Uric acid and gout as reflections of dysbiosis


Better blood and urine ranges of uric acid may cause gout (painful uric acid crystal deposition in joints) and kidney illness. Extra lately, uric acid has additionally been related to elevated threat for metabolic syndrome, kind 2 diabetes, heart problems, kidney and liver illness even within the absence of gout assaults, i.e., “asymptomatic hyperuricemia” or asymptomatic will increase in blood ranges of uric acid. Standard “remedies” contain decreasing the dietary consumption of purines, i.e., the genetic (DNA and RNA) materials current in animal merchandise, and prescribed drugs that block the enzyme, xanthine oxidase, that yields uric acid. As in so many different situations, the traditional options tackle “downstream” phenomena however fail to deal with the precise trigger—not food regimen, however disruptions of bowel flora composition with lack of microbial species which might be vigorous in metabolizing uric acid, thereby decreasing blood and urine ranges. This science has been unfolding for in regards to the previous decade, but it surely has lately galloped ahead with a flood of recent observations which might be yielding therapeutic prospects in managing uric acid. (It additionally addresses a basic flaw in standard considering: Why would people, genetically-adapted over three million years to consuming animal merchandise akin to meats, organs, and seafood, develop an intolerance to them? The issue shouldn’t be animal merchandise; it’s the capability to metabolize elements akin to uric acid, disrupted by shifts in gastrointestinal (G) microbiome composition because of trendy life and maybe worsened by a nutrient- and polyphenol-poor trendy food regimen.)

Folks with gout and hyperuricemia have been proven to have 1) disrupted gastrointestinal microbiome composition with elevated Proteobacteria (fecal species) and mucin-degraders akin to Bacteroides caccae, 2) elevated intestinal permeability, and three) elevated endotoxemia, all of which additional provides to irritation, insulin resistance, and susceptibility to heart problems. You’ll be able to recognize that gout and hyperuricemia aren’t nearly uric acid, however a constellation of phenomena, a lot of which may be backtracked to a disrupted GI microbiome.

The checklist of gastrointestinal microbes that metabolize uric acid in varied methods is rising quickly, largely Lactobacillus species which have developed to be environment friendly metabolizers of purines and different genetic materials. Among the many species/strains which have been related to lowered blood and urinary ranges of uric acid embody:

  • Lactobacillus brevis DSM9218
  • Lactobacillus plantarum WCFS1
  • Lactobacillus paracasei S12
  • Limosilactobacillus fermentum GR-3
  • Lacticaseibacillus paracasei MJM60396
  • Ligillactobacillus salivarius CECT 30632

A human research of the final microbe listed, L. salivarius CECT 30632 at a day by day dose of 1 billion CFUs per day for six months, demonstrated a marked discount in gout episodes, reliance on gout treatment, and lowered blood ranges of uric acid in comparison with placebo.

Along with over proliferation of fecal microbes and mucin-degrading species, lack of vital butyrate-producing species, Faecalibacterium prausnitzii and Bifidobacteria species, has additionally been documented. Though F. prausnitzii and Bifidobacteria species don’t themselves metabolize uric acid, they one way or the other assist people who do. Recall that prebiotic fibers akin to inulin/FOS trigger a “bloom” in these species, which will additionally add additional benefit. Additional, microbial metabolism of purines and different genetic materials is considerably elevated when glucose (sugar) is much less out there; in different phrases, a scenario wherein insulin resistance and blood glucose are introduced below management might additional improve the microbiome’s capability to rid your physique of purines and thereby uric acid.

In fact, you can attempt to get hold of and ferment a few of these species, as we do with our L. reuteri and L. gasseri yogurts to acquire excessive bacterial counts to make sure significant organic results akin to eradication of SIBO, smoother pores and skin, elevated libido, lowered intestinal permeability and decreased endotoxemia. However, as you may recognize, it turns into impractical to ferment each species we need to colonize our GI tracts. Curiously, the vast majority of species that metabolize purines and thereby cut back uric acid come from fermented meals akin to sauerkraut, pickles, and kimchi. Maybe in future we can get hold of a number of of these microbes akin to L. salivarius CECT 30632 that you can ferment as yogurt to amplify uric acid-reducing results. There may be sometimes a a number of 12 months lag going from laboratory statement to industrial availability, so these microbial strains aren’t but out there. Keep tuned.

By the best way, uric acid shouldn’t be the one issue that’s proving to be a metabolic consequence of a disrupted gastrointestinal microbiome. Add oxalates, homocysteine, vitamin B12 deficiency, folate deficiency and plenty of different conditions which might be yielding to insights into the microbiome that, like uric acid, ought to trigger us to rethink all we thought we knew about these phenomena.


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