Is there evidence for natural remedies?

Do you find yourself faced with clients reeling off lists of supplements you’ve never heard of? I do to! When doing some literature research into osteoarthritis I found this paper which is the topic of this Pain Update.

The reason I have put this together is not because I see firm evidence that we should be using these supplements, but rather as a useful list for quick reference if you are wondering what the potential benefit to any of these could be. And I emphasise the ‘potential’ there – to my knowledge there is no evidence to support the use of these in dogs and cats at the current time. A reference which supports that view is Barbeau-Gregoire et al (2022) which you can link to here. With the information provided here you can guide your clients when faced with those questions.

PS - the rose is just a pretty picture - I am not aware of rose extract being useful!

Watch webinar on Adjuncts to Chronic Pain Management

 

Curcumin

• Extracted from turmeric (Curcuma longa), curcumin is:

  • Antibacterial, antioxidant, and anti-inflammatory

  • Traditionally used in Ayurvedic medicine

• Mechanisms in OA:

  • Protects chondrocytes from inflammatory damage

  • Inhibits matrix metalloproteinases (MMPs) involved in cartilage breakdown

  • Enhances autophagy via the Akt/mTOR pathway

  • Activates NRF2/HO-1 signaling to combat oxidative stress

• Challenges:

  • Poor bioavailability and absorption

  • Limited high-quality RCTs in humans

• Solutions:

  • Nanoparticle encapsulation (e.g., silk fibroin) improves delivery and efficacy

  • Some studies in people show curcumin is as effective as ibuprofen, with better GI tolerance

Bromelain: A Proteolytic Enzyme from Pineapple

• Properties: A plant-derived enzyme with anti-inflammatory, analgesic, fibrinolytic, and immunomodulatory effects.

• Clinical Evidence:

  • Early studies showed limited efficacy when used alone.

  • Better outcomes observed when combined with other extracts like curcumin or Boswellia serrata.

  • Some trials showed no significant difference compared to NSAIDs like diclofenac in humans.

• Mechanism in OA:

  • Suppresses glycosaminoglycan (GAG) degradation.

  • Inhibits IL-1β and MMPs, reducing cartilage breakdown.

• Conclusion: Promising but inconsistent results; more research is needed to clarify its role and optimal use conditions.

Boswellia serrata: Anti-Inflammatory Resin Extract

• Source: Resin from the Boswellia tree, rich in terpenes and boswellic acids.

• Therapeutic Potential:

  • Used for inflammatory diseases like OA, asthma, and IBD.

  • Shown to reduce knee pain and swelling in RCTs in people.

  • May reduce NSAID use in human OA patients.

• Mechanism in OA:

  • Inhibits proinflammatory cytokines and enzymes like COX-1 and Cathepsin-G.

  • Encapsulation in lipid nanoparticles enhances efficacy.

• Limitations:

  • Lack of direct comparison with NSAIDs in many studies.

  • Bioactive concentrations may be low, but accumulation in tissues could explain effects.

Harpagophytum procumbens (Devil’s Claw)

• Composition: Contains harpagoside, phenolic acids, flavonoids, and iridoid glucosides.

• Mechanisms:

  • Suppresses IL-6 and NF-κB signaling.

  • Exhibits anti-inflammatory and analgesic effects in vitro.

• Clinical Evidence:

  • Comparable pain relief to NSAIDs in some studies in people.

  • Combined use in gels with conventional therapy improved pain and function.

• Limitations:

  • Long-term safety is not well established.

  • Some studies lack robust design or control groups.

Aescin (from Horse Chestnut)

• Composition: A terpenoid mixture of α-escin and β-escin.

• Mechanisms:

  • Promotes glucocorticoid receptor uptake.

  • Inhibits TNF-α, IL-1β, IL-6, and NF-κB.

• Clinical Evidence:

  • Topical and injectable forms showed pain relief and improved joint function in people.

  • Some studies suggest gastroprotective effects, making it suitable for long-term use.

• Limitations:

  • Few OA-specific studies.

  • Some trials lacked control groups or relied on physician-reported outcomes.

Matricaria chamomilla (Chamomile)

• Composition: Rich in flavonoids (e.g., apigenin, quercetin), terpenes, and phenolic acids.

• Pharmacological Properties:

  • Anti-inflammatory, antioxidant, analgesic, and antiplatelet.

  • Also beneficial for wound healing, anxiety, and organ protection.

• Mechanisms in OA:

  • Apigenin is the key anti-inflammatory agent.

  • Inhibits TNF-α, prostaglandin E2, and COX-2—similar to NSAIDs.

  • Topical application improves pain, stiffness, and physical activity.

• Clinical Evidence:

  • Traditional chamomile oil formulations have shown pain relief in knee OA.

  • Effective when applied topically, with good skin penetration.

Glycine soja (Wild Soybean)

• Composition: Contains isoflavones (e.g., genistein, daidzein), saponins, and flavonoids.

• Health Benefits:

  • Improves lipid profiles, reduces fat accumulation, and supports metabolic health.

• Mechanisms in OA:

  • Reduces inflammatory mediators (PGE2, IL-1β, IL-6, TNF-α).

  • Inhibits MMPs and collagen type II degradation.

  • Acts via NF-κB inhibition, offering chondroprotection.

• Clinical Potential:

  • Shown to reduce joint pain and inflammation in both in vitro and in vivo models.

  • Considered a promising therapeutic candidate for OA.

Zingiber officinale Roscoe (Ginger)

• Composition: Rich in phenolic compounds (e.g., gingerols, shogaols, zingerone) and essential oils.

• Mechanisms in OA:

  • Inhibits proinflammatory cytokines (TNF-α, IL-1β, IL-6, IL-17) and COX-2.

  • Suppresses NF-κB activation and oxidative stress.

  • Reduces NO production and iNOS expression in macrophages.

• Clinical Potential:

  • Effective in reducing pain, stiffness, and inflammation.

  • Considered a safer alternative to NSAIDs with fewer GI or renal side effects.

Quercetin

• Source: A flavonoid found in many fruits, vegetables, and herbs.

• Mechanisms in OA:

  • Anti-inflammatory via NF-κB, IRAK1/NLRP3, and p38 MAPK inhibition.

  • Promotes chondroprotection by reducing MMP activity, apoptosis, and cartilage degradation.

  • Enhances cartilage repair by promoting type II collagen and glycosaminoglycan synthesis.

  • Activates SIRT1/AMPK pathway to reduce ER stress.

• Clinical Potential:

  • Shown to prevent OA progression and support joint regeneration.

  • Recognized as a senolytic agent, targeting senescent cells in joint tissues.

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Zero Pain Reflect is our research roundup which aims to provide vet professionals with an easy-to-read digest on items of research in pain management which focus on one common subject area.

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This post was written by Matt Gurney.

Matt & Carl established Zero Pain Philosophy to provide educational resources & telemedicine to veterinary professionals globally, enabling optimal management of pain.

Matt sees referrals in the pain clinic at Eastcott Referrals. You can also receive telemedicine advice from us here if you have a pain case where you need a helping hand.

Matt Gurney is an RCVS & European Specialist in Veterinary Anaesthesia & Analgesia and works at Anderson Moores Veterinary Specialists. Matt is Past President of the European College of Veterinary Anaesthesia & Analgesia and works at Eastcott Referrals in the UK.

Carl Bradbrook is an RCVS & European Specialist in Veterinary Anaesthesia & Analgesia and is Past President of the Association of Veterinary Anaesthetists. Carl works at Anderson Moores Veterinary Specialists in the UK.

The intended audience for this pain update is veterinary professionals. This pain update is based on clinical experience and independent opinion.