This study aimed to investigate the therapeutic effects of camel milk (CM) on chronic fatigue syndrome (CFS) and elucidate the mechanisms underlying the microbiota–gut–brain axis. Using a murine model of CFS induced by chronic restraint and forced swimming stress, we administered lyophilized CM (1500 mg/kg/day, equivalent to approximately 121.5 mg/kg/day in humans based on body surface area conversion using the standard allometric scaling formula) orally. CM supplementation was significantly associated with ameliorated fatigue-like behaviors, as evidenced by prolonged swimming endurance and reduced immobility time. Metagenomic analysis revealed that CM was associated with reshaping of the small intestinal microbiota, including enrichment of beneficial Lactococcus lactis and suppression of pathobionts (H. hepaticus and H. typhlonius). These microbial shifts correlated with increased luminal lactic acid, improved intestinal barrier integrity (increased villus height, reduced crypt depth), and attenuated local inflammation (reduced TNF-α and IL-6, elevated IL-10). Consequently, CM was associated with reduced bacterial translocation and systemic inflammation, and normalization of hypothalamic–pituitary–adrenal (HPA) axis hyperactivity. We conclude that CM is associated with prevention of CFS-like symptoms through modulation of the gut ecosystem and strengthening of the intestinal barrier, potentially breaking the vicious cycle of gut inflammation and HPA axis dysfunction, although causality remains to be established through fecal microbiota transplantation or similar mechanistic studies.

Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a complex and debilitating disorder with limited treatment options. Camel milk (CM), known for its rich nutrients and anti-fatigue properties, may offer multi-target benefits for managing this condition. This study utilized an integrated approach combining metabolomics, network pharmacology, and animal experiments. CM metabolites were profiled and screened via ADME. Potential targets were predicted and intersected with CFS/ME-associated genes. Male BALB/c mice were subjected to chronic restraint and forced swimming to evaluate the effects of CM (1000 mg/kg) on behavioral, inflammatory, neuroendocrine, and metabolic parameters. CM administration significantly improved exhaustive swimming time and reduced immobility. It attenuated systemic inflammation (restored IL-10), normalized brain CREB and DRD2/OPRM1 mRNA, and enhanced skeletal muscle AKT/GLUT4 expression and glycogen levels. Camel milk alleviates CFS/ME symptoms through the multi-component, multi-target regulation of neuroendocrine, inflammatory, and energy metabolism pathways. These preclinical findings suggest that CM may have potential as a supportive nutritional intervention for alleviating chronic fatigue, pending validation in human studies.

Osteoporosis affects over 200 million people worldwide, with postmenopausal women at the highest risk. The treatment benefits of currently available drugs are constrained by safety concerns, and they lack bidirectional regulation of bone metabolism, driving growing interest in safe dietary interventions. Milk is rich in functional components, including minerals (calcium, phosphorus), casein phosphopeptide (CPP), lactoferrin (LF), osteopontin (OPN), and milk fat globule membrane (MFGM), that promote mineral absorption, regulate bone cell activity, and support intestinal health. This review examines their dual mechanisms in bone health regulation. Directly, LF activates Wnt/MAPK pathways to enhance osteogenesis and inhibit osteoclast activity, OPN modulates mineralization, and CPP synergizes with calcium and phosphorus to support bone formation. Indirectly, these components modulate gut microbiota via the gut–bone axis, raising short-chain fatty acids, lowering intestinal pH to boost calcium absorption, repairing the intestinal barrier, and reducing systemic inflammation. Remaining challenges lie in extraction, purification, and product development. Looking forward, the field must move from cell and animal-level evidence to human clinical validation and establish robust steady-state delivery of these bioactives. Successful translation along these lines is essential to turn milk-derived components into effective, evidence-based functional foods for bone health.