Oxalate is having a moment. An article linking dietary oxalate to intestinal inflammation started making the rounds this month, and if you have IBD, you may already be wondering: should I stop eating spinach and almonds?
My answer right now: No.
I’ll walk you through what the study actually found, and why it’s not changing what I recommend to patients.
Quick reminder: what is oxalate?
Oxalate is a naturally occurring compound found in plant foods, with some foods containing much higher amounts than others. Spinach and almonds are two commonly cited high-oxalate foods.
Previous research found an association between higher stool oxalate and greater intestinal inflammation in people with IBD. That led researchers to ask whether intestinal oxalate could contribute to inflammation.
What the study looked at
To explore that question, the researchers first looked at tissue and stool samples from people with Crohn’s disease and ulcerative colitis. Then they used mouse and cell models to dig deeper into what might be driving what they saw in people.
What they found
People with Crohn’s and ulcerative colitis had lower expression of intestinal transporters involved in oxalate absorption. This showed up in both inactive and active disease, but was more pronounced in inflamed tissue.
Stool oxalate was higher in a small group of people with Crohn’s, just 11 patients, despite no significant difference in reported dietary oxalate intake compared with controls. Importantly, diet and stool weren’t measured at the same time, so we can’t directly connect what someone ate with the amount of oxalate found in their stool. The study raises several possible explanations for higher intestinal oxalate, including altered oxalate transport and differences in oxalate-degrading gut microbes, but we don’t yet know how much dietary oxalate contributes. That’s not a gap we can fill with a dietary recommendation right now.
In mice, adding oxalate to the diet worsened experimental colitis. The amount of oxalate used was much higher than typical human intake, which the authors acknowledge. This is a common strategy in animal research to get a measurable effect, but it means we can’t extrapolate the dose directly to humans.
Bottom line
It’s always exciting to see research exploring the relationship between diet and IBD. But this is not sufficient evidence to recommend cutting almonds, spinach, or other oxalate-containing plant foods from your diet.
So what, if anything, should you do with this information?
Here’s what I’m doing, and not doing, with my own patients:
I’m not putting patients on low-oxalate diets. Most of my patients with active disease aren’t eating large amounts of oxalates as it is.
That said, this isn’t a blanket rule. I still consider a lower-oxalate approach in specific clinical situations, like fat malabsorption (for example, secondary to ileal resection) or a history of calcium-oxalate kidney stones. That guidance predates this study.
I’m watching for larger studies that directly compare dietary oxalate intake to human outcomes, and I’m especially curious about oxalate-degrading probiotics as a way to reduce intestinal oxalate without restricting food.
I’m making sure I’m paying attention to dietary calcium intake. Calcium binds oxalate in the intestine to escort it out, and people with IBD already tend to consume too little calcium.
Does that mean increasing calcium will prevent the intestinal inflammatory effects proposed in this study? We don’t know. The researchers didn’t assess calcium intake, and they specifically flag the interaction between oxalate and minerals like calcium as an area needing more study.
But ensuring adequate calcium intake is something we should already be doing.
For now, I’d rather correct a known nutritional inadequacy that may help reduce intestinal oxalate than create a new dietary restriction around a proposed mechanism with many unanswered questions.
