Best Probiotic For Kidney Stones

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THE GUT MICROBIOME, OXALATE INTOLERANCE AND YOUR KIDNEYS

My interest in oxalates began while conducting research for my doctoral dissertation on magnesium, drinking water and magnesium’s link to cardiovascular dis­ease. Magnesium is critical in over six hundred cellular reac­tions, including energy metabolism and protein synthesis.¹ The balance between magnesium and calcium is vital to health. As a natural calcium antagonist, magnesium influences calcium homeostasis and inhibits vascular calcification.² Many water treatment processes remove both magnesium and calcium to make the water softer. Around the globe, wherever the water is low in magnesium, there is a marked increase in conditions like cardiovascular disease, diabetes, obesity, cancer and kidney disease.

The kidneys play a vital role in magnesium and calcium reuptake and homeo­stasis. Magnesium deficiency is linked to kidney stone development, the progres­sion to chronic kidney disease (CKD) and other chronic diseases. Coincidently, the majority of kidney stones are composed of calcium and oxalate. Kidney stones are pertinent to the discussion of oxalates because they are the most manifest sign of oxalate intolerance or toxicity. Although oxalate intolerance or toxicity can present in other areas of the body, the kidneys are the most affected organ.

Although rare, evidence for kidney and bladder stones has been documented since antiquity. However, during the last century, kidney stones have become far more prevalent, more prevalent than bladder stones.³ In the U.S., kidney stone disease has increased by 70 percent within the past three decades alone.⁴ Today, approximately one in ten U.S. adults will experience a kidney stone incident in their lifetime, and up to 50 percent will have a recurrence within five to ten years.⁵ Globally, prevalence rates range between 5 to 20 percent with rising rates in women and children. In recent decades, pediatric rates of kidney stone incidents have increased five-fold.³

Western medicine refers to kidney stone disease as “nephrolithiasis” (stones within the kidneys) or “urolithiasis” (stones within the urinary tract and blad­der). Modern treatments such as sound waves or lasers are helpful in breaking up large stones and minimizing their associated pain. However, effective strategies for kidney stone prevention and recurrence continue to elude conventional medicine.

MICROBES AT THE CORE

Bacteria rely on minerals such as calcium and magnesium to provide energy, nutritional support and environmental protection.⁶ Each bacterium is surrounded by an envelope of water. When mineral concentration within the envelope gets high, precipitation occurs and crystals form—a process called biomineraliza­tion. It is through biomineralization that microbes have developed into fossils and other natural formations like stalactites and stalagmites.⁷ Advanced technology has enabled scientists to examine the core of sta­lactites, where they have found four of the five major bacterial groups that also reside in human intestines.⁸

Biomineralization, “the processes and products of mineral pre­cipitation,” has been active for billions of years occurring in and around all living organisms. These universal mechanisms uniting minerals, microbes and water bring a new understanding to kidney stone investigation.⁹ Ac­cording to a 2021 study in the journal Kidney360,¹⁰ the process of kidney stone formation reveals “definitive evidence of in vivo microbiome entombment.” Indeed, over 97 percent of kidney stones contain bacteria.¹¹

Recent advances in technology have resulted in an explosion of pub­lished research on microbes and the gut microbiome. In the past decade, a new scientific paradigm has emerged: the “holobiont” concept (meaning “whole unit of life”).^12-14 This new model broadens the research focus beyond host-environment interactions to include the gut microbiome (Figure 1).

Not simply another organ, the gut microbiome contains one hundred fifty times more genes than the human genome and functions indepen­dently.¹⁵ This imparts incredible flexibility to the gut microbiome. Gut microbes can rapidly change their DNA to help humans adapt and ac­climate to wherever they are on earth. In a study involving healthy young adults, researchers found that cycling between a vegetarian or carnivorous diet altered participants’ gut microbial communities “in a rapid, specific manner,” with observable changes in two to five days.¹⁶ In other words, gut bacteria quickly adjust to our diet, because they rely on us to feed them.

In return, gut bacteria produce 30 percent of the metabolites in our blood; they make short-chain fatty acids, hormones, vitamins and other compounds. They also modify and influence vitamin absorption. A recent finding indicates that if one type of bacteria lacks what another one has, they can share—the term is known as crosstalk. This crosstalk is also a cross-feeding—a sharing of “communal resources” recently designated by the term “pantryome.”¹⁷

Bacterial populations and diversity disap­pear when the gut is damaged or disrupted. This is “gut dysbiosis,” a well-recognized term. Dysbiosis produces both “gain of function” (meaning the addition of microbial pathogens and their toxins) and loss of function, or the loss of beneficial bacteria with their metabolic functions and products.

The scientific literature indicates that gut dysbiosis is associated with dozens of different diseases,^18,19 including kidney stones and chronic kidney disease (CKD) (see Figure 2).²⁰ In fact, kidney stone disease is an excellent example of loss of function connected to dysbiosis. Although there is a direct axis between the gut and every part of the body, the gut-kidney axis is unique because what occurs in the gut directly affects the kidneys.

 

Research suggests that antibiotic use, which alters the gut microbiome,²¹ plays a major role in the development of kidney stones.4 Cumu­lative antibiotic exposure also is associated with an increased risk of inflammatory bowel disease (IBD).²² It is not surprising that kidney stones are common complications of IBDs such as Crohn’s disease. Compared to the general population, individuals with IBD have a ten to one hundred times greater risk of developing kidney stones.²³

OXALATES AND OUR ANCESTORS

Oxalate is the ionized form of oxalic acid and occurs ubiquitously in nature. A key me­tabolite, oxalate is found in humans, plants, animals and microbes as well as in rocks and soils. The majority of oxalate within humans is produced by the body (endogenous oxalate) as a normal byproduct of metabolism. The food we eat can contain oxalates, which occur in varying levels in vegetables, fruits, nuts and grains. When consumed, these are referred to as exogenous oxalates.

Under normal physiological conditions, total body oxalate includes 60 to 80 percent endogenous oxalate (made in the liver, the pri­mary organ responsible for its production) and 20 to 40 percent exogenous oxalate (from the diet). Of the roughly 10 to 15 percent originating from the gastrointestinal tract, a small amount is absorbed.²⁴ Humans lack the enzymes to break down oxalate, but the gut bacteria can degrade it through multiple pathways. Importantly, how­ever, the right oxalate-degrading bacteria must be in the gut; without the right bacteria, oxalates can accumulate and cause toxicity.²⁵

Healthy kidneys eliminate the majority (90 to 95 percent) of the oxalate circulating in the blood, with the remainder excreted in the feces.²⁴ As indicated, kidney stones and kidney disease are common forms of oxalate toxicity. Oxalates bind to calcium, forming calcium oxalate stones. Calcium oxalate stones are the most common type of kidney stone—about 80 percent—al­though there are other types.²⁵

HIGH-OXALATE DIETS

As a long-time Weston A. Price Founda­tion member, my first question was, “How did our ancestors deal with oxalates?” Searching the words “high oxalate diet ancestors” led to a prehistoric site in the Lower Pecos Region of Texas.²⁶ There, archaeological evidence shows that for millennia, people ate cacti, which are exceedingly high in oxalates. The oxalate stones in cactus plants (also known as “phytoliths” or plant stones) are so hard—harder than dental enamel—that they would erode people’s teeth!²⁷ Scientists also examined coprolites (fossilized excrement) discovered in the back of a cave. These specimens also contained phytoliths from prickly pear cactus and other cacti. Interestingly, the presence of phytoliths in the stools indicates that these populations were able to pass the stones without problem.

Additional historical evidence includes a photograph taken circa 1900, which shows Native American women roasting agave hearts for consumption; agave, too, is very high in oxalates.

Turning to a different climate zone, we can examine the Inuit, who have had notoriously low rates of kidney stones. It is easy to assume that because their traditional diet consists primarily of animal foods, dietary oxalates are not an is­sue. However, according to the 1991 book Tra­ditional Plant Foods of Canadian Indigenous Peoples: Nutrition, Botany and Use,²⁸ Inuits, past and present, do eat plants—and again, these plants are high in oxalates. A traditional Inuit diet includes greens, berries, roots, wild celery, tall cottongrass, lichens, mosses, algae, kelp and other seaweeds, including an Eskimo “ice cream” made with berries and seal oil. These foods are consumed not just seasonally but all year long by preserving them through meth­ods like freezing, dehydrating, slow cooking, baking, fermenting or packing in seal oil. It is important to note that a rich source of omega-3 fatty acids found in fish oil and other seafoods protects against a number of risk factors for calcium oxalate kidney stone formation.²⁹

Likewise, traditional African peoples have also consumed high-oxalate foods. A 2016 article laments how during the colonial era, “exotic” Western crops such as cabbage and spinach displaced “African indigenous vegeta­bles,” which provide a much higher vitamin and mineral content. Foods like amaranth, African nightshade, spider plant, jute mallow and slen­der leaf can all be high in oxalates.³⁰ Africans knew how to prepare these foods properly to lower the oxalate content and increase mineral bioavailability, using methods like “thermal processing, germination, milling/household pounding, microbial fermentation, and soak­ing.”³⁰ In Africa, these indigenous vegetables and traditional processing techniques are cur­rently being reintroduced to counter malnutri­tion and increase food security.

The Mediterranean region shares a similar story, where wild edible plants high in oxalate have traditionally been important sources of nutrients. There, people once knew how to prepare these indigenous plant foods—through boiling, frying or simmering in stews—“to remove undesirable compounds, such as oxalic acid.”³¹ Unfortunately, as with many other cul­tures, modern people are losing the knowledge, literacy and ability to prepare these foods ac­cording to traditional processing methods.

FRIEND OR FOE?

In the environment, oxalate is the most oxi­dized carbon compound after carbon dioxide.³² As a 2020 article explains, when oxalate in soil is oxidized and degraded, carbonate is also formed—a process called the “oxalate carbon­ate pathway.” This cycle is critical—without oxalate, there would be no life. The oxalate carbonate pathway creates a carbon sink within the soil. It is nature’s CO2-trapping-and-removal system!³³

Shaping biological life above and below ground, bacteria and fungi are critical players in the oxalate carbonate pathway. Fungi are “oxalogenic,” that is, they produce oxalate and oxalic acid. They use oxalic acid to neutralize their environment by lowering pH. This helps make nutrients more available for plant uptake at the root level. Interestingly, oxalate produced by fungi will also chelate with heavy metals, making fungi attractive for biotransformation.³⁴ On the other hand, bacteria are “oxalotrophic,” meaning they consume oxalate. As bacteria devour and degrade oxalate, they raise the pH.³⁵ These two types of microbes work in harmony to balance the oxalate carbonate pathway.

So, what is the purpose of oxalate in hu­mans? Is it friend or foe? Early research suggests three potential physiological roles for oxalate in the human body. First, oxalate stimulates the absorption of water, sodium and chloride in the kidney tubules. Second, it assists with immune function, and third, it assists in RNA synthesis.²⁵ Interestingly, only super-high levels of oxalate (>5 mmol/L) cause renal necrotic cell death; normal physiological oxalate concentrations (≤ 1 mmol/L) do not.³⁶

To recap, under normal conditions, up to 95 percent of circulating oxalate will be excreted through the kidneys. The kidneys’ functional units are the nephrons, and each kidney con­tains about a million. Nephron count is unique to each individual and set in utero by about thirty-six weeks’ gestation; no new nephrons will be added over the lifespan.³⁷ The nephron’s filter, called the glomerulus, filters the blood; the nephron’s tubule then returns needed sub­stances to the blood and pulls out wastes.³⁸ Not all kidneys function at the same level, however. The “glomerular filtration rate” (GFR), which measures how well the kidneys are working, shows that the rate decreases by 1 percent per year starting at about age forty. In other words, an eighty-year-old will have about 50 percent of the kidney function of a forty-year-old.³⁷

When the nephrons can’t clear oxalate, buildup occurs, causing hyperoxaluria (high oxalate in the urine), the primary risk factor for kidney stones. There are several pathways to hyperoxaluria, including (1) supersaturation of urine with calcium oxalate (where “supersatu­ration” of a compound is “the concentration in solution above its solubility”), driving crystal­lization,³⁹ (2) increased intestinal absorption and (3) increased liver production.⁴⁰ Problems occur when bacteria and the supersaturation of miner­als cause stones to form. The supersaturation pathway is particularly important (see Figure 3). It’s interesting to recall the direct parallel between kidney stone formation and the forma­tion of fossils and stalactites.

Urine naturally contains specific elements that inhibit kidney stone formation. Inhibitors are substances that block stone formation, either directly by influencing supersaturation and other stone-forming processes or indirectly by modifying the urinary environment. Stone formation is determined by the balance of urine promoters and inhibitors. Because there is person-to-person variability in inhibitor concentrations and function, some people form stones while others do not.⁴¹

Recognized urinary inhibitors include magnesium and citrate (as well as potassium and other substances). Magnesium is well known for its ability to inhibit calcium oxalate crystals by blocking intestinal oxalate absorption and forming a soluble complex. Urinary citrate binds to calcium to decrease its concentration, while directly binding to calcium oxalate to inhibit crystal growth. Systemic pH balance influences urinary citrate production; alkalosis increases citrate synthesis and excretion, while an acidotic state decreases it.⁴²

IT’S DIET—BUT NOT DIETARY OXALATES

Overall, accumulating evidence reveals that kidney stones are fundamentally linked to a damaged gut, which impairs the body’s ability to clear oxalates. We must, therefore, consider the real culprits like refined sweeteners, ultra-processed foods and seed oils—hallmarks of the modern industrial diet.

For example, glucose intake significantly increases urine saturation with oxalate.^3,43 This may help explain the increased risk of kidney stones linked to diabetes and obesity (55 percent and 59 percent increased risk, respectively).⁴⁴ In fact, clinicians now test for glyoxylate, which is the immediate metabolic precursor to oxalate and a marker for diabetes.⁴⁵ Researchers have found that glyoxylate plasma levels can predict diabetes up to three years prior to a diagnosis of diabetes or even prediabetes before rising glucose levels.⁴⁶

Ironically, the elevated urinary oxalate ex­cretion associated with diabetes and obesity is shown to be independent of dietary oxalate in­take.46 Considering escalating diabetes rates and poor American dietary habits, it appears that gut dysbiosis and the overconsumption of industri­ally ultra-processed foods are more responsible for oxalate toxicity than the overconsumption of so-called “superfoods” like spinach or sweet potatoes. Simply put, it is not oxalate-containing foods like spinach that are increasing the pro­duction and absorption of oxalate. To address the oxalate problem, we must consider the impact of processed and ultra-processed industrial foods on gut and kidney health.

In a systematic review of severe, clinically-diagnosed cases of kidney damage (called “oxalate nephropathy”), fat malabsorption, due to gut damage, was more often reported (88 percent of cases) than excessive dietary oxalate consumption (20 percent of cases).⁴⁷ Fat malabsorption increases oxalate absorption in the small intestine and may also increase oxalate permeability in the colon. Normally, oxalates combine with calcium to form an insoluble complex, which blocks oxalate absorption. In cases of fat malabsorption, calcium binds with fat instead, increasing the number of free oxa­lates ready to be absorbed. Therefore, in patients with fat malabsorption, oxalate absorption can increase from the normal level of 5 to 10 percent to over 30 percent.⁴⁸

Surveys show that Americans are consum­ing three hundred times the recommended daily amount of added sugar.⁴⁹ When the body is in glucose homeostasis, typically just one teaspoon of glucose circulates in the blood. Imagine how much sugar is flooding the body during high sugar intake. For example, a popular Starbucks beverage can contain around eighteen teaspoons of sugar! Consuming one sugar-sweetened soda per day is associated with a 23 to 33 percent greater risk for kidney stone formation.⁴²

Research shows that high sugar consump­tion (especially fructose and high-fructose corn syrup) contributes to the formation of advanced glycation end products (AGEs). AGEs form when sugar molecules non-enzymatically fuse to proteins, which can cause damage in every organ.⁵⁰ In addition, AGEs are ubiquitously found in most ultra-processed foods, which account for over 60 percent of the calories in the American diet and make up 73 percent of the U.S. food supply.⁵¹ While gut bacteria use sugars to make more AGEs, AGEs may inhibit the growth of beneficial bacteria, which in turn “may contribute to the pathogenesis of ageing and diabetes-associated diseases.”⁵² Addition­ally, AGE-induced gut dysbiosis and inflamma­tion contribute to progressive kidney damage, including structural changes that further impair the kidneys’ filtering process.⁵³

In addition to excess sugar and fructose, overconsumption of industrial seed oils, high in omega-6 polyunsaturated fatty acids (PUFAs), contributes to AGE production (see Figure 4). The fatty acid ratio of omega-6 to omega-3 is a driving factor in kidney disease and many other chronic illnesses. In the past thirty years, dietary omega-6 consumption has increased in the face of omega-3 deficiency. The ideal ratio of omega-6 to omega-3 is about two to one, but today’s ratio is over twenty to one. Researchers have noted that a “USDA egg” has an omega-6 to omega-3 ratio of about 20:1.⁵⁴

Industrial seed oils and other sources of omega-6 weaken and soften the cell mem­branes,⁵⁵ which enhance oxalate binding to the nephrons and begin crystal formation.^56,57 Accumulating evidence shows a link between increased consumption of omega-6 fatty acids and kidney stone disease. In contrast, higher intakes of omega-3 fatty acid (mostly from seafood) protect against the risk of kidney stone formation, CKD and other degenerative dis­eases,^58,59 as evidenced by the diet of traditional Inuit populations, rich in omega-3 fatty acids.

OXALATE-DEGRADING BACTERIA

A species of oxalate-degrading bacteria was first discovered in 1980, when it was isolated in the domestic animal rumen. Further research led to the identification and naming of the new species, Oxalobacter formigenes. O. formigenes is unique in that it is the only bacteria species known to use oxalate as its primary energy source. In the healthy gut, O. formigenes is present only in small amounts, and its pres­ence is variable. Colonization with the “oxalate specialist” O. formigenes is associated with increased microbial diversity and decreased risk for kidney stones.^60,61

For decades, O. formigenes was presumed to be the sole player in oxalate degradation, keeping the research focus on it alone. However, with rapid advances in technology, scientists have learned that multiple bacterial species can degrade oxalate, working through a large network.²¹ For example, monitoring the gut bac­teria of over one thousand healthy participants, one study found that the majority (92 percent) of gut microbiomes contained several species of oxalate-degrading bacteria.⁶² Because of the complexity of the oxalate-degrading network, researchers now understand the importance of assessing gut health in its entirety rather than focusing on a single bacterial type such as O. formigenes.⁶³

Researchers note the specific ability of Bi­fidobacterium (B.) spp. and Lactobacillus (L.) spp. to degrade oxalate.⁶⁴ In a study examining food-based probiotics, researchers found seven different Lactobacillus strains isolated from dairy products (five strains of Lactobacillus fermentum and two of Lactobacillus gastricus) that showed significant oxalate-degrading abil­ity.⁶⁵ When present in the gastrointestinal tract, oxalate-degrading bacteria are able to decrease oxalate by up to 40 percent and achieve a sig­nificant reduction in kidney stone formation. Hence, a healthy gut is key to maintaining oxalate tolerance.

LOSS OF TOLERANCE

Consuming dietary oxalate helps maintain oxalate tolerance by feeding and sustaining oxalate-degrading bacteria. Therefore, when dietary oxalate intake stops, oxalate tolerance disappears. This phenomenon was dramatically illustrated in Utah in 1971 and involved the death of over twelve hundred sheep. Because atomic testing was happening in the region, scientists initially suspected that the testing was the cause of the sheep’s death. Upon further in­vestigation, they learned that the sheep had been voraciously grazing on Halogeton glomeratus, an extremely high-oxalate weed.⁶⁶ This was the herd’s first exposure to halogeton following a winter of abstinence. Oxalate poisoning was further compounded because the sheep had no access to water. The herd’s stomachs swelled, resulting in death due to the inability to clear the concentrated oxalate overload. In subsequent studies, researchers found that by gradually in­creasing sheep’s grazing exposure by two hours a day, the sheep could regain oxalate tolerance within a couple of days.

Maintaining tolerance by daily consuming some dietary oxalate is important. Ironically, when dietary oxalate intake is lower than fifty milligrams per day, oxalate absorption increases significantly.⁶⁷ At the same time, overconsuming high amounts of dietary oxalates, especially in the form of foods like spinach smoothies, can be hazardous. Acute kidney injury (AKI) can occur with an overload of dietary oxalate. However, most reported cases of dietary oxalate-induced kidney damage have had other AKI-related risk factors, including diabetes, gastric bypass surgery, CKD and dehydration.⁶⁷

HOW TO INCREASE OXALATE-DEGRADING BACTERIA

THE KEY STRATEGY FOR PREVENTION

Dehydration, or low fluid intake, is rec­ognized as the primary risk factor for kidney stone disease.42 Therefore, the universal rec­ommendation for prevention is increased fluid intake, with water being the preferred liquid.^43,68 Still, 65 percent of U.S. adults are chronically under-hydrated due to inadequate water intake.⁶⁹ Greater fluid intake increases urine volume, which in turn decreases the risk of supersatura­tion and calcium oxalate crystallization.

To prevent recurring kidney stones, the recommended intake is two and a half to three liters of fluid per day.^70,71 Most importantly, fluid should be consumed continuously throughout the day. It is especially critical to remain well hydrated at night when kidney filtration natu­rally declines. Although this may disrupt sleep, keeping hydrated during the night is essential in stone prevention.⁴³ Research shows that each two hundred millileters of fluid consumed per twenty-four-hour period is associated with a 13 percent decreased risk of stone formation.⁷²

Drinking water quality and mineral content are also important factors to consider. Higher mineral content is associated with increased urinary citrate, while lower mineral content is not. Mineral water frequently contains bicarbonate, which is absent in tap water.⁴² Gerolsteiner, a naturally sparkling mineral water, is a great source of magnesium and high in bicarbonate. As mentioned, magnesium is a natural stone inhibitor, while bicarbonate increases the ex­cretion of citrate, another important inhibitor. Mineral water provides the most bioavailable forms of magnesium and calcium. Because they are hydrated (ionic), these minerals are rapidly absorbed. Likewise, raw milk is a valuable source of bioavailable magnesium and calcium. Other liquids to increase hydration can include bone broths, soups, tea (depending on oxalate content) and limited amounts of sour kombucha.

WHAT’S NEXT?

Promising studies from China highlight the beneficial effects of vinegar (such as organic, unpasteurized apple cider vinegar) on kidney disease and other chronic illnesses. Research shows that acetic acid (5 percent), the bioactive ingredient in vinegar, can significantly impact and suppress kidney stone formation. In a study of over nine thousand people, one teaspoon (five milliliters) of vinegar, taken three times, daily decreased the risk of nephrolithiasis by 60 per­cent and the rate of recurrence by 50 percent.⁷³ In addition, daily vinegar intake was associated with an improved urinary profile, including increased urinary citrate, higher urine pH and reduced urinary calcium.⁷³ The same research group and others have repeated these findings in human, animal and in vitro studies.⁷⁴

Interestingly, Chinese vinegar factory workers reportedly have low rates of cancer and cardiovascular disease. Although the exact mechanism is unknown, researchers speculate that acetic acid can inhibit oxalate production because it has a similar structure.⁷⁵

As we have entered into a new era of gut microbiome research, attention to the impor­tance of probiotics therapy has increased rapidly. Growing evidence reveals several important lactic acid bacteria strains that consume oxalate and maintain oxalate homeostasis. Many of these strains can tolerate stomach acid, resist bile salts and survive antibiotics, making them attractive probiotic candidates.⁶⁵

Aside from taking commercial probi­otic pills, fermenting food for specific bacterial strains is gaining in popularity. In his 2022 book, Super Gut,⁷⁶ William Davis, MD outlines how to compound the potential of commercial probiotic supplements by using them to fer­ment dairy products and other foods. Using evidenced-based research, Dr. Davis offers a comprehensive guide to probiotics and how to transform them into high-powered fermented foods. Surprisingly, he includes oxalates in the discussion! Super Gut is a must-read for gut health.

FINAL THOUGHTS

Returning to the holobiont concept, we now know that demonizing dietary oxalates is an incomplete and outdated strategy. The link between the gut microbiome and kidney stone disease clearly shows that the host-gut microbi­ota relationship is critical to health and disease. Any research or health advice that disregards this vital relationship should be considered po­tentially obsolete, or at best, taken with caution.

Our ancestors’ ability to prepare and con­sume oxalates, even in high amounts, demon­strates that high-oxalate “superfoods” are not the issue; rather, the problem lies with improp­erly prepared foods and the modern, industrially disrupted, toxic gut. Therefore, rebuilding and maintaining a healthy gut microbiome is the utmost priority. A high-quality diet that includes fresh, minimally processed whole foods, a daily intake of fermented foods and adequate omega-3 PUFAs is key to gut health and protection against kidney stone disease and other diseases. Most importantly from a kidney standpoint, drinking plenty of naturally mineralized water and keeping well hydrated will ensure kidney health and longevity.

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SIDEBARS

 

DRUGS AND KIDNEY STONES

The gut is first to modify drugs, including antibiotics and other xenobiotics, before they reach the liver. In fact, due to its massive genetic potential, the gut microbiome’s enzyme count greatly exceeds that of the liver.⁷⁷ Initially, researchers thought that drugs were absorbed without impacting the gut.⁷⁸ However, they now know that in addition to the direct effects of antibiotics on gut bacteria, many non-antibiotic drugs exhibit antibiotic effects and also impact the gut.^18,79 According to recent evidence, over two hundred approved pharmacological compounds can inhibit the growth of at least one gut bacterium.⁸⁰

Non-antibiotic drugs affecting the gut microbiota include nonsteroidal anti-inflammatory drugs (NSAIDs), osmotic laxatives, hormones, benzodiazepines, antidepressants, antihistamines, irritable bowel drugs, proton pump inhibitors, metformin, statins and psychotropic drugs.¹⁸ In turn, gut bacteria have been shown to alter the effect of over thirty approved drugs.⁸⁰ Therefore, variation in gut composition is one explanation for individual reactions to drugs and other xenobiotics.

Alarmingly, antibiotic use has increased 65 percent worldwide within the past two decades.81 Increasing evidence shows that antibiotics can have a profound effect on both short-term and long-term gut health. In regards to kidney stone formation, one identified mechanism associated with antibiotic therapy is the rapid loss of microbial oxalate me­tabolism.⁴ A two-week course of antibiotics will eliminate 63 percent of Oxalobacter formigenes, with little recovery for oxalate metabolism thereafter. The presence of O. formigenes is an important indicator of gut health, while its absence is a clear sign of antibiotic damage.⁸² A second mechanism linking antibiotics to kidney stones is that some antibiotics may directly promote crystallization, which leads to kidney stone formation.⁸³ In one study, 70 percent of bacteria contained within calcium oxalate kidney stones were found to be multi-antibiotic-resistant, implicating bacteria in stone formation.⁴

Additionally, a connection between antibiotic therapy and fungal imbalance is widely recognized. Following antibiotic treatment, Candida albicans, a well-known fungus, can suppress the regeneration of Lactobacillus, a key bacterial player in the gastrointestinal tract.⁸⁴ It is important to remember that fungus produces oxalates to modify its environment. There­fore, more research is needed to see how fungal overgrowth contributes to oxalate excess and kidney stone formation.

FERMENTATION AND OXALATES

Fermentation is one of the oldest methods used in food preparation and production. Fermenting reduces antinutri­ents, improves nutritional quality and extends shelf life. Many countries rely on fermentation to transform cereals such as maize, rice, wheat, barley, millet and sorghum, as well as legumes such as chickpeas, lentils, groundnut seed, locust bean and soybean into palatable foods. In Africa and Asia, fermentation of indigenous cereals and legumes creates beverages, breads, pancakes, gruel, porridges, soups, side dishes, snacks, sauces, condiments and seasonings.

In addition to increasing nutrient bioavailability and bioaccessibility, fermentation is key in reducing oxalates and other antinutritional factors such as phytates, lectins and tannins. Fermentation reduces oxalates through microbes that use oxalate as a carbon source and by the hydrolytic action of enzymes produced during the fermentation process. According to a 2022 review article,⁸⁵ fermentation can reduce oxalates by significant percentages in flours made from sorghum (53 percent), groundnut (32 to 56 percent), African oil bean (62 to 77 percent), Lyon bean (16.5 to 68 percent), horse gram (66.8 percent) and lima bean (95 percent). Fermentation also reduces the oxalate content of several vegetables, including silver beet (fermented to make kimchi) by 38.5 percent,⁸⁶ cocoyam (an important food crop in Africa and Asia) by 58 to 65 percent, depending on the duration of fermentation,⁸⁷ and bamboo shoots by 37 to 56 percent.⁸⁸

 

CHAMPION OXALATE EATERS

The white-throated woodrat eats a large amount of oxalate but excretes 100 percent of the oxalate it consumes. For this reason, scientists have used the woodrat to study oxalate and the microbiome. Researchers who placed fecal transplants from these little animals into regular laboratory rats discovered that not only do the lab rats develop the same tolerance to oxalates as the woodrat, but the tolerance lasts for up to nine months!⁸⁹

 

HYPEROXALURIA: DYSREGULATED OXALATE HOMEOSTASIS

Oxalate homeostasis depends on the delicate balance of endogenous production, intake of exogenous sources from food and adequate bodily excretion. When this balance is disrupted, urinary oxalate increases, which leads to hyperox­aluria (high-oxalate urine).

Hyperoxaluria is the main risk factor for calcium oxalate kidney stone formation. It arises from two clinically identi­fied conditions: primary and secondary hyperoxaluria.⁷¹ Primary hyperoxaluria, quite rare and most often diagnosed in childhood, is due to inborn errors of glyoxylate metabolism resulting in oxalate overproduction. Secondary (or enteric) hyperoxaluria, more prevalent, is caused by increased intestinal oxalate absorption (dysbiosis), increased endogenous oxalate precursors (metabolic dysfunction) and excess dietary intake of oxalate-rich foods. It is frequently linked to de­hydration, multiple gastrointestinal disorders and other long-standing, hyperoxaluria-enabling conditions. In all cases, hyperoxaluria may lead to urine supersaturation of calcium oxalate, which may progress to crystal-induced kidney damage.

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This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Spring 2024

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