Camel Milk and Gastric Ulcer Management: Anti-Ulcerogenic and Healing Actions

Gastric ulcers, characterized by erosions in the stomach lining, arise from an imbalance between aggressive factors (like acid secretion, Helicobacter pylori infection, NSAID use) and defensive mucosal protections. Conventional treatments like proton pump inhibitors and antibiotics face challenges including side effects and antibiotic resistance, driving interest in natural alternatives. Camel milk (Camelus dromedarius) emerges as a promising adjunctive therapy, offering a multi-faceted approach to ulcer management through antibacterial, anti-inflammatory, cytoprotective, and tissue-repair mechanisms.

The pathogenesis of gastric ulcers frequently involves Helicobacter pylori colonization. Camel milk exerts potent antibacterial effects against this pathogen, primarily attributed to its high concentration of bioactive proteins. Lactoferrin, present in significant quantities (95-250 mg/dl), sequesters iron, creating an environment hostile to H. pylori, which has high iron requirements for growth. Furthermore, camel lactoferrin demonstrates direct anti-inflammatory effects on gastric mucosa. Unlike bovine lactoferrin, camel lactoferrin retains stability across a wider pH range, enhancing its efficacy in the acidic gastric environment. Camel milk is also rich in immunoglobulins (IgG, IgA, IgM, and unique heavy-chain-only antibodies – VHH domains) and lysozyme. These components act synergistically; lysozyme enzymatically disrupts bacterial cell walls, while immunoglobulins, particularly the stable VHH domains with their long Complementary Determining Region 3 (CDR3) loops, effectively bind and neutralize pathogens, including H. pylori. This broad-spectrum antimicrobial activity extends beyond H. pylori, helping control secondary infections and reducing microbial-driven inflammation within ulcerated tissue.

Chronic inflammation is a hallmark of active peptic ulcer disease. Camel milk modulates the inflammatory cascade at multiple points. Its lactoferrin potently inhibits the nuclear factor kappa B (NF-κB) signalling pathway. NF-κB is a master regulator of pro-inflammatory cytokine production; its suppression leads to decreased synthesis and release of interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), and other mediators implicated in gastric mucosal damage. Studies in rats with indomethacin-induced ulcers demonstrate that camel milk consumption (15 ml/kg) significantly lowers serum levels of IL-6 and TNF-α compared to controls. Additionally, camel milk components help restore the balance of prostaglandins (PGs). NSAID-induced ulcers often result from the inhibition of cyclooxygenase-1 (COX-1), reducing the synthesis of cytoprotective PGE2 in the stomach. Camel milk has been shown to counteract this by increasing mucosal PGE2 levels, promoting mucus and bicarbonate secretion, and enhancing mucosal blood flow – crucial factors in mucosal defence and healing.

Beyond combating infection and inflammation, camel milk actively promotes the healing of existing ulcerations. This wound-healing property is linked to several factors. Firstly, camel milk is exceptionally rich in zinc and magnesium. Zinc is a cofactor for numerous enzymes involved in DNA synthesis, cell proliferation, and tissue repair, accelerating the regeneration of the gastric epithelium. Magnesium contributes to the biosynthesis of glutathione, a key intracellular antioxidant that protects regenerating cells from oxidative stress. Secondly, the high vitamin C content (3-5 times higher than cow milk) acts as a powerful antioxidant, scavenging free radicals generated during the inflammatory process that can delay healing and damage cells. Thirdly, growth factors and bioactive peptides present in camel milk may stimulate angiogenesis (formation of new blood vessels) and fibroblast activity, facilitating tissue remodelling at the ulcer site. Histopathological examinations of gastric tissue from ulcer-induced rats treated with camel milk consistently show significant reductions in ulcer size, decreased inflammatory cell infiltration, and improved regeneration of glandular epithelium compared to untreated controls.

Camel milk also functions as a gentle, natural antacid and mucosal protectant. Its unique buffering capacity stems partly from its higher mineral content (sodium, potassium, magnesium, calcium) compared to bovine milk. While not as potent as pharmaceutical antacids, this buffering action can help neutralize excessive gastric acid, providing symptomatic relief. More importantly, camel milk enhances the stomach’s intrinsic mucosal defence barrier. It stimulates the production and secretion of gastric mucus, forming a thicker, more resilient gel layer that acts as a physical barrier against acid and pepsin. This effect, termed “cytoprotection,” is a key mechanism identified in rat models where camel milk showed remarkable healing effects (100% healing in indomethacin-induced ulcers), often outperforming the standard drug cimetidine (60.5% healing). The smaller size of camel milk fat globules (approximately 2.99 μm) compared to cow milk may also contribute to better digestibility and the formation of a protective coating on the mucosal surface.

Evidence from preclinical studies robustly supports camel milk’s anti-ulcerogenic potential. Key research published in Pharmacognosy Magazine demonstrated that camel milk (5 ml/kg orally) exhibited remarkable efficacy across diverse ulcer models in rats. It achieved 100% inhibition of lesions in the HCl/EtOH model, outperforming cimetidine (83.7% inhibition). In the water-restraint stress model, inhibition was 50%, and in the indomethacin-induced model, it was 33.3%. Most strikingly, camel milk achieved 100% healing of established indomethacin-induced ulcers, compared to 60.5% healing with cimetidine. These findings underscore its potent healing action. Furthermore, acute toxicity studies established a high safety margin, with no signs of toxicity or mortality observed in rats even at doses of 10 ml/kg, supporting the safety of the therapeutic dose (5 ml/kg) used. Studies specifically investigating indomethacin-induced ulcers confirmed that camel milk dose-dependently (5-15 ml/kg) elevated gastric levels of crucial cytoprotective enzymes (like superoxide dismutase and glutathione peroxidase) while significantly reducing the lipid peroxidation marker malondialdehyde (MDA), indicating a strong antioxidant effect at the ulcer site.

In conclusion, camel milk presents a compelling natural approach for managing and healing gastric ulcers. Its therapeutic strength lies in its multi-mechanistic action: direct antibacterial activity against H. pylori via lactoferrin and immunoglobulins; suppression of detrimental inflammation through NF-κB inhibition and cytokine modulation; potent stimulation of tissue repair facilitated by zinc, magnesium, vitamin C, and growth factors; and enhancement of mucosal defence via cytoprotection and buffering. While human clinical trials are needed to solidify dosing protocols and confirm efficacy in patients, the existing preclinical evidence, combined with its historical use and high safety profile, positions camel milk as a valuable adjunctive therapy within a comprehensive gastric ulcer management strategy. Its ability to simultaneously target infection, inflammation, and tissue healing, while strengthening the stomach’s natural defences, offers a holistic alternative to conventional mono-mechanistic drugs.

Glossary

1. Cytoprotection: A process whereby chemical compounds protect cells, particularly the gastric mucosal lining, from damaging agents without necessarily reducing gastric acid secretion. It involves enhancing intrinsic defence mechanisms like mucus and bicarbonate production 18.
2. Lactoferrin: An iron-binding glycoprotein found abundantly in camel milk. It exerts antibacterial effects (primarily against H. pylori via iron chelation), anti-inflammatory effects (e.g., inhibition of NF-κB), immunomodulatory properties, and promotes cell growth.
3. NF-κB (Nuclear Factor Kappa B): A pivotal transcription factor regulating the expression of genes involved in inflammation and immune responses. Its inhibition by camel milk lactoferrin reduces the production of pro-inflammatory cytokines like TNF-α and IL-6.
4. Prostaglandin E2 (PGE2): A key cytoprotective eicosanoid synthesized in the gastric mucosa. It stimulates mucus and bicarbonate secretion, maintains mucosal blood flow, and inhibits acid secretion. Its depletion by NSAIDs contributes to ulcer formation; camel milk helps restore protective levels.
5. VHH Domains (Nanobodies): Unique single-domain antibodies (heavy-chain-only) naturally occurring in camelids. They are highly stable and possess long antigen-binding loops (CDR3), enabling effective binding and neutralization of pathogens like H. pylori within the harsh gastric environment.
6. Cyclooxygenase (COX): An enzyme responsible for prostaglandin synthesis. COX-1 is constitutively expressed and produces protective prostaglandins in the stomach. NSAIDs inhibit COX-1, leading to reduced PGE2 and increased ulcer risk 13.
7. Cytokines (TNF-α, IL-6): Signalling proteins (e.g., Tumour Necrosis Factor-alpha, Interleukin-6) released by immune cells that mediate and amplify inflammation. Elevated levels are associated with gastric mucosal damage; camel milk consumption reduces their concentration.
8. Malondialdehyde (MDA): A marker of lipid peroxidation resulting from oxidative stress. Elevated MDA levels indicate tissue damage; camel milk reduces gastric MDA levels, demonstrating its antioxidant effect.
9. Cimetidine: A histamine H2-receptor antagonist drug used as a standard anti-ulcer treatment in comparative studies with camel milk.
10. Indomethacin: A potent non-steroidal anti-inflammatory drug (NSAID) frequently used in research to induce gastric ulcers in animal models by inhibiting cyclooxygenase and reducing protective prostaglandins.

References

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2. Rasheed, N., Alghasham, A., & Rasheed, Z. (2016). Lactoferrin from Camelus dromedarius inhibits nuclear transcription factor-kappa B activation, cyclooxygenase-2 expression and prostaglandin E2 production in stimulated human chondrocytes. Pharmacognosy Research, 8(2), 135–141. https://doi.org/10.4103/0974-8490.175612 
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