Microbiome and Salicylates and Oxalates (slides and video)

Dec 26, 2025
7 min read

For the Full Video and Explanation of these slides, please see:

You can also find me on Rumble account under Mastoqueen. (Please note, I was struggling with brain fog when I narrated and created the blog verbage.)

The next installment of the Cycle Of illness Series: Salicylates and Oxalates. In these slides we discuss how Oxalates and Salicylates don’t “cause” the illness (although sure do make things a lot worse for us), but it highlights where in the Cycle of Illness you have hiccups, deficiencies, and processes failing.

This video is about how salicylates and oxalates affect the body, and where in the Cycle of Illness it stems from, how it keeps the cycle of illness misfiring, and how you can get back into healing verus harm.

Oxalates are organic compounds found in many of the foods we eat, including healthy greens and delicious chocolate.

We can also produce oxalates in the body through certain pathways. Oxalates can bind with calcium and be excreted through the intestines, or they can enter the bloodstream and eventually be excreted through the kidneys.

Oxalate levels in the body need to be balanced with the breakdown and excretion, matching the production and intake. When oxalate levels are out of balance, problems can arise with oxalate crystal formation, which can cause kidney stones, joint pain, or other problems.

When we eat plants high in oxalates, the gut microbiome metabolizes some of the oxalates, and then our intestines absorb some of the oxalates we have eaten. Oxalates are absorbed as free oxalate; however, if calcium is available in the intestines (e.g., from consuming dairy products), it easily binds to oxalates and prevents absorption

We can also synthesize oxalate in our bodies through the metabolism of different substances. The biosynthesis of oxalates in the liver accounts for 50-80% of the body’s oxalate pool. Dietary intake accounts for the remainder.

Precursors of oxalates produced in the body include amino acids and carbohydrate sources.

Hydroxyproline, from collagen breakdown, and glycine are amino acid sources that can be metabolized to form oxalates. Glycolate, glyoxylate, and glyoxal are derived from carbohydrates and can form oxalates in the body through their catabolic pathway.

Oxalates don’t just stress the gut — they leave their mark across multiple systems.

First, they exit through the kidneys, where they can cause stones, nephrocalcinosis, and filtration stress. This increases stone risk and reduces the kidneys’ ability to clear toxins.

Second, oxalates bind key minerals like calcium, magnesium, and even iron in mitochondria. This lowers available levels, which worsens cramps, arrhythmias, bone loss, and fatigue.

Third, oxalates disrupt the gut–brain axis. They can lodge in nerves and contribute to peripheral neuropathy, and they worsen brain inflammation when the glymphatic system is already slowed.

So where do oxalates leave their mark? On the gut lining, the kidneys, the mitochondria, the nervous system, and the immune system.

Again, they don’t create a new cycle — they accelerate breakdown across all the existing loops of dysbiosis, mitochondrial collapse, neuroinflammation, and autoimmunity.

Oxalates are compounds that normally get broken down by healthy gut bacteria, like Oxalobacter formigenes. But when the microbiome is weakened and those bacteria are lost, oxalates start to build up.

Once oxalates accumulate, they act like tiny glass shards. They damage the gut lining and mitochondria, which irritates mast cells and triggers histamine release.

This amplifies inflammation, increases pain, and worsens neuro symptoms.

Oxalates also bind minerals like calcium and magnesium, which blocks mitochondrial enzymes and drains energy. The result is muscle wasting and fatigue, feeding directly into the cachexia loop.

On top of that, when tissues are damaged by oxalates, the immune system can mistake self-proteins as foreign. This confusion fuels autoimmune targeting and keeps the inflammation cycle going.

So the trigger point here is loss of oxalate-degrading microbes. From there, oxalates pour into the system, irritate mast cells, increase histamine, worsen cytokine storms, and accelerate both cachexia and autoimmunity.

In other words, oxalates don’t create a brand-new cycle — they accelerate the ones already in motion: dysbiosis, histamine, cachexia, and autoimmunity.

Joint pain, eye involvement, and skin deposition

Oxalates don’t just affect the kidneys. When levels rise, calcium oxalate crystals can deposit throughout the body — including joints, skin, and even the retina. These sharp crystals can lodge in synovial fluid, cartilage, tendons, bone, and surrounding soft tissue, provoking a local inflammatory response.

The result can look very similar to gout: joint pain, swelling, stiffness, and reduced mobility. This condition is often referred to as oxalate-induced arthritis, where crystal deposition inside the joint space triggers inflammation. It’s most commonly seen in people with genetic or metabolic factors that lead to elevated oxalate levels.

Joint involvement may be acute and flare-like, or it may develop into a chronic inflammatory process. Ankles, knees, elbows, and knuckles are most often affected. In some cases, imaging shows visible calcifications in joints, tendons, or nearby soft tissue. Oxalate deposition can also contribute to bursitis and synovitis.

Animal models of hyperoxaluria show clear evidence of tissue remodeling and fibrosis, which likely explains the persistent joint and skin issues seen in people with high oxalate burden.

Skin manifestations associated with oxalates include small papules or nodules (often on the hands or face), acrocyanosis (bluish discoloration of hands or feet), and livedo reticularis.

Mitochondrial dysfunction

Mitochondria generate ATP through tightly regulated processes within their inner membrane. Oxalate has been shown to disrupt this system by depolarizing the inner mitochondrial membrane and increasing reactive oxygen species (ROS), leading to oxidative stress and impaired energy production.

Studies also show that calcium oxalate crystals directly induce mitochondrial dysfunction in immune cells such as macrophages. In humans, high dietary oxalate intake results in measurable declines in mitochondrial metabolic function in some — but not all — individuals.

Animal models consistently demonstrate increased mitochondrial ROS production with elevated oxalates, particularly when glutathione is insufficient. For individuals with mast cell activation, CBS upregulation, or impaired sulfur handling, this oxidative stress burden is often amplified. Not surprisingly, mitochondrial dysfunction is frequently observed in people with hyperoxaluria.

MRI contrast (gadolinium): long-term effects

Some individuals experience persistent symptoms following MRI scans that use contrast agents. These symptoms commonly include joint pain, skin changes, kidney issues, and cognitive dysfunction or “brain fog.” The contrast agent involved is gadolinium — a heavy metal used to enhance imaging.

A 2025 study found that oxalic acid can chemically interact with certain gadolinium-based contrast agents (including Omniscan and Dotarem), forming gadolinium oxalate nanoparticles. Researchers suspect that accumulation of these particles in tissues may underlie the chronic symptoms reported after contrast exposure.

Importantly, activation of the NLRP3 inflammasome following gadolinium contrast exposure has been documented for over a decade, linking contrast reactions directly to inflammatory signaling pathways.

Endothelial damage and atherosclerosis (in your cardiovascular system and lymphatic system)

Endothelial cells line the interior of blood and lymphatic vessels and play a critical role in vascular health. Oxalic acid is taken up by many tissues, but in endothelial cells it disrupts calcium signaling, leading to cellular injury.

Endothelial dysfunction is a key driver of atherosclerosis. People with hyperoxaluria show increased risk for vascular abnormalities, including hypertension and plaque formation. Oxalate crystals have even been identified within some atherosclerotic plaques.

Long-term studies support this connection. One 8-year prospective study found that higher dietary oxalate intake — especially when calcium intake was low — significantly increased the risk of hypertension and kidney disease. Another 10-year follow-up study showed a 50% increase in cardiovascular disease risk with higher oxalate intake, again worsened by inadequate calcium.

Mast cells:

Mast cells are immune cells designed to respond rapidly to threats. When activated, they release histamine, tryptase, and inflammatory cytokines — sometimes appropriately, and sometimes excessively.

Oxalate sensitivity and mast cell activation overlap in several important ways. Tissue samples from patients with calcium oxalate kidney stones show significantly higher mast cell counts compared to healthy controls. Medications that stabilize mast cells, such as ketotifen, have been shown to reduce calcium oxalate stone formation.

Even more telling: stinging nettles cause intense skin irritation largely because they contain oxalic and tartaric acids — both of which are known mast cell activators.

Inflammation: (macrophage activation by oxalate crystals)

Macrophages can exist in two primary states:

M2 (anti-inflammatory, tissue repair)
M1 (pro-inflammatory, high ROS production)

Calcium oxalate crystals are interpreted by macrophages as foreign particles, pushing them into the pro-inflammatory M1 state — even in the absence of infection. This creates inflammation without a pathogen, which leads to tissue damage rather than healing.

A 2021 study examined inflammatory responses to dietary oxalates. Participants followed a low-oxalate diet for three days, then consumed a high-oxalate vegetable smoothie. Within five hours, crystalline oxalate levels rose, and certain individuals showed clear shifts toward macrophage-driven inflammation.

In the liver, oxalates contribute to metabolic dysfunction–associated steatohepatitis (MASH). In liver dysfunction, oxalate production via lactate dehydrogenase increases, while AGXT activity declines. The result is rising oxalate levels, increased inflammation, and progressive fibrosis.

NLRP3 inflammasome activation:

Oxalate crystals and elevated ROS strongly activate the NLRP3 inflammasome, a central driver of inflammatory cytokine release. In kidney stone disease, this leads to pain, inflammation, and worsening renal damage.

Targeting NLRP3 is now an active area of research. Recent studies show that inhibiting NLRP3 activation reduces stone formation by preventing calcium oxalate crystal adhesion within the kidneys.

Breast tissue and cancer risk:

Chronic oxalate exposure increases the likelihood that normal breast epithelial cells undergo malignant transformation. Studies examining breast tumor samples consistently show higher oxalate concentrations in tumor tissue compared to adjacent non-tumor tissue.

Calcium oxalate microcalcifications in the breast are associated with invasive carcinomas, though they are also seen in benign breast cysts — suggesting oxalates play a role in tissue irritation and remodeling long before malignancy develops.

When you eat foods that contain oxalates, your gut microbiome plays a big role in how much of the oxalates you will absorb. The bacteria Oxalobacter formigenes uses oxalates as a primary energy source, so the presence of this bacterium can protect against oxalate absorption.

One study found that people who had Oxalobacter formigenes in their gut microbiome had lower urinary oxalate levels. The same study found that the absence of Oxalobacter formigenes correlated with higher plasma oxalate levels.

The kidneys play a key role in maintaining the balance of oxalates in the body. Free oxalates are excreted by the kidneys, or they can combine with calcium ions in the kidneys to form calcium oxalate crystals. If the calcium oxalate crystals infiltrate the vessel walls in the kidneys, this can lead to the formation of kidney stones or even kidney disease.

Oxalates can also be eliminated in feces when levels are higher in the body. This excretion into the intestine can then be degraded by the gut microbiome and eliminated, or oxalates can be reabsorbed into the body under certain conditions.

Oxalate levels in the body are carefully regulated through a balance of dietary absorption, endogenous production, kidney filtration, intestinal secretion, and reabsorption. When any part of this system is disrupted, oxalate levels can rise abnormally high.