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In this episode, you will learn about the impact of oxalates on health and how oxalates may be a secondary mycotoxin.

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About My Guest

My guest for this episode is Emily Givler.  Emily Givler is a Functional Genomic Nutrition Consultant, researcher, and lecturer with a thriving clinical practice at Tree of Life Health in Lancaster County, Pennsylvania.  She holds advanced certifications in Nutrition, Herbalism, and Nutrigenomics from the Holt Institute of Medicine, PanAmerican University of Natural Health, and Functional Genomic Analysis where she now serves as an adviser and supplement formulator.  In her practice, she utilizes personalized lifestyle changes, dietary, and nutritional protocols based on genetic predispositions, environmental and epigenetic influences, and functional lab testing to help her clients regain their health.  In addition to her clinical work, she lectures on behalf of Functional Genomic Analysis, teaching weekend intensives on advanced interpretation of SNP data to practitioners ranging from Acupuncturists, Chiropractors and Naturopaths to Psychologists, Internists, and Anesthesiologists.  She offers practitioner mentoring through the BeyondProtocols.org platform, helping colleagues navigate the complex web of genetic polymorphisms to develop more efficacious protocols for their chronically ill or complex cases.  She sits on the advisory board for the Nutrigenomic Research Institute as well as lending her services as an independent researcher. 

Key Takeaways

  • What are oxalates?
  • What are the symptoms and conditions associated with oxalates?
  • What is the role of oxalates in hypermobility or Ehlers Danlos Syndrome?
  • What is the role of oxalates in autism?
  • Do oxalates trigger Mast Cell Activation Syndrome?
  • How are oxalates tested for?
  • What is the role of genetics in hyperoxaluria?
  • Why are sulfate levels important in hyperoxaluria?
  • How can Oxalobacter be supported in our microbiome?
  • How might oxalates be considered a secondary mycotoxin?
  • What type of diet may be appropriate in hyperoxaluria?
  • How might oxalates be treated?
  • Can glycine or Vitamin C be problematic in those with oxalate issues?

Connect With My Guest


Interview Date

November 18, 2020


Transcript Disclaimer: Transcripts are intended to provide optimized access to information contained in the podcast.  They are not a full replacement for the discussion.  Timestamps are provided to facilitate finding portions of the conversation.  Errors and omissions may be present as the transcript is not created by someone familiar with the topics being discussed.  Please Contact Me with any corrections.    

[00:00:01.12] Welcome to BetterHealthGuy Blogcasts, empowering your better health. And now, here's Scott, your Better Health Guy.

[00:00:14.10] The content of this show is for informational purposes only and is not intended to diagnose treat or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice, or as information to facilitate self-treatment. As always, please discuss any potential health-related decisions with your own personal medical authority.

[00:00:34.16] Scott: Hello everyone, and welcome to episode number 131 of the BetterHealthGuy Blogcasts series. Today's guest is Emily Givler, and the topic of the show is Oxalates. Emily Givler is a Functional Genomic Nutrition consultant, researcher, and lecturer with a thriving clinical practice at Tree of Life Health in Lancaster County, Pennsylvania.

She holds advanced certifications in nutrition, herbalism, and nutrigenomics from the Holt Institute of Medicine, Pan-American University of Natural Health and Functional Genomic Analysis where she now serves as an advisor and supplement formulator. In her practice, she utilizes personalized lifestyle changes, dietary and nutritional protocols based on genetic predispositions, environmental, and epigenetic influences and functional lab testing, to help her clients regain their health.

In addition to her clinical work, she lectures on behalf of Functional Genomic Analysis, teaching weekend intensives on advanced interpretation of SNP data to practitioners ranging from acupuncturists, chiropractors, and naturopaths to psychologists, internists, and anesthesiologists.

She offers practitioner mentoring through the BeyondProtocols.org platform, helping colleagues navigate the complex web of genetic polymorphisms to develop more efficacious protocols for their chronically ill or complex cases. She sits on the advisory board for the Nutrigenomic Research Institute, as well as lending her services as an independent researcher.

And now, my interview with Emily Givler.

You have been on the podcast previously in a powerful and thought-provoking discussion with Beth O’Hara, Dr. Neil Nathan on Precision Mycotoxin Detoxification. It's an honor for me to have you back on the show today as a solo guest, thanks so much for being here today Emily.

[00:02:32.17] Emily: Well, thank you so much for having me; it really is such a treat to be here.

[00:02:36.13] Scott: Tell us what drew you to working with clients today that have complex chronic conditions, did you have some personal health journey that led you to your passion today?

[00:02:46.28] Emily: I did, and it's great that we're talking about oxalates because I did not know it at the time. But oxalates have been a big underlying source of a lot of challenging health issues in my life. And I’m really glad we're talking in November because this is kind of the central point in time for me with my own health journey.

When I was 14, the Thanksgiving of the year that I was 14, we were driving to my aunt's house, and I started noticing a really gnawing pain in my hip that had never been there before. And it just grew and spread from there to full right side pain, all the way down my leg, across my low back. It started spreading to my upper back. So I went through about five years of testing and physical therapy, and nothing showing up.

And then 20 years ago, this month, I made my way to a rheumatologist who diagnosed me with Fibromyalgia at age 19. And at that point, she told me that the good news was that it wouldn't shorten my lifespan or cause any type of disfigurement. But that I would be in progressively increasing pain for the rest of my non-shortened, non-disfigured life.

So I was glad to have a label but really disheartened to think that there was only a label and no explanation, and no hope for a better future. So at that same appointment, she wrote me a really, what felt like a really extreme prescription for narcotic painkillers. And told me to take six to eight a day regardless of pain. Double it on days that I was in pain, and I was in so much pain every day at that point.

So I kindly requested to have a liver and kidneys by the time I turned 40, at which point she also wrote me a prescription for antidepressants. And I feel like this is so similar to the journey that a lot of your listeners have probably been on. Where we get a label if we're lucky, and then we get Band-Aids and no actual root cause explanation. So I decided not to go the painkiller route, not to go the antidepressant route. And to see if I could just get myself feeling better.

And so I took a lot of horrible missteps along the way, including 17 years as a vegetarian which since we'll be talking oxalates, we'll figure out why that was such a bad idea. But eventually, I realized that oxalates were driving this pain and dysfunction. So now I’m exactly 20 years post that diagnosis, and I have about two percent of the pain that I had - with no painkillers. And I have about 8,000 times the energy that I had as a teenager, as I’m closing in on 40.

So this has been a long road for me, because of having to figure it out all out for myself. So if I can take that experience, and help other people avoid the many missteps that I took, and help them find that root cause as opposed to just the label, then it really validates a lot of the journey that I have been on.

[00:06:04.24] Scott: Amen to that. Yes, it's frustrating that so many years go by, and then we ultimately identify something that could have been implemented relatively simply in many cases. But we just didn't know.

And so the beauty of it is your experience now I know is helping many people. And so while that maybe doesn't make your pain go away that you suffered, you certainly are helping people minimize their own struggle and their own pain today.

[00:06:30.13] Emily: And being able to sit here on the other side, hopefully, if nothing else I can give people hope. And I would not change a day of it, because I get to work with people and give them the hope that I struggled to find and that definitely makes it all worthwhile.

[00:06:46.08] Scott: Yes. I feel the same; I wouldn't change my journey either. As difficult as it was, there's definitely some gifts. Talk to us about what are oxalates for people that have never heard of it and where do we find them. And then are they always bad or is there a role, is there some benefit of us having a certain amount of exposure to oxalate.

[00:07:07.18] Emily: So oxalates are compounds that are produced largely by plants. They are naturally occurring, and they're produced by plants as a type of defense mechanism. Largely against stressors like insect activity that would eat the part of the plant that the plant needs to live. So largely the leaves and the roots are going to be the biggest producers of oxalate in nature.

So it's this natural toxin, and we do produce small amounts of oxalate in our body endogenously as part of the Krebs cycle. But oxalic acid itself is a mineral chelator, so it gets bound up with different minerals and metals things like calcium, magnesium, iron, and aluminum. And it forms these insoluble crystalline precipitates that are like little razor blades or shards of glass in the body. These are tiny little precipitates; they're micron size and nanoparticles.

And they shred surrounding tissue and create a whole host of health concerns depending on where those precipitates are deposited. Generally, when they are in excessive levels, then they are a detriment to health. But there are reasons that we make them endogenously. For the plants, there's a lot of reasons that they make them; it's a huge protective mechanism. For ourselves, they are chelators; they can bind up some heavy metals.

And so that binding may sequester those metals. They also may act as a bit of a hormetic stress. But typically, it's only when we have genetic polymorphisms that our endogenous production of oxalates really gets high. So our body is only supposed to produce very small amounts of them. But the potential benefit to the human body I think is pretty minimal. But for the plants, they are definitely a good thing.

[00:09:15.05] Scott: So you mentioned that we endogenously produce these in small amounts. For people that are dealing with high levels of oxalates, what are some of the common sources where we would exogenously introduce them into the body?

[00:09:27.25] Emily: So one of the biggest places that we see this is actually fat maldigestion. So if our dietary fats are not being properly emulsified, if we don't have adequate bile flow, then those undigested, non-emulsified fats will actually get bound up with our dietary minerals. And they form almost a soapy like compound in the gastrointestinal tract. And we will end up excreting unused, the minerals along with the fats. And that binding of minerals in the gastrointestinal tract will actually increase the gastrointestinal absorption of dietary oxalates.

This gallbladder bile flow component is the number one place that we see excessive oxalates coming from outside of the genetics. We can also see overconsumption of dietary oxalates in someone with leaky gut, that increased gut permeability plus that increase of dietary oxalates can be a disaster for over absorption. But then one place that I don't think enough people are looking at those exogenous oxalates is from things like mold.

And certain mold species like Aspergillus niger, in particular, will produce oxalate as a fermentation byproduct. So we can get oxalates there. And then we can see overproduction of oxalates within the Krebs cycle for a number of reasons outside of genetic polymorphisms. Just dietary insufficiencies and things like sulfate, B6, or B1 can contribute to hyperoxaluria as well.

[00:11:13.08] Scott: So when we have dietary consumption of things like spinach and beets and Swiss chard and rhubarb, that combined with leaky gut or intestinal hyperpermeability for example, then allows us to absorb more of those oxalates than we otherwise would.

[00:11:31.06] Emily: Exactly. And we can throw into that picture dysbiosis. And if we are missing certain microbes in the gut that would degrade dietary oxalate, which normally would allow people to eat these plants without problems, then they become more problematic for us. And most of these things are not mutually exclusive.

So one of the reasons I struggled with oxalates so much was I had gallbladder and bile flow issues, I had some mold exposure. I had some antibiotics that disrupted my microbiome. And I had endogenous production from genetic polymorphisms. So we can have all of the above.

[00:12:09.12] Scott: And we're going to talk about all of those in more detail. So let's talk a little bit more about the difference between primary and secondary hyperoxaluria. So which one of those is more common, what's the difference between those two conditions?

[00:12:24.29] Emily: So primary hyperoxaluria is when it is a genetically driven condition. And there are two primary sets of SNPs or single nucleotide polymorphisms that are most closely associated with primary hyperoxalurias type 1 and 2. They are AGXT which is sometimes coded as just AXT - Alanine Glyoxylate Transferase.

And then another set of snips called GRHPR. So those are going to be the two big drivers for primary hyperoxaluria. So there is a type 3, and those are the HOGA1 genes. Most of the time, people with high oxalates are dealing with secondary hyperoxaluria meaning it's not hardwired into your genetic code, it's coming from other places. And again, we can have both of those simultaneously. But most of the time, we're going to be seeing people with secondary hyperoxaluria.

[00:13:26.00] Scott: Let's talk a little bit more about what oxalates do in the body that's detrimental to our health. So you mentioned that they create these crystals that essentially kind of can tear tissue, leading to pain. But what are some of the other things they do in the body that either impair function or lead to other challenges?

[00:13:45.24] Emily: So we have to get the elephant out of the room first, and that's kidney stones. So this is the most obvious and most medically recognized form of hyperoxaluria. About anywhere from 60 to 80 percent of all kidney stones are calcium oxalate stones. There can be a few other types in there. But most kidney stone formers are having some type of issue with oxalates.

That can cause a lot of pain and do a lot of damage to the kidney, the bladder, the urethra during the process of excreting this crystal. But only about half a percent of everyone with hyperoxaluria will develop kidney stones. So this is a really small percentage of people. But the medical community is great if you're physically peeing this thing out, at picking it up putting it on a slide and going aha, I figured out why you have all this pain.

But if you have those same precipitates but much smaller micron-sized, nanoparticle size attached to the sulfate receptors in your body. They are not going to show up on traditional imaging, so they're very difficult to see.

You won't see them on CT scans or ultrasounds or MRIs until they have formed very large precipitants. So they bind up with the sulfate receptor sites, and the damage that they do depends on where they are located. So we have a lot of sulfate receptors in connective tissue. So many people with high levels of oxalates will develop various structural instability, joint pain.

The fascia is really impacted by high oxalate. So often, we'll see a lot of muscular pain going along with that when the oxalates are spread throughout the connective tissue and the fascia. Many people experience ocular issues; there are types of cataracts that are associated with high oxalates. And increased ocular pressure can be associated with high oxalates, as well as stye formation.

So people who are frequent stye formers or who have things like blepharitis should consider potentially looking at oxalates as a driver. And if they're in the lungs, you can see things like pulmonary fibrosis and COPD. When they are in the pelvic floor, we'll see issues in women like vulvodynia and interstitial cystitis. And men we may see enlarged and inflamed prostates.

So the symptomatology is really going to be very dependent on where the precipitates are, what is bound up with that oxalate. We may see things like oxalate induced anemia if the oxalate is getting bound up with all of our iron and pulling it out of hemoglobin production. But generally, we're looking at inflammatory conditions, very painful conditions.

And oxalates also have a detrimental effect on the mitochondria. They shred and destroy the mitochondria; they interfere with the Krebs cycle at several different points through disruption primarily of B1 levels. And so we'll see these fatigue, chronic fatigue type of presentations going along with hyperoxaluria as well.

[00:17:14.04] Scott: So it's a pretty broad list of things that it can do in the body, especially when it's impacting the mitochondria and shifting redox and depleting antioxidants. I mean so many different things. Are there different types of oxalates? And does the type matter in terms of its potential to create specific symptoms in the body?

[00:17:35.02] Emily: Well, there are different types of oxalate precipitates. So we have oxalic acid, which by itself is not really going to give us too many problems. But when that oxalic acid, which is that potent chelating agent, that gets bound with certain minerals or metals, then we're going to have various issues. So oxalic acid has the strongest affinity for calcium; this is part of why so many of the kidney stones that we see are calcium oxalate.

But it has a nearly equal affinity for magnesium. So this will pull that magnesium out of circulation. Even without oxalates, about 80 percent of Americans are magnesium deficient. It is a critical cofactor for hundreds of different enzymatic reactions. And you can lose a substantial amount of it due to elevated oxalate. And just a moment ago, I mentioned oxalate-induced anemias.

So I’ve worked with a number of clients who have really struggled with low iron, like low serum iron, low ferritin, low hemoglobin, low hematocrit; all of our markers. And when they we start mobilizing oxalates, they end up excreting what looks like rust-colored sand because of that iron oxalate being excreted from the body.

So we can see various anemic presentations associated with hyperoxaluria. And then you can see having metals being bound up with high oxalates as well so if you have someone who is really struggling with hyperoxaluria, who is also say eating a lot of tuna or other large fish. They may hold on to more mercury than someone who does not have high oxalate because they do have that additional chelator bound up in their system holding on to it.

[00:19:26.15] Scott: So in that case, it's not necessarily a good thing that the oxalates are being bound to the metals, because they're not necessarily getting excreted. So we're not thinking of oxalates like a binder, and even if they were, the trade-off with pain and so on obviously it's not going to be worth it. But it sounds like they're actually causing retention of metals, not so much that they're helping with excretion.

[00:19:47.12] Emily: It can go either way, if we're trying to get the oxalates out and we have someone with heavy metals, we should consider that we could be pulling some of the metals out and vice versa. If we're working on metals, we should consider whether they're dealing with high oxalates, because that may be an additional wrinkle in trying to do a heavy metal detox. They go hand in hand. 

[00:20:11.12] Scott: So you mentioned a number of conditions, I want to just kind of throw a few of them out that I know I picked up from one of your prior conversations so people kind of think about this. So you mentioned kidney stones and cataracts, and pulmonary fibrosis, Fibromyalgia. But they can also play a role in things like breast cancer, endometriosis, uterine fibroids which seem to be very common.

PCOS which seems to be very common, issues with the thyroid, you mentioned interstitial cystitis and vulvodynia. But even arthralgias, osteopenia, osteoporosis, vertigo, which is also very common. I mean I hear lots of people in this realm of Lyme and mold dealing with vertigo and hadn't made that connection to oxalates. Diverticulitis or diverticulosis, sarcoidosis, so I mean that's a huge list of conditions that people in our community are dealing with.

[00:21:01.18] Emily: And it is worth noting, that these are all conditions that we will find associations with oxalates in the published literature. So this is not anecdotal, observational. There are studies that show these associations very definitively. When I started looking into all of these pathologies and their associations with oxalates, I was floored that we would see all of these serious pathologies associated with the stuff that causes kidney stones, which are certainly painful.

But we don't typically draw associations between kidney stones and breast cancer. Or kidney stones and Hashimoto's, and yet they're there. So a number of different things are happening. And one of the most significant is the relationship between sulfate and oxalate. So these are antagonistic compounds that will have a very dynamic relationship with one another, much like copper and zinc or sodium and potassium. So as we increase oxalic acid in the body, we will push out sulfate and vice versa.

As we increase sulfate, we decrease oxalate and cause the excretion of in the urine. So oxalates hijack the sulfation system. They move through the body on sulfate transporters, and they get bound up with sulfate receptor sites. And sulfate is the fourth most abundant nutrient in the body; we need it for so many other things. And so the increase in oxalate, not only has this mechanical shredding mechanism, but it also causes the loss of that critical sulfate molecule, which can then have a negative impact on things like hormones.

So many of our hormones need to be sulfated, like DHEA sulfate and pregnenolone sulfate. So when we lose that sulfation component, we will see dysregulation of hormones which can come into play in things like PCOS and endometriosis. And then we combine that with the physical shredding in the tissue, and we see things like uterine fibroids and ovarian cysts developing because the body is responding both to the inflammation and the mechanical shredding, and dealing with the hormonal dysregulation. So it's really messing things up at very deep levels.

In terms of the thyroid, the thyroid actually can become a repository for oxalate crystals. There was a series of autopsy studies done in the 70s and 80s where they actually dissolved the thyroids of people who had passed away after having Hashimoto's, and they found them just riddled with calcium oxalate crystals. So these are physical things that get embedded into tissue, as well as creating systemic inflammation and dysregulating many of these other systems.

[00:24:05.04] Scott: And we'll talk more about the sulfate piece later, but Stephanie Seneff talks a lot about sulfate deficiency. Unfortunately, it's sometimes challenging to reintroduce sulfate into the body, because a lot of times people don't tolerate those sulfur-containing compounds, right? So we'll talk a little more about that. But let's get into the connection between oxalates and Mast Cell Activation Syndrome. Do we know if oxalates can serve as triggers for mast cell activation?

[00:24:34.04] Emily: We do, and you just really hit the nail on the head with that. Oxalates are a very direct trigger for the mast cells to create more inflammation, so it's almost a one to one. Now there are many other things that can also cause mast cell activation; it is rarely just oxalates doing it. But if we fail to address the oxalic component in someone with mast cell activation, then they're going to stay stuck in this cycle.

[00:25:05.00] Scott: Some people suggest that Burning Mouth Syndrome is a Mast Cell Activation Syndrome symptom. Oxalates have also been implicated. And so what are your thoughts on oxalates and mast cell activation in those that are dealing with Burning Mouth Syndrome.

[00:25:21.25] Emily: So my general feeling for just about everything is that there's not one right answer for everyone, and especially with some of these broad labels like Burning Mouth Syndrome or Fibromyalgia. Sometimes they're just a good description of symptoms, and not everyone who has that label may be dealing with it for the same reason.

So there may be people out there with Fibromyalgia, who it's not driven by oxalates the way mine was. But we do see a few things causing us to think that maybe in some people, oxalates may be a factor. Now if there is something like in Lichen planus in the mouth, which would cause patches and sores that can cause burning in the mouth as well.

And we do find some associations between various Lichen presentations like in planus and benefit from a low oxalate diet. So for some people that may be where lowering their oxalate level helps with the burning mouth. We often see this presentation in people with low estrogen and low thyroid. It's often women who present with burning mouth.

And those are two things that may be driven by high oxalate. So the oxalate may be the upstream driver if that dysregulation is causing the burning mouth. And then Dr. Afrin had done a study with women with burning mouth. And giving them mast cell stabilizers, and the majority of the women in that study noticed a significant reduction in the burning mouth symptoms. So there probably is a mast cell activation component.

And again for some people, oxalates may influence that. So if your oxalates are dysregulating your thyroid and your estrogen and causing mast cell activation, triggering burning mouth, then oxalates reducing them in the diet may be beneficial for you. But again, there may be mold or Lyme disease or any other number of things triggering that mast cell activation either in addition to or independent of oxalate.

[00:27:31.23] Scott: Let's talk a little bit about the impact of oxalates on structural integrity. So if we look at things like hypermobility or Ehlers-Danlos Syndrome, which to me seems to, I don't know if there's just more awareness or if the environment is changing, it's becoming a bigger issue, but I’m hearing more and more about Ehlers-Danlos Syndrome. So what role might oxalates play in those conditions where there is some structural integrity component?

[00:27:55.29] Emily: So I think this really comes back to the relationship between oxalate and sulfate because sulfate is very important for structural integrity. So I mentioned things like DHEA sulfate. But we also need things like chondroitin sulfate for healthy cartilage, healthy connective tissue, healthy inner vertebral discs.

So we can point to a few places in the genetics, where there may be some issues that relate to both sulfate and oxalate. And SNPs that I look at in people with hypermobility and EDS would include things like collagen synthesis SNPs. But also, the CHST3s, which are a chondroitin sulfate related SNP. And people who have variants here don't sulfate chondroitin can join properly, they don't form stable, healthy cartilage, particularly along the spinal column.

So we see a high level of structural instability. These are people with a lot of, they've identified that they have structural issues, potentially things like hypermobility and EDS. They're seeing chiropractors, all the time and they're told oh, you just don't hold your adjustments, and they can't figure out why. They're doing all the exercises, they're doing everything they should be, yet they keep sliding out of place. These are people who will often benefit from repletion of sulfate; the absence of sulfate will allow an increase in oxalate in that tissue.

So there's kind of a vacuum that's created, and oxalate gets sucked back in. You mentioned Stephanie Seneff’s lecture on this topic, and she really has spoken quite extensively about this dynamic relationship. But if sulfate is low, oxalate will be high. And if oxalate is high, it will push sulfate out. So we can get to that structural instability either from low sulfate and the genetics as a driver or from high oxalates for any of the reasons that we identified previously as a driver.

And this is probably part of why we see so many people with mold toxicity developing hypermobility. That oxalate from the molds destabilizes the connective tissue, and you see this progressive hypermobility presenting.

[00:30:25.14] Scott: Is there a connection between oxalates and some of the dysautonomias that are very common like POTS, for example?

[00:30:33.04] Emily: Potentially, and some of this may have more to do with the mineral chelation and an imbalance in the electrolytes. With pots, more so than oxalates, I think we should really pay close attention to things like choline levels and the phospholipids that cell membrane integrity.

And because we so often see this connection between poor fat digestion and high oxalates. I think the fat component is probably more the driver, and the oxalates are another symptom or comorbidity. More so than the driver of the dysautonomia. But we do often see them hand in hand.

[00:31:18.00] Scott: Let's talk about the connection between oxalates and SIBO. If we have SIBO, does that then impact our dietary consumption and absorption of oxalates? I’ve heard that people with SIBO often have high levels of oxalate, so is there a connection there as well?

[00:31:33.27] Emily: I feel like my answer for everything from this point is going to be it depends. So for some people, there certainly can be. The microbiome is such a critical part in degrading dietary oxalates. There are a number of beneficial organisms in the gut that can do this if the pH is right. But when we have something like SIBO, we may see an imbalance in our oxalate degrading organisms, in particular the Oxalobacter formigenes.

And that will make it more difficult for us to break down oxalate, and so that can cause over-absorption. Additionally, if SIBO is potentiating leaky gut, we can end up over absorbing oxalates in that way. But it is not necessarily a one-to-one, it's something to consider with SIBO, but not everyone with SIBO needs to worry about oxalates.

[00:32:30.01] Scott: I know that oxalates are very common in autism. What do we think is the reason for high oxalates in children on the autism spectrum?

[00:32:38.26] Emily: We're getting into a lot of speculation here. Some of it may be a genetic component. We do see a lot of yeast and fungal exposures, either in parents of autistic children where it may have been passed from mother to child or in the children themselves. And so we do have that potential for high oxalate production from mold exposure.

It may be related to high aluminum, which we will often see in this population as well. I think the genetics are probably pretty minimal. I think the gastrointestinal comorbidities are more likely tied into that over absorption and high deposition of oxalates, particularly in the brain.

So a lot of autistic kids who do a lot of the eye rubbing and eye-poking, well are almost always having issues with oxalates as well as kids who have a lot of sensory issues with fabrics, tags, things like that. As we reduce the oxalate burden in their bodies, we often see a lot of those symptoms abating.

[00:33:56.03] Scott: Beautiful. Let's move on to talking about testing, how we explore this condition. So how can we test for the potential of oxalates? And then is an elevated oxalic acid, if we're looking at organic acids for example. Is that something we should always be concerned about? Or could we make an argument similar to urine mycotoxins that lower levels might be healthy excretion? Is there a scenario where a high level on a test might actually not be something that you need to address?

[00:34:27.03] Emily: High is going to be a relative term here. So I think the foundational piece of that question even beyond oxalates is that we, as practitioners, need to know the context of the test that we're interpreting. So if I ate a spinach salad with a bunch of beets on it, and then the next morning did my urine organic acid test.

I would anticipate seeing a slightly elevated level of oxalic acid, because I’ve had a high intake of oxalic acid, and I want it to be coming out. So that would not be concerning, but that would be a small elevation if you see extremely high elevations, five times, ten times higher than your upper limit on an organic acid test. This is going to be more than oral absorption and dietary absorption of oxalates. And it is going to be something that we want to be aware of, and concerned about.

But the testing is imperfect, so organic acid test is my go-to test for oxalates because it gives us three different at least the Great Plains test, gives us three different metabolic markers for oxalate. So that we can determine whether there is endogenous production, as well as measuring the oxalic acid itself, but it is a snapshot, you can also do 24-hour urine collection to see your total oxalic acid excretion.

And this will give you a bigger picture of whether you are dumping more than you should be, and when other oxalates are an issue. But neither of these methods are perfect because they're excretion tests. And we've been talking about how oxalates get bound up with those sulfate receptors. So retained oxalates are much more of an issue than those that are being excreted.

And so not seeing an elevated marker doesn't always mean that oxalates are not an issue. So we have to then turn to our clinical expertise and look for some of these other signs and symptoms, and there are a few other little subtle places that you can cross-reference to see are you thinking the right thing with oxalates. And in serum, there are two markers that we can look at. The first is LDH or Lactate Dehydrogenase, and when this is low, like 160 or lower, it is an indicator that we want to be thinking about the potential for hyperoxaluria.

And then the other marker we could look at is our calcium level. And if that is on the higher end, it is an increased risk for calcium oxalate stone formation. So we can look at the calcium, we can look at the LDH, we can look at the urine excretion. But I will say the people that I see with the biggest issues with oxalates, often have extremely low levels of excretion and that's part of the problem.

[00:37:35.27] Scott: I love all the connections that you're making, even for me having looked at some of this before. Like my mom, for example, had elevated calcium in her blood tests, and also very commonly deals with kidney stones.

So it makes total sense. One of the things that I have seen on the Great Plains organic acid test is the oxalic acid may be high. I have not commonly seen glyceric or glycolic being high, or maybe even low. And so I’m wondering how commonly do you see those being out of the normal range. And then what do they tell us when they're either high or low, and do they somehow shift your treatment direction.

[00:38:16.09] Emily: So I see those elevated quite frequently, but this is probably based on the nature of the clients who find their way to me. So most of the time, you will only see oxalic acid elevated. And when it's just the oxalic acid, then we know it's a secondary hyperoxaluria. That it's not coming from the genetics, it's coming from the gut one way or the other.

Whether it's yeast or fungal overgrowth, other types of dysbiosis, the fat issue or overconsumption, it's coming from the gut. When glyceric or glycolic acid are elevated, then we want to consider a primary hyperoxaluria. Although, new research is showing that in cases of mold toxicity, the glyceric and glycolic can elevate when there's Aspergillus.

So there we would cross-reference with the first nine markers on the urine organic acid test, to see whether we find any indications of colonized molds in the system. But if we're not seeing colonized mold, and we do see elevated glyceric or glycolic acid. I’m always going to turn to the genetics and look for polymorphisms on AGXT or GRHPR potentially SPP1 and HOGA1. But the AGXT and the GRHPR homozygous variants, you will not see this with heterozygous polymorphisms.

But when you see homozygous polymorphisms along those pathways, enzymatically the body is going to produce more oxalate and less glycine. So we would take different approaches there because it's coming from a different direction.

The times that I am most concerned with those tests if I see elevations on glyceric or glycolic, and low or normal oxalic acid, this is someone who is making a huge quantity of oxalate, and none of it's coming out. So they're going to have more inflammatory problems, more pain presentations. And with them, we're going to have to go really slow to get this high body burden down safely.

[00:40:29.26] Scott: And we're going to talk more about treatment, and how you approach this in general. But when we're looking at those people that have specific SNPs that explain their hyperoxaluria, are there then nutrients or supplements that help to bypass those genetic predispositions? Or how is the treatment approach different when it is more genetic?

[00:40:52.07] Emily: Sure. So B6 is our biggest intervention when it is a genetic predisposition along the AGXT or GRHPR. Because B6 is the cofactor for each of those enzymes. And the research on B6 and hyperoxaluria is interesting.

They have not yet found an upper limit. So every amount of B6 that they have given in studies for people who are kidney stone formers, the benefit just goes up as the B6 level goes up. And again, this is in people who have a primary hyperoxaluria, where it is this enzymatic insufficiency that's driving it. And that's the minority of people. For everybody else, we're going to use totally different interventions.

[00:41:42.19] Scott: It's interesting because that leads me to a question I wasn't planning to ask. But in these people that are depleted with B6 and that potentially being a reason why some of these genes are expressing in such a way that it leads to hyperoxaluria.

It makes me wonder if there's a connection between hyperoxaluria and Kryptopyrroluria, where your Zinc and B6 then is depleted. And could that then potentially cause this genetic expression to be more of a focus.

[00:42:11.18] Emily: Oh, absolutely. And these are the connections that I love making. It's that stone that gets tossed in, and then all of these other ripples that we see. So I’m always thinking well, what else happens if we're low in B1, what else happens if we're low in B6 and does that connect with these other things that we're seeing.

And so often, we see things like mold causing and triggering things like porphyrias which are going to be driven in for some people by low B6 and low zinc and things like Kryptopyrroluria. So we can get there in a number of different ways. But when we have colonized mold that is making oxalates, that is a driver for so many of these other things.

[00:43:03.10] Scott: And we're going to talk about that in just a few minutes, that really is this idea of oxalates as a secondary mycotoxin is what really excited me about our conversation today. So I think people are going to be really surprised to hear that connection being made. As much as I had heard about oxalates over the years, I had not heard that until I heard you presenting on it.

And so we're going to get there in just a few minutes. Let's talk more about the low sulfate contribution to hyperoxaluria. And do you then see that restoring the sulfate levels helps with the oxalate issue? And what are some of the ways that people can tolerate increasing sulfate? So can they do Epsom salt baths, or are there other things that might help with replenishing the sulfate in the body.

[00:43:51.09] Emily: So the sulfate is a really critical piece when oxalates are high because if your oxalates are high, your sulfate is already low. So we do need to work on replenishing it, and this is one of the most powerful ways for getting rid of the existing body stores of oxalate.

So remember, the oxalic acid is traveling through the body on those sulfate transporters, and it's bound on sulfate receptor sites. So as we reintroduce sulfate, we shift the gradient in these cells along the SLCs, the solute carriers that control both sulfate and oxalate. And we push that oxalate off of that sulfate receptor and into excretion pathways. So that we can get it out of the body, so introducing sulfate slowly and progressively can be hugely helpful.

But high oxalates, I really believe are a big reason why so many people feel very sensitive to sulfur. So oxalate excretion and oxalate reduction always need to be done slowly; otherwise, you can cause more harm. Remember that these are physical precipitates that we have to get out of the body. So much like with heavy metals, it's not enough to move them, they have to get all the way out. And what we're trying to move are like tiny little shards of glass. So if we move too many of them too quickly, they're going to shred the surrounding tissue as they get out of the body.

And we excrete oxalates through the kidneys, through the colon, through the tear ducts and through the pores. And if they are coming out too quickly, we can see things like kidney stone formation or diverticulosis, diverticulitis, stye formation, eye irritation.

And things like cystic acne and other types of skin-related cysts as and rashes as the oxalates are coming out too quickly through any of those areas.

[00:45:58.00] Scott: So that's another beautiful connection that I had not made before. So what you're saying is that as we introduce more sulfate into the body, that's potentially then helping these elevated oxalate levels to reduce leading to excretion.

And that if we don't tolerate some of the sulfur type components that are introducing sulfate into the body, it might be that substance was actually beneficial to us, but that the symptoms that we're having could be the result of oxalate mobilization or oxalates in the process of excretion. I understand correctly?

[00:46:32.18] Emily: Exactly. So when we're moving oxalates out too quickly, there's something we call oxalate dumping. Where we push them off of those receptor sites into those excretion pathways, and oxalate will aggregate or clump together.

So if we get a lot of oxalate in one place at one time, we're more likely to form a larger and larger stone, which is going to cause many more problems on its path out of the body. So we always want to go very slowly with the introduction of these, particularly sulfate-containing compounds. Things like chondroitin sulfate, glucosamine sulfate, MSM these can be amazing for people with high oxalates.

But we want to start with a slow introduction and progressively increase them. I often start people with high oxalates with Epsom salt soak. So for those of your listeners who may not know, Epsom salts are magnesium sulfate, and we absorb a tremendous amount of both magnesium and sulfate transdermally when we soak either our whole bodies or even just our feet and Epsom salts.

And this can be wonderful; it's a big part of why so many people feel joint relief and musculoskeletal relief when they do Epsom salt soaks. But there are people who two minutes in an Epsom salt soak, and they are going to have more pain rather than less. It floored me the first time I had someone who said I soaked my feet and Epsom salts, and then I felt like I was walking on glass.

And it took me a little while to realize that it was that push of oxalates out from where they were retained, into those excretion pathways, causing the uptick in pain. So even at something as seemingly as innocuous as Epsom salts in a very sensitive person, it's not a negative sulfate reaction. It's not that sulfur reaction that we hear a lot of people talk about with things like CBS polymorphisms. It's more that push of the oxalate too quickly out of the body.

[00:48:41.11] Scott: And we're going to talk more about mold as a contributor to endogenous oxalate formation in the body. But while we're talking about sulfation, if oxalates are impacting sulfation. I would assume then that impacts sulfation in such a way that some of the mycotoxins are going to be cleared from the body less efficiently or less effectively, correct?

[00:49:05.03] Emily: Correct. And there are not a whole lot of mycotoxins that need to be sulfated. However, high levels of oxalate will also reduce your glutathione and NADPH levels. So we would also see a potential negative impact on our mycotoxins that need to be conjugated with glutathione, to be cleared from the body as well.

[00:49:28.01] Scott: So let's talk then about the connection between low citrate levels and oxalates, and is that why we might use things like magnesium citrate or calcium citrate in an oxalate protocol?

[00:49:39.13] Emily: Exactly. So adequate levels of citrate will prevent some of our oxalates from forming endogenously, but citrate can also help prevent the aggregation of oxalate from micron-sized particles into larger precipitates that are more challenging to excrete and be eliminated. This is one area where conventional medicine is actually pretty good at recognizing the relationship between spontaneous kidney stone formers and citrate levels.

And I work with one really sweet little boy who at age two, spontaneously formed thousands of kidney stones. It was so heartbreaking to see. He needed a series of six surgeries to put stents in his kidneys, to drain them all because let me tell you, no one is going to pass thousands of kidney stones without some major issues. And when all was said and done, the driver of that spontaneous kidney stone formation was low citrate levels.

And the long-term intervention that he needed was just potassium citrate. So his medical team started on potassium citrate, after having eliminated all of these oxalates through this horrible series of surgeries. And he was in the clear for a long time, so his parents got a little lax with the potassium citrate. And the stones started coming right back.

So it's a very important piece, it's one that we should not overlook. And this is why the preferred form of calcium for people with oxalates is typically calcium citrate. Now there are some people who are sensitive to that, because of how it's produced. So we can potentially use other forms. But we get that additional benefit from the citrate as well as the calcium.

[00:51:44.21] Scott: Dr. Klinghardt has talked about oxalates as a protective response in agriculture against aluminum, you mentioned that earlier in our conversation as well. He suspects that humans upregulate oxalate production as well as a result of inhaled aluminum exposure from whatever outdoor sources we might encounter.

And he suggests that a protocol that focuses on detoxifying aluminum leads to lowering of oxalate levels. And so I’m wondering if you've seen that connection between environmental toxins, aluminum potentially contributing to oxalate levels. And maybe even glyphosate, for example, is that as another environmental toxin, could that be another reason that we're experiencing these hyperoxalurias.

[00:52:32.24] Emily: Well, Dr. Klinghardt has some methods for testing that I don't have at my disposal, like ART. And so as a researcher, I have to defer to what's in the published literature, and there's not enough out there that would point to oxalate as a protective mechanism being up-regulated in the body for me to really weigh in too strongly.

I do see oxalates and high aluminum sometimes going together. But I see high oxalates for so many other reasons. So I think that there is a subset of people who this is probably the issue. But I don't think that it is the case for the majority of people with high oxalates. Glyphosate may be a slightly different story though because glyphosate does break down into oxalic acid in the body.

And Professor Seneff has spoken quite extensively about the potential role of glyphosate as a glycine mimic. So there and glycine and oxalate are pretty closely tied to one another. So there may be actually multiple ways that glyphosate is contributing to bio-accumulation of oxalic acid.

[00:53:54.10] Scott: So we do have this bacteria in our healthy microbiome, you mentioned at the Oxalobacter formigenes that's intended to help break down oxalates in the diet. A lot of people in this community may be dealing with Lyme disease, for example, have been on long-term antibiotics, that potentially shifts our microbiome.

Are there ways that we can support or fortify our Oxalobacter populations? I see online lots of different probiotics that have Oxalobacter in them, but they all seem to be in other countries. And I’m wondering why can we not get those here?

[00:54:30.13] Emily: So Oxalobacter is a really sensitive organism. And there has been a lot of really robust research on it. And there are some studies that show that as little as a single dose of tetracycline antibiotics like doxycycline or fluoroquinolones like Cipro, can obliterate your Oxalobacter.

So in the Lyme community, we see so many people who have done months and months and months or years of antibiotics, but even people who just growing up got a lot of tetracyclines, or got a tick bite and did prophylactic Doxycycline, just that one round.

They may have really done some significant damage to the Oxalobacter. And because it is such a sensitive organism, there have been a lot of challenges in getting it into a probiotic, in a form that can actually recolonize in our gut in any type of meaningful way. So I think this is a case where most people are not going to be able to take it.

So we have to do what we can to encourage that regrowth within the microbiome and the recolonization. And so there are some stool tests that actually measure this level, the Genova GI Effects test I believe measures it. And what I have observed, and this is just observational on my part. So the approach that I’ve been using that I’ve been seeing work pretty well is to use probiotics like MegaSpore with those spore-based probiotics.

When we use those organisms, and we do subsequent GI Effects testing, I'm seeing those levels rebound very nicely. So whether it is providing the fuel or just the healthy microbial environment, allowing whatever remaining organisms are still present to repopulate. I am seeing those levels come up pretty nicely with products and that thing.

[00:56:41.12] Scott: Beautiful, two capsules a day right here, love MegaSpore.

Okay, now we're going to get into what I was probably most excited about here, in making this connection for people, which is what you presented at the nutrigenetic research institute conference on mycotoxins recently. I believe you presented it first about a year prior at that similar event.

So this was a new concept to me that we could be colonized with things like Aspergillus or Penicillium, and I understood the idea of colonization. But I didn't know that those colonized organisms potentially can then create oxalates. And you've now termed oxalates as a secondary mycotoxin. So help make that connection for us.

[00:57:24.09] Emily: Sure. So some of that may be me just trying to get people's attention because I think that oxalates are really big and very overlooked factor in our chronic health conditions. And when we think about what mycotoxins are, is this metabolic, toxic byproduct from mold species. We think about what oxalate is in relationship with mold.

Molds like Aspergillus, especially Aspergillus niger, but not limited to only that organism produce oxalic acid as a fermentation byproduct. So as these organisms are living and proliferating and feeding and growing inside of us, they produce very high levels of oxalic acid.

And as we dig into the published literature, there are some really frightening studies that we can find, found a whole series of pathology reports on people who had died from Aspergillus colonization in their lungs. And they found that the cause of death was actually due to the damage from the oxalate produced by the molds, and not by the molds themselves.

So that production of oxalate by those colonized molds can be very significant, and tremendously damaging. And so if we are seeing colonized Aspergillus, colonized Penicilliums we really need to be thinking about not only the conventional mycotoxins. But then the other things they're producing like the oxalic acid. Because as bad as the mycotoxins themselves things like mycophenolic acid and ochratoxin, as bad as they are, the oxalic acid is just as bad and just as damaging.

It can also trigger things like cancer and autoimmune conditions. So if we pay attention to the ochratoxin and the aflatoxin, and ignore the oxalic acid, that's also being produced, we are unlikely to see robust healing. Because even after we get rid of that colonized organism, we still have to make sure we eliminate the residual oxalate just like we would have to eliminate any residual mycotoxins that are also produced. 

[00:59:47.28] Scott: So just to make the connection for listeners, so exposure to molds from water-damaged buildings, living in a moldy house, school wherever you're getting exposure. Has the potential to colonize the sinuses and gut, and then what we're talking about here is those endogenous fungal organisms now being able to create oxalic acid or oxalates that can then lead to all of the things that we're talking about in this conversation.

So another reason why it's so important to really consider the environment around us when we're looking to improve our health. One of the debates that I’ve seen on this conversation around oxalates and fungal contributors is whether or not Candida or Candida also leads to the production of oxalate. So do you want to weigh in on that conversation?

[01:00:34.23] Emily: So I would say there is not subtle, this is definitely not settled science. There is currently no published study that I am aware of that conclusively shows that Candida is an oxalate-producing organism.

So from a what's published perspective, we don't know that type of yeast is causing high oxalate in the same way something like Aspergillus or Penicillium could. Anecdotally, we often see them going together, but that could be for any number of reasons. This is a place where correlation may not be causation.

So there may be other aspects of dysbiosis that are contributing to the hyperoxaluria, there may be fat malabsorption contributing to the hyperoxaluria. And there might be Candida present. So there might be a temptation to say I’m seeing these together a lot of the time. But there's not enough in the research to tell us that the Candida is making the oxalate.

[01:01:42.19] Scott: Beautiful. Given what about oxalates, what portion of the problem would you say comes from diet versus fungal, mold colonization? So if we kind of split out the exogenous, or outside of us, versus endogenous or coming from inside of us. What do you think the contribution of each of those is in hyperoxaluria?

[01:02:03.22] Emily: So I can only speak to my client population, and right now, most of the people that I work with are dealing with a lot of mold. And their oxalates, I would say are coming almost 50/50 from the mold in their system.

And the fat malabsorption and maldigestion issues that the mold has created. So the mold's the driver just for a couple of different reasons. But I see those two factors, the gallbladder, bile flow, fat malabsorption, and the mold and being the two major contributing factors.

Every now and then, I see someone who's over-consuming dietary oxalates really horribly, and that's the driver. Every now and then I see genetic polymorphisms. But they're a very small percentage of the people that I’m working with.

[01:03:01.08] Scott: Plus it's tricky because some may not necessarily be one or the other. So for example, if mold exposure is leading to leaky gut or intestinal hyperpermeability, we may be getting more from what we're consuming, but we may be getting more because we already had this gut issue from molds that are colonizing us. And so then it's a little bit of both, right? Contributors?

[01:03:22.21] Emily: Oh, absolutely. And this is where all of those different reasons that we laid out, in the beginning, are not mutually exclusive. And as I mentioned, my own oxalate issues were a beautiful combination of genetics and mold and diet and antibiotics. So I feel like everything in the universe was saying you will deal with oxalates. So we have to peel back those layers and address often all of the above.

[01:03:50.02] Scott: When you see high oxalate indicators on the OAT, do you then look at the furans to consider the potential for colonization as a contributor? And how accurate has that been in terms of looking at some of those two, four, five, nine type markers on the OAT in terms of giving you some indication for the potential of colonization contributing to the hyperoxaluria?

[01:04:14.01] Emily: One of the reasons that I love the Great Plains urine organic acid test, is it does give us all of these different places where we can cross-reference and being able to do that, I find much more valuable than looking at any of these markers in isolation. So anytime I’m seeing oxalates high, my first thought is always to cross-reference with those furan markers. And I do find there to be very strong associations.

But then I also on that same test with cross-reference, with some of the ketone and fatty acid markers. Especially the subarate, and I would cross-reference with the orotic acid, which is an ammonia or choline marker. To see whether there's a bile flow issue, and a fat malabsorption issue in addition to the potential for colonized mold.

We would cross-reference with the lactic acid marker, to see whether there is a B1 insufficiency that may be contributing. So we can cross-reference with a lot of these places to get a bigger picture of all of these different areas where we might be getting elevated oxalates.

[01:05:30.20] Scott: If we think of mycotoxins as a protective mechanism, we know that when molds are threatened, they often produce more mycotoxins to try to protect themselves. And so that leads me to the question when we're using antifungals, for example, to deal with fungal colonization in the body, does that have the potential to increase the production of oxalic acid from these colonized fungal organisms?

[01:05:57.13] Emily: We don't know definitively, because there's not solid research on this. But oxalic acid is produced by Aspergillus as a fermentation byproduct. So I do think that there is, to some degree, less likelihood of oxalate being increased kind of in the death throes of these organisms.

However, when we think about why they are produced in other plants like spinach and beets, it is as a defense mechanism. So there may be some small increase. But I don't tend to see people having oxalate flares or oxalate dumping issues, in conjunction with antifungal, in the same way, we would if there's an too high of a toxic burden because of other mycotoxins.

[01:06:52.15] Scott: Beautiful. Let's talk a little bit about diet, so what type of diet do you recommend for people that have elevated oxalates? And then talk a little, you mentioned the oxalate dumping. So when you start limiting the intake of oxalates, there is this potential for oxalate dumping, which can make symptoms worse.

So talk to us about some of the considerations and things that are important for us to understand, before we jump into what I’ve seen some people do which is okay, I’m going to go from a hundred to zero and actually make themselves worse from an oxalate perspective.

[01:07:23.17] Emily: So if I have someone who is eating a lot of dietary oxalates, to begin with, and I need them to reduce it. Especially if it's someone who I suspect is not going to listen, and they're going to try to go cold turkey. I always ask them which of their kidneys they like best. Because if you cut oxalates out too quickly or try to get rid of them too quickly, you might lose one of them.

I mean the damage that can be caused by oxalate dumping can be very severe. So it is not something that I think we should ever aim for. I’m going to think about this as like the tortoise and the hare, and a slow progression is going to allow us to cross the finish line faster. Than if we just keep trying to race forward and end up falling backwards again and again.

So we're thinking about these stored little razor blades or shards of glass that will clump together when they get around more of their similar compounds. So we have to go slowly, and we have to stay hydrated as we're doing this whole process. So we want to slowly decrease dietary oxalates by only about five to ten percent total per week.

So this isn't like a food allergy, where you can never eat these foods again, it's a cumulative level in the system. So we want to gradually tick down on the amount of oxalate that we're eating, and we can do that in two different ways. We can do it either by physically reducing the amount of those oxalate-containing foods, or we can add dietary calcium when we eat those high oxalate foods and allow that connection between the oxalate and the calcium to occur in the digestive tract.

That will prevent the oxalic acid from being absorbed into the body; instead, we will excrete those minerals and the oxalic acid harmlessly in stool. So that's reducing your intake of oxalates. So if we try to cut down our diet and we add a supplement to bind the oxalates at the same time that can for some people be too rapid of a reduction.

If we also threw in some glucosamine and chondroitin, because our knees have been hurting us, now we're pushing more oxalates out from that sulfate. So as we layer these interventions, we increase the risk of dumping, because we have more coming out of the body at one time. And they're going to clump together. So if you have tiny little micron-sized particulates being excreted in urine, other than seeing some cloudy urine, you'll probably never know that they are coming out or that they're an issue.

But if they start clumping and forming larger crystals, then you may notice some like flank pain over the kidney areas. You may notice burning with urination, increased urgency for urination. Burning bowel movements, sandy bowel movements. Some people will get blood in their urine from the shredding that occurs from the oxalates. I mentioned earlier the eye-type symptoms.

So the potential for styes and other types of irritations the eyes as well as irritation to the skin. If you get these oxalates coming out too quickly. I have been fortunate to only have one episode that I can clearly say was oxalate dumping, and it was one of the most painful experiences of my life, including childbirth. And it was from taking too much B1 too quickly and pushing too many oxalates out. I had one of the worst migraines ever.

I literally passed out from pain and the only time in my entire life. I was completely disoriented. I had kidney pain for three days afterwards, just from that little bit of a push. So we always want to layer all of these interventions, both the dietary restriction of oxalates, as well as the addition of things like B6, B1, and sulfate-containing compounds. If we suspect oxalates, it has to be a progression and not all at once. So with the diet, we slowly phase these oxalate foods out. 

[01:11:53.04] Scott: And it's interesting too, I mean a lot of times we look in the mast cell arena for example. We look at how fermented foods used to be the best thing ever we could do, and now we kind of go oh, maybe not.

Similar for years, the green shake marketing company kind of like the MTHFR marketing company was out really promoting green shakes. Lots of spinach, and obviously that can be a contributor to oxalates. And so maybe not as healthy for some people as we think it might be.

Similarly, chia seeds. I kind of balance that, I try to put them into my power shake every morning. But chia seeds are another one that potentially can contribute to the burden of oxalates.

So what are your thoughts on the celery juice? Lots of people have daily celery juice; there's a well-known proponent of that. I know some people feel great on it, but then it also potentially could be a source of oxalates as I understand. So what are your thoughts on the celery juice?

[01:12:52.03] Emily: So I think that there's not one right answer for everyone. And everybody wants a quick and easy answer, and things like celery juice for some people is a quick and easy answer. And there are people who it is genuinely good for. And there are other people who it will take their health in completely the wrong direction.

So if you are having issues with high oxalates, celery juice should definitely be avoided. It doesn't mean you should never eat any celery; it doesn't mean that you should never have any type of green juice. I mean, my body feels really good on certain green juices, even with my oxalate issues. I just have to be really mindful about what I put in them.

Things like romaine or green leaf or oak leaf lettuces, poor lettuce gets so overlooked. But lettuce is very low in oxalate. And I will peel and seed a cucumber and put that in, because most of the oxalate and cucumber will be in the seeds or the peel, so we can eliminate that part. And I might put a single piece of celery in my juice.

But certainly not a whole head of celery. And so we'll layer in these pieces that are on the lower oxalate so that I can get the other good benefits because oxalate is not the only component in these otherwise healthy foods. And that's why it shouldn't be avoided for everyone.

But if you are having issues with oxalates, then those really high rapid oxalate intervention or oxalate foods like the celery juice or anything with spinach should be avoided, at least until you deal with whatever is causing the oxalate issue in the first place.

[01:14:42.15] Scott: And do you find that if people need to be a little more strict, granted phasing into that but a little more strict with reducing high oxalate foods. That as they then deal with their colonization of organisms potentially that are producing oxalates internally, that over time they can become less restrictive with the dietary changes?

[01:15:02.28] Emily: Absolutely. And I know there are a lot of voices in the high oxalate community who will probably disagree with me because they feel very strongly that oxalates should just be reduced long-term. But so few people are truly dealing with a primary hyperoxaluria.

If this is a secondary issue, if you fix the issue, you should be able to get these otherwise healthy foods in. Or find ways to compensate for whatever insufficiency is creating that issue in the first place. But I’m a firm believer that if we fix the upstream issues, we can normalize the diet in a lot of wonderful ways.

[01:15:43.26] Scott: In our last few minutes together, I’m going to jump into treatment. You've talked about calcium citrate and how that reduces the potential for oxalates being absorbed. When would someone take the calcium citrate in relationship to the foods, and what are some of the other supplements that might be helpful in dealing with hyperoxaluria?

[01:16:03.01] Emily: So you want your calcium and your oxalate to be together in the gut. And primarily in the stomach is where you want them to be together. So many people will advocate for taking your calcium about 30 minutes prior to eating so that it's there to kind of catch that oxalate from food. I think there are a number of variables that come into play.

And one of the biggest ones is what else are you eating, and are you taking any other supplements with your meals? So I see a lot of people whose main dietary oxalate issue is this fat malabsorption, and they need more help with bile flow.

And so I may have them taking something like a liposomal bitters or phosphatidylcholine about 10 minutes prior to eating to encourage bile flow. And I learned a number of years ago from Dr. Klinghardt that we should not take our fat-based supplements and our minerals at the same time. So if the priority is to get that bile flowing before the meal, and we're using those fat-based supplements to do that, then we want to wait until we start eating to take our minerals like calcium.

So that the calcium doesn't just emulsify with the fat instead, so for most people, if you're not taking a fat first, you can take the calcium about 30 minutes before eating. If you are taking like a liposomal formula or like a pantethine and a gel cap before your meal, then you want to wait and take the minerals towards the end. But we can use other minerals, not just calcium.

Magnesium has nearly as strong of an affinity towards oxalic acid. But you don't want to think about that as magnesium towards your like RDA level. Whatever magnesium or calcium we're putting in with our oxalate food, is ending up in our toilet bowl, that's the goal here. To bind them up and excrete it harmlessly. So this is where calcium kind of shines a little bit above magnesium. We really want to be absorbing some of that magnesium.

[01:18:19.26] Scott: So things like calcium citrate, magnesium citrate, you've talked about B6, things to support bile flow; whether it's ox bile or PC or even taurine potentially. Let's talk a little bit about glycine. So many people use glycine to help deal with chemical or solvent toxicity, but glycine can also potentially turn into oxalate. So is there a need in some people to restrict glycine supplementation if they're dealing with oxalates?

[01:18:51.06] Emily: I think this is probably a little overblown, because while your total glycine reserves do contribute in a very small way to oxalic acid. It's something like less than 0.1% of glycine will be converted into oxalic acid. So it's very minimal.

And when we're talking about genes like AGXT, when that polymorphism is expressing, we make more oxalate and less glycine. So there's often a glycine insufficiency already in people with high oxalate. And if we have glyphosate contributing to that oxalate burden, and kind of inserting itself in place of glycine. Now we've got two different mechanisms by which we may be high in oxalate and benefit from having a little bit of glycine.

[01:19:51.00] Scott: Beautiful. Right now with the pandemic that's going on, lots of people are taking high doses of vitamin c. That potentially can also be an issue, because of the contributor to oxalates. What are your thoughts on vitamin C and those that already have elevated oxalates?

[01:20:05.23] Emily: Well, Dr. Sandeep Gupta and I have been doing a deep dive into the published research on vitamin C and oxalate for about a year. And what we found is that a lot of the literature really conflates oral doses and IV doses. And doesn't make important distinctions between the two. So some ascorbic acid does get converted into oxalic acid, and it seems to occur at a higher rate with oral supplementation than intravenous supplementation. So if you have a disrupted microbiome and you have genetic polymorphisms on AGXT, HOHA1 or GRHPR. I would use caution with high dose vitamin C across the board. We're talking 8 grams plus per day.

I would also use caution with oral supplementation of ascorbic acid if you have any type of oxalate issue because that's where we'll see that higher rate of conversion. But if your oxalates are coming from, diet coming from the gut, not being driven by genetics then things like IV vitamin C is likely quite safe.

Obviously, this is something that people need to discuss with their practitioner just to make sure. But if we're using things like a Ascorbyl palmitate or Camu Camu which is a rain forest berry, that's a great whole food source of vitamin C. If we're using a liposomal C or iv vitamin C, these seem to be the safest ways to go. It's really that oral ascorbic acid, where we might get ourselves into some trouble.

[01:21:57.00] Scott: Beautiful. You were involved in the formulation of a supplement called OXA-BLOX, and I’d like to hear a little bit about the ingredients in that product. One listener asked why the OXA-BLOX has magnesium glycinate versus magnesium citrate. I’m really excited about this product. I want you to share it with us.

[01:22:15.22] Emily: So I love this product. It's something I use myself; I actually have my bottle of it right here with me. But this is probably not the place that most people should start if they are starting to reduce oxalates. Because this is a combination product that's going to address a lot of the different factors that we've been talking about today.

So there's calcium and magnesium in it to bind that incoming dietary oxalate. So this is a product that should always only be taken with food. So calcium is somewhat counter-intuitive if we're thinking that it's the calcium oxalate that's giving us problems. How would taking calcium fix those problems? By binding the oxalate and eliminating it.

So we don't actually want a super bioavailable form of calcium. We don't want it to be absorbed; we want it to sit in the gut. So it's a very different way of thinking about any of our minerals than how we typically think of them. So we have those binding minerals in there, we never want to take calcium on an empty stomach if we're dealing with oxalates.

So we have the binders to reduce that incoming oxalate. We have B6 to help support the reduction of oxalic acid through these two genetic pathways. We have B1, which helps to support the Krebs cycle and healthy transketolase levels. That B1 can be a very powerful intervention for reducing existing stores of oxalates and pushing them out of the body.

Then there's also a little bit of MSM in the product. Again, as that gentle sulfate source to start pushing out the existing oxalates. And then there's some red clover in it as well. And red clover has been shown to help with proper calcium utilization. It's very good for bone density. But it's also very nourishing and supportive of the kidneys.

And we do want to make sure we take care of our kidneys as we are working on eliminating oxalates. In terms of the mag glycinate, as we just discussed, I am not really overly concerned about glycine and oxalate.

And if anything I see a little bit of a need to support healthy glycine levels, and people with high oxalates. And we see so many people with connective tissue issues and anxiety when oxalates are high. So the mag glycinate is a little bit more calming, and it can help support musculoskeletal integrity as well.

[01:24:57.23] Scott: So should I not take OXA-BLOX with food if that meal is already low oxalate?

[01:25:03.04] Emily: Correct.

[01:25:05.04] Scott: Okay.

[01:25:05.10] Emily: So this is one place where people get mixed up. They're so low in dietary oxalate, but then they're still taking a calcium supplement. You need, it's basically a one to one between calcium and oxalate.

You and I are no longer drinking our milk so that we grow up big and strong. We're not looking at growing new bone; we're looking at maintaining integrity of our bones and eliminating those chelating agents that are going to steal the calcium from them. So again, it's a very different way of thinking about calcium in adulthood versus in adolescence, when we are growing very rapidly.

[01:25:48.07] Scott: Any benefits that you've seen in taking homeopathic oxalicum acidum relative to hyperoxaluria?

[01:25:55.12] Emily: Especially in people who are very sensitive to either sulfur or to oxalate. This can be a way to kind of dip their toe in. And this is not going to be everyone who's dealing with high oxalates, but especially people who are in the throes of mast cell activation, and oxalate is an active contributing factor because of that level of increased sensitivity.

The homeopathic can act as a desensitizing agent and help calm down some of the inflammatory processes. Some people also do really well with homeopathic sulfur kind of titrate it up as well. 

[01:26:34.20] Scott: Beautiful. One of the things that I commonly see people do is look at a supplement, look at a capsule and say oh, I can't have that because it has milk thistle or it has ABC and ABC is higher in oxalates.

And so my thought process has always been that the amount they're likely getting in a capsule of something is fairly small, and that milk thistle is helpful just as an example for many other things in the body. And so what are your thoughts when people that are dealing with hyperoxaluria jump to oh, I can't take any of these things, because they might have a small amount of oxalate in them?

[01:27:12.00] Emily: So I tend to think the way that you think on this. That it is a cumulative effect, and things like stinging nettle, big part of that sting is oxalic acid. So there's a lot of beneficial herbs in particular that do contain some oxalic acid. And here, it is definitely a cost-benefit analysis. And we need to think about what other things are in that formula.

Does the formula contain other minerals that would bind up the oxalic acid component? It may not have bioavailable oxalic acid that's going to have a detrimental effect. But if we are taking tons and tons and tons of stinging nettle, because it's the only thing that we know to do for our histamine reactions. Then we could potentially be creating some issues with oxalates. And in the Lyme and mold community, in these communities of chronic health dysfunction, some of us end up taking an awful lot of supplements. So there are certainly people who the cumulative total may be more than they can handle.

But I would caution people against discounting an otherwise beneficial supplement, just because one ingredient in it may contain some oxalic acid.

[01:28:34.17] Scott: Beautiful. So my last question is the same for every guest, and that is what are some of the key things that you do on a daily basis in support of your own health?

[01:28:42.25] Emily: So, for my own health, I have learned that movement and gratitude are the two biggest things that I can do to keep myself going every day. And it both of those feel even more important as we get more and more locked down.

So I’m taking advantage of every bit of sunshine and getting out in the sun and riding my bike and being out in the fresh air. And every day, I start my day with a gratitude practice, and I focus on all of the good things that I have moving forward in my life. And I like to reflect back on where I was 20 years ago, and how far I’ve come.

Because that perspective, even when things are not great. It's helpful to remember where they were and where they could have been. And one other thing that I am so grateful for is the ability to get to do this work and help other people find these answers. So those two things keep me centered and grounded, and with that, I can handle anything else that comes at me.

[01:29:44.17] Scott: Such an amazing conversation. So many dots that were connected, even a few things that I hadn't considered that you really helped connect the dots and I think this is going to be a powerful conversation for people.

And so my gratitude practice for today is being grateful for you, not only for being here, sharing your knowledge with everybody, and helping to connect the dots. But for all of the people that you work with and health, we appreciate you and so honor you and all that you do, so thank you.

[01:30:11.29] Emily: Thank you so much, Scott, it was such a pleasure.

[01:30:14.02] To learn more about today's guests, visit TOLHealth.com or BeyondProtocols.org. That's T-O-L Tree of Life Health.com or BeyondProtocols.org TOLHealth.com or BeyondProtocols.org.

[01:30:32.02] Thanks for listening to today's episode. If you're enjoying the show, please leave a positive rating or review which will help the show reach a broader audience. To follow me on Facebook, Instagram or Twitter, you can find me there as better health guy.

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[01:31:08.06] Thanks for listening to this BetterHealthGuy Blogcast, with Scott, your Better Health Guy. To check out additional shows and learn more about Scott's personal journey to better health, please visit BetterHealthGuy.com.


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