Bile Acids and Gut Health: Everything You Need to Know

A smiling young woman seen from the front, casually eating a wedge of fresh white cheese in a bright, relaxed setting.

Summary

Bile acids are for more than just breaking down fat in the gastrointestinal tract; they’re signaling molecules shaped by the gut microbiome. Specific gut microbes convert bile acids into unconjugated and secondary forms, influencing metabolism, immunity, and overall wellness. This FAQ answers common questions, highlights the key gut microbes involved, and explains why these interactions matter for patient care.

As a refresher, the liver produces many important compounds daily, and bile acids are among the most versatile. They do much more than help with digestion—they affect metabolism, immune function, and cell signaling throughout the body. Their broad influence also means they are implicated in a surprising range of health conditions.

Did you know that bile acids share a dynamic, two-way relationship with the gut microbiome? Not only do bile acids influence the composition and activity of gut bacteria, but these microbes also transform bile acids into entirely new forms, each with unique properties and functions. In this article, we'll explore frequently asked questions about bile acids, how gut microbes are involved, and why they matter for overall health.

.
.

What are bile acids?

Bile acids are molecules the liver creates from cholesterol. The liver produces two main primary bile acids: cholic acid and chenodeoxycholic acid.

Before these primary bile acids leave the liver, they get conjugated, or tagged, with the amino acids glycine or taurine. This conjugation process creates bile salts, which are stored in the gallbladder until a meal containing fats is eaten. When fats reach the small intestine, the gallbladder releases bile salts to break them into smaller droplets. This makes it easier for pancreatic lipase to turn them into fatty acids and glycerol for absorption. Without this process, the small intestine struggles to absorb dietary fats and fat-soluble vitamins, such as A, D, E, and K [1].

How is the microbiome involved? 

Once bile salts have finished emulsifying fat in the small intestine, most travel to the terminal ileum (the last part of the small intestine), where they're reabsorbed and sent back to the liver through the portal vein. This recycling process, called enterohepatic circulation, is remarkably efficient—about 95% of bile acids get reused [2]. But what happens to the remaining 5% that isn’t reabsorbed and passes into the colon? That’s where the gut microbiome takes control.

Certain gut bacteria produce enzymes called bile salt hydrolases (BSHs). These enzymes can "deconjugate" bile salts, essentially removing those amino acid tags we mentioned earlier. This process creates unconjugated bile acids (uBAs).

This might seem like a small change, but it has big effects. uBAs behave differently than their conjugated counterparts and can even act as antimicrobials because they can slip through bacterial cell walls more easily because they repel water [3]. Since uBAs can be harmful to certain microbes, some bacterial species have evolved mechanisms to further modify them, converting uBAs into secondary bile acids (sBAs).

How do gut microbes convert uBAs into sBAs?

There are two primary ways this conversion process happens:

1. Dehydroxylation requires specific genes (bai genes) in the microbiome: 

  • Cholic acid (uBA) → deoxycholic acid (sBA)
  • Chenodeoxycholic acid (uBA) → lithocholic acid (sBA)

2. Oxidation and epimerization use enzymes called hydroxysteroid dehydrogenases (HSDHs). Sometimes, existing sBAs get changed into new forms: 

  • Chenodeoxycholic acid (uBA) → ursodeoxycholic acid (sBA)
  • Deoxycholic acid (sBA) → isodeoxycholic acid (sBA)
  • Lithocholic acid (sBA) → isolithocholic acid (sBA)

These transformations require specific bacterial species and enzymes [4]. Not all gut microbiomes can do these transformations equally well. This means the types and amounts of sBAs vary a lot from person to person. The science on sBAs is mixed: both high and low levels can be problematic.

Are there specific microbes that metabolize bile acids?

Four major bacterial phyla (which encompass many species) can create unconjugated bile acids because they have BSHs: Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria [5], [6].

But only a few taxa can turn those unconjugated bile acids into secondary bile acids [7], [8]:

  • Dehydroxylation is possible in just a few bacterial taxa: Lachnospiraceae, Peptostreptococcaceae, and Clostridium.
  • Oxidation and epimerization are also limited to a few bacterial genera such as Clostridium, Mycobacterium, Eggerthella, Ruminococcus, and Collinsella. 

A diverse gut microbiome supports not only digestive health but also plays a key role in shaping the bile acid profile. Remarkably, a recent study reported that only 37 bacterial species can produce both unconjugated and secondary bile acids [8]. Having a more diverse gut microbiome increases the likelihood of having the right enzymes for these complex transformations.

How do different bile acids interact with the body?

Bile acids are more than digestive detergents—they're signaling molecules that regulate inflammation, protect the gut barrier, and influence the microbiome [9], [10]. How they interact with your body depends on their chemical form: conjugated, unconjugated, or secondary.

Conjugated bile acids

Conjugated primary bile acids (attached to glycine or taurine) emulsify dietary fats for absorption and signal through FXR receptors to regulate their own synthesis [11]. At normal levels, they support intestinal barrier function [12].

Unconjugated bile acids

At moderate levels:

  • Support barrier function and provide antimicrobial protection against pathogenic microbes [13].

At elevated levels:

  • Stimulate water secretion, causing diarrhea [14].
  • Disrupt epithelial cells, increasing permeability and triggering inflammation [15].
  • Released taurine feeds problematic bacteria like Bilophila wadsworthia [16].

Secondary bile acids

At moderate levels:

  • Activate TGR5 receptors, reducing inflammatory cytokines [17].
  • Promote tight junction integrity and mucus production [18], [19]. 
  • Resist pathogen colonization, including C. difficile [18], [20].

At elevated levels:

  • May contribute to DNA damage and oxidative stress [21].
  • Associated with increased colonic inflammation and colorectal cancer risk [22].

What health issues commonly affect bile acid balance?

Certain conditions can alter total fecal bile acid levels or impair the microbiome’s ability to convert them into unconjugated and secondary forms. 

Table comparing bile acid metabolism changes across diseases and conditions such as IBD, diabetes, cancer, and antibiotic use.
  • Inflammatory bowel disease, which includes Crohn’s disease and ulcerative colitis, was associated with higher levels of bile salts (or conjugated bile acids) and unconjugated bile acids and lower levels of secondary bile acids [6], [8], [23]-[29]. However, the microbiome’s capacity to metabolize bile acids appears to shift in both directions in these conditions, indicating that maintaining a balance of bile acids is important [6], [8], [23]. Altered metabolism results in a more toxic bile acid pool, which can disrupt the integrity of the intestinal barrier. 
  • In people with colorectal cancer, the enzyme responsible for creating unconjugated bile acids, BSH, was at lower levels [8]. However, there was also an increase in oxidation and epimerization via the HSDH enzyme, suggesting an increase in some types of secondary bile acids [8]. These specific secondary bile acids are known to antagonize intestinal receptors, which typically suppress tumor growth. 
  • Non-alcoholic fatty liver disease patients had altered potential for secondary bile acid production, which may disrupt lipid metabolism and contribute to hepatic fat accumulation [8], [30], [31].
  • Patients with type 2 diabetes had reduced metabolism of bile acids altogether, likely resulting in more conjugated bile salts, leading to reduced insulin sensitivity [6].
  • Antibiotic use was associated with decreased deconjugation potential of the microbiome via BSH, driven by changes in its composition [32], [33]. 

Scientists haven't yet figured out what an "ideal" bile acid profile looks like. The key to supporting healthy bile acid metabolism is maintaining a diverse microbiome capable of performing all necessary transformations in a balanced manner.

What is bile acid malabsorption? 

As we discussed, under normal circumstances, approximately 95% of bile acids are efficiently reabsorbed in the terminal ileum and returned to the liver via enterohepatic circulation. However, several conditions can disrupt this process, leading to bile acid malabsorption (BAM), where more than 5% of bile acids pass into the colon. BAM can be caused by:

  • Crohn’s disease [34]
  • Surgical resection of the terminal ileum [35]
  • Radiation injury [35]
  • Celiac disease [35]
  • Chronic pancreatitis and exocrine pancreatic insufficiency [35]
  • Microscopic colitis [36]
  • Small intestine bacterial overgrowth [35]
  • Post-cholecystectomy [34]

When excess bile acids reach the colon, they act as potent secretagogues, stimulating water and electrolyte secretion into the colonic lumen [37]. This results in bile acid diarrhea (BAD), characterized by chronic watery diarrhea that can significantly impact quality of life. 

When elevated levels of bile acids pass into the colon due to malabsorption, you might assume this would simply increase secondary bile acid production. However, the reality is more complex, as microbiome dysbiosis may leave an individual without the capacity to produce secondary bile acids, and accelerated intestinal transit time may not even allow for bacterial bile acid metabolism.

As a result, unconjugated bile acids can accumulate in the colon, with significant implications, including disruption of the epithelial barrier, promotion of inflammation, and microbial dysbiosis.

What is the difference between fecal and urinary bile acid levels? 

Bile acids show up in stool because the recycling system (enterohepatic circulation) isn't 100% efficient. Remember how about 5% of bile acids make it to the colon? After microbiome-powered deconjugation and transformations occur, about half of this portion is absorbed in the colon and then returned to the liver. The rest is lost through stool. This is completely normal.

Bile acids in urine happen for a different reason. After the liver produces bile acids, they should be sent to the gallbladder to wait until fat is consumed. If this transport system fails, bile acids build up in the blood. Eventually, they overwhelm the kidneys and are excreted in the urine. This is not normal and may signal liver or bile duct problems.

Are there ways to improve the bile acid profile?

Yes, several approaches can help balance your bile acids.

Diet

  • Drink teas with epigallocatechin. This antioxidant powerhouse is found in many green teas, and preliminary rodent studies suggest it may alter bile acid levels, both increasing and decreasing them [38].
  • Prioritize high-fiber foods. Fiber feeds the beneficial gut bacteria that metabolize bile acids to support bile acid balance [39], [40]. 
  • Limit excess fat intake to avoid strain on the liver, where bile acids are produced [41].
  • Try Konjac glucomannan-enriched noodles. They are a great alternative to gluten noodles, and have been shown to reduce levels of secondary bile acids [42].

Probiotic supplements

  • A probiotic containing three strains of Lactiplantibacillus plantarum reduced levels of both conjugated and secondary bile acids in serum in overweight adults [43]. 
  • A Lactobacillus reuteri probiotic increased levels of unconjugated bile acids [44]. 

Therapeutics for bile acid malabsorption and diarrhea 

  • Bile acid sequestrants are a first-line treatment for bile acid diarrhea that typically require a prescription [45]. They act by binding bile acids in the intestine, preventing their secretagogue effect in the colon.
  • An herbal blend known as rikkunshito is also recommended for bile acid malabsorption due to its ability to adsorb bile acids [46]. 

Where can I find the uBA and sBA metrics in Tiny Health’s Gut Health Test results?

You’ll find them in the Microbial Enzymes & Metabolites section under Modified Bile Acid Production Capacity. Our metric measures the microbiome's ability to produce unconjugated and secondary bile acids via the presence of genes.

  • Deconjugation via BSH (BS -> uBA) is indicated by the presence of the cbh gene.
  • Dehydroxylation (uBA -> sBA) is measured by the presence of the genes baiB, baiH, baiCD, and baiF. 
  • Oxidation and Epimerization (uBA -> sBA) are measured by the presence of the genes hdhA, E1.1.1.201, E1.1.1.393, and E1.1.1.52. 

What does it mean if the uBA or sBA capacities are imbalanced on a Tiny Health test? 

  • Low uBA: Reduced barrier integrity and antimicrobial defense against pathogens like C. difficile [13].
  • High uBA: Increased diarrhea risk, barrier damage, and dysbiosis promotion [14]-[16].
  • Low sBA: Loss of anti-inflammatory signaling, weakened barrier, reduced antimicrobial activity [17], [18].
  • High sBA: Context-dependent—may be beneficial if moderate, but very high levels increase inflammation and cancer risk [22].

Are these metrics available in the PRO Gut Health Test?

Yes. To find unconjugated and secondary bile acid results, navigate to the All Insights page and look for the Microbial Enzymes & Metabolites section under Modified Bile Acid Production Capacity.

Disclaimer: For educational purposes only. Tiny Health does not diagnose, treat, or cure any conditions. Each practitioner is responsible for their own clinical decisions. We provide microbiome interpretation support, not personalized medical advice.

References

[1] A. Di Ciaula et al., “Bile Acid Physiology,” Ann. Hepatol., vol. 16, no. Suppl. 1: s3-105., pp. s4–s14, Nov. 2017, doi: 10.5604/01.3001.0010.5493. 

[2] A. Wahlström, S. I. Sayin, H.-U. Marschall, and F. Bäckhed, “Intestinal Crosstalk between Bile Acids and Microbiota and Its Impact on Host Metabolism,” Cell Metab., vol. 24, no. 1, pp. 41–50, July 2016, doi: 10.1016/j.cmet.2016.05.005. 

[3] M. Begley, C. G. M. Gahan, and C. Hill, “The interaction between bacteria and bile,” FEMS Microbiol. Rev., vol. 29, no. 4, pp. 625–651, Sept. 2005, doi: 10.1016/j.femsre.2004.09.003. 

[4] J. A. Winston and C. M. Theriot, “Diversification of host bile acids by members of the gut microbiota,” Gut Microbes, vol. 11, no. 2, pp. 158–171, 2020, doi: 10.1080/19490976.2019.1674124. 

[5] Z. Song et al., “Taxonomic profiling and populational patterns of bacterial bile salt hydrolase (BSH) genes based on worldwide human gut microbiome,” Microbiome, vol. 7, no. 1, p. 9, Jan. 2019, doi: 10.1186/s40168-019-0628-3. 

[6] A. Labbé, J. G. Ganopolsky, C. J. Martoni, S. Prakash, and M. L. Jones, “Bacterial bile metabolising gene abundance in Crohn’s, ulcerative colitis and type 2 diabetes metagenomes,” PloS One, vol. 9, no. 12, p. e115175, 2014, doi: 10.1371/journal.pone.0115175. 

[7] M. Vital, T. Rud, S. Rath, D. H. Pieper, and D. Schlüter, “Diversity of Bacteria Exhibiting Bile Acid-inducible 7α-dehydroxylation Genes in the Human Gut,” Comput. Struct. Biotechnol. J., vol. 17, pp. 1016–1019, 2019, doi: 10.1016/j.csbj.2019.07.012. 

[8] Y. Yang et al., “Systematic identification of secondary bile acid production genes in global microbiome,” mSystems, vol. 10, no. 1, p. e0081724, Jan. 2025, doi: 10.1128/msystems.00817-24. 

[9] J. M. Ridlon, D. J. Kang, P. B. Hylemon, and J. S. Bajaj, “Bile acids and the gut microbiome,” Curr. Opin. Gastroenterol., vol. 30, no. 3, pp. 332–338, May 2014, doi: 10.1097/MOG.0000000000000057. 

[10] L. Shi, L. Jin, and W. Huang, “Bile Acids, Intestinal Barrier Dysfunction, and Related Diseases,” Cells, vol. 12, no. 14, p. 1888, July 2023, doi: 10.3390/cells12141888. 

[11] M. Schoeler and R. Caesar, “Dietary lipids, gut microbiota and lipid metabolism,” Rev. Endocr. Metab. Disord., vol. 20, no. 4, pp. 461–472, Dec. 2019, doi: 10.1007/s11154-019-09512-0. 

[12] D. K. Li et al., “Inhibition of microbial deconjugation of micellar bile acids protects against intestinal permeability and liver injury,” Sci. Adv., vol. 8, no. 34, p. eabo2794, Aug. 2022, doi: 10.1126/sciadv.abo2794. 

[13] T. Inagaki et al., “Regulation of antibacterial defense in the small intestine by the nuclear bile acid receptor,” Proc. Natl. Acad. Sci. U. S. A., vol. 103, no. 10, pp. 3920–3925, Mar. 2006, doi: 10.1073/pnas.0509592103. 

[14] M. Camilleri and P. Vijayvargiya, “The Role of Bile Acids in Chronic Diarrhea,” Am. J. Gastroenterol., vol. 115, no. 10, pp. 1596–1603, Oct. 2020, doi: 10.14309/ajg.0000000000000696. 

[15] L. K. Stenman, R. Holma, A. Eggert, and R. Korpela, “A novel mechanism for gut barrier dysfunction by dietary fat: epithelial disruption by hydrophobic bile acids,” Am. J. Physiol. Gastrointest. Liver Physiol., vol. 304, no. 3, pp. G227-234, Feb. 2013, doi: 10.1152/ajpgi.00267.2012. 

[16] S. Devkota et al., “Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice,” Nature, vol. 487, no. 7405, pp. 104–108, July 2012, doi: 10.1038/nature11225. 

[17] C. Zhou, Y. Wang, C. Li, Z. Xie, and L. Dai, “Amelioration of Colitis by a Gut Bacterial Consortium Producing Anti-Inflammatory Secondary Bile Acids,” Microbiol. Spectr., vol. 11, no. 2, p. e0333022, Mar. 2023, doi: 10.1128/spectrum.03330-22. 

[18] W. Sheng, G. Ji, and L. Zhang, “The Effect of Lithocholic Acid on the Gut-Liver Axis,” Front. Pharmacol., vol. 13, p. 910493, 2022, doi: 10.3389/fphar.2022.910493. 

[19] A. B. Larabi, H. L. P. Masson, and A. J. Bäumler, “Bile acids as modulators of gut microbiota composition and function,” Gut Microbes, vol. 15, no. 1, p. 2172671, 2023, doi: 10.1080/19490976.2023.2172671. 

[20] Z. He et al., “Gut microbiota-derived ursodeoxycholic acid from neonatal dairy calves improves intestinal homeostasis and colitis to attenuate extended-spectrum β-lactamase-producing enteroaggregative Escherichia coli infection,” Microbiome, vol. 10, no. 1, p. 79, May 2022, doi: 10.1186/s40168-022-01269-0. 

[21] H. Bernstein, C. Bernstein, C. M. Payne, and K. Dvorak, “Bile acids as endogenous etiologic agents in gastrointestinal cancer,” World J. Gastroenterol., vol. 15, no. 27, pp. 3329–3340, July 2009, doi: 10.3748/wjg.15.3329. 

[22] L. Liu et al., “Deoxycholic acid disrupts the intestinal mucosal barrier and promotes intestinal tumorigenesis,” Food Funct., vol. 9, no. 11, pp. 5588–5597, Nov. 2018, doi: 10.1039/c8fo01143e. 

[23] P. Das, S. Marcišauskas, B. Ji, and J. Nielsen, “Metagenomic analysis of bile salt biotransformation in the human gut microbiome,” BMC Genomics, vol. 20, no. 1, p. 517, June 2019, doi: 10.1186/s12864-019-5899-3. 

[24] S. R. Sinha et al., “Dysbiosis-Induced Secondary Bile Acid Deficiency Promotes Intestinal Inflammation,” Cell Host Microbe, vol. 27, no. 4, pp. 659-670.e5, Apr. 2020, doi: 10.1016/j.chom.2020.01.021. 

[25] S. Sommersberger et al., “Altered fecal bile acid composition in active ulcerative colitis,” Lipids Health Dis., vol. 22, no. 1, p. 199, Nov. 2023, doi: 10.1186/s12944-023-01971-4. 

[26] H. Duboc et al., “Connecting dysbiosis, bile-acid dysmetabolism and gut inflammation in inflammatory bowel diseases,” Gut, vol. 62, no. 4, pp. 531–539, Apr. 2013, doi: 10.1136/gutjnl-2012-302578. 

[27] D. Peterson, C. Weidenmaier, S. Timberlake, and R. Gura Sadovsky, “Depletion of key gut bacteria predicts disrupted bile acid metabolism in inflammatory bowel disease,” Microbiol. Spectr., vol. 13, no. 2, p. e0199924, Feb. 2025, doi: 10.1128/spectrum.01999-24. 

[28] A. Heinken, D. A. Ravcheev, F. Baldini, L. Heirendt, R. M. T. Fleming, and I. Thiele, “Systematic assessment of secondary bile acid metabolism in gut microbes reveals distinct metabolic capabilities in inflammatory bowel disease,” Microbiome, vol. 7, no. 1, p. 75, May 2019, doi: 10.1186/s40168-019-0689-3. 

[29] J. Lloyd-Price et al., “Multi-omics of the gut microbial ecosystem in inflammatory bowel diseases,” Nature, vol. 569, no. 7758, pp. 655–662, May 2019, doi: 10.1038/s41586-019-1237-9. 

[30] E. Smirnova et al., “Metabolic reprogramming of the intestinal microbiome with functional bile acid changes underlie the development of NAFLD,” Hepatol. Baltim. Md, vol. 76, no. 6, pp. 1811–1824, Dec. 2022, doi: 10.1002/hep.32568. 

[31] N. Jiao et al., “Alterations in bile acid metabolizing gut microbiota and specific bile acid genes as a precision medicine to subclassify NAFLD,” Physiol. Genomics, vol. 53, no. 8, pp. 336–348, Aug. 2021, doi: 10.1152/physiolgenomics.00011.2021. 

[32] K. Korpela et al., “Intestinal microbiome is related to lifetime antibiotic use in Finnish pre-school children,” Nat. Commun., vol. 7, p. 10410, Jan. 2016, doi: 10.1038/ncomms10410. 

[33] B. H. Mullish, A. Pechlivanis, G. F. Barker, M. R. Thursz, J. R. Marchesi, and J. A. K. McDonald, “Functional microbiomics: Evaluation of gut microbiota-bile acid metabolism interactions in health and disease,” Methods San Diego Calif, vol. 149, pp. 49–58, Oct. 2018, doi: 10.1016/j.ymeth.2018.04.028. 

[34] A. N. Barkun, J. Love, M. Gould, H. Pluta, and H. Steinhart, “Bile acid malabsorption in chronic diarrhea: pathophysiology and treatment,” Can. J. Gastroenterol. J. Can. Gastroenterol., vol. 27, no. 11, pp. 653–659, Nov. 2013, doi: 10.1155/2013/485631. 

[35] J. M. Nieto, “Bile Acid Malabsorption: A Concise Review,” Gastroenterol. Hepatol. Open Access, vol. 4, no. 2, Feb. 2016, doi: 10.15406/ghoa.2016.04.00091. 

[36] F. Fernandez-Bañares et al., “Bile acid malabsorption in microscopic colitis and in previously unexplained functional chronic diarrhea,” Dig. Dis. Sci., vol. 46, no. 10, pp. 2231–2238, Oct. 2001, doi: 10.1023/a:1011927302076. 

[37] A. L. Ticho, P. Malhotra, P. K. Dudeja, R. K. Gill, and W. A. Alrefai, “Bile Acid Receptors and Gastrointestinal Functions,” Liver Res. Beijing China, vol. 3, no. 1, pp. 31–39, Mar. 2019, doi: 10.1016/j.livres.2019.01.001. 

[38] J. Huang et al., “Green Tea Polyphenol EGCG Alleviates Metabolic Abnormality and Fatty Liver by Decreasing Bile Acid and Lipid Absorption in Mice,” Mol. Nutr. Food Res., vol. 62, no. 4, Feb. 2018, doi: 10.1002/mnfr.201700696. 

[39] B. N. R. Ginos et al., “Circulating bile acids in healthy adults respond differently to a dietary pattern characterized by whole grains, legumes and fruits and vegetables compared to a diet high in refined grains and added sugars: A randomized, controlled, crossover feeding study,” Metabolism., vol. 83, pp. 197–204, June 2018, doi: 10.1016/j.metabol.2018.02.006. 

[40] A. Kastl et al., “Dietary fiber-based regulation of bile salt hydrolase activity in the gut microbiota and its relevance to human disease,” Gut Microbes, vol. 14, no. 1, p. 2083417, 2022, doi: 10.1080/19490976.2022.2083417. 

[41] Y. Wan et al., “Unconjugated and secondary bile acid profiles in response to higher-fat, lower-carbohydrate diet and associated with related gut microbiota: A 6-month randomized controlled-feeding trial,” Clin. Nutr. Edinb. Scotl., vol. 39, no. 2, pp. 395–404, Feb. 2020, doi: 10.1016/j.clnu.2019.02.037. 

[42] W.-T. Wu, H.-C. Cheng, and H.-L. Chen, “Ameliorative effects of konjac glucomannan on human faecal β-glucuronidase activity, secondary bile acid levels and faecal water toxicity towards Caco-2 cells,” Br. J. Nutr., vol. 105, no. 4, pp. 593–600, Feb. 2011, doi: 10.1017/S0007114510004009. 

[43] T. Padro et al., “Lactiplantibacillus plantarum strains KABP011, KABP012, and KABP013 modulate bile acids and cholesterol metabolism in humans,” Cardiovasc. Res., vol. 120, no. 7, pp. 708–722, May 2024, doi: 10.1093/cvr/cvae061. 

[44] M. L. Jones, C. J. Martoni, and S. Prakash, “Cholesterol lowering and inhibition of sterol absorption by Lactobacillus reuteri NCIMB 30242: a randomized controlled trial,” Eur. J. Clin. Nutr., vol. 66, no. 11, pp. 1234–1241, Nov. 2012, doi: 10.1038/ejcn.2012.126. 

[45] G. Marasco et al., “Pathophysiology and Clinical Management of Bile Acid Diarrhea,” J. Clin. Med., vol. 11, no. 11, p. 3102, May 2022, doi: 10.3390/jcm11113102. 

[46] Y. Araki, K.-I. Mukaisho, Y. Fujiyama, T. Hattori, and H. Sugihara, “The herbal medicine rikkunshito exhibits strong and differential adsorption properties for bile salts,” Exp. Ther. Med., vol. 3, no. 4, pp. 645–649, Apr. 2012, doi: 10.3892/etm.2012.478.Â