We all know glutathione, vitamin C, vitamin E, selenium, quercetin, sulforaphane and bioflavonoids, nutrients like B vitamins and magnesium — and helping our patients make healthy choices.
Okay, so all of that. And here we are now back at the OAT in the mitochondrial section. So 22 to 32 — it’s like, wow, okay, there’s a lot of markers — this is a chunk it. I just take 22 to 32 and I’m looking at it as a block. I’m gonna look for multiple high values. For me, that’s kind of like three or four or more. And I’m definitely starting to get worried that my patient has got mitochondrial dysfunction and needs some support and I need to kind of dig into some of those other issues that we just talked about — figure out what’s the problem in the mitochondria.
So we know it can be higher with toxins. That might be an issue. These mitochondrial markers — actually I do a lot of pediatric stuff, especially eczema and stuff — it can be higher in babies. So I’m not actually concerned if this was an infant like three or four months old. I’m not gonna actually be super concerned about this. They just tend to kind of have high mitochondrial function. They’re just babies. It’s just pretty normal.
But in an adult — I mean, look how many highs there are — like this adult, we really need to figure out what is going on. And one way I like to support with mitochondrial dysfunction, particularly for fatigue, is through CoQ10 and L-carnitine. I do find that it’s very helpful for patients with the mitochondrial dysfunction.
So as we said, it’s occurring in the Krebs cycle. And just like an example, if you wanted to drill down on the biochemistry, you can see here — so succinic, fumarate — you know, these are saying Krebs cycle metabolites. We can see it’s from the Krebs cycle, like succinate, succinic acid, fumarate, fumaric acid, malate, malic acid. So you can see where the biochemistry is coming from.
And again, if you really want to drill down into the biochemistry of all this and go line by line, you certainly can. There’s resources at Mosaic and upcoming again — that upcoming full day OAT analysis with Dr. Woeller where you could dig down into the more nitty gritty of each line. Sometimes it’s helpful — like suberic acid elevation can be linked with like an environmental chemical exposure. But again, for me, I’m not going through 74 lines. I’m really kind of, you know, I see a lot of patients and for this I’m kind of just chunking it — and it’s perfectly fine to do that.
The neurotransmitter section — this is another pretty dense section. And again, this isn’t the area where I spend usually a lot of my resources or where a lot of my patients are coming up with issues. So being 101, we’re going to cover it at a high level. And if this is an area of interest to you, there’s lots of resources again where you can really dive down much more in depth onto the neurotransmitter section.
But let’s talk about it kind of high level. And okay, so here we have, you know, from 33 to 40, but it’s kind of split into two. So split into the phenylalanine and tyrosine metabolites, and then it’s split into the tryptophan metabolites.
At a high level, you know, I think we know that dopamine, norepinephrine and epinephrine are get-up-and-go neurotransmitters, and serotonin is the more kind of calming transmitter — kind of that happy hormone type serotonin. So that’s just at a high level.
But let’s kind of drill down into these two sections and we’ll start with the top. So we’re going to start with the phenylalanine and tyrosine metabolites. And so the metabolites that are being measured in the urine are HVA, VMA, and DOA. And then 35 and 37 are just ratios that they’re giving you — what is the HVA to VMA? And then what is the HVA to DOA ratio?
Okay, so what does this mean? HVA stands for homovanillic acid. We see it here. That’s a metabolite of dopamine. VMA is vanillylmandelic acid and that’s a metabolite of epinephrine and norepinephrine.
And let’s keep in mind again that these are only metabolites of the neurotransmitters. We’re not measuring the neurotransmitters themselves. So we can make extrapolations, but if you were to really want to get heavy into the system, you might want to be measuring neurotransmitters themselves directly if you find some of these markers are off on the OAT.
But let’s take a high-level look at kind of what’s going on on this chart. So we said that these are phenylalanine and tyrosine metabolites because as we can see, the process for making dopamine comes from phenylalanine and tyrosine. Then DOPA is made with the help of vitamin B6, dopamine is created, and then dopamine can go one of two ways.
If we have the enzyme dopamine beta hydroxylase along with copper and vitamin C, we can convert dopamine into norepinephrine and then we can convert norepinephrine into epinephrine. And the breakdown product of norepinephrine and epinephrine is the VMA, vanillylmandelic acid. Or dopamine can take a different path. It can go up to DOA and then get broken down into homovanillic acid or HVA.
So again, we’re measuring the HVA. The DOA is measured and the VMA is being measured.
There’s factors that can impact the body’s ability to metabolize and excrete these neurotransmitters — things like genetics and the enzymes (the MAO and COMT enzymes), nutrient cofactors — are they deficient in copper or vitamin C or vitamin B6? Supplements that they’re taking and bacteria.
So we’re gonna come back to those clostridia in a minute — or now. We’re doing it now. Okay, so this is one of those connect sections where I said when we were in the clostridia we’re gonna come back to this because it’s going to impact the dopamine.
So here we are. So remember on the first page under the bacterial section there’s general bacteria and there’s the not-good-guy clostridia. So we’re looking at the bad-guy clostridia. And let’s focus in on 16 and 17 — HPHPA and 4-cresol. These are going to be the ones we’re going to be looking at.
There’s a connection between high levels of either of these clostridia and what you’re going to see in this phenylalanine and tyrosine metabolites — so that dopamine section. It is a common finding when the clostridia is high to have HVA high or DOA high or the ratios high — and then to have the VMA more kind of either low or suppressed.
What in the world is going on here? Clostridia is inhibiting dopamine beta hydroxylase.
Let’s look at this so that it makes sense because I think it’s easier to visualize it.
Related Tests and Panels
Okay, so remember we’ve got the two types. We’ve got Clostridium difficile, which breaks down into 4-cresol, and there’s some other clostridia species that are not good guys that break down into HPHPA. Both of these will inhibit the enzyme dopamine beta hydroxylase. This is just a different representation of this, but we already talked about dopamine needs dopamine beta hydroxylase to be converted into norepinephrine.
So if this DBH is being inhibited by clostridia, then it’s going to choke off the ability for dopamine to go down this pathway. So that’s going to lower this and lower VMA, and now it is going to choose to go this way. That’s going to raise DOA and raise HVA. So that is what’s happening with the clostridia.
Again, if this happens and your patient’s high in clostridia and these neurotransmitters are off and it looks like they’re high in dopamine and DOA and low in norepinephrine/epinephrine, usually when you treat the clostridia down it goes away.
But dopamine can be high for other reasons too. If there’s low copper or low vitamin C, it’s going to have trouble converting. DOA can be elevated if you’re lacking magnesium, SAMe, or COMT. So again, just because some of these metabolites are high doesn’t necessarily mean there’s problems with the neurotransmitters. So you might want to check it.
Now why might HVA be elevated?
Well, if somebody is supplementing with L-DOPA, dopamine, tyrosine, or phenylalanine, that could elevate the HVA. Ingestion of things like aspartame or salicylates, either high salicylate food or aspirin. Toxic metal exposure can do it. The effects of truly elevated dopamine can be damaging to neurons and mitochondria and can deplete glutathione.
The next section — the tryptophan metabolites.
Now we see the serotonin metabolite 5-HIAA, and we’ll look at quinolinic and kynurenic. Okay, just a quick reminder — serotonin, it’s a neurotransmitter, and a lot of the serotonin is actually created in the gut by the intestinal enterochromaffin cells. Some in the brain as well, but there’s definitely a gut-brain connection with serotonin.
And serotonin regulates — well, we’re learning more and more about it — everything from gastrointestinal motility (so if you’ve got a SIBO patient, maybe they’ve got a motility issue), peripheral vascular tone, cerebral vascular tone, platelet function. It could be connected with mood disorders, migraines, IBS, hypertension — it impacts a lot of systems. And again, the 5-HIAA is the metabolite marker on the OAT.
So let’s go look at this.
Now of course it’s called tryptophan metabolites because this is not part of that tyrosine pathway. This is tryptophan. So tryptophan in the body can go down two pathways. It can go down the serotonin pathway — and we can see that we actually also make melatonin from serotonin — or it can go down the quinolinic pathway.
We can’t control which way tryptophan is gonna go. Stress, infection, and immune stimulation are all gonna trigger tryptophan to go down this quinolinic pathway. So you might want to think twice before you supplement with tryptophan if you’re trying to increase serotonin, because you may actually be increasing quinolinic acid in a patient.
5-HTP might be a better option because 5-HTP cannot go this way, become tryptophan, and then become quinolinic. 5-HTP is going to continue down this pathway to serotonin and/or melatonin and 5-HIAA.
But before you start supplementing with 5-HTP or tryptophan, just be aware of something called serotonin syndrome. It is a potentially life-threatening reaction that can result from medication or supplements that build up toxic levels of serotonin in the body.
So of course serotonin is good — we talked about all the benefits — but too much serotonin is bad. There can be mild symptoms like dilated pupils or rapid heartbeat, but there can be severe symptoms and even death with serotonin syndrome.
Drugs that can cause serotonin syndrome are SSRIs — antidepressants like fluoxetine, escitalopram, sertraline — very commonly prescribed ones. So check and make sure if your patient is on some of these drugs, you may want to think twice before you start supplementing with 5-HTP or tryptophan. Certainly if you’re seeing any of these symptoms, you’re gonna want to action on that pretty quickly.
Okay, so let’s go back. We talked about this pathway — let’s talk about this quinolinic pathway.
So it’s a downstream product of the kynurenine pathway. We know it’s involved with tryptophan and it’s a marker of inflammation. So quinolinic acid can be neurotoxic. It’s produced by macrophages and activated microglia. One example: phthalates in the body. So toxic exposure can drive quinolinic acid.
We know it acts as a neurotoxin, a pro-inflammatory mediator, a pro-oxidant — creating unstable radical molecules — and can alter the integrity of the blood-brain barrier. More and more research seems to be coming out about the role of quinolinic acid in neuroinflammatory diseases. So again, if your specialty or your interest is in neuroinflammatory diseases, brain stuff, this is an area where you’d want to drill down into it. And again, Mosaic has resources to help you drill down on this pathway and get more detail beyond just a 101.
And then that last marker in the block — kynurenic — I kind of use it, you know, a high kynurenic could mean that the vitamin B6 is low. We’re going to look at vitamin B6 in the next section.
Now folate metabolism — we’re in our next section.
So we’re moving on from the neurotransmitters into folate metabolism. And there are two markers in here — the purine metabolites — which are kind of giving us an indicator of how folate might be doing: uracil and thymine. Purine nucleosides are building blocks of RNA. So this is kind of showing us the activity of cellular turnover. It can indicate if these are high, high cellular turnover or issues with methylation.
We’re going to talk about methylation a lot towards the end with marker 59. But this is a connect. So if you’ve got high levels here, go to the end of the OAT and check out the methylation toxic exposure marker — we’ll be talking about it in a minute.
It’s actually normal — I see these one or two elevated a lot in babies and children. I think there’s just high cellular turnover — babies are undergoing rapid growth and they need a lot of RNA and DNA. So again, this is something in like a very young pediatric population, I’m not concerned about high marker 41 or 42.
But in adults, I do want to kind of figure out: is this a methylation issue? What’s going on here? I mean, in the worst case scenario, it could be cancer. Now of course we’re not going to jump to that conclusion, but — and do not say to your patients, “you might have cancer” — but just something at the back of your mind. If these are high, you’re going to want to kind of drill down a little bit and figure out what’s going on. And it might just be that they need some folate support.
The next section we’re going to go into is the B vitamin markers. So here we see vitamin B12, B6, and B5. And we’re going to see methylmalonic acid, xanthurenic acid, and pantothenic acid.
So methylmalonic acid is that functional marker for B12. We talked about methylmalonic acid earlier in the webinar in relation to propionic acid, right? So if propionic acid is high and MMA is high, well, that’s two markers that could be indicating B12. So for me, that’s just more confidence that this patient is needing B12 support.
Xanthurenic acid is the B6 marker. Again, B6 is important in neurotransmitter metabolism, and B6 is involved in a ton of enzymatic reactions. So this is kind of your one shot on the OAT to check in on B6 status.
Pantothenic acid is vitamin B5, and this is a bit more of an intake marker. I don’t see this come up very much, honestly. I find the MMA and the xanthurenic acid to be more functionally useful.
Then we go into the methylation section — and that’s marker 59 — figlu, formiminoglutamic acid. This is really important and you’re going to want to correlate this with your other methylation labs if you’re doing MTHFR or homocysteine, etc. I actually really like having this figlu marker on the OAT, and I find it to be helpful.
When figlu is high, it’s a marker that there may be insufficient folate to carry out methylation and the metabolism of histidine. So it is an indirect marker of methylation status. You can see this elevated in folate deficiency or folate dysfunction. Again, if I’m seeing this high, I’m going back and checking my folate metabolism markers and then considering methylation support.
We’ve got a few detoxification markers in the next section. This includes pyroglutamic acid, orotic acid, and sulfate. These are 60 through 62. These are going to show how detoxification is happening. For me, sulfate is one of the more helpful ones. That’s marker 62.
So this is part of phase II liver detox. Sulfate is used in the sulfation pathway. A low level of sulfate can impair that sulfation pathway, and I find that to be very clinically relevant. So I do supplement with sulfate, typically in the form of magnesium sulfate — Epsom salt baths. That’s my go-to with patients who have low sulfate levels. It’s a really nice way to replenish.
Then we move into the oxidative stress section. That’s markers 63 through 65. These are some of the most important markers on the OAT for me — glutathione status and oxidative stress.
The one I really like here is marker 63, pyroglutamic acid. This is a marker that can reflect glutathione recycling. So a high level of pyroglutamic acid can indicate that glutathione is being turned over — maybe there’s oxidative stress — and the body is trying to replenish.
I use this as a marker for antioxidant needs. If this is elevated, I think about glutathione support — maybe IV or liposomal — and other antioxidants like vitamin C.
We also have 8-hydroxy-2-deoxyguanosine (8-OHdG), but that’s not on the OAT — it’s on the MycoTOX Profile. So if you want to dig more into oxidative stress or DNA damage, you might want to run that test as well.
The final section before the case study is amino acid metabolism. This is where I’ll admit I don’t spend a ton of time in this section. It’s mostly markers of abnormal amino acid metabolism — things like phenylalanine, tyrosine, and branched-chain amino acids.
This section becomes more helpful in patients with inborn errors of metabolism or if you’re dealing with a pediatric or metabolic case. For most adults in a general clinical population, this section is less useful.
Okay, let’s move into the case study. I want to show you how we put all of this together.
So here’s a pediatric patient, an 8-year-old male who came in with eczema. The eczema started as a baby. It was itchy, flared often. His mother said it was sometimes triggered by foods, but it was always there to some degree.
On physical exam, he had widespread eczema lesions — cheeks, back of arms, behind the knees. He also had allergic shiners, nasal congestion, and a white-coated tongue. That white-coated tongue had me suspicious for fungal overgrowth.
His diet was mostly a standard American diet. He ate a lot of packaged foods. A lot of sugar. And his mother noted that he craved carbs and sugar. That’s a big clue for me when I’m thinking about fungal overgrowth.
So we ran an OAT and here’s what we found.
Related Tests and Panels
In the yeast/fungal section, look at marker 2 — arabinose — elevated. That’s the main candida marker. This, combined with his symptoms and white tongue, confirmed fungal overgrowth for me.
We also saw high oxalic acid. That’s marker 21. Remember what we said earlier — oxalates often go up when candida is high. So that was another confirmation.
In the bacterial section, his general markers were okay, but marker 16 — HPHPA — was elevated. That clostridia marker. I knew that was going to have implications in the neurotransmitter section.
Sure enough, in neurotransmitters, his HVA was elevated. DOA was elevated. And the ratio of HVA to VMA was high. VMA itself was low-normal. So this matched that clostridia picture — high dopamine metabolites, low norepinephrine/epinephrine metabolites.
In the mitochondrial section, he had several elevations. I didn’t count every one, but it looked like more than three or four were high. So that told me there was likely some mitochondrial dysfunction, probably due to oxidative stress and fungal overgrowth.
In the vitamin markers, his xanthurenic acid was high. That’s B6. I wanted to make sure he was getting enough of that. His methylmalonic acid was borderline — not too high — so I wasn’t worried about B12.
In the detox section, his sulfate was low. I started him on Epsom salt baths to support sulfation and detox.
So here was my plan: I started with antifungal herbs and probiotics to crowd out the candida. I gave him NAC to support glutathione and oxidative stress, and magnesium sulfate baths for detox. I also cleaned up his diet — reduced sugar and added more whole foods.
We re-ran the OAT after about 12 weeks.
Arabinose came down significantly. Oxalic acid came down. HPHPA was now in range. Neurotransmitters looked better. Mitochondrial markers were down.
And clinically, his eczema improved dramatically. The itch was gone. His skin was mostly clear. His mother said his focus and behavior improved too.
This case shows how the OAT can connect multiple systems. We saw fungal overgrowth, neurotransmitter imbalance, oxidative stress, and mitochondrial dysfunction — all from one test. And treatment based on those findings helped resolve the root cause.
Thank you so much for attending this OAT 101 webinar.
I hope this gave you a better understanding of how to approach the Organic Acids Test and how to apply it clinically in your own practice. Remember, you don’t need to understand every single line item to use this test effectively. Learn the main sections, find your clinical anchors, and build from there.
There are more advanced trainings available if you want to go deeper, and you can always contact Mosaic Diagnostics for further support.
Thanks again, and I wish you the best in helping your patients heal.
