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.

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.