Introduction. Vitamin D regulates approximately 3% of the human genome, which helps explain its roles in the musculoskeletal, cardiovascular, and immune systems, as well as in the development of malignant diseases and diabetes. Its deficiency may cause rickets in children and osteomalacia and osteoporosis in adults. Every 3 seconds, an osteoporotic fracture occurs, affecting 1 in 3 women and 1 in 5 men over the age of 50 years. The study aimed to evaluate serum vitamin D concentrations in postmenopausal women with osteopenia and osteoporosis and to assess the association between vitamin D status and bone mineral density. Material and Methods. This retrospective study included medical records of 100 postmenopausal women diagnosed with osteopenia or osteoporosis by dual-energy X-ray absorptiometry. Participants were divided into three groups by serum 25-hydroxyvitamin D concentrations (< 50 nmol/L; 50-75 nmol/L; ≥ 75 nmol/L) and four age groups (≤ 49; 50-59; 60-69; ≥ 70 years). Results. The mean age of the participants was 67.14 years. The mean 25-hydroxyvitamin D concentration was 50.28 nmol/L in women with osteoporosis and 54.98 nmol/L in women with osteopenia. A statistically significant positive correlation was observed between 25-hydroxyvitamin D concentration and hip bone mineral density. Conclusion. Serum vitamin D concentrations in postmenopausal women with osteopenia and osteoporosis were below the desirable range. A positive and statistically significant correlation was found between serum vitamin D concentration and hip bone mineral density. Older age was associated with a higher prevalence of fractures among women with osteopenia and osteoporosis.

Obesity is characterized by chronic low-grade inflammation (meta-inflammation) and metabolic dysregulation. Adipose tissue acts as an immunometabolic organ, with macrophages playing a central role. This review examines inflammatory memory in adipose tissue, focusing on CD68+ macrophages and their role in cardiometabolic and cancer risk during weight cycling. (2) Narrative synthesis of evidence from immunology, obesitology, and oncology, with emphasis on macrophage polarization and signaling pathways. (3) Weight cycling induces persistent immune memory in adipose tissue, characterized by exaggerated macrophage responses upon weight regain. CD68+ macrophages contribute to extracellular matrix remodeling, tumor signaling, and metabolic dysfunction. Key mechanisms include PI3K/AKT/mTOR dysregulation, FOXO1/KLF10 axis impairment, and CREB-mediated transcription. This inflammatory memory promotes atherosclerosis progression, insulin resistance, and increased cancer risk, despite prior weight loss. (4) Macrophage-driven inflammatory memory represents a key mechanistic link between obesity, cardiometabolic disease, and cancer. Targeting meta-inflammation independent of body weight should be integral to future therapies.