Recall that, up until about 50 years ago, most people harbored our favorite bacterial species, Lactobacillus reuteri, in their bowel flora, obtained from our moms via breastfeeding and passage through the birth canal. But 96% of modern Americans have lost L. reuteri due to antibiotic exposure, glyphosate, other herbicides, pesticides, antibiotic residues in meat, etc., not to mention increasing reliance on synthetic formulas in place of breastfeeding and increasing use of C-sections. Another bacterial species, Oxalobacter formigenes, also appears to be a casualty of such modern microbiome-altering factors.
Oxalates are compounds commonly found in foods such as nuts, peanuts, spinach, beets, and chocolate. A substantial number of people are unable to manage higher intakes of dietary oxalates and develop painful calcium oxalate kidney stones with their consumption. The incidence of calcium oxalate kidney stones has increased four-fold over the past 50 years, including in children.
Over the last few years, however, it has become clear that the presence of the bacterial species, Oxalobacter formigenes, and other oxalate-metabolizing species substantially influence intestinal and urinary levels of oxalate. Oxalobacter uses oxalate as its sole nutrition source, thereby reducing intestinal and urinary oxalates. You can find Oxalobacter formigenes in in the majority of hunter-gatherers such as the Hadza and Yanomami, as well as in people in Western society who do not develop calcium oxalate kidney stones.
Here is a graph from a recent study comparing the presence of Oxalobacter in modern American children compared to hunter-gatherer populations such as the Hadza.
(From PeBenito 2019)
But it has also become clear that, beyond loss or reduction of Oxalobacter, there are other changes in intestinal microbiome composition at work that allow higher intestinal and urinary levels of oxalates: some species are lost, some species are present at abnormally high levels. For example, a relative reduction in Lactobacillus plantarum may also contribute to stone formation, as well as increases in Archaea such as Methanobrevibacter smithii and fungal species. There are also hints that SIBO may underlie higher urinary oxalate levels and thereby calcium oxalate kidney stone formation.
Here is a terrific graphic from Suryavanshi 2018 that illustrates the changes in microbiome composition in stone forming vs. non-stone forming people:
No doubt: We need more information to craft a microbiome-modifying program to reduce urinary oxalates and thereby potential for calcium oxalate kidney stones. But one thing is becoming crystal clear: Calcium oxalate kidney stones are largely a disease of disrupted bowel flora.