Greater blood and urine levels of uric acid can cause gout (painful uric acid crystal deposition in joints) and kidney disease. More recently, uric acid has also been associated with increased risk for metabolic syndrome, type 2 diabetes, cardiovascular disease, kidney and liver disease even in the absence of gout attacks, i.e., “asymptomatic hyperuricemia” or asymptomatic increases in blood levels of uric acid. Conventional “treatments” involve reducing the dietary intake of purines, i.e., the genetic (DNA and RNA) material present in animal products, and pharmaceuticals that block the enzyme, xanthine oxidase, that yields uric acid. As in so many other conditions, the conventional solutions address “downstream” phenomena but fail to address the actual cause—not diet, but disruptions of bowel flora composition with loss of microbial species that are vigorous in metabolizing uric acid, thereby reducing blood and urine levels. This science has been unfolding for about the past decade, but it has recently galloped forward with a flood of new observations that are yielding therapeutic possibilities in managing uric acid. (It also addresses a fundamental flaw in conventional thinking: Why would humans, genetically-adapted over three million years to consuming animal products such as meats, organs, and seafood, develop an intolerance to them? The problem is not animal products; it’s the capacity to metabolize components such as uric acid, disrupted by shifts in gastrointestinal (G) microbiome composition due to modern life and perhaps worsened by a nutrient- and polyphenol-poor modern diet.)
People with gout and hyperuricemia have been shown to have 1) disrupted gastrointestinal microbiome composition with increased Proteobacteria (fecal species) and mucin-degraders such as Bacteroides caccae, 2) increased intestinal permeability, and 3) increased endotoxemia, all of which further adds to inflammation, insulin resistance, and susceptibility to cardiovascular disease. You can appreciate that gout and hyperuricemia are not just about uric acid, but a constellation of phenomena, much of which can be backtracked to a disrupted GI microbiome.
The list of gastrointestinal microbes that metabolize uric acid in various ways is growing rapidly, mostly Lactobacillus species that have evolved to be efficient metabolizers of purines and other genetic material. Among the species/strains that have been associated with reduced blood and urinary levels of uric acid include:
- Lactobacillus brevis DSM9218
- Lactobacillus plantarum WCFS1
- Lactobacillus paracasei S12
- Limosilactobacillus fermentum GR-3
- Lacticaseibacillus paracasei MJM60396
- Ligillactobacillus salivarius CECT 30632
A human study of the last microbe listed, L. salivarius CECT 30632 at a daily dose of one billion CFUs per day for 6 months, demonstrated a marked reduction in gout episodes, reliance on gout medication, and reduced blood levels of uric acid compared to placebo.
In addition to over proliferation of fecal microbes and mucin-degrading species, lack of important butyrate-producing species, Faecalibacterium prausnitzii and Bifidobacteria species, has also been documented. Although F. prausnitzii and Bifidobacteria species do not themselves metabolize uric acid, they somehow support those that do. Recall that prebiotic fibers such as inulin/FOS cause a “bloom” in these species, that may also add further advantage. Further, microbial metabolism of purines and other genetic material is substantially increased when glucose (sugar) is less available; in other words, a situation in which insulin resistance and blood glucose are brought under control may further enhance the microbiome’s capacity to rid your body of purines and thereby uric acid.
Of course, you could try to obtain and ferment some of these species, as we do with our L. reuteri and L. gasseri yogurts to obtain high bacterial counts to ensure meaningful biological effects such as eradication of SIBO, smoother skin, increased libido, reduced intestinal permeability and decreased endotoxemia. But, as you can appreciate, it becomes impractical to ferment each and every species we want to colonize our GI tracts. Interestingly, the majority of species that metabolize purines and thereby reduce uric acid come from fermented foods such as sauerkraut, pickles, and kimchi. Perhaps in future we will be able to obtain one or more of these microbes such as L. salivarius CECT 30632 that you could ferment as yogurt to amplify uric acid-reducing effects. There is typically a several year lag going from laboratory observation to commercial availability, so these microbial strains are not yet available. Stay tuned.
By the way, uric acid is not the only factor that is proving to be a metabolic consequence of a disrupted gastrointestinal microbiome. Add oxalates, homocysteine, vitamin B12 deficiency, folate deficiency and a number of other situations that are yielding to insights into the microbiome that, like uric acid, should cause us to reconsider all we thought we knew about these phenomena.
