Metabolic syndrome (MetS) is defined by a combination of metabolic abnormalities, such as central obesity, insulin resistance, hypertension, and dyslipidemia, and significantly increases the risk of cardiovascular diseases and type 2 diabetes. The high prevalence of MetS is a public health concern, necessitating rapid identification and intervention strategies to prevent this emerging epidemic. Diagnosing MetS requires the presence of three or more of these abnormalities, underscoring the need for effective management approaches. Despite a growing body of literature, limited reviews have critically evaluated the complex interplay between metabolic dysfunction, inflammation, and coagulation, particularly in the context of dietary interventions. Therefore, this article reviews the relationship between metabolic syndrome, inflammation, and thrombotic diseases, with an emphasis on their impacts on hematological health. Furthermore, this review explores the potential role of vegetarian and vegan dietary patterns in controlling these processes and improving hematological outcomes. This narrative review aims to critically evaluate current research on the inflammatory and thrombotic implications of MetS and assess the potential modulating role of vegan and plant-based diets within this context.

Leukemia represents a heterogeneous group of hematologic malignancies characterized by the dysregulated proliferation, differentiation, and survival of hematopoietic cells. Vitamin D (VD), a fat-soluble secosteroid hormone, is increasingly recognized not only as a regulator of calcium–phosphate metabolism but also as an important immune–metabolic modulator involved in hematopoietic homeostasis, inflammatory signaling, and cellular fate determination. Growing evidence suggests that VD deficiency may influence leukemogenesis, disease progression, treatment responsiveness, and supportive-care outcomes in patients with leukemia. Mechanistic studies indicate that the active metabolite, 1,25-dihydroxyvitamin D₃ (calcitriol), modulates leukemic cell biology by activating the vitamin D receptor (VDR) and regulating genomic and non-genomic signaling pathways, including MAPK, PI3K/AKT/mTOR, JAK/STAT, NF-κB, and β-catenin. Through these pathways, VD may affect transcriptional programs governing proliferation, differentiation, apoptosis, autophagy, immune regulation, and treatment resistance. Clinical and observational studies suggest that low 25-hydroxyvitamin D levels may be associated with adverse outcomes in selected leukemia subtypes, including poorer treatment responses, shorter overall survival and relapse-free survival, and shorter time to treatment. However, the available data remain heterogeneous, and causality has not been established. This review provides an integrated translational synthesis of VD deficiency in leukemia, linking molecular mechanisms with subtype-specific clinical evidence and supportive-care implications. Although VD supplementation should not be considered an independent anti-leukemic therapy, individualized assessment and correction of deficiency may represent a rational, low-toxicity component of supportive care. Further prospective and interventional studies are needed to define optimal supplementation strategies, identify responsive patient subgroups, and clarify the clinical relevance of VD status in leukemia.