bims-vitmet Biomed News
on Vitamin metabolism
Issue of 2025–08–17
eight papers selected by
Onurkan Karabulut, Berkeley City College



  1. Biol Trace Elem Res. 2025 Aug 14.
      Alzheimer's disease (AD) is a growing global public health concern, particularly affecting the elderly population. It is clinically characterized by progressive memory loss, cognitive decline, and impaired daily functioning. Given the multifactorial etiology of AD, increasing attention has been directed toward modifiable risk factors, including deficiencies in essential micronutrients such as selenium and vitamin D. This narrative review aims to examine the current evidence on the potential roles of selenium and vitamin D in the onset and progression of AD, with an emphasis on the underlying biochemical and neuroprotective mechanisms. A comprehensive literature search was conducted across databases including PubMed, MEDLINE, Cochrane Library, Web of Science, ScienceDirect, BMJ, EMBASE, and Google Scholar using combinations of relevant keywords related to Alzheimer's disease, selenium, vitamin D, neuroprotection, oxidative stress, and micronutrient deficiency. Selenium and vitamin D have been implicated in mitigating several pathological features of AD, such as amyloid-beta plaque accumulation, tau hyperphosphorylation, oxidative stress, and neuroinflammation. Observational studies indicate that low levels of selenium (below 70-90 μg/L) and vitamin D (below 20 ng/mL) are associated with an increased risk of cognitive decline and dementia. However, most findings stem from preclinical or observational studies, and the evidence remains inconclusive due to variations in study design, dosage, sample size, and duration of supplementation. While emerging evidence suggests a neuroprotective role for selenium and vitamin D in AD pathology, current findings are limited by methodological heterogeneity and a lack of high-quality randomized clinical trials. Further mechanistic and interventional studies are warranted to clarify the causal relationship and therapeutic potential of these micronutrients in Alzheimer's disease management.
    Keywords:  Alzheimer’s Disease; Amyloid beta peptide; Micronutrient deficiency; Neuroprotection; Oxidative stress; Selenium; Vitamin D
    DOI:  https://doi.org/10.1007/s12011-025-04788-7
  2. Biol Open. 2025 Aug 11. pii: bio.062017. [Epub ahead of print]
      Vitamin B12 is an essential micronutrient produced only by prokaryotes, and animals must acquire it from their diet. Vitamin B12 is critical for the synthesis of methionine and propionyl-CoA metabolism. In humans, vitamin B12 deficiency has been linked to many disorders, including infertility and developmental abnormalities. The growing trend towards plant-based diets and the ageing populations increases the risk of vitamin B12 deficiency, and therefore, there is an increasing interest in understanding vitamin B12 biology. Accurate approaches for detecting and quantifying vitamin B12 are essential in studying its complex biology, from its biogenesis in Bacteria and Archaea to its effects in complex organisms. Here, we present an approach using the commonly available E. coli methionine auxotroph strain B834 (DE3) and a multi-well spectrophotometer to detect and estimate the levels of vitamin B12 from biological samples at picomolar concentrations. We further show that our method is sufficient to reveal important differences in the production of vitamin B12 from vitamin B12-synthesising bacteria commonly found in the microbiome of wild Caenorhabditis elegans isolates. Our results establish a high-throughput and simple assay platform for detecting and estimating vitamin B12 levels using the E. coli B834 (DE3) strain.
    Keywords:  C. elegans; Caenorhabditis elegans; CemBio; Cobalamin; E. coli; MetE; Vitamin B12
    DOI:  https://doi.org/10.1242/bio.062017
  3. Int J Mol Sci. 2025 Jul 24. pii: 7146. [Epub ahead of print]26(15):
      Cognitive function is critical for overall health, with vitamin D's impact under extensive investigation. This review explores the association between vitamin D and cognitive health, its neuroprotective mechanisms, and the therapeutic potential of supplementation in cognitive decline. Observational studies link low vitamin D levels to increased cognitive deterioration risk, particularly in Alzheimer's disease, vascular dementia, Parkinson's disease, and schizophrenia. Clinical trial results on vitamin D supplementation's cognitive benefits are inconclusive. Vitamin D's neuroprotective effects are complex, influencing cognitive abilities by interacting with neuronal and glial cells, modulating immune responses, and regulating key molecular pathways. Challenges remain in clinical applications, including determining optimal vitamin D levels, effective supplementation forms and doses, and identifying responsive populations. The review advocates for robust clinical trials to address these gaps, facilitating informed use of vitamin D in cognitive health. Future research should focus on the optimal timing, duration, and target groups for supplementation to enhance cognitive outcomes and reduce risks.
    Keywords:  VD; cognition; inflammation; neurodegenerative disease; neuroprotection; vitamin D analogs
    DOI:  https://doi.org/10.3390/ijms26157146
  4. Behav Neurol. 2025 ;2025 7888243
      As one of the seven primary nutrients in the human body, vitamins are vital to maintaining good health. In recent years, there has been a completely new understanding of vitamins, and researchers have conducted more thorough investigations on them. These compounds, once viewed simply as supplemental nutrients, are now believed to play a more complex and critical role in human health. On the other hand, ingesting too much vitamins may cause negative health effects. Multiple studies have demonstrated a strong correlation between neurological problems and excessive vitamin intake. The purpose of this paper is to review the toxic effects of excessive vitamin intake on the nervous system, focusing on vitamin A and some of the B vitamins. It also analyzes the relationship between excessive vitamin intake and neurological dysfunction by reviewing the research findings in recent years, mainly including their possible mechanisms of action, clinical manifestations, and preventive measures, to provide ideas and inspiration for the subsequent clinical research.
    Keywords:  folic acid; nervous system; pyridoxine; retinoic acid; toxicity; vitamins
    DOI:  https://doi.org/10.1155/bn/7888243
  5. Nutrients. 2025 Aug 05. pii: 2559. [Epub ahead of print]17(15):
      Background/objectives: Chronic kidney disease (CKD) affects up to 15% of the global population and is driven by vascular and interstitial damage, and is most prevalent in persons with hypertension and diabetes. Vitamin K, a necessary cofactor for activation of vitamin K-dependent proteins may modulate these processes. It is well established that vitamin K deficiency is associated with CKD, but the therapeutic effects of supplementation on kidney function are still uncertain. We aimed to review the current evidence on the effect of vitamin K deficiency and supplementation on any marker of renal function and kidney disease, across general adult populations and CKD patient populations. Methods: A search was conducted in PubMed, targeting terms related to vitamin K status and CKD. Studies were included if they reported data on vitamin K status or supplementation in relation to kidney function outcomes. Results: A total of 16 studies were included. Nine interventional studies were included and confirmed that vitamin K supplementation improves biomarkers of vitamin K status but showed no consistent beneficial effects on renal function. Seven observational studies across populations found significant associations between vitamin K status and decline in kidney function; however, associations were often attenuated after adjustments. Conclusions: No clear effect of supplementation was observed on the reported kidney markers in patient populations. A clear association between low vitamin K status and impaired kidney function was confirmed. Studying heterogeneity makes the comparability and generalizability of the results difficult. Our review highlights the need for more cohort studies and clinical trials in general or patient populations.
    Keywords:  chronic kidney disease; supplementation; vitamin K
    DOI:  https://doi.org/10.3390/nu17152559
  6. Nutr Res. 2025 Jul 14. pii: S0271-5317(25)00092-2. [Epub ahead of print]141 1-9
      Metabolic syndrome (MetS) comprises a constellation of dysregulated cardiometabolic parameters. This study assessed associations between MetS and vitamin C in the US National Health and Nutrition Examination Survey (NHANES) to determine vitamin C requirements in people with a range of MetS severity, the hypothesis being that people with higher MetS severity would have higher requirements for the vitamin. Data for non-supplementing, fasting adults (n = 4,832) was extracted from NHANES 2003-6 and 2017-18 and included demographic and lifestyle variables, cardiometabolic laboratory variables, vitamin C dietary intakes and serum concentrations. MetS severity score was calculated using sex, waist circumference, systolic blood pressure, HDL cholesterol, triglycerides and fasting glucose concentrations. The mean (range) MetS severity score for the group was 0.19 (-4.0 to 6.8). There was a negative association between MetS severity score and serum vitamin C (r=-0.203, p < 0.001). Participants who met the vitamin C adequacy threshold of ≥50 µmol/L had a mean MetS severity score of 0.00 vs 0.38 in those who did not meet the threshold (p < 0.001). When the group was stratified by MetS severity score tertiles, the participants with the highest scores required an intake >100 mg/d, equating to an additional 65 mg/d (or 2.7-fold higher intake requirement) to meet the adequacy threshold relative to those with the lowest scores. Comparable relationships were observed between the individual MetS severity score components and vitamin C status and requirements. Overall, the results indicate that increased metabolic dysregulation results in decreased vitamin C status and a higher intake requirement for the vitamin to meet adequate circulating concentrations.
    Keywords:  Ascorbic acid; Metabolic syndrome; NHANES; Vitamin C; Vitamin C intake
    DOI:  https://doi.org/10.1016/j.nutres.2025.07.003
  7. Nurs Res Pract. 2025 ;2025 2137328
      Infertility significantly impacts individuals and society, necessitating effective strategies for its management. Among the various factors influencing female fertility, micronutrients play a crucial role in reproductive health by supporting oocyte quality, hormonal balance, and implantation processes. This narrative review examines the importance of optimal preconception micronutrient intake in enhancing female fertility. By analyzing research from various scientific databases, including PubMed, Google Scholar, and ScienceDirect, spanning from 2000 to April 2024, we highlight the impact of key micronutrients such as folate, vitamin D, iron, selenium, and antioxidants on fertility outcomes. Deficiencies in these nutrients have been associated with impaired ovarian function, disrupted menstrual cycles, and increased risk of pregnancy complications. Given the prevalence of micronutrient inadequacies among women of reproductive age, this review underscores the need for evidence-based nutritional interventions and standardized supplementation guidelines. The findings aim to bridge the gap between research and clinical practice, providing healthcare professionals with insights to optimize fertility care through targeted nutritional strategies.
    DOI:  https://doi.org/10.1155/nrp/2137328
  8. bioRxiv. 2025 Aug 06. pii: 2025.08.05.668752. [Epub ahead of print]
      Ferroptosis, a regulated form of cell death driven by excessive lipid peroxidation, has emerged as a promising therapeutic target in cancer. Ferroptosis suppressor protein 1 (FSP1) is a critical regulator of ferroptosis resistance, yet the mechanisms controlling its expression and stability remain mostly unexplored. To uncover regulators of FSP1 abundance, we conducted CRISPR-Cas9 screens utilizing a genome-edited, dual-fluorescent FSP1 reporter cell line, identifying both transcriptional and post-translational mechanisms that determine FSP1 levels. Notably, we identified riboflavin kinase (RFK) and FAD synthase (FLAD1), enzymes which are essential for synthesizing flavin adenine dinucleotide (FAD) from vitamin B2, as key contributors to FSP1 stability. Biochemical and cellular analyses revealed that FAD binding is critical for FSP1 activity. FAD deficiency, and mutations blocking FSP1-FAD binding, triggered FSP1 degradation via a ubiquitin-proteasome pathway that involves the E3 ligase RNF8. Unlike other vitamins that inhibit ferroptosis by scavenging radicals, vitamin B2 supports ferroptosis resistance through FAD cofactor binding, ensuring proper FSP1 stability and function. This study provides a rich resource detailing mechanisms that regulate FSP1 abundance and highlights a novel connection between vitamin B2 metabolism and ferroptosis resistance with implications for therapeutic strategies targeting FSP1 in cancer.
    DOI:  https://doi.org/10.1101/2025.08.05.668752