ABSTRACT
Type 2 diabetes mellitus (T2DM) is a complex metabolic disorder with a multifactorial etiology and a significant global burden. In recent years, emerging evidence has suggested a potential link between T2DM and vitamin B12 deficiency, raising concerns about its impact on disease progression, management, and associated complications. This comprehensive review critically examines the current understanding of the prevalence, risk factors, clinical implications, and management strategies related to vitamin B12 deficiency in individuals diagnosed with T2DM. The review begins by providing an overview of the epidemiology of T2DM and its associated complications, underscoring the need for comprehensive management approaches. Subsequently, it delves into the physiology of vitamin B12, including its sources, absorption mechanisms, and biological functions, laying the groundwork for understanding the potential implications of deficiency in T2DM. A thorough analysis of the literature is conducted to elucidate the prevalence and risk factors of vitamin B12 deficiency in individuals with T2DM, considering factors such as age, duration of diabetes, medication use (e.g., metformin), dietary patterns, and comorbidities. Special attention is given to the role of metformin, the first-line therapy for T2DM, in precipitating or exacerbating vitamin B12 deficiency through mechanisms involving alterations in the gut microbiota and intestinal absorption. The review further explores the clinical manifestations and diagnostic challenges associated with vitamin B12 deficiency in the context of T2DM, emphasizing the importance of recognizing subtle symptoms and implementing appropriate screening protocols. It discusses the potential implications of vitamin B12 deficiency on glycemic control, diabetic neuropathy, cognitive function, cardiovascular health, and overall quality of life in individuals with T2DM. In addressing the management of vitamin B12 deficiency in T2DM, the review examines various therapeutic strategies, including oral and parenteral supplementation, dietary modifications, and lifestyle interventions. It critically evaluates the evidence supporting routine screening for vitamin B12 deficiency in individuals with T2DM and discusses controversies surrounding optimal supplementation protocols, dosing regimens, and monitoring strategies. Furthermore, the review highlights gaps in current knowledge and identifies areas for future research, such as the long-term effects of vitamin B12 supplementation on clinical outcomes in T2DM, the impact of genetic factors on vitamin B12 metabolism, and the potential role of personalized interventions. Overall, this review consolidates existing evidence and provides insights into the complex relationship between T2DM and vitamin B12 deficiency, aiming to inform clinical practice, enhance patient care, and guide future research endeavors in this important area of metabolic medicine.
ABSTRACT
Sudden infant death is a complex event characterized by biochemical features that are difficult to understand in general settings. Herein, we present a case report of a three-month-old infant who succumbed to sudden infant death syndrome (SIDS), focusing on the biochemical abnormalities identified through post-mortem analysis. The infant, previously healthy and meeting developmental milestones, was found lifeless in the crib during sleep. An autopsy revealed no anatomical abnormalities or signs of external trauma, consistent with SIDS diagnosis. Biochemical analysis of SIDS continued after post-mortem samples revealed dysregulation in neurotransmitter pathways, particularly serotonin, within the brain stem. These findings suggest a potential disruption in serotonin signaling, which may contribute to the vulnerability of infants to sudden death during sleep. Furthermore, metabolic profiling revealed deficiencies in enzymes involved in mitochondrial energy metabolism, particularly those related to fatty acid oxidation. These metabolic disturbances may compromise cellular function and contribute to the pathogenesis of SIDS. Environmental factors were also explored, with analysis revealing elevated levels of nicotine metabolites in post-mortem samples, suggesting maternal smoking exposure during pregnancy. Nicotine and its derivatives have known effects on neurotransmitter systems, potentially exacerbating underlying biochemical vulnerabilities in susceptible infants. This case report underscores the complex interplay of biochemical factors in the pathogenesis of SIDS and highlights the importance of multidisciplinary approaches in unraveling its mysteries. Further research is warranted to elucidate the precise mechanisms underlying these biochemical abnormalities and to develop targeted interventions aimed at reducing the incidence of SIDS and safeguarding infant health.
