The Gut-Liver Axis in Dogs – Supporting Vital Detoxification

· by Glendon Lloyd

The Gut-Liver Axis in Dogs – Supporting Vital Detoxification

How Gut Health Shapes Liver Function, Detoxification Capacity, and Whole-Body Wellness

“The gut-liver axis represents your dog’s frontline detoxification partnership, with the portal vein carrying gut-derived substances directly to the liver before they reach the rest of the body. While we cannot remove every environmental toxin your dog encounters, we can profoundly influence the gut microbiome that controls which substances reach the liver and how effectively they are neutralised.“

Summary

A dog’s gut health determines how effectively their liver can detoxify. The portal vein carries blood directly from the intestines to the liver before it reaches the rest of the body, meaning gut dysbiosis translates immediately into increased endotoxin burden, impaired bile acid metabolism, and chronic hepatic inflammation. This anatomical arrangement makes the liver the first line of defence against gut-derived toxins, but also renders it uniquely vulnerable to gut dysfunction.

The gut microbiome profoundly influences liver health through multiple mechanisms: production of beneficial short-chain fatty acids (SCFAs) that support hepatic metabolism and reduce inflammation; conversion of primary bile acids to secondary bile acids essential for cholesterol homeostasis and metabolic regulation; and maintenance of intestinal barrier integrity that prevents harmful endotoxins from overwhelming hepatic detoxification capacity. When gut dysbiosis disrupts this delicate balance, the consequences for liver health are significant – increased endotoxin translocation, altered bile acid metabolism, enhanced oxidative stress, and chronic low-grade inflammation that can contribute to hepatic disease progression.

At Bonza, the gut-liver axis is one of the eight gut-organ axes underpinning the “One Gut. Whole Dog.” philosophy, with the Biotics Triad in Bioactive Bites supporting the intestinal barrier integrity and bile acid metabolism that directly determines hepatic toxic load, and Superfoods & Ancient Grains providing the prebiotic fibre diversity that feeds the beneficial bacteria responsible for butyrate production and hepatoprotective SCFA signalling.

At a glance

The liver receives 70-80% of its blood supply directly from the gut via the portal vein – meaning everything absorbed from your dog’s intestines arrives at the liver first. When the gut is unhealthy, the liver bears the consequences before any other organ.

What the science shows

  • Dogs with chronic hepatobiliary disease show marked reductions in beneficial bacteria critical to gut-liver function, including Clostridium hiranonis – the primary species responsible for converting primary bile acids to secondary forms essential for metabolic regulation.
  • The 2026 Waltham catalogue identified two previously unknown Peptacetobacter species in the canine gut with the specific molecular machinery for secondary bile acid conversion – a discovery the researchers described as significant in the context of chronic gastrointestinal disease in dogs.
  • When intestinal barrier integrity fails, bacterial LPS enters the portal vein and activates Kupffer cells – the liver’s resident macrophages that comprise 80% of all fixed macrophages in the body – triggering inflammatory cascades that can progress to fibrosis if the endotoxin burden is sustained.
  • A randomised case-control study demonstrated that synbiotic supplementation in dogs with chronic hepatobiliary disease produced significant reductions in liver enzyme markers and resolved gastrointestinal signs in treated dogs compared to controls.
  • Dogs need dog-specific microbiome science – prior to the Waltham catalogue, existing databases built from human research captured only approximately 25% of the bacteria present in canine faeces, explaining why human gut health approaches applied to dogs so frequently underperform.

How to support it

  • Maintain gut barrier integrity as the primary liver protection strategy – reducing endotoxin translocation via the portal vein is the single most impactful intervention available for reducing chronic hepatic inflammatory burden.
  • Feed diverse prebiotic fibres to sustain the bacteria responsible for bile acid transformation and SCFA production – both pathways directly determine how much metabolic and inflammatory work the liver must perform daily.
  • Consider clinoptilolite as an endotoxin binding strategy – this natural zeolite binds LPS within the gut lumen before it can be absorbed, providing a protective layer even when some degree of intestinal permeability exists.
  • Support hepatic detoxification capacity with milk thistle silymarin, B vitamins, zinc, and taurine – taurine is the primary bile acid conjugate in dogs and serves dual roles as both a digestive aid and a hepatocyte antioxidant.

Key insight

The liver can only do its job effectively when the gut is doing its job. Every meal that nourishes beneficial gut bacteria, every intervention that strengthens the intestinal barrier, is simultaneously a direct investment in hepatic health.

Introduction: The Body’s Central Detoxification Partnership

Every moment of every day, your dog’s body faces an onslaught of substances that require processing, neutralisation, or elimination – from the natural byproducts of metabolism to environmental toxins, from the beneficial compounds in food to the potentially harmful bacterial products that inevitably arise in the gut. Managing this continuous chemical challenge falls primarily to two organ systems that have evolved to work in remarkably close partnership: the gastrointestinal tract and the liver.

The connection between gut and liver health in dogs has moved from theoretical to proven. In January 2026, researchers from the Waltham Petcare Science Institute published the most comprehensive mapping of the canine gut microbiome ever undertaken – analysing over 500 faecal samples from 107 dogs across the USA and Europe. Among their discoveries: two novel bacterial species (Peptacetobacter species) with the specific capacity to regulate bile acid metabolism. The researchers described this as “an important finding in the context of chronic GI disease in pets.”

This discovery illuminates a fundamental truth about canine health: the gut and liver are in constant biochemical conversation, with gut bacteria serving as essential intermediaries.

This partnership – the gut-liver axis – represents one of the most critical and underappreciated relationships in canine physiology. Unlike other gut-organ connections that communicate through general circulation, the gut and liver share a unique anatomical intimacy: the portal vein carries blood directly from the intestines to the liver, bypassing systemic circulation entirely. This means that virtually everything absorbed from your dog’s gut – nutrients, microbial metabolites, bacterial toxins, and more – arrives at the liver before reaching any other organ.

This anatomical arrangement confers significant advantages. The liver serves as a highly effective filter and processing plant, extracting nutrients for storage or distribution, neutralising potentially harmful compounds, and preventing gut-derived toxins from reaching sensitive tissues throughout the body. When functioning optimally, this system protects your dog’s brain, heart, kidneys, and other organs from substances that would otherwise cause damage.

However, this same arrangement means the liver bears the brunt of gut dysfunction. When intestinal barrier integrity fails, when gut bacteria become imbalanced, or when the microbiome’s beneficial functions are compromised, the liver faces an increased toxic burden that can exceed its detoxification capacity. The result is a cascade of inflammation, oxidative stress, and metabolic dysfunction that can progress to clinical liver disease if left unaddressed.

Understanding the gut-liver axis empowers us to take a proactive approach to hepatic health. Rather than waiting for liver problems to manifest – often detected only when disease has significantly progressed – we can support this vital partnership through targeted nutrition that maintains gut barrier integrity, promotes beneficial bacterial populations, and provides the nutrients essential for optimal liver function.

Key Takeaways

  • The gut-liver axis operates through the portal vein, which carries 70-80% of the liver’s blood supply directly from the intestines, delivering nutrients alongside gut-derived microbial products that the liver must process and detoxify.¹,²
  • Gut dysbiosis significantly impacts liver health, with dogs diagnosed with chronic hepatobiliary disease showing marked reductions in beneficial bacteria including Clostridium hiranonis and Ruminococcus faecis, alongside increased potentially pathogenic species.³,⁴
  • Bacterial endotoxin (lipopolysaccharide/LPS) translocation from the gut to the liver via the portal system represents a major pathway of hepatic inflammation, with increased intestinal permeability directly increasing the toxic burden on hepatic Kupffer cells.⁵,⁶
  • Bile acid metabolism depends on gut bacteria, with microbial enzymes converting primary bile acids to secondary bile acids essential for lipid digestion, cholesterol regulation, and metabolic signalling – disruption of this pathway contributes to hepatobiliary dysfunction.⁷,⁸
  • Short-chain fatty acids (SCFAs) produced by beneficial gut bacteria support liver health through anti-inflammatory effects, enhanced gut barrier function, and direct hepatoprotective properties.⁹
  • Synbiotic supplementation (combining prebiotics and probiotics) has demonstrated significant benefits in dogs with chronic hepatobiliary disease, including reduction of liver enzyme markers and resolution of gastrointestinal signs.¹⁰
  • The liver performs over 500 essential functions including detoxification of drugs and environmental toxins, nutrient metabolism, protein synthesis, hormone regulation, and immune complex clearance – all of which depend on healthy gut-liver axis function.
  • Kupffer cells – the liver’s resident macrophages – represent approximately 80% of the body’s fixed macrophages and serve as the primary defence against gut-derived endotoxins and pathogens.¹,²
  • Nutritional interventions including prebiotics, probiotics, postbiotics, hepatoprotective botanicals, and targeted nutrients can support gut-liver axis function by maintaining intestinal barrier integrity, promoting beneficial bacterial populations, and providing direct liver support.
  • A comprehensive gut-liver support approach combining microbiome optimisation with hepatoprotective ingredients offers the most effective strategy for maintaining detoxification capacity and metabolic health throughout your dog’s life.

Table of Contents

Understanding the Gut-Liver Axis

The gut-liver axis encompasses the bidirectional anatomical, functional, and biochemical communication between the gastrointestinal tract and the liver. This relationship is mediated by multiple pathways including the portal venous system, biliary secretions, and systemic circulation carrying inflammatory mediators and metabolites. Understanding these pathways reveals why gut health is inseparable from liver function.

The Portal Vein: A Direct Highway

The portal vein provides the anatomical foundation of the gut-liver axis, delivering approximately 70-80% of the liver’s blood supply directly from the Splanchnic circulation – blood draining from the intestines, colon, pancreas, and spleen.¹,² This arrangement is fundamentally different from other organ relationships: the liver receives nutrient-rich but potentially toxin-laden blood before it enters general circulation.

The blood flowing through the portal system carries a complex cargo:

Nutrients: Amino acids, carbohydrates, fatty acids, vitamins, and minerals absorbed from digested food travel to the liver for processing, storage, or distribution to the body.

Hepatotrophic factors: Substances from the pancreas including insulin and glucagon maintain normal hepatocyte size and function – portal diversion, as seen in portosystemic shunts, leads to hepatic atrophy.

Microbial metabolites: Short-chain fatty acids, secondary bile acids, vitamins synthesised by gut bacteria, and other beneficial compounds that support liver and whole-body health.

Potentially harmful substances: Bacterial endotoxins (particularly lipopolysaccharide), intact bacteria that have translocated across the gut barrier, food-derived antigens, and environmental toxins absorbed from the intestine.

The 2023 Roberts/Swanson trial documented significantly lower faecal phenol and indole concentrations in dogs fed plant-based diets, reducing the precursor load for hepatic conjugation to p-cresyl sulphate and indoxyl sulphate. For the full peer-reviewed evidence on plant-based canine nutrition and liver-relevant outcomes, see the Bonza evidence review on plant-based dog food research.

Kupffer Cells: Guardians at the Gate

Within the hepatic sinusoids – the specialised capillaries that carry portal blood through the liver – reside Kupffer cells, the largest population of fixed macrophages in the body, comprising approximately 80% of all tissue-resident macrophages.¹,² These sentinel cells perform crucial immune surveillance functions:

Pathogen clearance: Kupffer cells continuously sample portal blood, capturing and destroying bacteria, viruses, and parasites that have breached the intestinal barrier.

Endotoxin neutralisation: Perhaps their most critical function, Kupffer cells bind and neutralise lipopolysaccharide (LPS) from gram-negative bacteria, preventing it from triggering systemic inflammatory responses.

Immune modulation: Through cytokine production, Kupffer cells coordinate hepatic immune responses and communicate with other liver cells including hepatocytes and stellate cells.

When functioning normally, Kupffer cells efficiently clear the low levels of bacterial products that inevitably reach the liver through the portal system. However, when gut dysbiosis or barrier dysfunction significantly increases the load of bacterial translocation, Kupffer cell capacity can become overwhelmed, leading to inflammatory cytokine release and hepatic injury.

Bidirectional Communication

The gut-liver axis operates in both directions. While the gut influences the liver through the portal system, the liver profoundly shapes gut health through bile secretion:

Bile acids: Synthesised by hepatocytes from cholesterol, bile acids are essential for lipid digestion and absorption. They also serve as signalling molecules and antimicrobial agents that shape gut microbiome composition.

Immunoglobulin A (IgA): The liver secretes IgA into bile, which travels to the intestine where it provides immune protection against pathogens and helps maintain tolerance to food antigens.

Antimicrobial peptides: Bile contains compounds that inhibit bacterial overgrowth in the upper small intestine and influence microbial population dynamics throughout the gut.

This bidirectional communication means that liver dysfunction can cause gut problems, just as gut dysfunction can cause liver problems – a relationship that can create self-perpetuating cycles of deterioration when either organ system is compromised.

The Liver: Your Dog’s Master Metaboliser

The liver is your dog’s largest internal organ, comprising approximately 3-5% of body weight and performing over 500 distinct biochemical functions essential for survival. Understanding these functions illuminates why gut health matters so profoundly for hepatic wellbeing.

Essential Liver Functions

Detoxification: The liver transforms fat-soluble toxins, drugs, hormones, and metabolic waste products into water-soluble compounds that can be excreted via urine or bile. This includes neutralising ammonia (from protein metabolism) into urea, metabolising medications, and processing environmental toxins.

Nutrient metabolism: The liver regulates carbohydrate metabolism (converting glucose to glycogen for storage and back again as needed), processes dietary fats, synthesises cholesterol and lipoproteins, and manages amino acid availability throughout the body.

Protein synthesis: Virtually all plasma proteins are synthesised by the liver, including albumin (essential for maintaining blood pressure and transporting substances), clotting factors (essential for blood coagulation), and transport proteins for hormones and minerals.

Bile production: Hepatocytes continuously produce bile – approximately 10ml per kg body weight daily – which is concentrated in the gallbladder and released into the small intestine to facilitate fat digestion and absorption.

Nutrient storage: The liver stores glycogen (the body’s glucose reserve), fat-soluble vitamins (A, D, E, K), vitamin B12, and essential minerals including iron, copper, and zinc.

Immune function: Beyond Kupffer cell activity, the liver produces acute-phase proteins during infection, removes immune complexes from blood, and coordinates inflammatory responses.

Hormone regulation: The liver metabolises and inactivates many hormones including thyroid hormones, cortisol, and sex steroids – it also converts thyroid hormone T4 to the active T3 form.

Phase I and Phase II Detoxification

The liver’s detoxification system operates through a sophisticated two-phase process, with each phase depending on specific nutrient cofactors:

Phase I (Activation/Modification): This phase, primarily performed by cytochrome P450 enzymes, converts fat-soluble toxins into intermediate compounds through oxidation, reduction, and hydrolysis reactions. While necessary, these intermediates are often more reactive and potentially more harmful than the original toxins. Phase I requires adequate supplies of:

Phase II (Conjugation): This phase attaches water-soluble molecules to Phase I intermediates, rendering them harmless and suitable for elimination via urine or bile. Six major conjugation pathways exist, each requiring specific nutrients:

  • Glutathione conjugation: Requires glutathione (synthesised from glycine, cysteine, and glutamic acid)
  • Amino acid conjugation: Requires glycine, taurine, and other amino acids
  • Methylation: Requires methyl donors (SAMe, methylfolate, B12)
  • Sulfation: Requires sulfur-containing amino acids (methionine, cysteine, taurine)
  • Glucuronidation: Requires UDP-glucuronic acid
  • Acetylation: Requires acetyl-CoA

When Detoxification Becomes Overwhelmed

Problems arise when the toxic load exceeds detoxification capacity, when Phase I proceeds faster than Phase II (accumulating harmful intermediates), or when nutrient deficiencies impair enzyme function. Gut dysbiosis contributes to this burden in several ways:

Increased endotoxin exposure: Dysbiosis and intestinal permeability increase LPS delivery to the liver, consuming detoxification resources and triggering inflammation.

Reduced SCFA production: Short-chain fatty acids from beneficial bacteria support hepatocyte function and reduce oxidative stress – their absence impairs liver resilience.

Altered bile acid metabolism: Dysbiosis disrupts the microbial conversion of bile acids, affecting cholesterol homeostasis and metabolic signalling.

Nutrient malabsorption: Gut dysfunction can impair absorption of the very nutrients required for detoxification enzymes.

Bile Acids and the Enterohepatic Circulation

Bile acids occupy a unique position in gut-liver communication, serving as digestive aids, antimicrobial agents, metabolic regulators, and signalling molecules. Their metabolism depends intimately on gut bacteria, making bile acid homeostasis a direct reflection of gut-liver axis health.

Primary and Secondary Bile Acids

The liver synthesises primary bile acids – cholic acid (CA) and chenodeoxycholic acid (CDCA) – from cholesterol through a multi-step enzymatic process. These primary bile acids are conjugated with either taurine or glycine (dogs predominantly use taurine) before secretion into bile. After release into the small intestine, bile acids facilitate the emulsification and absorption of dietary fats and fat-soluble vitamins.

Approximately 95% of secreted bile acids are actively reabsorbed in the terminal ileum and returned to the liver via the portal vein – a process called enterohepatic circulation. This recycling occurs 6-8 times daily, conserving these metabolically expensive molecules while ensuring adequate bile acid availability for digestion.

Microbial Bile Acid Metabolism

The small fraction of bile acids (approximately 5%) that escape ileal reabsorption enter the colon, where gut bacteria dramatically transform them through several enzymatic processes:⁷,⁸

Deconjugation: Bacterial bile salt hydrolases (BSH) remove the taurine or glycine conjugates, producing unconjugated bile acids.

7α-dehydroxylation: This critical transformation, performed by specific bacterial species including Clostridium scindens and Clostridium hiranonis, converts primary bile acids to secondary bile acids – cholic acid becomes deoxycholic acid (DCA), and chenodeoxycholic acid becomes lithocholic acid (LCA).

Epimerisation: Bacterial enzymes can convert chenodeoxycholic acid to ursodeoxycholic acid (UDCA), a secondary bile acid with notable hepatoprotective properties.

These microbial transformations are not merely incidental – they produce secondary bile acids with distinct biological activities that influence metabolism, immunity, and even microbiome composition itself. Secondary bile acids bind to specific receptors (FXR, TGR5) that regulate glucose metabolism, lipid homeostasis, and inflammatory responses.

The Gut Bacteria That Speak to Your Dog’s Liver

Bile acids are produced by the liver and released into the small intestine to help digest fats. But their journey doesn’t end there. Specific gut bacteria transform these primary bile acids into secondary bile acids – a conversion that profoundly influences both gut and liver health.

The Waltham catalogue study identified two previously unknown Peptacetobacter species in dogs with this exact capability. These bacteria carry both bile salt hydrolase (BSH) enzymes and genes within the bai operon – the molecular machinery required for secondary bile acid conversion.

This matters because secondary bile acids:

  • Help regulate the growth of potentially harmful bacteria (including E. coli and C. perfringens)
  • Signal back to the liver to regulate bile acid production
  • Influence glucose and lipid metabolism throughout the body
  • Support healthy inflammatory responses

When this bacterial population is disrupted, the gut-liver axis communication breaks down – a pattern consistently observed in dogs with chronic enteropathy.

Disrupted Bile Acid Signalling in Disease

Dogs with chronic liver disease show significant alterations in faecal bile acid profiles, reflecting disruption of the gut-liver axis:⁸

Reduced secondary bile acids: Dogs with hepatobiliary disease, particularly those with biliary tract involvement, show decreased conversion of primary to secondary bile acids – indicating reduced populations or activity of 7α-dehydroxylating bacteria.

Altered primary-to-secondary ratios: The ratio of primary to secondary bile acids in faeces serves as a marker of microbial bile acid metabolism; elevated ratios indicate dysbiosis affecting this pathway.

Bile acid diarrhoea: When bile acid malabsorption occurs (due to ileal disease or biliary dysfunction), excess bile acids reaching the colon cause secretory diarrhoea – a condition that may be underdiagnosed in dogs with liver disease.

Research demonstrates that dogs with chronic hepatobiliary disease (CHD) show marked reduction in bacteria responsible for bile acid metabolism, including Clostridium hiranonis and Ruminococcus faecis.³ This creates a self-reinforcing cycle: liver disease alters bile composition and flow, which changes gut microbiome composition, which further disrupts bile acid metabolism, which impacts liver health.

Endotoxemia: When the Gut Threatens the Liver

Lipopolysaccharide (LPS), also called endotoxin, is a structural component of the outer membrane of gram-negative bacteria. While contained within the gut, LPS poses no threat. However, when gut barrier function is compromised, LPS can translocate into the portal circulation, triggering inflammatory responses that directly damage the liver and contribute to systemic illness.

Understanding Metabolic Endotoxemia

Metabolic endotoxemia refers to elevated circulating LPS levels that, while lower than those seen in acute sepsis, are sufficient to trigger chronic low-grade inflammation. This condition has emerged as a significant factor in numerous chronic diseases affecting both humans and dogs.⁵,⁶

Several factors contribute to metabolic endotoxemia:

Increased intestinal permeability: When tight junctions between intestinal epithelial cells become compromised – due to inflammation, dysbiosis, dietary factors, or stress – LPS can pass between cells into the lamina propria and portal circulation.

Transcellular transport: LPS can also hitch a ride with dietary fats, being incorporated into chylomicrons during fat absorption and transported directly through enterocytes to lymphatic vessels and eventually to the liver.

Bacterial overgrowth: Small intestinal bacterial overgrowth (SIBO) increases the amount of gram-negative bacteria in the upper gut, increasing LPS availability for absorption.

Reduced clearance: When liver function is impaired, Kupffer cells may be unable to efficiently clear the normal low levels of LPS that reach the portal system, allowing it to spill over into systemic circulation.

LPS and Toll-Like Receptor 4 Activation

LPS exerts its inflammatory effects through activation of Toll-like receptor 4 (TLR4), a pattern recognition receptor expressed on immune cells, hepatocytes, and other cell types.⁶ The activation cascade proceeds as follows:

  1. LPS binds to LPS-binding protein (LBP) in circulation
  2. This complex interacts with CD14 on cell surfaces
  3. MD-2 assists in presenting LPS to TLR4
  4. TLR4 activation triggers intracellular signalling cascades
  5. NF-κB pathway activation leads to inflammatory cytokine production
  6. TNF-α, IL-1β, IL-6, and other mediators cause tissue inflammation

Research in dogs with congenital portosystemic shunts (CPSS) has demonstrated that portal LPS is increased in these patients, consistent with decreased hepatic clearance due to portal blood bypassing the liver.⁶ Hepatic TLR4 expression was significantly associated with portal blood flow, supporting the concept that LPS delivery via the portal system is important for hepatic function and regeneration.

The Inflammation-Hepatic Damage Cycle

Chronic LPS exposure creates a self-perpetuating cycle of liver damage:

Initial inflammatory insult: LPS activates Kupffer cells, which release inflammatory cytokines (TNF-α, IL-6, IL-1β) and reactive oxygen species.

Hepatocyte injury: These mediators damage hepatocytes directly and induce oxidative stress that overwhelms antioxidant defences.

Stellate cell activation: Inflammatory signals activate hepatic stellate cells (Ito cells), transforming them into myofibroblasts that produce collagen – the beginning of liver fibrosis.

Impaired detoxification: Damaged hepatocytes have reduced capacity to clear subsequent LPS exposure, amplifying future inflammatory responses.

Worsened gut barrier: Hepatic inflammation and altered bile production affect gut health, increasing intestinal permeability and LPS translocation – completing the vicious cycle.

Breaking this cycle requires addressing both the gut source of the problem (maintaining barrier integrity and healthy microbiome composition) and supporting the liver’s capacity to manage and recover from inflammatory challenges.

Gut Dysbiosis and Hepatic Disease

The connection between gut microbiome disruption and liver disease has emerged as a significant area of veterinary research, with studies demonstrating consistent alterations in gut bacterial populations in dogs with various hepatobiliary conditions.

Why Dogs Need Dog-Specific Science

Prior to the Waltham catalogue, researchers attempting to study the canine microbiome faced a significant problem: existing databases – built primarily from human research – captured only about 25% of the bacteria present in dog faeces. The remaining 75% was essentially invisible to science.

The new catalogue achieves mapping rates of up to 95%, revealing that the canine microbiome is fundamentally distinct from humans. It has evolved alongside dogs over millennia, adapting to their specific diet, physiology, and environment.

This explains why simply applying human gut health research to dogs often fails. Dogs need nutritional approaches built on canine-specific science.

Microbiome Alterations in Canine Liver Disease

Research examining gut microbiome composition in dogs with chronic hepatobiliary disease (CHD) has revealed several consistent patterns:³,⁴

Reduced beneficial bacteria: Dogs with CHD show marked reductions in bacteria associated with healthy gut function, including:

  • Clostridium hiranonis – critical for secondary bile acid production
  • Ruminococcus faecis – an important SCFA producer
  • Other Firmicutes typically associated with eubiosis

Increased potentially pathogenic species: Conversely, dogs with liver disease show elevated populations of:

  • Escherichia and Shigella species
  • Serratia species
  • Other Proteobacteria associated with dysbiosis

Reduced microbial diversity: Overall bacterial diversity tends to decrease in dogs with hepatic disease, a pattern consistently associated with worse health outcomes across multiple conditions.

The Cholestasis Connection

Cholestasis – impaired bile flow – appears particularly associated with gut-liver axis disruption. Research has found that dogs with ultrasonographic and biochemical evidence of cholestatic liver disease show deeper microbiome alterations than dogs with non-cholestatic liver conditions.³

This connection likely operates bidirectionally:

Bile acid effects on microbiome: Bile acids have antimicrobial properties and influence bacterial growth. Reduced or altered bile flow changes the gut environment, allowing shifts in bacterial populations.

Microbial effects on bile acids: As discussed, gut bacteria are essential for converting primary bile acids to secondary forms. Dysbiosis disrupts this conversion, altering the bile acid pool composition and potentially exacerbating cholestatic conditions.

Inflammatory amplification: Cholestasis increases intestinal permeability, enhancing bacterial translocation and LPS exposure to an already-stressed liver.

Chronic Hepatobiliary Disease and Gut Health

The recognition that gut-liver interaction leads to dysbiosis in dogs with CHD has significant clinical implications.³,⁴ For dogs being managed for chronic liver conditions, attention to gut health becomes an important adjunctive consideration:

Synbiotic supplementation benefits: A randomised case-control study examining synbiotic (combined probiotic/prebiotic) administration in dogs with chronic hepatobiliary disease demonstrated significant reductions in biochemical markers of liver injury (including ALT) and resolution of gastrointestinal signs in treated dogs compared to controls.¹⁰

Qualitative microbiome improvements: While dramatic changes in overall microbiome diversity may take time, qualitative shifts toward healthier bacterial populations can occur relatively quickly with appropriate intervention.

Clinical sign resolution: Gastrointestinal symptoms including diarrhoea – often present in dogs with liver disease – frequently improve with gut-targeted therapies, reflecting the intimate gut-liver connection.

Nutritional Modulation of the Gut-Liver Axis

Understanding the gut-liver axis’s importance naturally leads to the question of how we can nutritionally support this vital partnership. Research increasingly supports multi-targeted approaches that address both gut health and direct hepatic support simultaneously.

Prebiotics for Gut-Liver Health

The Waltham research demonstrated that dietary interventions show “promising results in modulating aspects of canine GI function.” Supporting the bacteria that maintain healthy bile acid metabolism requires targeted nutritional strategies.

The study identified extensive carbohydrate-degrading capacity across the canine microbiome, with an average of 71 carbohydrate-active enzymes (CAZymes) per bacterial species. Populations capable of breaking down cellulose (36% of species), starch (22%), chitin (75%), and hemicellulose (37%) were identified – demonstrating the microbiome’s remarkable capacity to process diverse plant fibres. These fibres serve as fuel for beneficial bacteria, including those involved in bile acid transformation and SCFA production.

The bacterial species most enriched in functional capacity belonged to families associated with fibre fermentation – suggesting that dietary diversity supports metabolic diversity in the microbiome. This scientific foundation supports the use of:

Prebiotics – non-digestible food components that selectively nourish beneficial gut bacteria – support liver health by promoting bacterial populations that produce beneficial metabolites and maintain gut barrier integrity:

Fructooligosaccharides (FOS): These prebiotic fibres promote Bifidobacteria and Lactobacilli populations while supporting SCFA production. FOS has demonstrated hepatoprotective effects in various models by reducing endotoxin exposure and supporting healthy bile acid metabolism.

Mannan-oligosaccharides (MOS): Derived from yeast cell walls, MOS binds to pathogenic bacteria preventing their adhesion to intestinal walls while supporting beneficial bacterial growth. By reducing pathogen populations, MOS decreases LPS production at its source.

Beta-glucans: These prebiotic polysaccharides from yeast and fungi support beneficial bacteria while also directly binding to immune cells, modulating inflammatory responses that affect both gut and liver.

Inulin: A longer-chain fructan fermented slowly through the colon, inulin provides sustained prebiotic effects and supports butyrate production – particularly important for gut barrier integrity.

Probiotics and Postbiotics

Probiotics introduce beneficial bacteria directly, while postbiotics deliver their beneficial metabolites:

Bacillus species: Spore-forming probiotics like Bacillus velezensis (Calsporin®) survive gastric transit reliably and support overall microbiome balance. Their ability to produce antimicrobial compounds helps control potentially pathogenic bacteria.

Lactobacillus species: Various Lactobacillus strains support gut barrier function, produce beneficial metabolites including lactic acid that inhibits pathogens, and have demonstrated benefits in inflammatory conditions affecting both gut and liver. A probiotic strain that supports detoxification.

Postbiotic metabolites: Heat-inactivated probiotics and their fermentation products (such as TruPet™ and Diamond V®) deliver beneficial compounds regardless of individual microbiome variability, providing consistent gut-liver axis support.

Hepatoprotective Botanicals

Several botanicals have demonstrated direct hepatoprotective effects through multiple mechanisms:

Milk Thistle (Silybum marianum): The silymarin complex – comprising silybin, silychristin, and silydianin – represents the most extensively studied hepatoprotective botanical:¹¹,¹²,¹³

  • Antioxidant effects: Silymarin scavenges free radicals and enhances cellular glutathione levels, protecting hepatocytes from oxidative damage
  • Anti-inflammatory properties: Inhibits NF-κB activation and reduces inflammatory cytokine production
  • Membrane stabilisation: Protects hepatocyte membranes from toxin-induced damage
  • Regenerative support: Stimulates protein synthesis and promotes hepatocyte regeneration
  • Choleretic effects: Supports healthy bile flow and composition

Studies in dogs confirm silymarin’s hepatoprotective properties, with research demonstrating protection against various hepatotoxic challenges and support for dogs with elevated liver enzymes.¹²,¹³

Artichoke (Cynara scolymus): Contains cynarin and chlorogenic acid with documented hepatoprotective, bile-stimulating, and lipid-lowering effects. Artichoke supports healthy bile production and flow while providing antioxidant protection.¹¹

Turmeric/Curcumin: Beyond its broad anti-inflammatory effects, curcumin demonstrates specific hepatoprotective properties including protection against heavy metal-induced liver damage and support for healthy bile production. Combining curcumin with black pepper extract (piperine) dramatically enhances its bioavailability.

Dandelion Root (Taraxacum officinale): Traditional use for liver support is validated by research showing polysaccharides in dandelion root help increase bile flow from the liver and support detoxification processes.¹¹

Supporting liver function becomes especially important for dogs using pharmaceutical antihistamines – natural alternatives can reduce this metabolic burden

Essential Nutrients for Liver Function

Optimal liver function requires adequate supplies of specific nutrients that serve as cofactors for detoxification enzymes and support hepatocyte health:

S-Adenosyl-L-Methionine (SAMe): A crucial methyl donor and glutathione precursor, SAMe supports Phase II methylation reactions and helps maintain hepatocyte membrane integrity. SAMe is produced naturally in the body but may become depleted during liver stress.¹¹

B-Complex Vitamins: Essential cofactors for Phase I and Phase II detoxification enzymes. B6, B12, and folate are particularly important for methylation reactions, while B2 and B3 support cytochrome P450 function.

Zinc (glycinate form): Supports over 300 enzymatic reactions including several involved in detoxification. Zinc also supports gut barrier integrity, addressing the gut-liver axis at both ends. Chelated forms like zinc glycinate offer superior absorption.

Vitamin E (RRR-alpha-tocopherol): The natural form of vitamin E provides essential antioxidant protection for hepatocyte membranes, protecting against lipid peroxidation induced by toxins and inflammatory processes.

Vitamin C: Supports glutathione regeneration and provides direct antioxidant protection. Vitamin C also serves as a cofactor for collagen synthesis, important for maintaining hepatic connective tissue integrity.

Taurine: This amino acid is essential for bile acid conjugation in dogs and also serves as an antioxidant and membrane stabiliser in hepatocytes. Adequate taurine supports both bile metabolism and hepatocyte protection.

L-Glutamine: Beyond its role in gut barrier support, glutamine is utilised by hepatocytes during stress and serves as a nitrogen carrier essential for ammonia detoxification.

Choline: Essential for phosphatidylcholine synthesis and VLDL formation, choline supports fat export from the liver and helps prevent hepatic lipid accumulation. Phosphatidylcholine (lecithin) itself has demonstrated hepatoprotective effects.¹¹

Endotoxin Binding Strategies

Given the central role of LPS translocation in gut-liver axis dysfunction, ingredients that bind and neutralise endotoxins before they can be absorbed offer a direct protective approach:

Clinoptilolite: This natural zeolite mineral binds bacterial endotoxins including LPS within the gut lumen, preventing their translocation across the intestinal barrier. By reducing the endotoxin load reaching the liver via the portal system, clinoptilolite provides prophylactic support even when some degree of gut permeability exists.

Yucca schidigera: Contains steroidal saponins that bind endotoxins and ammonia in the gut, reducing their absorption and the subsequent burden on hepatic detoxification pathways.

Omega-3 Fatty Acids

The marine-derived omega-3 fatty acids EPA and DHA support gut-liver axis health through multiple mechanisms:

Anti-inflammatory effects: Omega-3s reduce inflammatory cytokine production and support resolution of inflammation – benefiting both gut barrier function and hepatic inflammatory responses.

Membrane fluidity: Incorporation into cell membranes improves membrane function in both enterocytes and hepatocytes.

Lipid metabolism: Omega-3s support healthy lipid metabolism and may help prevent hepatic fat accumulation.

Algal sources of omega-3s (such as DHAgold®) provide these benefits in highly bioavailable form whilst avoiding the sustainability and contamination concerns associated with fish oils, like salmon oil.

Practical Implementation for Dog Owners

Translating gut-liver axis science into practical action involves several key considerations:

Choose foods supporting gut-liver health: Select diets containing prebiotic fibres (FOS, MOS, inulin), probiotics, and postbiotics that support beneficial bacterial populations. Look for foods with omega-3 fatty acids and anti-inflammatory botanicals.

Consider hepatoprotective supplementation: For dogs with known liver stress (medication use, exposure to toxins, breed predisposition) or existing hepatic conditions, targeted supplements containing milk thistle, B vitamins, and antioxidants may provide meaningful support.

Support gut barrier integrity: Include nutrients that maintain tight junction function – glutamine, zinc, and omega-3s help keep the intestinal barrier intact, reducing endotoxin translocation to the liver.

Minimise liver toxic burden:

  • Avoid unnecessary medications where possible
  • Use natural pest prevention alternatives when appropriate
  • Minimise exposure to environmental toxins (lawn chemicals, household cleaners)
  • Ensure clean, filtered drinking water

Be mindful of dietary fat quality: While dietary fat itself isn’t problematic, the type matters. Plant-based omega-3s and moderate, high-quality fat intake support gut-liver health better than excessive saturated fats that may increase LPS absorption.

Maintain healthy body weight: Excess body weight is associated with chronic low-grade inflammation and increased intestinal permeability. Weight management supports gut-liver axis function.

Monitor for early signs of liver stress: Watch for subtle signs including decreased appetite, increased thirst, occasional vomiting, lethargy, or changes in stool quality. Early intervention supports better outcomes.

Work with your veterinarian: If your dog has existing liver conditions or is on medications metabolised by the liver, discuss gut-liver axis support strategies and appropriate monitoring.

Supporting Your Dog’s Gut-Liver Axis: The Bonza Approach

Bonza’s “One Gut. Whole Dog.” philosophy recognises that true liver health cannot be separated from gut health — the portal vein ensures that every disruption in gut microbiome balance translates directly into increased toxic burden on the liver before it reaches any other organ. The gut-liver axis is one of the eight gut-organ axes underpinning Bonza’s formulation framework, informing both Superfoods & Ancient Grains and the Bioactive Bites supplement range. The daily food provides foundational gut-liver axis support through Calsporin®, TruPet™ postbiotic, prebiotic chicory, yeast-derived MOS and beta-glucans, DHAgold® algae-derived omega-3, and the PhytoPlus® botanical blend including turmeric and ginger, working together through the Biotics Triad to maintain the microbiome balance, SCFA production, and gut barrier integrity that determines the endotoxin load the liver must process daily.

For dogs requiring targeted gut-liver axis support, Biotics Bioactive Bites is formulated to reduce the gut-derived toxic burden on hepatic tissue, combining the complete Biotics Triad at therapeutic concentrations — TruPet™ postbiotic (285mg), Calsporin® (4.5 × 10⁴ CFU), and Lactobacillus helveticus (2.7 × 10⁹ CFU) — alongside L-glutamine and zinc glycinate for gut barrier repair to reduce endotoxin translocation via the portal vein, clinoptilolite (144mg) for direct endotoxin binding within the gut lumen, and a concentrated anti-inflammatory botanical network of turmeric, boswellia, and ginger reducing inflammatory burden on both gut and liver simultaneously. Used together with Superfoods & Ancient Grains, Biotics addresses the gut-liver axis at both ends simultaneously, from the microbial regulation of bile acid metabolism and SCFA hepatoprotection to the barrier integrity that determines what the liver’s Kupffer cells must defend against.

Frequently Asked Questions

What is the gut-liver axis and why does it matter for my dog?

The gut-liver axis describes the intimate bidirectional relationship between the gastrointestinal tract and the liver. It matters because the liver receives 70-80% of its blood supply directly from the intestines via the portal vein, meaning gut health directly determines what the liver must process and detoxify. A healthy gut microbiome produces beneficial metabolites that support liver function, maintains barrier integrity that prevents endotoxin exposure, and metabolises bile acids essential for digestive and metabolic health. When gut function is compromised, the liver bears the consequences through increased toxic burden and inflammatory exposure.

How does gut health affect liver function?

Gut health affects liver function through several mechanisms. First, gut bacteria produce short-chain fatty acids that provide direct hepatoprotective effects and support energy metabolism. Second, intestinal barrier integrity determines how much bacterial endotoxin (LPS) reaches the liver – leaky gut dramatically increases hepatic inflammatory burden. Third, gut bacteria convert primary bile acids to secondary forms essential for metabolic regulation. Fourth, a balanced microbiome prevents overgrowth of pathogenic bacteria that produce harmful toxins. When any of these functions are compromised, liver health suffers.

What is metabolic endotoxemia and how does it affect the liver?

Metabolic endotoxemia refers to elevated levels of bacterial lipopolysaccharide (LPS) in circulation – lower than acute sepsis but sufficient to cause chronic low-grade inflammation. LPS from gut bacteria can cross a compromised intestinal barrier or be absorbed with dietary fats. When LPS reaches the liver via the portal vein, it activates Kupffer cells and hepatocytes through Toll-like receptor 4, triggering inflammatory cytokine release, oxidative stress, and potentially hepatocyte damage. Chronic metabolic endotoxemia contributes to liver inflammation, fibrosis progression, and impaired detoxification capacity.

Can prebiotics and probiotics help my dog’s liver?

Yes, research supports the benefits of prebiotics and probiotics for liver health. Prebiotics nourish beneficial bacteria that produce SCFAs with hepatoprotective properties, maintain gut barrier integrity, and support healthy bile acid metabolism. Probiotics introduce beneficial strains that compete with pathogenic bacteria, support barrier function, and produce beneficial metabolites. Studies in dogs with chronic hepatobiliary disease have shown that synbiotic supplementation (combining prebiotics and probiotics) significantly reduced liver enzyme markers and resolved gastrointestinal signs.¹⁰

What is milk thistle and how does it support liver health?

Milk thistle (Silybum marianum) contains silymarin, a complex of flavonolignans with extensively documented hepatoprotective properties.¹¹,¹²,¹³ Silymarin works through multiple mechanisms: it scavenges free radicals and boosts glutathione levels (antioxidant protection), inhibits inflammatory pathways (anti-inflammatory effects), stabilises hepatocyte membranes (protection against toxins), stimulates protein synthesis (regenerative support), and enhances bile flow (choleretic effects). Studies in dogs confirm silymarin’s ability to protect against hepatotoxic challenges and support dogs with elevated liver enzymes.

How do bile acids connect gut and liver health?

Bile acids are synthesised by the liver and secreted into the intestine where they aid fat digestion. Approximately 95% are reabsorbed and returned to the liver (enterohepatic circulation), but the remaining 5% are transformed by gut bacteria into secondary bile acids with distinct biological activities. These microbial transformations are essential – secondary bile acids regulate metabolism, immunity, and even microbiome composition itself. Dogs with liver disease show disrupted bile acid profiles reflecting loss of bile-acid-metabolising bacteria, creating a cycle where liver dysfunction worsens gut health and vice versa.⁷,⁸

What signs might indicate gut-liver axis dysfunction in my dog?

Signs that might indicate gut-liver axis dysfunction include digestive issues (intermittent vomiting, diarrhoea, decreased appetite), subtle behaviour changes (lethargy, reduced enthusiasm), changes in coat quality, and occasionally visible signs like mild jaundice or changes in stool colour. However, the liver has substantial reserve capacity, so overt symptoms often don’t appear until significant dysfunction exists. Regular veterinary check-ups including bloodwork can detect liver enzyme elevations that might indicate problems before clinical signs develop.

My dog is on long-term medications. Should I be concerned about liver health?

Many medications are metabolised by the liver, and long-term use can increase hepatic workload. While this doesn’t mean medications shouldn’t be used when needed, it does highlight the importance of supporting liver function during chronic medication use. Discuss with your veterinarian about appropriate monitoring (periodic liver enzyme panels) and consider hepatoprotective supplementation. Gut health support is particularly relevant since it reduces additional inflammatory burden on an already-working liver.

Are certain breeds more prone to liver problems?

Yes, certain breeds have genetic predispositions to specific liver conditions: Yorkshire Terriers and Maltese are prone to portosystemic shunts; Doberman Pinschers are predisposed to chronic hepatitis and copper storage disease; Bedlington Terriers have high risk for copper storage disease; Labrador Retrievers can develop copper-associated hepatitis; West Highland White Terriers may develop chronic liver inflammation; and Cocker Spaniels are susceptible to chronic active hepatitis. Dogs of predisposed breeds may particularly benefit from proactive gut-liver axis support throughout life.

How does diet affect the gut-liver axis?

Diet profoundly influences the gut-liver axis at multiple levels. Dietary fibre provides substrate for beneficial bacteria to produce SCFAs that support liver health. The type and amount of dietary fat influences LPS absorption – excessive saturated fat may increase endotoxin translocation. Protein quality affects ammonia production and detoxification burden. Phytonutrients and antioxidants from plant ingredients provide direct hepatoprotective effects. A balanced diet rich in diverse plant fibres, quality proteins, and beneficial phytonutrients supports optimal gut-liver axis function.

Can gut-liver axis support help senior dogs?

Absolutely. Ageing is associated with declining liver function, reduced microbiome diversity, and increased intestinal permeability – all factors that stress the gut-liver axis. Senior dogs may particularly benefit from prebiotic and probiotic support to maintain beneficial bacterial populations, hepatoprotective nutrients to support declining detoxification capacity, and antioxidants to combat age-related oxidative stress. Proactive nutritional support becomes increasingly important as dogs age to maintain metabolic resilience and quality of life.

What role does clinoptilolite play in gut-liver health?

Clinoptilolite is a natural zeolite mineral with strong binding affinity for bacterial endotoxins including LPS. By binding these toxins within the gut lumen, clinoptilolite prevents their absorption and subsequent delivery to the liver via the portal system. This provides a safety net even when some degree of intestinal permeability exists – the endotoxins are captured before they can trigger hepatic inflammation. Clinoptilolite thus addresses gut-liver axis dysfunction at its source by reducing the toxic burden before it reaches the liver.

How long does it take to see benefits from gut-liver axis support?

Timeframes vary depending on the condition being addressed. Acute digestive improvements (reduced gas, firmer stools) may occur within days as gut bacteria adjust. Liver enzyme improvements typically require 4-8 weeks to become measurable, reflecting the time needed for hepatocyte recovery and reduced inflammatory burden. Significant changes in microbiome composition require consistent intervention over weeks to months. For dogs with established liver conditions, ongoing support is typically necessary rather than short-term intervention.

Should I use gut-liver axis support alongside veterinary treatment for liver disease?

Nutritional support should complement, never replace, appropriate veterinary care for liver disease. However, evidence suggests that gut-directed therapies can provide meaningful adjunctive benefits for dogs with hepatobiliary conditions.¹⁰ Always inform your veterinarian about supplements your dog receives – they can help coordinate a comprehensive management plan and advise on any potential interactions with medications. The combination of appropriate medical treatment with targeted nutritional support often yields better outcomes than either approach alone.

Can gut health support prevent liver problems?

While we cannot prevent all liver conditions (particularly those with genetic origins), maintaining optimal gut-liver axis function provides significant protective benefits. A healthy microbiome reduces endotoxin exposure, supports bile acid metabolism, and produces hepatoprotective metabolites. Adequate antioxidant status protects against oxidative damage from environmental toxins. Strong gut barrier integrity prevents inappropriate immune activation. These factors collectively support hepatic resilience and may reduce the likelihood or severity of liver problems, particularly those related to inflammation, toxin exposure, or metabolic dysfunction.

Conclusion

The gut-liver axis represents one of the most critical yet underappreciated relationships in canine physiology. The unique anatomical connection via the portal vein – delivering gut-derived blood directly to the liver before it reaches any other organ – creates an intimate partnership where gut health directly determines hepatic wellbeing. When this axis functions optimally, the liver efficiently processes nutrients, neutralises toxins, maintains metabolic homeostasis, and protects the entire body from gut-derived threats. When disrupted, the consequences ripple outward to affect virtually every organ system.

Understanding this connection transforms how we approach both gut and liver health. Rather than viewing these as separate concerns, we recognise them as inseparable partners in maintaining metabolic resilience. Gut dysbiosis doesn’t just cause digestive problems – it increases the toxic burden on the liver through endotoxin translocation, disrupts bile acid metabolism, and promotes chronic inflammation that can progress to hepatic disease. Conversely, liver dysfunction impairs bile production and immune function, destabilising the gut environment and worsening dysbiosis.

The good news is that nutrition offers powerful tools for supporting this vital partnership. Prebiotics nourish the beneficial bacteria that produce hepatoprotective SCFAs and maintain barrier integrity. Probiotics and postbiotics directly support healthy microbiome function. Hepatoprotective botanicals like milk thistle provide targeted liver support with documented benefits. Essential nutrients supply the cofactors required for detoxification enzymes. Endotoxin binders reduce the inflammatory burden reaching the liver. And omega-3 fatty acids support both gut barrier function and hepatic anti-inflammatory mechanisms.

As our understanding of the gut-liver axis continues to advance, we can expect increasingly sophisticated approaches to supporting canine metabolic health through nutrition. The recognition that gut health profoundly influences hepatic function empowers dog owners to take meaningful action for their companions’ long-term wellbeing – through diet, supplementation, and the understanding that caring for the gut means caring for the liver, and caring for both means supporting whole-body health.

Explore the Gut-Organ Axes

References

  1. Merck Veterinary Manual. Anatomy of the Hepatobiliary System in Small Animals. 2024.
  2. Hepatic Disease. In: Ettinger SJ, Feldman EC, editors. Textbook of Veterinary Internal Medicine. 7th ed. Saunders Elsevier; Philadelphia, PA, USA: 2010. pp. 1472–1502.
  3. Habermaass V, Olivero D, Gori E, Mariti C, Longhi E, Marchetti V. Intestinal Microbiome in Dogs with Chronic Hepatobiliary Disease: Can We Talk about the Gut-Liver Axis? Animals. 2023;13:3174. doi:10.3390/ani13203174
  4. Kim H, Chae Y, Cho JH, Song M, Kwak J, Doo H, Choi Y, Kang J, Yang H, Lee S, Keum GB, Wattanaphansak S, Kim S, Kim HB. Understanding the diversity and roles of the canine gut microbiome. Journal of Animal Science and Biotechnology. 2025;16:95. doi:10.1186/s40104-025-01235-4
  5. Tivers MS, Lipscomb VJ, Smith KC, Wheeler-Jones CPD, House AK. Lipopolysaccharide and toll-like receptor 4 in dogs with congenital portosystemic shunts. The Veterinary Journal. 2015;206(3):404-413. doi:10.1016/j.tvjl.2015.07.006
  6. Page MJ, Kell DB, Pretorius E. The Role of Lipopolysaccharide-Induced Cell Signalling in Chronic Inflammation. Chronic Stress. 2022;6:24705470221076390. doi:10.1177/24705470221076390
  7. Rowe JC, Winston JA. Collaborative Metabolism: Gut Microbes Play a Key Role in Canine and Feline Bile Acid Metabolism. Veterinary Sciences. 2024;11(2):94. doi:10.3390/vetsci11020094
  8. Habermaass V, Bartoli F, Gori E, et al. Fecal Bile Acids in Canine Chronic Liver Disease: Results from 46 Dogs. Animals. 2024;14(21):3051. doi:10.3390/ani14213051
  9. Pilla R, Suchodolski JS. The Role of the Canine Gut Microbiome and Metabolome in Health and Gastrointestinal Disease. Frontiers in Veterinary Science. 2020;6:498. doi:10.3389/fvets.2019.00498
  10. Habermaass V, Biolatti C, Bartoli F, et al. Effects of Synbiotic Administration on Gut Microbiome and Fecal Bile Acids in Dogs with Chronic Hepatobiliary Disease: A Randomized Case-Control Study. Veterinary Sciences. 2024;11(8):364. doi:10.3390/vetsci11080364
  11. Marchegiani A, Fruganti A, Gavazza A, Mangiaterra S, Candellone A, Fusi E, Rossi G, Cerquetella M. Evidences on Molecules Most Frequently Included in Canine and Feline Complementary Feed to Support Liver Function. Veterinary Medicine International. 2020;2020:9185759. doi:10.1155/2020/9185759
  12. Hackett ES, Twedt DC, Gustafson DL. Milk Thistle and Its Derivative Compounds: A Review of Opportunities for Treatment of Liver Disease. Journal of Veterinary Internal Medicine. 2013;27(1):10-16. doi:10.1111/jvim.12002
  13. Tedesco DEA, Guerrini A. Use of Milk Thistle in Farm and Companion Animals: A Review. Planta Medica. 2023;89(6):584-607. doi:10.1055/a-1969-2440
  14. Albillos A, de Gottardi A, Rescigno M. The gut-liver axis in liver disease: Pathophysiological basis for therapy. Journal of Hepatology. 2020;72(3):558-577. doi:10.1016/j.jhep.2019.10.003
  15. Shalaby N, Samocha-Bonet D, Kaakoush NO, Danta M. The Role of the Gastrointestinal Microbiome in Liver Disease. Pathogens. 2023;12(9):1087. doi:10.3390/pathogens12091087
  16. Balouei, F.; Stefanon, B.; Martello, E.; Atuahene, D.; Sandri, M.; Meineri, G. Supplementation with Silybum marianum Extract, Synbiotics, Omega-3 Fatty Acids, Vitamins, and Minerals: Impact on Biochemical Markers and Fecal Microbiome in Overweight Dogs. Animals 2024, 14, 579. doi.org/10.3390/ani14040579
  17. Castillo-Fernandez J, Gilroy R, Jones RB, Honaker RW, Whittle MJ, Watson P, Amos GCA. Waltham catalogue for the canine gut microbiome: a complete taxonomic and functional catalogue of the canine gut microbiome through novel metagenomic based genome discovery. Microbiome. 2026;14(1):25. https://link.springer.com/article/10.1186/s40168-025-02265-w

Editorial Information

FieldDetail
PublishedJanuary 2026
Last Updated12 May 2026 (Added evidence-review framing on plant-based canine nutrition and hepatic outcomes.)
Reviewed byGlendon Lloyd, Dip. Canine Nutrition (Distinction), Dip. Dog Nutrigenomics (Distinction)
Next ReviewNovember 2026
AuthorGlendon Lloyd
DisclaimerThis article is for informational purposes only and does not constitute veterinary advice. Always consult a qualified veterinarian before making changes to your dog’s diet or supplement regimen.

Glendon Lloyd is the founder of Bonza. He holds Diplomas in Dog Nutrigenomics and Canine Nutrition (both with Distinction) and is a SFTR accredited member. He is committed to advancing evidence-based canine nutrition through continuous study of peer-reviewed research. His expertise spans evidence-based canine nutrition, nutrigenomics, and the connections between diet, the gut microbiome, and long-term health outcomes.
Through the Bonza Health Hub for Dogs, Glendon shares evidence-based articles on preventative canine health, making complex nutritional science accessible to dog owners seeking to make informed decisions about their companions’ wellbeing.

Glendon Lloyd

About Glendon Lloyd

As the founder and CEO of Bonza, I am challenging one of the most overlooked truths in canine health: the gut is not just part of the system. It is the system.

I hold Diplomas in Canine Nutrition and Dog Nutrigenomics, both awarded with Distinction, and I formulate every Bonza recipe in-house alongside our board of canine veterinary nutritionists. The gut microbiome sits at the centre of immune regulation, inflammation, metabolic function and neurological health, yet much of modern dog nutrition still treats food as fuel rather than biology. I am working to change that.

At Bonza we take a systems-biology approach to canine nutrition. We design food and supplements that actively shape the microbiome through plant diversity, functional fibres, and named, regulatory-authorised bioactives with full strain-level transparency: the Biotics Triad of prebiotics, probiotics and postbiotics, alongside phytonutrients and adaptogens. Each works through the eight gut-organ axes that connect the gut to the skin, joints, immune system, behaviour, heart, metabolism, liver and longevity.

This is about more than better ingredients. It is about redefining food as a controllable input for health outcomes, shifting from reactive care to precision nutrition that supports resilience, longevity and disease prevention.

We are building what canine nutrition should have been all along.

One Gut. Whole Dog.

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