Walnuts: Gut Microbiome and Urolithins

Table of Contents

1. What Reaches the Colon
2. From Ellagitannin to Urolithin
3. Urolithin Metabotypes A, B and 0
4. The Human Walnut Feeding Trials
5. Short-Chain Fatty Acids and Butyrate Producers
6. Secondary Bile Acids
7. Links to Cholesterol and Blood Pressure
8. What the Pooled Reviews Conclude
9. Urolithins Beyond the Gut: Early Human Associations
10. Animal and Laboratory Work
11. Urolithin Supplements Are a Separate Question
12. What Is Not Known
13. Who the Research Raises Concerns For
14. Connections
15. Key Research Papers
16. Featured Videos

What Reaches the Colon

Three parts of a walnut matter for gut bacteria.

• Ellagitannins. These are large polyphenols built around a core called ellagic acid. A 2024 systematic review of walnut ellagitannin research found glansreginin A, pedunculagin and casuarictin to be the ones reported most often in walnut kernels. Because the molecules are large, very little is absorbed intact; the same review describes their bioavailability as limited and points to their gut-made metabolites, the urolithins, as the forms that reach the body.
• Fibre. A review from a colon-cancer research group gives walnuts about 2 grams of fibre per ounce (28 g). Gut bacteria ferment fibre into short-chain fatty acids such as acetate, propionate and butyrate.
• Fat, including alpha-linolenic acid (ALA). Walnuts are the common nut richest in this plant omega-3 (covered on the ALA, Omega-3 and Brain page). One feeding trial, discussed below, was designed specifically to ask whether walnut fats or the rest of the walnut drive the bacterial changes.

Processing changes the starting material. A food-chemistry study that baked walnut kernels found that heating at 165 °C for 30 minutes roughly doubled the free ellagic acid (an increase of 99.5%) while the tannin-bound fractions fell, meaning roasting shifts walnut tannins toward free ellagic acid before they are eaten. Whether that changes urolithin production in people was not tested.

From Ellagitannin to Urolithin

The chain runs in three steps.

1. Tannin to ellagic acid. In the gut, ellagitannins such as pedunculagin are broken apart and release ellagic acid. A 2023 review describes this release as hydrolysis that happens at low pH.
2. Ellagic acid to urolithins, by bacteria. Ellagic acid itself is poorly absorbed. Colon bacteria strip it down, ring by ring, into urolithins (chemically, hydroxy-dibenzopyranones). Intermediate forms such as urolithins C and D are made along the way; the end products most often measured are urolithin A, isourolithin A and urolithin B.
3. Absorption and conjugation. Urolithins are absorbed, and the body attaches sugar-acid (glucuronide) or sulfate groups to them. The forms found in blood and urine are mostly these conjugates.

The proof that bacteria, not human enzymes, do step two came from the Spanish research group that first described urolithins in humans. In 2005, Cerdá and colleagues incubated stool samples from six volunteers with ellagic acid, the pomegranate tannin punicalagin, and a walnut ellagitannin extract under oxygen-free conditions. All three produced urolithin A in every volunteer's stool culture, but at very different rates and amounts from person to person. That same year the group fed 40 healthy volunteers a single serving of one of four tannin foods (strawberries 250 g, red raspberries 225 g, walnuts 35 g, or oak-aged red wine 300 mL). Neither the tannins nor ellagic acid appeared in urine; a urolithin B conjugate appeared in every participant 32–56 hours later. Walnuts gave the highest recovery — on average 16.6% of the ingested ellagitannins, against 2.8% for strawberries — and every group split into "high" and "low" excreters.

Later work identified some of the bacteria involved. Species of Gordonibacter make intermediate urolithins; in 2018 the group described a new genus, Ellagibacter isourolithinifaciens, isolated from healthy human stool, that converts ellagic acid into isourolithin A. Both belong to the Eggerthellaceae family. A 2022 review by the same group counts 13 urolithins and their conjugates described to date, found variously in urine, blood, stool, breast milk, prostate, colon and breast tissue. The same review cautions that many laboratory experiments used urolithin forms and concentrations that do not match what is found in the body, "making some reported urolithin activities questionable."

Walnuts are not the only source. Pomegranate (see Pomegranate: Punicalagins and Antioxidants), strawberries, raspberries and blackberries also carry ellagitannins, and the same bacteria convert them to the same urolithins.

Urolithin Metabotypes A, B and 0

When researchers looked at urolithins in urine across many feeding trials, people consistently fell into three groups, now called urolithin metabotypes (UM). A 2014 summary of intervention trials with walnuts and other nuts, strawberries, raspberries, other berries and pomegranate described them this way:

• Metabotype A (UM-A) — produce urolithin A conjugates only. Between 25% and 80% of volunteers, depending on the trial.
• Metabotype B (UM-B) — produce isourolithin A and/or urolithin B in addition to urolithin A. Between 10% and 50%.
• Metabotype 0 (UM-0) — none of these urolithins detected. Between 5% and 25%.

The three groups appeared regardless of age, sex, body mass index, and the amount or type of tannin food eaten. The same summary noted a higher share of metabotype B among volunteers with metabolic syndrome or colorectal cancer, conditions associated with altered gut bacteria. Put plainly: two people can eat the same handful of walnuts and end up with different urolithins in their blood, or none at all, because their gut bacteria differ.

Do metabotypes track heart-risk markers?

Two studies from the Spanish group examined this, and both describe correlations, not cause and effect.

• Selma et al., 2018. Metabotypes were measured in 20 healthy normal-weight people eating walnuts (30 g a day), 49 overweight or obese people taking a pomegranate extract (450 mg a day), and 25 people with metabolic syndrome eating mixed nuts (15 g walnuts, 7.5 g hazelnuts and 7.5 g almonds a day). In the overweight-obese group, urolithin A was positively correlated with apolipoprotein A-I (the main HDL protein), while urolithin B and isourolithin A — the metabotype B markers — were positively correlated with total cholesterol, LDL cholesterol, apolipoprotein B and oxidized LDL. In the metabolic syndrome group, urolithin A correlated inversely only with glucose. Statin-treated metabolic syndrome patients with metabotype A had lipid profiles resembling healthy normal-weight people, while those with metabotype B responded poorly to lipid-lowering treatment. The authors call metabotypes "potential" cardiometabolic biomarkers needing larger cohorts. Note that the overweight-obese findings came from pomegranate extract, not walnuts.
• Romo-Vaquero et al., 2019. In the stool of 249 healthy people, almost half the bacterial groups separating metabotype A from B belonged to the Coriobacteriaceae family. Metabotype B individuals had higher blood cholesterol and higher bacterial diversity; Coriobacteriaceae abundance correlated positively with total and LDL cholesterol and body mass index. The authors propose this bacterial family as a possible link between metabotype and cholesterol.

Metabotype appears to start early in life. In a study of breastfeeding mothers who ate walnuts, total urolithins in breast milk ranged from 8.5 to 176.9 nanomolar, were absent in the milk of three mothers, and followed each mother's metabotype. When their infants' guts were tracked over the first year, the pattern of Gordonibacter colonisation followed the mother's metabotype, and neither breastfeeding nor vaginal birth was required for it; the authors suggest close mother–baby contact as the likely route.

The Human Walnut Feeding Trials

Below is every human walnut trial found for this page that sequenced stool bacteria, measured short-chain fatty acids or bile acids, or related bacteria to urolithins. Most are small, and several are crossover designs in which each person serves as their own control. "Relative abundance" means a bacterial group's share of all the bacteria sequenced — a rise in one group's share is not the same as more of that bacterium in absolute terms, and neither is a health outcome.

Holscher et al., 2018 (United States)

A controlled-feeding crossover trial in 18 healthy men and women (mean age 53, mean BMI 28.8). All food was provided; diets contained 0 or 42 g of walnuts a day for two 3-week periods with a 1-week washout. Compared with the control period, walnuts produced 49–160% higher relative abundance of Faecalibacterium, Clostridium, Dialister and Roseburia, and 16–38% lower relative abundance of Ruminococcus, Dorea, Oscillospira and Bifidobacterium. Stool secondary bile acids fell (see below) and LDL cholesterol was 7% lower. The authors note that Faecalibacterium and Roseburia belong to butyrate-producing Clostridium clusters IV and XIVa.

Bamberger et al., 2018 (Germany)

The largest trial: 194 healthy adults (134 women, mean age 63) in a randomised crossover design, 43 g of walnuts a day for 8 weeks against 8 weeks nut-free. Participants were told to cut fat, carbohydrate or both to make room for the walnut calories. Stool from 135 participants was sequenced. Walnut eating shifted overall bacterial composition by roughly 5% (p = 0.02). Ruminococcaceae and Bifidobacteria rose, while species of Clostridium cluster XIVa (Blautia, Anaerostipes) fell. Which macronutrient people swapped out made only a marginal difference. The authors call for longer studies and for linking the changes to the lipid improvements seen in the same trial. Note the opposite direction for Bifidobacterium compared with Holscher's trial. This trial was funded by a walnut industry body, which the authors state had no role in the analysis.

Tindall et al., 2020 (United States)

The cleverest design. Forty-two adults at raised cardiovascular risk (mean BMI 30, blood pressure 121/77, LDL 120 mg/dL) ate a 2-week standard Western diet, then three controlled diets for 6 weeks each in random order: a walnut diet (57–99 g walnuts a day, scaled to energy needs); a diet matching walnut fatty acids without any walnuts; and a diet in which oleic acid replaced the ALA. All three were low in saturated fat. Roseburia rose on both the walnut diet and the walnut-fatty-acid-matched diet, which the authors say the fat profile could explain. Only the whole-walnut diet enriched Gordonibacter relative to the fatty-acid-matched diet — the urolithin-producing genus, suggesting a non-fat walnut component (most plausibly the tannins) at work. After the walnut diet, Lachnospiraceae abundance was inversely correlated with blood pressure and lipid measures.

Petersen et al., 2023 (same trial, gene activity)

An exploratory analysis in 35 participants from the Tindall trial looked not at which bacteria were present but at which bacterial genes were being actively expressed (metatranscriptomics). The walnut diet (57 g per 2,100 kcal, 18% of energy) increased the diversity of expressed genes compared with both walnut-free diets, though the diversity of active species did not differ. Gordonibacter showed more active genes, including higher expression of glycine amidinotransferase, an enzyme on the pathway to homoarginine. The authors propose this as a "novel mechanism" but stress that it was exploratory and needs replication. The work was funded by a walnut industry body.

García-Mantrana et al., 2019 (Spain)

A short study: 27 healthy people ate 33 g of peeled raw walnuts a day for three days. Stool bacteria and short-chain fatty acids were measured, and participants were sorted by urinary metabotype. The bacteria of metabotype B people responded more: Gordonibacter rose only in metabotype B, while some Lachnospiraceae fell in metabotype A. Coprococcus and Collinsella rose in both, and acetate and propionate production increased. No control diet was used, so the three-day changes are before-and-after comparisons.

Liu et al., 2024 (United States)

Thirty-nine people ate 2 ounces (about 56 g) of walnuts a day for 21 days, with stool and urine collected before and after. Overall bacterial composition and diversity changed (both significant). The 13 genera most enriched after walnuts included Roseburia, Butyricicoccus, Eubacterium eligens, Lachnospira and Gordonibacter — but also Bilophila and Ruminococcus torques, groups not usually described as beneficial, a reminder that "walnuts changed the microbiome" covers mixed shifts. Twenty-six genera were associated with seven of the nine urolithins measured in urine, 22 of them positively after walnut eating. There was no walnut-free control group.

Herselman et al., 2022 (Australia)

A randomised trial in university students studying the effects of academic stress and daily walnuts. Academic stress was associated with lower gut bacterial diversity in female students, and walnut eating improved it. Effects in male students could not be established because there were too few of them.

Short-Chain Fatty Acids and Butyrate Producers

Short-chain fatty acids are what gut bacteria make when they ferment fibre. Butyrate is the main fuel for the cells lining the colon, and acetate and propionate are absorbed and used elsewhere. The walnut evidence on them comes in two kinds.

• Measured directly, in people: only the three-day García-Mantrana study above reported stool short-chain fatty acids from a walnut-only intervention, finding higher acetate and propionate after walnuts. The 2025 pooled review (below) found that across five nut trials that measured them, propionate was the one consistently raised.
• Inferred from bacteria: several trials found more Roseburia, Faecalibacterium, Butyricicoccus or Ruminococcaceae, groups known to produce butyrate. A rise in butyrate producers is suggestive, but stool butyrate itself was not reported in those trials' abstracts.
• In a laboratory gut model: when Schlörmann and colleagues digested and then fermented five nuts with human stool bacteria in vitro, every nut produced 1.9 to 2.8 times more short-chain fatty acids than the control and shifted the mix toward butyrate. Only walnut samples produced vaccenic acid and the conjugated linoleic acid isomer c9,t11-CLA, which the authors call a potential chemopreventive metabolite. This was a test-tube system, not a human result.

Secondary Bile Acids

The liver makes bile acids to help digest fat (see the bile acids animation). Those that reach the colon are converted by bacteria into "secondary" bile acids, chiefly deoxycholic acid and lithocholic acid. High levels of these two in the colon have been studied as possible contributors to colon inflammation and cancer.

Holscher's 2018 trial is the only human walnut trial in this set that measured them: after three weeks of 42 g a day, stool deoxycholic acid was 25% lower and lithocholic acid 45% lower than after the control diet. The authors describe these as proinflammatory secondary bile acids. In the in-vitro fermentation study, deoxycholic and iso-deoxycholic acid were also lower in fermented nut samples than in the control. One three-week trial in 18 people is the whole of the human evidence; it has not been repeated in a larger group, and it did not measure colon outcomes.

Links to Cholesterol and Blood Pressure

Several of these trials also measured heart-risk markers, which invites the question of whether the bacterial changes help explain them. What the studies report are associations within small groups; none showed that the bacteria caused the changes.

• LDL cholesterol. In Holscher's trial, LDL was 7% lower and the plant sterol campesterol 6% lower after walnuts. The same period saw lower secondary bile acids, and the authors suggest the microbiota "may contribute" to the walnut effect. (The wider walnut–LDL evidence is covered on the Heart Health and PREDIMED page.)
• Blood pressure and lipids, Tindall trial. The parent report of the trial found that the primary outcome, central systolic blood pressure, did not change on any diet and arterial stiffness did not change. Central diastolic pressure fell more on the walnut diet than on the oleic-acid diet (−1.78 vs +0.15 mm Hg), but not more than on the walnut-fatty-acid-matched diet. All three diets lowered total, LDL and non-HDL cholesterol. The follow-up microbiome analysis then found Lachnospiraceae inversely correlated with blood pressure and lipid measures after the walnut diet.
• Metabotypes and lipids. As described above, metabotype B markers tracked higher LDL and apolipoprotein B in one study (mostly in a pomegranate-extract group), and Coriobacteriaceae tracked cholesterol in another.

For context, a 2020 meta-analysis of 18 walnut trials (1,799 participants) found no overall effect of walnuts on systolic or diastolic blood pressure. Small subgroup effects were seen at doses of 40 g or less and with interventions of 8 weeks or longer, but the authors concluded the changes were too slight to matter clinically and that the analysis "does not support walnut consumption as a BP-lowering strategy."

What the Pooled Reviews Conclude

Three reviews have pooled nut-and-microbiome trials. Each includes walnut trials alongside almonds, pistachios and others, so their findings apply to nuts as a group.

• Creedon et al., 2020 (meta-analysis of 9 randomised trials in 8 reports: 5 almond, 3 walnut, 1 pistachio, healthy adults). Nuts increased Clostridium, Dialister, Lachnospira and Roseburia and decreased Parabacteroides. There was no effect on bacterial phyla, diversity or stool output. The first author's fellowship was funded by an almond industry body.
• Fitzgerald et al., 2021 (systematic review of 8 sequencing studies of almonds, walnuts, hazelnuts or pistachios). Nuts had a "modest" effect on diversity: two studies found a shift in within-person diversity and four a shift in overall composition. Walnuts appeared to explain composition shifts more often than other nuts. Results were inconsistent across studies.
• Snelson et al., 2025 (systematic review and meta-analysis of 28 intervention trials, almonds most studied). Most trials found no significant change in diversity and no significant change in most bacterial groups. Several found more Clostridium and Roseburia; results for Bifidobacterium were mixed after almonds or walnuts. Propionate rose in the five trials that measured short-chain fatty acids. There was no effect on stool pH or gut permeability, and an "unfavorable" effect on stool moisture. The authors conclude that nuts have a modest effect on gut health and that heterogeneity between studies limits firmer conclusions.

For the same question about other nuts, see Pistachios: Gut Microbiome and Almonds: Gut Microbiome and Prebiotic.

Urolithins Beyond the Gut: Early Human Associations

Because urolithins are absorbed, researchers have begun asking whether urinary urolithin levels track anything outside the gut in walnut trials. These are correlations within trials, and each is a single study.

• Metabolic syndrome, 2012. In people with metabolic syndrome given a nut-enriched diet for 12 weeks (walnuts, hazelnuts and almonds), urinary urolithins A and B rose significantly, with urolithins C and D also detected; proanthocyanidin breakdown products did not rise. Urolithins were the main urinary microbial metabolites that distinguished nut eaters from controls.
• Mood, 2026. In a randomised crossover trial, 31 healthy young adults (90% women) ate 40 g of walnuts a day for 8 weeks and had an 8-week nut-free period. Total mood disturbance scores fell by 4.85 points with walnuts. Urinary urolithins rose and correlated with rises in urinary 5-HIAA, a serotonin breakdown product. The trial was open-label (participants knew when they were eating walnuts), and the authors say the mechanism needs further work.
• Brain structure, 2026. In an MRI sub-study of the 2-year Walnuts and Healthy Aging trial (104 older adults from the Barcelona centre), among those assigned to walnuts (n = 55), greater increases in urinary urolithin A, urolithin C and a urolithin C conjugate were associated with better-preserved cortical thickness, more so in metabotype B. Cognitive results of this trial are on the Cognitive Aging page.

Animal and Laboratory Work

Much of the walnut-microbiome literature is in animals or cells. These studies help generate ideas but do not show what happens in people.

• Rats. Byerley and colleagues fed 20 male rats either a walnut diet or a diet with the walnut's fat, fibre and protein replaced by corn oil, casein and cellulose, for up to 10 weeks. Walnut-fed rats had greater bacterial diversity, more Firmicutes and fewer Bacteroidetes, more Lactobacillus, Ruminococcaceae and Roseburia, and less Bacteroides and Anaerotruncus.
• Mice, colon cancer model. Nakanishi and colleagues gave mice a chemical carcinogen. A standard diet with 9.4% walnuts gave a modest (1.3-fold) reduction in tumour numbers; higher walnut levels lacked this effect, particularly in female mice. Specific bacterial groups correlated with tumour presence and number.
• Mice, colitis models. A polyphenol extract from the walnut septum (the woody divider inside the shell, not the kernel people eat) eased chemically induced colitis in mice and shifted bacteria. A walnut-derived peptide (LPF) and an isolated walnut protein also altered mouse gut bacteria. These are walnut by-products or isolated fractions, not whole walnuts.
• Test-tube fermentation. The Schlörmann study described above.

A 2024 review of walnut-derived compounds and intestinal inflammation gathers this preclinical work and frames it as a theoretical basis for future study in inflammatory bowel disease; it does not report human trials showing walnuts treat that disease.

Urolithin Supplements Are a Separate Question

Purified urolithin A is sold as a supplement, and the 2022 urolithin review notes that the first human intervention trials giving urolithin A itself have been carried out. Those trials are not walnut research, and their findings cannot be transferred to walnuts for three reasons:

• A supplement delivers a fixed dose of one urolithin to everyone, including metabotype 0 people who make none from food.
• Walnuts deliver tannins, fibre, fats and other compounds together, and the urolithin dose each person ends up with varies widely.
• No study in this set measured how much urolithin A a typical serving of walnuts produces compared with a supplement dose.

The same caution applies to the large literature on urolithin A in cell lines and animals: those experiments often use concentrations or unconjugated forms that differ from what circulates in people, a limitation the urolithin research group itself highlights.

What Is Not Known

• Whether any of it changes health outcomes. No walnut trial has shown that the bacterial shifts reduce disease. The studies measured stool bacteria, metabolites and blood markers over weeks.
• Which shifts are consistent. Roseburia and Clostridium-type increases recur; Bifidobacterium went up in one large trial and down in another. Most trials, and the pooled reviews, found little or no change in overall diversity.
• Absolute versus relative change. Almost all results are relative abundances from 16S sequencing, which can shift when other groups change.
• Long-term effects. Trials ran from three days to eight weeks. Whether the changes persist with years of eating walnuts is untested.
• Whether metabotype can change. Metabotypes are stable enough to be seen across trials, but whether a metabotype 0 person can become a producer, and whether that matters, is not established in these studies.
• Which walnut component does what. Tindall's design suggests fats drive some changes (Roseburia) and non-fat components others (Gordonibacter), but this comes from one trial.
• Funding. Several trials were funded by nut industry bodies. The authors state that funders had no role in analysis; independent replication is limited.

Who the Research Raises Concerns For

• People with tree nut allergy. Walnut is a common tree nut allergen; none of the microbiome findings apply to people who react to walnuts.
• People with digestive conditions. The trials above enrolled mostly healthy adults or adults with raised cardiovascular risk. They do not tell us how people with inflammatory bowel disease, irritable bowel syndrome or other gut disorders respond; the colitis evidence is in mice. The 2025 pooled review reported an unfavourable effect of nuts on stool moisture.
• People reading supplement claims. Claims that walnuts "boost urolithin A" rest on the fact that some people make urolithin A from walnut tannins; the 5–25% of people in metabotype 0 made none in the trials summarised.

Decisions about diet changes for a medical condition belong with a clinician.

Connections

• Nuts — all nuts on the site
• Walnuts — the main topic page
• Walnuts — Benefits Deep Dive — the hub for every walnut article
• ALA Omega-3 and Brain — the walnut fat story
• Cognitive Aging — the Walnuts and Healthy Aging trial
• Heart Health and PREDIMED — the lipid evidence
• Soaking and Phytates — preparation and polyphenols
• Walnuts: Nutrient Profile — the composition table
• Pistachios: Gut Microbiome — the parallel pistachio evidence
• Almonds: Gut Microbiome and Prebiotic — the most-studied nut
• Ellagic Acid — the urolithin precursor
• Pomegranate — the other major urolithin source
• Gut Health — the gut health section
• Microbiome — the gut bacteria overview
• Dietary Fiber — what gut bacteria ferment
• Gut Barrier and Microbiome (animation)
• Lipid Panel — the markers these trials measured

Key Research Papers

1. Holscher HD, Guetterman HM, Swanson KS, et al. Walnut Consumption Alters the Gastrointestinal Microbiota, Microbially Derived Secondary Bile Acids, and Health Markers in Healthy Adults: A Randomized Controlled Trial. The Journal of nutrition. 2018;148(6):861-867. PubMed PMID: 29726951
2. Bamberger C, Rossmeier A, Lechner K, et al. A Walnut-Enriched Diet Affects Gut Microbiome in Healthy Caucasian Subjects: A Randomized, Controlled Trial. Nutrients. 2018;10(2):244. PubMed PMID: 29470389
3. Tindall AM, McLimans CJ, Petersen KS, et al. Walnuts and Vegetable Oils Containing Oleic Acid Differentially Affect the Gut Microbiota and Associations with Cardiovascular Risk Factors: Follow-up of a Randomized, Controlled, Feeding Trial in Adults at Risk for Cardiovascular Disease. The Journal of nutrition. 2020;150(4):806-817. PubMed PMID: 31848609
4. Tindall AM, Petersen KS, Skulas-Ray AC, et al. Replacing Saturated Fat With Walnuts or Vegetable Oils Improves Central Blood Pressure and Serum Lipids in Adults at Risk for Cardiovascular Disease: A Randomized Controlled-Feeding Trial. Journal of the American Heart Association. 2019;8(9):e011512. PubMed PMID: 31039663
5. Petersen KS, Chandra M, Chen See JR, et al. Walnut consumption and gut microbial metabolism: Results of an exploratory analysis from a randomized, crossover, controlled-feeding study. Clinical nutrition (Edinburgh, Scotland). 2023;42(11):2258-2269. PubMed PMID: 37826992
6. García-Mantrana I, Calatayud M, Romo-Vaquero M, et al. Urolithin Metabotypes Can Determine the Modulation of Gut Microbiota in Healthy Individuals by Tracking Walnuts Consumption over Three Days. Nutrients. 2019;11(10):2483. PubMed PMID: 31623169
7. Liu H, Birk JW, Provatas AA, et al. Correlation between intestinal microbiota and urolithin metabolism in a human walnut dietary intervention. BMC microbiology. 2024;24(1):476. PubMed PMID: 39548408
8. Herselman MF, Bailey S, Deo P, et al. The Effects of Walnuts and Academic Stress on Mental Health, General Well-Being and the Gut Microbiota in a Sample of University Students: A Randomised Clinical Trial. Nutrients. 2022;14(22):4776. PubMed PMID: 36432461
9. Selma MV, González-Sarrías A, Salas-Salvadó J, et al. The gut microbiota metabolism of pomegranate or walnut ellagitannins yields two urolithin-metabotypes that correlate with cardiometabolic risk biomarkers: Comparison between normoweight, overweight-obesity and metabolic syndrome. Clinical nutrition (Edinburgh, Scotland). 2018;37(3):897-905. PubMed PMID: 28347564
10. Romo-Vaquero M, Cortés-Martín A, Loria-Kohen V, et al. Deciphering the Human Gut Microbiome of Urolithin Metabotypes: Association with Enterotypes and Potential Cardiometabolic Health Implications. Molecular nutrition & food research. 2019;63(4):e1800958. PubMed PMID: 30471188
11. Tomás-Barberán FA, García-Villalba R, González-Sarrías A, et al. Ellagic acid metabolism by human gut microbiota: consistent observation of three urolithin phenotypes in intervention trials, independent of food source, age, and health status. Journal of agricultural and food chemistry. 2014;62(28):6535-8. PubMed PMID: 24976365
12. Cerdá B, Tomás-Barberán FA, Espín JC. Metabolism of antioxidant and chemopreventive ellagitannins from strawberries, raspberries, walnuts, and oak-aged wine in humans: identification of biomarkers and individual variability. Journal of agricultural and food chemistry. 2005;53(2):227-35. PubMed PMID: 15656654
13. Cerdá B, Periago P, Espín JC, et al. Identification of urolithin a as a metabolite produced by human colon microflora from ellagic acid and related compounds. Journal of agricultural and food chemistry. 2005;53(14):5571-6. PubMed PMID: 15998116
14. Beltrán D, Romo-Vaquero M, Espín JC, et al. Ellagibacter isourolithinifaciens gen. nov., sp. nov., a new member of the family Eggerthellaceae, isolated from human gut. International journal of systematic and evolutionary microbiology. 2018;68(5):1707-1712. PubMed PMID: 29583112
15. Cortés-Martín A, García-Villalba R, García-Mantrana I, et al. Urolithins in Human Breast Milk after Walnut Intake and Kinetics of Gordonibacter Colonization in Newly Born: The Role of Mothers' Urolithin Metabotypes. Journal of agricultural and food chemistry. 2020;68(45):12606-12616. PubMed PMID: 33135412
16. García-Villalba R, Giménez-Bastida JA, Cortés-Martín A, et al. Urolithins: a Comprehensive Update on their Metabolism, Bioactivity, and Associated Gut Microbiota. Molecular nutrition & food research. 2022;66(21):e2101019. PubMed PMID: 35118817
17. Mateș L, Banc R, Zaharie FA, et al. Mechanistic Insights into the Biological Effects and Antioxidant Activity of Walnut (Juglans regia L.) Ellagitannins: A Systematic Review. Antioxidants (Basel, Switzerland). 2024;13(8):974. PubMed PMID: 39199220
18. Fan N, Fusco JL, Rosenberg DW. Antioxidant and Anti-Inflammatory Properties of Walnut Constituents: Focus on Personalized Cancer Prevention and the Microbiome. Antioxidants (Basel, Switzerland). 2023;12(5):982. PubMed PMID: 37237848
19. Guo X, Gu F, Yang T, et al. Quantitative conversion of free, acid-hydrolyzable, and bound ellagic acid in walnut kernels during baking. Food chemistry. 2023;400:134070. PubMed PMID: 36084595
20. Creedon AC, Hung ES, Berry SE, et al. Nuts and their Effect on Gut Microbiota, Gut Function and Symptoms in Adults: A Systematic Review and Meta-Analysis of Randomised Controlled Trials. Nutrients. 2020;12(8):2347. PubMed PMID: 32781516
21. Fitzgerald E, Lambert K, Stanford J, et al. The effect of nut consumption (tree nuts and peanuts) on the gut microbiota of humans: a systematic review. The British journal of nutrition. 2021;125(5):508-520. PubMed PMID: 32713355
22. Snelson M, Biesiekierski JR, Chen S, et al. Effects of Nut Intake on Gut Microbiome Composition and Gut Function in Adults: A Systematic Review and Meta-analysis. Advances in nutrition (Bethesda, Md.). 2025;16(7):100465. PubMed PMID: 40518048
23. Li J, Jiang B, O Santos H, et al. Effects of walnut intake on blood pressure: A systematic review and meta-analysis of randomized controlled trials. Phytotherapy research : PTR. 2020;34(11):2921-2931. PubMed PMID: 32510725
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PubMed Topic Searches

1. Walnut and gut microbiota trials
2. Walnut and urolithins
3. Urolithin metabotypes
4. Walnut ellagitannins and pedunculagin
5. Nuts and the gut microbiome: pooled analyses
6. Urolithin-producing bacteria

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