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Oxalates and Autoimmunity: The Hidden Connection to Microbial Imbalance

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KEY NOTES
  • Oxalates come from both dietary sources AND microbial production inside the body
  • Specific microorganisms (Candida, Aspergillus, and certain parasites) are significant oxalate producers
  • Oxalates can trigger autoimmunity through tissue damage, molecular mimicry, intestinal permeability, and mitochondrial dysfunction
  • Testing for both oxalates AND microbial markers is essential for comprehensive treatment
  • Addressing the microbial component is critical for patients who don’t respond to dietary interventions alone

What Are Oxalates and How Do They Contribute to Autoimmunity?

When discussing autoimmunity and autoimmune disorders, one of the most focused on areas is food. Rightly so, as there are many compounds in food that can precipitate autoimmunity and exacerbate existing autoimmune diseases.
Oxalates are naturally occurring compounds found throughout the plant kingdom, serving as plant defense mechanisms against consumption. Ancestrally, we understood how to mitigate the effects of oxalates in food, but as dietary preferences have changed and we have lost some of this wisdom on food preparation, the oxalate issue has become more prevalent.
These small, sharp crystal structures bind to minerals like calcium and can accumulate in human tissues, triggering immune responses that extend far beyond their well-known role in kidney stones. When oxalate crystals deposit in tissues, they can damage cell membranes and mitochondria, unleashing inflammatory cascades that disrupt immune regulation. This cellular damage exposes previously hidden tissue proteins to immune surveillance, potentially activating self-reactive immune cells. The resulting chronic inflammation and molecular mimicry (where the immune system confuses self-tissues with foreign substances) create the perfect storm for autoimmune development, where the body essentially loses the ability to distinguish between self and non-self.

Specific Autoimmune Conditions Linked to Oxalate Accumulation

Research and clinical observation have shown that oxalate accumulation may play a role in several specific autoimmune conditions:

  1. Multiple Sclerosis (MS): Studies have found oxalate crystal deposits in brain tissues of MS patients. These deposits can trigger neuroinflammation and contribute to demyelination processes. The mitochondrial dysfunction caused by oxalates may accelerate neurodegeneration.
  2. Rheumatoid Arthritis (RA): Oxalate crystals have been detected in synovial fluid and joint tissues of RA patients. These crystals can activate the NLRP3 inflammasome pathway, contributing to joint inflammation and cartilage degradation.
  3. Hashimoto’s Thyroiditis: Clinical observations suggest that oxalate accumulation in thyroid tissue may trigger antibody responses against thyroid peroxidase (TPO) and thyroglobulin through molecular mimicry mechanisms.
  4. Systemic Lupus Erythematosus (SLE): The systemic nature of SLE makes it particularly susceptible to widespread oxalate crystal deposition, potentially contributing to multi-organ inflammation.
  5. Inflammatory Bowel Disease (IBD): Oxalates can directly damage intestinal mucosa, exacerbating intestinal permeability issues already present in Crohn’s disease and ulcerative colitis.
  6. Psoriasis and Psoriatic Arthritis: Skin manifestations of oxalate accumulation have been documented, potentially contributing to the characteristic skin lesions in psoriasis.
  7. Autoimmune Thyroid Conditions: Both Graves’ disease and Hashimoto’s thyroiditis patients have shown improvement with oxalate reduction protocols in clinical settings.
It’s worth noting that oxalates may not be the primary cause of these conditions, but rather an exacerbating factor that can trigger flares and worsen progression when other toxins, stressors and environmental factors are present.

Beyond Food Sources - The Overlooked Oxalate Equation

When discussing oxalates and their impact on health, the conversation typically centers around diet. Health practitioners routinely advise patients to avoid high-oxalate foods like spinach, almonds, beets, and chocolate. We create extensive lists of dietary culprits, meticulously tracking intake and recommending elimination protocols.
But what if we’re only addressing half the equation?
While dietary sources of oxalates are significant, there’s a critical and often overlooked piece of the oxalate puzzle: microbial production.
I’ve had countless patients come into our office who diligently followed low-oxalate diets with only partial improvement.
The missing link?
The oxalates being generated by microorganisms within their own bodies, completely independent of their dietary choices.
This overlooked connection between microbes and oxalate production may explain why some patients with oxalate-related symptoms don’t respond fully to dietary interventions alone. Certain microbes, particularly Candida and Aspergillus species can manufacture oxalates as metabolic byproducts, potentially contributing significantly to total oxalate burden.
In this article, we’ll explore this crucial yet underappreciated dimension of oxalate-related health issues, revealing why addressing microbial imbalances is just as important as dietary modifications when tackling oxalate-driven inflammation and autoimmunity.
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High-Oxalate Foods: The Usual Suspects

Before diving deeper into the microbial connection, it is well established that many foods contain significant amount of oxalates and in many cases they should be avoided until the body can better handle them. It is also worth noting that many of these foods are also often sprayed heavily with pesticides (which I discussed here) so when reintroducing these foods it is imperative to opt for organic options.
These are often the dietary sources that typically receive the most attention.
Very High Oxalate Foods (>50mg per serving):
  • Spinach (raw, 1 cup): 750mg
  • Swiss chard (cooked, 1 cup): 102mg
  • Beet greens (cooked, 1 cup): 91mg
  • Rhubarb (cooked, 1 cup): 86mg
  • Almonds (1/4 cup): 122mg
  • Almond butter (2 Tbsp): 79mg
  • Almond milk (1 cup): 65mg
  • Cashews (1/4 cup): 49mg
  • Potatoes with skin (1 medium): 97mg
  • Sweet potatoes (1 medium): 56mg
  • Beets (1/2 cup): 76mg
  • Navy beans (1/2 cup): 52mg
  • Dark chocolate (1 oz): 65mg
  • Black tea (8 oz): 55mg
Moderately High Oxalate Foods (20-50mg per serving):
  • Kale (raw, 1 cup): 36mg
  • Peanuts (1/4 cup): 27mg
  • Peanut butter (2 Tbsp): 25mg
  • Quinoa (1/2 cup cooked): 48mg
  • Blueberries (1/2 cup): 33mg
  • Blackberries (1/2 cup): 25mg
  • Raspberries (1/2 cup): 22mg
  • Okra (1/2 cup): 26mg
  • Celery (1 cup): 19mg
  • Dried figs (3 medium): 24mg
  • Sesame seeds (1 Tbsp): 35mg
  • Brown rice (1/2 cup): 24mg
Many patients are surprised to learn that some of their “healthiest” dietary choices like green smoothies with spinach, almond milk, berry bowls, and chocolate protein shakes can actually contribute to a significant oxalate burden when consumed regularly.
But while modifying preparation and intake of these foods is important, we must expand our focus beyond diet alone to truly understand and address oxalate-related health issues.

The Microbial Connection: When Microorganisms Produce Oxalates

What many practitioners and patients don’t realize is that oxalates don’t just come from food. A wide variety of microorganisms in our body can actually produce oxalates independently of our diet. This is a critical piece of the puzzle when addressing oxalate-related health issues.

Microorganisms Organized by Clinical Significance in Oxalate Production
Highest Clinical Significance (Primary Treatment Targets)
  1. Candida albicans
    • The most common fungal pathogen in humans
    • Produces significant amounts of oxalates as metabolic byproducts
    • Often proliferates after antibiotic use or with high-sugar diets
    • Clinical studies show direct correlation between Candida overgrowth and urinary oxalate levels
  2. Aspergillus niger
    • One of the most prolific oxalate producers among all microorganisms
    • Can colonize the respiratory tract and sinuses
    • Studies show it can produce up to 20x more oxalates than other Aspergillus species
    • Often found in patients with chronic sinusitis and respiratory conditions
  3. Cryptosporidium species
    • Parasitic infection strongly associated with hyperoxaluria
    • Studies show altered oxalate metabolism during infection
    • Often missed in conventional parasitology testing
    • Frequently found in patients with unexplained oxalate issues despite dietary changes
Moderate Clinical Significance (Secondary Treatment Targets)
  1. Other Candida species
    • Candida glabrata and Candida tropicalis
    • Significant oxalate producers, though typically less prevalent than C. albicans
    • Often co-occur with Candida albicans in systemic fungal overgrowth
  2. Aspergillus fumigatus
    • Common cause of respiratory infections
    • Produces oxalates as part of its virulence mechanisms
    • More commonly problematic in immunocompromised individuals
  3. Pseudomonas aeruginosa
    • Opportunistic bacterial pathogen
    • Produces oxalates through alternative metabolic pathways
    • Often resistant to conventional antimicrobial treatments
    • Frequently found in chronic respiratory and urinary tract infections
  4. Giardia lamblia
    • During giardiasis, patients show increased oxalate levels
    • Disrupts normal gut flora balance, reducing oxalate-degrading species
    • May persist chronically in some patients despite treatment
  5. Blastocystis hominis
    • Some strains associated with increased oxalate levels in patients
    • Connection to irritable bowel syndrome where oxalate issues are sometimes observed
    • Controversial parasite with varying pathogenicity between strains
Lower but Relevant Clinical Significance
  1. Penicillium species
    • Penicillium chrysogenum and Penicillium oxalicum
    • Environmental fungi that can colonize the GI tract
    • Notable oxalate producers, though less commonly found than Candida/Aspergillus
  2. Streptomyces species
    • Several soil bacteria in this genus that can colonize the gut
    • Produce oxalates as secondary metabolites
  3. Lactobacillus species
    • Some strains of these otherwise beneficial bacteria can produce oxalates under certain conditions
    • Highlights the importance of strain-specific probiotic selection
  4. Bifidobacterium species
    • Some species can produce oxalates while others degrade them
    • Strain-specific effects important in probiotic therapy
  5. Helminth parasites
    • Including Schistosoma and Ascaris species
    • May contribute to oxalate issues through multiple mechanisms
    • More common in individuals with travel history to endemic regions
These microorganisms produce oxalates through several metabolic pathways:
  1. Glyoxylate cycle – In this pathway microbes use when in glucose-limited environments, the enzyme glyoxylate oxidase directly converts glyoxylate (a two-carbon compound) to oxalate
  2. Krebs cycle intermediates – The Krebs cycle is the central metabolic pathway for aerobic organisms. Some microbes have enzymatic pathways that convert malate and succinate (Krebs cycle intermediates) into precursors that eventually form oxalate.
  3. Glycolate pathway – This pathway that microbes use in high oxygen environments involves the conversion of glycolate to oxalate.
  4. Ascorbic acid metabolism – Some microorganisms (especially Aspergillus) can metabolize ascorbic acid (vitamin C) through pathways that generate oxalate as an end product. This pathway explains why high-dose vitamin C supplementation can increase oxalate levels in susceptible individuals.
Mechanisms of Microbial Oxalate Production
Parasites and other microorganisms may contribute to oxalate issues through several mechanisms:
  1. Direct production – Many microbes directly synthesize oxalates as metabolic byproducts
  2. Indirect mechanisms:
    • Damaging intestinal mucosa, altering oxalate absorption
    • Disrupting the gut microbiome, reducing populations of oxalate-degrading bacteria
    • Causing inflammation that alters normal metabolic processes
    • Increasing intestinal permeability, allowing greater oxalate absorption
    • Creating localized pH changes that affect oxalate solubility
  3. Secondary effects:
    • Inducing oxidative stress that can increase endogenous oxalate production
    • Metabolizing host nutrients in ways that generate oxalate precursors
When these microorganisms overgrow in the gut or elsewhere in the body due to dysbiosis or infection, they can significantly increase the total oxalate burden.
This explains why some patients continue to show elevated oxalate levels on testing despite rigorous dietary restriction as their internal microbial factories are still producing oxalates regardless of what they eat. This becomes particularly relevant in cases of:
  • Chronic fungal overgrowth
  • Small intestinal bacterial overgrowth (SIBO)
  • Post-antibiotic dysbiosis
  • Chronic parasitic infections
  • Immunocompromised states where opportunistic infections flourish

How Oxalates Trigger Autoimmune Responses

The pathway from oxalate accumulation (whether from diet or microbial) to autoimmunity involves several mechanisms:
  1. Tissue Damage and Inflammation: When oxalate crystals form in tissues, they can cause physical damage and trigger localized inflammation.
  2. Molecular Mimicry: The immune response to oxalate crystals may sometimes cross-react with the body’s own tissues through a process called molecular mimicry, potentially triggering autoimmune reactions.
  3. Increased Intestinal Permeability: Oxalate crystals can damage the intestinal lining, contributing to “leaky gut,” which allows larger molecules to enter the bloodstream and potentially trigger immune responses.
  4. Disruption of Mitochondrial Function: Oxalates can interfere with cellular energy production in mitochondria, leading to oxidative stress and cellular dysfunction that may contribute to autoimmune processes.

The Vicious Cycle: Infection, Oxalates, and Immune Dysregulation

When infections or microbial imbalances are present, they can create a self-perpetuating cycle:
  1. Microbial overgrowth produces oxalates
  2. Oxalates damage tissues and trigger inflammation
  3. Inflammation alters immune function and gut permeability
  4. Increased gut permeability allows more microbes to translocate
  5. More inflammation leads to further immune dysregulation

Clinical Approaches to Breaking the Cycle

Addressing oxalate-related autoimmunity requires a comprehensive approach:
  1. Identify and address underlying infections or dysbiosis
  2. Support detoxification pathways to help clear accumulated oxalates
  3. Support healthy oxalate metabolism with calcium, magnesium, and vitamin B6
  4. Gradually reduce dietary oxalates (sudden reduction can cause “dumping” symptoms)
  5. Restore beneficial gut bacteria that can degrade oxalates, particularly Oxalobacter formigenes

Testing for Oxalates: The Power of Organic Acid Testing

How Organic Acid Testing Detects Oxalates
Organic Acid Testing (OAT) is one of our most valuable tools for assessing oxalate burden in the body. This urine test provides a comprehensive metabolic snapshot by measuring over 70 organic acid compounds excreted by the body.
Specifically for oxalates, the OAT test measures:
  1. Oxalic Acid: Direct measurement of oxalate levels in the urine. Elevated levels can indicate either high dietary intake, increased endogenous production, or impaired oxalate metabolism.
  2. Glyceric Acid: Elevated levels may indicate issues with glyoxylate metabolism, which can lead to increased oxalate production.
  3. Glycolic Acid: Another metabolite in the glyoxylate pathway, elevated levels can suggest increased endogenous oxalate production.
What makes OAT testing particularly valuable is its ability to simultaneously detect markers of microbial overgrowth that may be contributing to oxalate issues:
  • Arabinose: Elevated levels suggest Candida overgrowth, which can produce oxalates
  • Tartaric Acid: Often elevated with certain fungal infections
  • Citramalic Acid: Associated with certain bacterial imbalances
  • Furan compounds: Indicators of intestinal dysbiosis
Interpreting OAT Results for Oxalate-Related Issues
When analyzing OAT results in the context of potential oxalate-related autoimmunity, I look for specific patterns:
  1. Elevated Oxalates with Normal Microbial Markers: May suggest primarily dietary sources or genetic factors affecting oxalate metabolism (such as Primary Hyperoxaluria).
  2. Elevated Oxalates with Elevated Fungal Markers: Strongly suggests fungal contribution to oxalate burden, requiring targeted antifungal therapies along with oxalate reduction.
  3. Elevated Oxalates with Multiple Dysbiosis Markers: Indicates complex gut ecology issues contributing to oxalate problems, requiring comprehensive gut restoration.
  4. Moderately Elevated Oxalates with Mitochondrial Dysfunction Markers: May indicate that oxalates are impacting cellular energy production, potentially contributing to fatigue and chronic inflammation.
To find out more…
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Interpreting OAT Results for Oxalate-Related Issues
While OAT testing provides excellent insight into oxalate metabolism, I often recommend additional testing as I do not believe an OAT is a standalone test:
  • Autonomic Response Testing: to identify precisely which foods and microbes are triggering oxalate fueled inflammation
  • Comprehensive stool analysis: To identify specific microbial imbalances
  • Inflammatory markers: To assess the degree of systemic inflammation
  • Autoimmune panels: To evaluate for specific autoimmune markers that may be related to oxalate burden

Conclusion

Understanding the relationship between oxalates, microbial imbalance, and autoimmunity provides a new lens through which to view certain chronic health conditions. By addressing not just dietary oxalates but also the underlying microbial factors that contribute to oxalate burden, we can develop more effective, personalized treatment approaches for patients with autoimmune conditions.
Remember your health journey is unique, and addressing oxalate burden is just one piece of a comprehensive approach to autoimmunity. If you’re struggling with autoimmune symptoms, I encourage you book a complimentary call with us so we can learn more about your health journey and work to develop a personalized healing program that’s right for you.

References

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  2. Abratt VR, Reid SJ. Oxalate-degrading bacteria of the human gut as probiotics in the management of kidney stone disease. Adv Appl Microbiol. 2010;72:63-87. doi:10.1016/S0065-2164(10)72003-7
  3. Jayaram N, Sharma RK, Nagarathna R, Nagendra HR. Role of fungal oxalates in the formation of calcium oxalate kidney stones in Hyperoxaluria. Int Urol Nephrol. 2021;53(4):697-706. doi:10.1007/s11255-020-02695-5
  4. Peck AB, Canales BK, Nguyen CQ. Oxalate-degrading microorganisms or oxalate-degrading enzymes: Which is the future therapy for enzymatic dissolution of calcium-oxalate uroliths in recurrent stone disease? Urolithiasis. 2016;44(1):45-50. doi:10.1007/s00240-015-0797-x
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