Avocado-Soybean Unsaponifiables – Evidence-Based Benefits for Dog Joints
Summary
Avocado-soybean unsaponifiables (ASU) are natural plant extracts derived from avocado (Persea americana) and soybean (Glycine max) oils that have demonstrated significant chondroprotective and anti-inflammatory properties in canine joint health research. Classified as a slow-acting disease-modifying osteoarthritis agent (DMOAA), ASU works through multiple mechanisms to protect cartilage from degradation, reduce inflammatory signalling in joint tissues, and support the synthesis of key structural components including collagen and aggrecan.¹ ² In the landmark canine anterior cruciate ligament (ACL) model of osteoarthritis, ASU treatment significantly reduced cartilage lesion severity, preserved subchondral bone volume, and decreased synovial inflammation.¹ ASU is generally well tolerated in dogs, with no significant adverse effects reported in published research, and its plant-based origin makes it suitable for dogs on any dietary protocol.²
Key Takeaways
- ASU is a natural extract from avocado and soybean oils, combined in a 1:2 ratio, containing bioactive phytosterols that protect joint cartilage and reduce inflammation in dogs.¹ ²
- In a controlled canine osteoarthritis study, ASU significantly reduced cartilage lesion severity (P = 0.0002), preserved subchondral bone volume (P < 0.05), and decreased synovial inflammation (P = 0.04) compared to placebo.¹
- ASU works through multiple complementary mechanisms: inhibiting cartilage-degrading enzymes (MMP-13), suppressing inflammatory mediators (IL-1β, TNF-α, COX-2, iNOS), and stimulating collagen and aggrecan synthesis — with canine studies confirming increased TGF-β1 and TGF-β2 levels in joint fluid following ASU treatment.¹ ³ ⁴ ¹⁵
- The phytosterols in ASU, particularly β-sitosterol, influence gut microbiota composition and short-chain fatty acid production, connecting ASU to the emerging gut-joint axis in osteoarthritis management.⁵ ⁶
- Bonza includes ASU at 10mg per chewy in Bounce Bioactive Bites, working synergistically with glucosamine, chondroitin, boswellia, and other joint-support ingredients for comprehensive multi-pathway joint protection.
In this guide:
- What Are Avocado-Soybean Unsaponifiables?
- Bioactive Compounds and How They Work
- Health Benefits for Dogs
- ASU and Gut Health
- Why Bonza Includes ASU in Bounce
- Safety Profile
- How to Give ASU to Your Dog
- Dosage Guidelines
- Practical Considerations
- Frequently Asked Questions
- Related Reading
- References
- Editorial Information
- About the Author
What Are Avocado-Soybean Unsaponifiables?
Avocado-soybean unsaponifiables are the fraction of avocado and soybean oils — approximately 1% of the total oil content — that remains after saponification, the chemical process of making soap. This concentrated extract is produced by combining one-third avocado unsaponifiables with two-thirds soybean unsaponifiables (a 1:2 ratio), creating a complex mixture of bioactive lipid compounds with documented therapeutic properties for joint health.² ⁷
The use of avocado and soybean oils for their healing properties has roots in traditional folk medicine, where both oils were valued for soothing joint discomfort and supporting connective tissue health. Modern scientific investigation into ASU began in earnest in France during the mid-20th century, when researchers isolated the unsaponifiable fractions and began systematic evaluation of their effects on joint tissues. This work led to the development of Piascledine 300, a pharmaceutical-grade ASU preparation that has been prescribed in France and other European countries as an adjunctive treatment for osteoarthritis since the 1990s.⁷ ⁸
The recognition that ASU’s benefits extend beyond human medicine came with the pivotal work of Boileau and colleagues (2009), who demonstrated in a rigorous canine model of osteoarthritis that oral ASU treatment significantly reduced the development of structural joint damage — providing direct evidence of chondroprotective effects in dogs.¹ This canine research, combined with extensive in vitro and human clinical data, has established ASU as one of the more thoroughly researched natural joint-support compounds available for veterinary use.²
Bioactive Compounds and How They Work
ASU is a complex mixture of lipid-soluble bioactive compounds, and its therapeutic effects are attributed to the combined actions of several classes of molecules rather than any single active ingredient.⁴ ⁷
Phytosterols are the primary bioactive constituents and include β-sitosterol, campesterol, and stigmasterol. These plant-derived sterols are structurally similar to cholesterol and are rapidly incorporated into cell membranes, where they modulate inflammatory signalling pathways. β-Sitosterol, the most abundant phytosterol in ASU, has been shown to inhibit NF-κB activation and suppress pro-inflammatory cytokine production in immune and joint cells.⁴ ⁹ The sterol content of ASU preparations is considered the primary driver of biological activity in articular chondrocytes.⁴
Tocopherols (forms of vitamin E) contribute antioxidant protection, scavenging reactive oxygen species (ROS) that accelerate cartilage degradation in osteoarthritic joints. Oxidative stress is a recognised driver of chondrocyte dysfunction and matrix breakdown, and the tocopherol content of ASU provides a complementary layer of cellular protection.⁷
Triterpene alcohols and furan fatty acids are also present in the unsaponifiable fraction. While their individual contributions are less well characterised, they are thought to contribute to ASU’s overall anti-inflammatory profile. Researchers have noted that the total unsaponifiable fraction (used “in toto”) demonstrates greater therapeutic activity than isolated individual components, suggesting synergistic interactions among its constituents.⁷
The mechanisms through which these compounds protect joint tissues operate on multiple levels simultaneously:
Anticatabolic effects: ASU inhibits the release and activity of matrix metalloproteinases (particularly MMP-13, the primary collagen-degrading enzyme in osteoarthritis), reduces expression of ADAMTS-4 and ADAMTS-5 (aggrecanases that break down cartilage matrix), and increases tissue inhibitors of metalloproteinases (TIMP-1).¹ ⁴ These actions directly slow the enzymatic destruction of cartilage.
Anti-inflammatory effects: ASU suppresses multiple inflammatory mediators including interleukin-1β (IL-1β), tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), prostaglandin E2 (PGE₂), and nitric oxide (NO). This is achieved partly through inhibition of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression, and partly through modulation of NF-κB, a master regulator of inflammatory gene expression.¹ ³ ⁴
Anabolic effects: ASU stimulates chondrocytes to increase synthesis of collagen and aggrecan — the two primary structural components of cartilage matrix. It also corrects growth factor abnormalities by increasing transforming growth factor-beta (TGF-β) in synovial fluid, promoting cartilage repair processes. Importantly, this anabolic effect has been confirmed directly in dogs: Altinel et al. (2007) demonstrated that canine joints treated with ASU showed significantly increased levels of both TGF-β1 and TGF-β2 in joint fluid, with elevated TGF-β associated with enhanced production of collagen and proteoglycans by cartilage cells.⁴ ¹⁵
Subchondral bone protection: Beyond cartilage effects, ASU has been shown to reduce loss of subchondral bone volume and preserve calcified cartilage thickness, addressing the bone remodelling component of osteoarthritis that is often overlooked by conventional joint supplements.¹
Health Benefits for Dogs
Joint Cartilage Protection
The strongest evidence for ASU’s benefits in dogs comes from the canine ACL transection model, considered the gold standard for studying osteoarthritis progression. In this controlled study, dogs receiving ASU at 10 mg/kg per day for eight weeks showed significantly reduced cartilage lesion severity on both tibial plateaus and femoral condyles compared to placebo-treated animals (P = 0.0002). Macroscopic examination revealed smaller lesion areas on the tibial plateaus (P = 0.04), whilst histological analysis confirmed better preservation of cartilage architecture with less fibrillation and surface damage.¹
Inflammation Reduction
ASU’s multi-target anti-inflammatory action addresses the chronic low-grade inflammation that drives osteoarthritis progression. The canine study demonstrated significantly reduced cellular infiltration in the synovial membrane (P = 0.04), indicating less synovial inflammation.¹ In vitro studies using canine-relevant cell models confirm that ASU suppresses the production of key inflammatory mediators including TNF-α, IL-1β, COX-2, iNOS, and PGE₂ in both articular chondrocytes and monocyte/macrophage cells.³
Subchondral Bone Preservation
Osteoarthritis involves not just cartilage but also the bone beneath it. ASU-treated dogs showed significantly preserved subchondral bone volume (P < 0.05) and maintained calcified cartilage thickness (P = 0.01) compared to placebo. This dual protection of both cartilage and bone is particularly relevant for managing the structural progression of the disease.¹
Reduced NSAID Dependence
Clinical evidence in humans — which has translational relevance given the conserved joint biology across mammals — indicates that ASU supplementation can reduce the need for non-steroidal anti-inflammatory drugs (NSAIDs). A meta-analysis of randomised controlled trials found that ASU provided symptomatic relief in osteoarthritis, reducing pain and improving joint function.⁸ Canine cell-based evidence further supports this potential: Grzanna et al. (2020) demonstrated that the combination of ASU, glucosamine, and chondroitin sulfate significantly enhanced the anti-inflammatory effect of the veterinary NSAID carprofen in canine chondrocyte cultures, with the combination suppressing PGE₂ production more effectively than either carprofen or ASU+glucosamine+chondroitin alone.¹⁶ This NSAID-sparing potential is particularly valuable for dogs on long-term joint management protocols, where minimising pharmaceutical load supports better overall health outcomes.
Synergy with Glucosamine and Chondroitin
ASU has been shown to complement and enhance the effects of glucosamine and chondroitin sulfate. Research demonstrates that the combination produces greater chondroprotective effects than any single agent alone, with ASU’s anti-inflammatory and anabolic actions amplifying the structural support provided by glucosamine and chondroitin.² ⁴ In canine chondrocyte cultures, the ASU+glucosamine+chondroitin sulfate combination significantly suppressed production of multiple inflammatory mediators — including IL-6, IL-8, and MCP-1 — more effectively than the NSAID carprofen alone, confirming this synergistic relationship in a canine-specific cell model.¹⁶ This combination approach is a key consideration in formulation design.
ASU and Gut Health
The connection between ASU and gut health centres on two interrelated pathways: the direct effects of ASU’s phytosterol constituents on the intestinal environment, and the broader gut-joint axis through which gut health influences joint inflammation and osteoarthritis progression.
Phytosterols and the Gut Microbiome
The phytosterols in ASU — particularly β-sitosterol, campesterol, and stigmasterol — interact meaningfully with the gut microbiome. Research demonstrates that β-sitosterol attenuates intestinal inflammation by inhibiting the binding of lipopolysaccharide (LPS) to toll-like receptor 4 (TLR-4) in the NF-κB pathway, directly supporting gut barrier integrity.⁹ This is significant because compromised intestinal barrier function (commonly termed “leaky gut“) allows bacterial endotoxins to enter systemic circulation, driving inflammatory processes that affect distant organs — including joints.
Studies in animal models show that phytosterols modulate gut microbiota composition in several beneficial ways. Phytosterol supplementation has been associated with increased production of short-chain fatty acids (SCFAs) including acetate and butyrate.⁵ Butyrate is the primary energy source for colonocytes (the cells lining the large intestine) and plays a critical role in maintaining gut barrier function, regulating local and systemic immune responses, and suppressing inflammatory signalling.
Furthermore, β-sitosterol has been shown to reshape the gut microbial community structure, enriching beneficial genera including Eubacterium, Lactobacillus, and Butyricicoccus whilst reducing potentially harmful taxa.⁶ ¹⁰ These shifts favour an anti-inflammatory microbial profile that supports both gut integrity and systemic immune regulation.
The Gut-Joint Axis
The gut-joint axis is an increasingly recognised pathway through which intestinal health directly influences joint disease, and it has particular relevance for dogs with osteoarthritis. Research using dogs as a translational model for osteoarthritis has revealed that LPS-binding protein (LBP) — a marker of intestinal barrier dysfunction — is positively associated with the number of joints experiencing OA-related pain.¹¹ This finding aligns with human data showing that elevated circulating LPS levels correlate with increased osteoarthritis severity.¹²
The mechanisms connecting gut health to joint inflammation operate through several pathways. When the intestinal barrier is compromised, bacterial products including LPS translocate into the bloodstream, activating immune cells and triggering systemic low-grade inflammation. This inflammatory state increases the production of cytokines (IL-1β, TNF-α, IL-6) that directly promote cartilage degradation in joints.¹² Additionally, gut dysbiosis reduces the microbial production of anti-inflammatory metabolites such as SCFAs, removing a natural brake on systemic inflammation.¹³
Research in dogs with chronic arthritis has confirmed altered gut microbiome composition compared to healthy animals, with arthritic dogs showing elevated C-reactive protein (CRP, a systemic inflammation marker), lower serum vitamin B12 and folate concentrations, and shifts in bacterial populations including increased abundance of Megamonas and reduced levels of several protective bacterial families.¹³
By supporting gut barrier integrity through phytosterol-mediated TLR-4 inhibition, promoting beneficial microbial composition, and enhancing SCFA production, ASU’s gut-level actions create a complementary pathway to its direct chondroprotective effects — addressing joint health from both the systemic inflammatory environment and the local joint tissue level simultaneously.
Relevance to Bonza’s Gut-Joint Axis Approach
ASU’s dual action — working directly on joint tissues while simultaneously supporting gut health — aligns with Bonza’s gut-joint axis approach to mobility support. Rather than targeting joint symptoms alone, this strategy recognises that optimal joint health requires addressing the systemic inflammatory environment shaped by intestinal health, microbiome composition, and gut barrier integrity.
Why Bonza Includes ASU in Bounce Bioactive Bites Joint Supplement
Bonza includes avocado-soybean unsaponifiables at 10mg per chewy in Bounce Bioactive Bites as a key component of a comprehensive, multi-pathway approach to joint and mobility support. The decision to include ASU reflects several evidence-based considerations:
Chondroprotective evidence in dogs. ASU is one of relatively few natural joint-support compounds with direct evidence of structural cartilage protection in a controlled canine model.¹ The Boileau et al. (2009) study demonstrated protection of both cartilage and subchondral bone — addressing two critical components of osteoarthritis progression that many single-ingredient approaches miss.
Multi-mechanism action. ASU’s simultaneous anticatabolic, anti-inflammatory, and anabolic effects on joint tissues mean it contributes to cartilage protection through complementary pathways. This aligns with Bonza’s formulation philosophy of addressing joint health through multiple mechanisms rather than relying on any single approach.
Synergy with Bounce’s formulation partners. ASU has demonstrated synergistic effects when combined with glucosamine and chondroitin sulfate, with canine cell evidence confirming enhanced anti-inflammatory activity of this combination.⁴ ¹⁶ In Bounce, ASU works alongside glucosamine HCl (240mg), chondroitin sulphate from Greendroitin (80mg), MSM (120mg), Boswellia serrata (10mg), and Turmeric (curcuma longa) (10mg) to create a comprehensive joint-support matrix. ASU’s proven ability to increase TGF-β levels in canine joint fluid — stimulating collagen and proteoglycan synthesis — complements the structural support provided by glucosamine and chondroitin.¹⁵ The combination of ASU’s chondroprotective effects with Boswellia’s 5-lipoxygenase inhibition and curcumin’s NF-κB modulation provides multi-pathway inflammation control.
Gut-joint axis support. ASU’s phytosterol content contributes to Bounce’s gut-joint axis approach, complementing the prebiotic action of Fibrofos 60 FOS (80mg), the postbiotic benefits of TruPet (83mg), and the β-glucan immune modulation of Biolex MB40 (83mg). Together, these ingredients support the intestinal environment alongside direct joint tissue protection.
Plant-based formulation compatibility. As a natural extract from avocado and soybean oils, ASU aligns with Bonza’s 100% plant-based formulation commitment, providing chondroprotective benefits typically associated with animal-derived ingredients through an entirely plant-sourced compound.
Safety Profile
ASU has a well-established safety profile across both veterinary and human research. In the canine ACL transection study, dogs received ASU at 10 mg/kg per day orally for eight weeks with no reported adverse effects.¹ Human clinical trials using ASU at 300mg/day for periods of up to six months have consistently reported no clinically significant adverse effects, with only infrequent mild gastrointestinal complaints occurring at rates comparable to placebo.² ⁷ ⁸
Both avocado and soybean are generally recognised as safe (GRAS) as food ingredients, and their unsaponifiable fractions carry no known toxicity concerns at supplemental doses.² No drug interactions have been well documented for ASU, though as with any supplement, veterinary consultation is recommended for dogs on concurrent NSAID therapy or other medications.
Important clarification regarding avocado safety in dogs: ASU is derived from the oil fraction of avocado fruit and does not contain persin, the fungicidal toxin found in avocado skin, leaves, seeds, and bark that can be harmful to some animal species. The unsaponifiable extraction process isolates the bioactive lipid compounds whilst excluding potentially harmful plant components.
How to Give ASU to Your Dog
How to introduce ASU (avocado-soybean unsaponifiables) supplementation for your dog’s joint health safely and effectively, from veterinary consultation through to ongoing monitoring.
- Consult your veterinarian
Discuss ASU supplementation with your vet before starting, particularly if your dog has existing health conditions, takes NSAIDs, or is recovering from joint surgery.
- Choose a synergistic formulation
Select an ASU supplement that combines it with complementary joint-support ingredients such as glucosamine, chondroitin sulphate, and anti-inflammatory botanicals for enhanced efficacy.
- Administer daily with food
Give ASU consistently with meals. As a lipid-based compound, co-administration with dietary fats supports optimal absorption.
- Allow 4–8 weeks for effect
ASU is a slow-acting chondroprotective agent. Meaningful improvements in mobility and comfort typically emerge after 4–8 weeks of consistent daily supplementation.
- Monitor mobility and comfort
Track changes in your dog’s willingness to exercise, ease of rising, post-rest stiffness, and fluidity of movement during walks.
- Maintain ongoing supplementation
Continue daily supplementation for sustained benefit. ASU’s protective effects require continuous presence, and stopping may allow inflammatory processes and cartilage vulnerability to return.
Dosage Guidelines
ASU dosage in veterinary practice is typically guided by the canine research literature and commercial formulation standards:
| Dog Size | Body Weight | Typical ASU Dose Range |
|---|---|---|
| Small | Under 10 kg | 10–30 mg/day |
| Medium | 10–25 kg | 30–60 mg/day |
| Large | 25–40 kg | 60–90 mg/day |
| Giant | Over 40 kg | 90–120 mg/day |
The canine ACL transection study used 10 mg/kg per day, which provides a research-validated reference point.¹ Commercial veterinary joint supplements containing ASU typically provide 45–90mg per dose depending on the product and target dog size.
Bonza Bounce Bioactive Bites provide 10mg of avocado unsaponifiables per 3g chewy, formulated to work synergistically within the complete Bounce blend. Feeding guidelines are based on body weight (1 soft chew/10kg bodyweight per day)— consult the Bounce packaging or product page for specific recommendations.
Dosage information is provided for educational purposes. Always follow the feeding guidelines on your chosen supplement’s packaging and consult your veterinarian for individualised recommendations.
Practical Considerations
Onset of action. ASU is classified as a slow-acting symptomatic ‘drug’ for osteoarthritis, meaning visible benefits develop gradually. Dog owners should be prepared for a 4–8 week supplementation period before assessing efficacy, rather than expecting immediate results comparable to pharmaceutical pain relief.
Best started early. Research and veterinary consensus suggest that ASU and other chondroprotective agents deliver the greatest benefit when started early in the course of joint disease — ideally at the first signs of stiffness or mobility changes, following joint surgery, or as preventive support in breeds predisposed to osteoarthritis.
Soy sensitivity. While rare, some dogs may have sensitivities to soy-derived products. If your dog has a known soy allergy, consult your veterinarian before supplementation with ASU-containing products, though the extensive processing involved in producing unsaponifiable extracts removes the protein fractions typically responsible for allergic responses.
Storage. ASU-containing supplements should be stored in a cool, dry environment away from direct sunlight to preserve the integrity of the lipid-soluble bioactive compounds.
Complementary support. ASU works best as part of a comprehensive joint-management approach that includes appropriate body weight management, regular low-impact exercise, and veterinary oversight. No single supplement replaces the need for professional veterinary assessment and an integrated care plan.
Frequently Asked Questions
Unsaponifiables are the small fraction (roughly 1%) of vegetable oils that resists saponification — the chemical reaction that converts fats into soap. This fraction is concentrated with bioactive lipid compounds including phytosterols, tocopherols, and triterpene alcohols. In avocado and soybean oils, these compounds have demonstrated significant anti-inflammatory and chondroprotective properties, protecting cartilage from degradation and supporting joint tissue repair through multiple biological mechanisms.¹ ⁴
No. ASU is a highly concentrated extract of the unsaponifiable fraction, which constitutes only about 1% of the total oil. Whole avocado or soybean oil would not provide therapeutically meaningful levels of the bioactive phytosterols and other compounds responsible for ASU’s joint-protective effects. The extraction and concentration process is essential to achieving the biological activity demonstrated in research.⁷
ASU is classified as a slow-acting agent, and research suggests 4–8 weeks of consistent daily supplementation before meaningful clinical improvement becomes apparent. The Boileau et al. canine study used an 8-week treatment period to demonstrate significant structural protection.¹ Unlike fast-acting pain medications, ASU works by gradually modulating inflammatory pathways and supporting cartilage repair processes.
ASU should not be used as a direct replacement for prescribed NSAID therapy without veterinary guidance. However, human clinical evidence suggests that consistent ASU supplementation may reduce the need for NSAIDs over time.⁸ Any changes to your dog’s prescribed medications should be discussed with and supervised by your veterinarian.
The unsaponifiable extraction process removes the vast majority of protein content — which is typically responsible for allergic responses to soy. However, trace residues may remain, so dogs with confirmed soy allergies should only use ASU-containing supplements under veterinary supervision.
Research suggests ASU works synergistically with glucosamine and chondroitin sulfate, meaning the combination produces greater chondroprotective effects than any single agent alone.⁴ Canine chondrocyte studies confirm that the ASU+glucosamine+chondroitin combination suppresses key inflammatory mediators more effectively than either the combination or the NSAID carprofen alone, and that combining both may allow reduced NSAID dosing.¹⁶ ASU is commonly formulated alongside these ingredients in veterinary joint supplements for this reason.
Veterinary orthopaedic specialists generally recommend starting chondroprotective supplementation early — ideally before significant joint damage has occurred. ASU’s ability to protect cartilage from degradation and support healthy matrix synthesis suggests potential value as a preventive measure for breeds predisposed to osteoarthritis, active sporting dogs, and dogs recovering from joint surgery.
The toxicity concern with avocado relates to persin, a fungicidal compound found in the skin, leaves, seeds, and bark of the avocado plant. ASU is extracted from the oil of the avocado fruit flesh, and the unsaponifiable extraction process does not carry persin into the final product. There is no evidence of persin-related toxicity from ASU supplementation in any published research.
Related Reading
- The Gut-Joint Axis: How Your Dog’s Gut Health Affects Their Joints
- The Dog Gut Microbiome: Vital Key to Dog Health
- Best Probiotics for Dogs: A Canine Nutritionist’s Guide
- Best Prebiotics for Dogs: Canine Nutritionist’s Complete Guide
References
- Boileau C, Martel-Pelletier J, Caron J, et al. Protective effects of total fraction of avocado/soybean unsaponifiables on the structural changes in experimental dog osteoarthritis: inhibition of nitric oxide synthase and matrix metalloproteinase-13. Arthritis Research & Therapy. 2009;11(2):R41. doi: 10.1186/ar2649
- Sabucedo-Suárez A, López-Peña M, Permuy M, Muñóz F. Soybean and avocado unsaponifiables: a review of their potential use in the treatment of osteoarthritis. Front Vet Sci. 2025 Jan 15;11:1473688. doi: 10.3389/fvets.2024.1473688. PMID: 39881723; PMCID: PMC11776088.
- Au RY, Al-Talib TK, Au AY, Phan PV, Frondoza CG. Avocado soybean unsaponifiables (ASU) suppress TNF-α, IL-1β, COX-2, iNOS gene expression, and prostaglandin E2 and nitric oxide production in articular chondrocytes and monocyte/macrophages. Osteoarthritis and Cartilage. 2007;15(11):1249–1255. doi: 10.1016/j.joca.2007.07.009
- Christiansen BA, Bhatti S, Goudarzi R, Emami S. Management of osteoarthritis with avocado/soybean unsaponifiables. Cartilage. 2015;6(1):30–44. doi: 10.1177/1947603514554992
- Wasilewski T, Kamińska B, Zakrzewski B, et al. Phytosterols and the digestive system: a review study from insights into their potential health benefits and safety. Pharmaceuticals. 2024;17(5):557. doi: 10.3390/ph17050557
- Wu W, Liu W, Wang H, Wang W, Chu W, Jin J. β-sitosterol inhibits trimethylamine production by regulating the gut microbiota and attenuates atherosclerosis in ApoE-/- mice. Front Cardiovasc Med. 2022 Nov 1;9:986905. 10.3389/fcvm.2022.986905. PMID: 36386330; PMCID: PMC9663806.doi:
- Cruz-Martins N, Ferreres F, Catarino MD, et al. Avocado–soybean unsaponifiables: a panoply of potentialities to be exploited. Molecules. 2020;25(16):3672. doi: 10.3390/molecules25163672
- Christensen R, Bartels EM, Astrup A, Bliddal H. Symptomatic efficacy of avocado-soybean unsaponifiables (ASU) in osteoarthritis (OA) patients: a meta-analysis of randomized controlled trials. Osteoarthritis Cartilage. 2008 Apr;16(4):399-408. doi: 10.1016/j.joca.2007.10.003. Epub 2007 Nov 26. PMID: 18042410.
- Kim KA, Lee IA, Gu W, Hyam SR, Kim DH. β-Sitosterol attenuates high-fat diet-induced intestinal inflammation in mice by inhibiting the binding of lipopolysaccharide to toll-like receptor 4 in the NF-κB pathway. Mol Nutr Food Res. 2014 May;58(5):963-72. 10.1002/mnfr.201300433. Epub 2014 Jan 9. PMID: 24402767.
- Lv WJ, Huang JY, Lin J, Ma YM, He SQ, Zhang YW, Wang TZ, Cheng K, Xiong Y, Sun FG, Pan ZC, Sun JB, Mao W, Guo SN. Phytosterols Alleviate Hyperlipidemia by Regulating Gut Microbiota and Cholesterol Metabolism in Mice. Oxid Med Cell Longev. 2023 Apr 26;2023:6409385. doi: 10.1155/2023/6409385. PMID: 37151603; PMCID: PMC10156461.
- Stevens BJ, Lascelles BDX, Guo A, et al. Gut microbiome and osteoarthritis: insights from the naturally occurring canine model of osteoarthritis. Arthritis & Rheumatology. 2024;76(12):1813–1822. doi: 10.1002/art.42956
- Wei Z, Li F, Pi G. Association Between Gut Microbiota and Osteoarthritis: A Review of Evidence for Potential Mechanisms and Therapeutics. Front Cell Infect Microbiol. 2022 Mar 16;12:812596. doi: 10.3389/fcimb.2022.812596. PMID: 35372125; PMCID: PMC8966131.
- Cintio M, Scarsella E, Sgorlon S, et al. Gut microbiome of healthy and arthritic dogs. Veterinary Sciences. 2020;7(3):92. doi: 10.3390/vetsci7030092
- Maheu E, Cadet C, Marty M, et al. Randomised, controlled trial of avocado-soybean unsaponifiable (Piascledine) effect on structure modification in hip osteoarthritis: the ERADIAS study. Annals of the Rheumatic Diseases. 2014;73(2):376–384. doi: 10.1136/annrheumdis-2012-202485
- Altinel L, Saritas ZK, Kose KC, Pamuk K, Aksoy Y, Serteser M. Treatment with unsaponifiable extracts of avocado and soybean increases TGF-β1 and TGF-β2 levels in canine joint fluid. Tohoku Journal of Experimental Medicine. 2007;211(2):181–186. doi: 10.1620/tjem.211.181
- Grzanna MW, Secor EJ, Fortuno LV, Au AY, Frondoza CG. Anti-inflammatory effect of carprofen is enhanced by avocado/soybean unsaponifiables, glucosamine and chondroitin sulfate combination in chondrocyte microcarrier spinner culture. Cartilage. 2020;11(1):108–116. doi: 10.1177/1947603518783495
Editorial Information
| Field | Detail |
|---|---|
| Published | February 2026 |
| Last Updated | February 2026 — Added canine TGF-β (Altinel et al. 2007) and canine chondrocyte NSAID-sparing synergy (Grzanna et al. 2020) references |
| Reviewed by | Glendon Lloyd, Dip. Canine Nutrition, Dip. Canine Nutrigenomics (Distinction) |
| Next Review | August 2026 |
| Author | Glendon Lloyd |
| Disclaimer | This 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. |
