Abstract

In recent decades, the increased incidence of cardiovascular disease (CVD) mortality among young adults has raised concerns. Although clinical manifestations of CVD typically occur later in life, the underlying pathological processes emerge early on. Numerous studies have demonstrated that elevated homocysteine levels serve as an independent risk factor for endothelial dysfunction and arterial stiffness, which are key contributors to CVD. Notably, vitamin B deficiency, particularly deficiencies in Vitamins B9 and B12, emerges as a significant factor in childhood hyperhomocysteinemia, initiating the development of subclinical atherosclerosis in early life. In this narrative review, we summarize the association between vitamin B deficiency-induced hyperhomocysteinemia and subclinical atherosclerosis in adolescents. We conducted a comprehensive review of relevant literature from prominent bibliographic databases, including PubMed/MEDLINE, PMC Central, Google Scholar, and Cochrane database. Four cross-sectional studies were included and reviewed as part of our analysis. The reviewed studies, focusing on homocysteine levels as an exposure variable and markers of atherosclerosis as outcome measures, demonstrate a strong correlation between homocysteine levels and markers of atherosclerosis, including increased carotid intima-media thickness (CIMT) and endothelial dysfunction. Particularly, adolescents with vitamin B12 deficiency exhibit a significant positive correlation between homocysteine levels and CIMT. These findings underscore the potential of hyperhomocysteinemia as an early marker for detecting subclinical atherosclerosis in adolescents with vitamin B deficiency. Despite limited research in this area, recognizing the importance of early detection and management of subclinical atherosclerosis in adolescents can help mitigate the risk of severe cardiovascular and cerebrovascular events in young adulthood.

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