Overview
SCIENTIFIC SCORE
Possibly Effective
Based on 16 Researches
7.4
USERS' SCORE
Good
Based on 2 Reviews
8.5
Supplement Facts
Serving Size: 1 Lozenge
Amount Per Serving
%DV
Folate
167 mcg DFE(100 mcg folic acid)
42%
Vitamin B-12 (as Cyanocobalamin)
1 mg (1,000 mcg)
41,667%
Top Medical Research Studies
9
Folate treatment aids liver fat reduction
We investigated the effects of folic acid treatment on nonalcoholic fatty liver disease (NAFLD), a condition where excess fat builds up in the liver, often linked to obesity and insulin resistance. Our research revealed that giving folic acid to mice on a high-fat diet helped improve their glucose tolerance and insulin sensitivity, alongside reducing unhealthy fat levels in their liver cells.
By diving into the mechanisms, we discovered that folic acid works by changing the DNA methylation patterns that regulate the expression of a protein called ALKBH5. This reduction in ALKBH5 levels led to an increase in a specific type of RNA modification and subsequently boosted the production of a protein called ATG12, which is vital for autophagy – the process that cleans up and recycles cellular components.
When we inhibited ATG12 through overexpression of ALKBH5, autophagy was impeded, showcasing how crucial ATG12 is for allowing folic acid to effectively reduce fat accumulation in the liver. Overall, these findings indicate that folic acid could be a promising nutritional ally in fighting NAFLD, revealing a clear mechanism by which it protects liver health.
By diving into the mechanisms, we discovered that folic acid works by changing the DNA methylation patterns that regulate the expression of a protein called ALKBH5. This reduction in ALKBH5 levels led to an increase in a specific type of RNA modification and subsequently boosted the production of a protein called ATG12, which is vital for autophagy – the process that cleans up and recycles cellular components.
When we inhibited ATG12 through overexpression of ALKBH5, autophagy was impeded, showcasing how crucial ATG12 is for allowing folic acid to effectively reduce fat accumulation in the liver. Overall, these findings indicate that folic acid could be a promising nutritional ally in fighting NAFLD, revealing a clear mechanism by which it protects liver health.
Read More
9
We explored how methylcobalamin, a form of vitamin B12, impacts liver disease, particularly in the context of cholestatic liver failure. The study utilized high-throughput screening to identify methylcobalamin as a specific inhibitor of gasdermin E (GSDME), a protein that plays a key role in pyroptotic cell death—a form of inflammatory cell death contributing to liver damage.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Read More
9
Methylcobalamin improves nerve myelination
We delved into the effects of methylcobalamin, a form of vitamin B12, on nerve myelination in rats suffering from moderate hepatic encephalopathy, a condition caused by ammonia toxicity due to liver dysfunction. In our study, we established a model of hepatic encephalopathy by administering thioacetamide to induce liver damage, subsequently leading to changes in nerve myelination in specific brain regions.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
Read More
Most Useful Reviews
9
Supports liver health
Cyanocobalamin (vitamin B12) is vital for preventing fatty infiltration of the liver and has significant lipotropic effects. It enhances phagocytic activity, boosts immunity, and regulates hematopoietic functions. By reducing homocysteine levels, it helps lower the risk of heart disease. A deficiency can double the likelihood of liver disease in individuals with AIDS. This essential nutrient supports reproductive health and increases sperm count. It's a remarkable supplement for maintaining overall health.
Read More
7.5
Improves B12 deficiency
I bought these for my dad, who has diabetes and B12 deficiency. He believes it is good quality and contains the necessary ingredients for his health. This supplement aids in alleviating his symptoms associated with liver disease.
Read More
Medical Researches
SCIENTIFIC SCORE
Possibly Effective
Based on 16 Researches
7.4
- All Researches
9
Folate treatment aids liver fat reduction
We investigated the effects of folic acid treatment on nonalcoholic fatty liver disease (NAFLD), a condition where excess fat builds up in the liver, often linked to obesity and insulin resistance. Our research revealed that giving folic acid to mice on a high-fat diet helped improve their glucose tolerance and insulin sensitivity, alongside reducing unhealthy fat levels in their liver cells.
By diving into the mechanisms, we discovered that folic acid works by changing the DNA methylation patterns that regulate the expression of a protein called ALKBH5. This reduction in ALKBH5 levels led to an increase in a specific type of RNA modification and subsequently boosted the production of a protein called ATG12, which is vital for autophagy – the process that cleans up and recycles cellular components.
When we inhibited ATG12 through overexpression of ALKBH5, autophagy was impeded, showcasing how crucial ATG12 is for allowing folic acid to effectively reduce fat accumulation in the liver. Overall, these findings indicate that folic acid could be a promising nutritional ally in fighting NAFLD, revealing a clear mechanism by which it protects liver health.
By diving into the mechanisms, we discovered that folic acid works by changing the DNA methylation patterns that regulate the expression of a protein called ALKBH5. This reduction in ALKBH5 levels led to an increase in a specific type of RNA modification and subsequently boosted the production of a protein called ATG12, which is vital for autophagy – the process that cleans up and recycles cellular components.
When we inhibited ATG12 through overexpression of ALKBH5, autophagy was impeded, showcasing how crucial ATG12 is for allowing folic acid to effectively reduce fat accumulation in the liver. Overall, these findings indicate that folic acid could be a promising nutritional ally in fighting NAFLD, revealing a clear mechanism by which it protects liver health.
Read More
9
We explored how methylcobalamin, a form of vitamin B12, impacts liver disease, particularly in the context of cholestatic liver failure. The study utilized high-throughput screening to identify methylcobalamin as a specific inhibitor of gasdermin E (GSDME), a protein that plays a key role in pyroptotic cell death—a form of inflammatory cell death contributing to liver damage.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Our findings showed that when tested on mouse models with liver failure due to cholestasis, cisplatin, or concanavalin A, methylcobalamin effectively reduced liver damage. It significantly lowered liver transaminase levels, indicating less liver inflammation and cellular injury, and helped alleviate overall liver cell death.
Furthermore, methylcobalamin worked by preventing the cleavage of GSDME, which is essential for uncontrolled inflammatory cell death. By binding to a specific site on the GSDME protein, it blocked the interactions that trigger this damaging process. Overall, our study highlighted the potential of methylcobalamin as a promising therapeutic option for managing cholestatic liver failure and related conditions.
Read More
9
Methylcobalamin improves nerve myelination
We delved into the effects of methylcobalamin, a form of vitamin B12, on nerve myelination in rats suffering from moderate hepatic encephalopathy, a condition caused by ammonia toxicity due to liver dysfunction. In our study, we established a model of hepatic encephalopathy by administering thioacetamide to induce liver damage, subsequently leading to changes in nerve myelination in specific brain regions.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
We focused on the hippocampus, an area crucial for memory and learning, where we noted significant reductions in myelin levels and myelin basic protein (MBP) quantities in the affected rats. However, after administering methylcobalamin for a week, we observed a remarkable recovery in the myelination status, alongside normalized levels of harmful homocysteine, which is regulated by the enzyme methionine synthase that methylcobalamin helps activate.
Our findings suggest that methylcobalamin effectively restores nerve myelination in the context of liver disease by addressing underlying biochemical changes. The treatment not only improved myelination but also showed promise in restoring neurobehavioral functions in the rats. This research indicates a potential therapeutic role for vitamin B12 in managing liver-related nerve damage, making it worth further exploration in human studies.
Read More
9
We explored the intriguing question of whether vitamin B12 can provide a protective effect against liver damage caused by acetaminophen, a common painkiller known for its potential hepatotoxicity. In our study, we used male Wister rats and organized them into three groups: one receiving acetaminophen, another treated with vitamin B12, and a control group given distilled water. Each group was administered their respective treatments for a week before we evaluated their liver health.
Our findings indicate that vitamin B12 supplementation significantly improved hepatic health in the rats exposed to acetaminophen. We observed a notable reduction in liver enzyme levels, which is a key marker of liver damage. Additionally, vitamin B12 helped boost antioxidant levels in the body, compensated for a decline in tissue glutathione, and reduced harmful inflammatory markers such as TNF-α and interleukin-6.
Overall, the results of our study suggest that vitamin B12 effectively mitigates acetaminophen-induced liver toxicity by enhancing liver function and reducing inflammation. This insight opens up interesting avenues for considering vitamin B12 as a supportive treatment in managing liver health in cases of acetaminophen exposure.
Our findings indicate that vitamin B12 supplementation significantly improved hepatic health in the rats exposed to acetaminophen. We observed a notable reduction in liver enzyme levels, which is a key marker of liver damage. Additionally, vitamin B12 helped boost antioxidant levels in the body, compensated for a decline in tissue glutathione, and reduced harmful inflammatory markers such as TNF-α and interleukin-6.
Overall, the results of our study suggest that vitamin B12 effectively mitigates acetaminophen-induced liver toxicity by enhancing liver function and reducing inflammation. This insight opens up interesting avenues for considering vitamin B12 as a supportive treatment in managing liver health in cases of acetaminophen exposure.
Read More
8
We explored how genetic variations in folate metabolism might influence survival rates in patients with hepatocellular carcinoma (HCC), a common form of liver cancer. Our study involved a large group of 970 HCC patients who provided genetic information on six specific single nucleotide polymorphisms (SNPs). We further looked at the relationship between these genetic factors and serum folate levels to understand their combined impact on overall survival and liver cancer-specific outcomes.
Interestingly, we found that a particular SNP known as rs1801394 showed a significant connection with better survival rates. In various models, including additive, co-dominant, and dominant types, carrying the G allele of this SNP was linked to improved overall survival. We also noticed that the more protective alleles a person carried, the better their liver cancer-specific survival and overall survival became.
Moreover, we observed that having higher levels of serum folate interacted positively with this genetic variant, enhancing the prognosis for those carrying the G allele. This suggests a promising link between folate metabolism and liver cancer outcomes, highlighting the importance of genetic factors in how folate may affect survival in liver disease patients.
Interestingly, we found that a particular SNP known as rs1801394 showed a significant connection with better survival rates. In various models, including additive, co-dominant, and dominant types, carrying the G allele of this SNP was linked to improved overall survival. We also noticed that the more protective alleles a person carried, the better their liver cancer-specific survival and overall survival became.
Moreover, we observed that having higher levels of serum folate interacted positively with this genetic variant, enhancing the prognosis for those carrying the G allele. This suggests a promising link between folate metabolism and liver cancer outcomes, highlighting the importance of genetic factors in how folate may affect survival in liver disease patients.
Read More
User Reviews
USERS' SCORE
Good
Based on 2 Reviews
8.5
- All Reviews
- Positive Reviews
- Negative Reviews
9
Supports liver health
Cyanocobalamin (vitamin B12) is vital for preventing fatty infiltration of the liver and has significant lipotropic effects. It enhances phagocytic activity, boosts immunity, and regulates hematopoietic functions. By reducing homocysteine levels, it helps lower the risk of heart disease. A deficiency can double the likelihood of liver disease in individuals with AIDS. This essential nutrient supports reproductive health and increases sperm count. It's a remarkable supplement for maintaining overall health.
Read More
7.5
Improves B12 deficiency
I bought these for my dad, who has diabetes and B12 deficiency. He believes it is good quality and contains the necessary ingredients for his health. This supplement aids in alleviating his symptoms associated with liver disease.
Read More
Frequently Asked Questions
No FAQs are available for this product and symptom.
References
- Huang C, Luo Y, Liu Y, Liu J, Chen Y, et al. DNA hypermethylation-induced suppression of ALKBH5 is required for folic acid to alleviate hepatic lipid deposition by enhancing autophagy in an ATG12-dependent manner. J Nutr Biochem. 2025. 10.1016/j.jnutbio.2025.109870
- Christensen KE, Faquette ML, Leclerc D, Keser V, Luan Y, et al. Folic Acid and Methyltetrahydrofolate Supplementation in the Mouse Model with Hepatic Steatosis. Nutrients. 2024;17. 10.3390/nu17010082
- Zhu J, Liao X, Du L, Lv P, Deng J. Associations of serum folate and vitamin B levels with all-cause mortality among patients with metabolic dysfunction associated steatotic liver disease: a prospective cohort study. Front Endocrinol (Lausanne). 2024;15:1426103. 10.3389/fendo.2024.1426103
- India-Aldana S, Midya V, Betanzos-Robledo L, Yao M, Alcalá C, et al. Impact of metabolism-disrupting chemicals and folic acid supplementation on liver injury and steatosis in mother-child pairs. J Hepatol. 2024. 10.1016/j.jhep.2024.11.050
- Dong J, Li Z, Wang C, Zhang R, Li Y, et al. Dietary folate intake and all-cause mortality and cardiovascular mortality in American adults with non-alcoholic fatty liver disease: Data from NHANES 2003 to 2018. PLoS One. 2024;19:e0314148. 10.1371/journal.pone.0314148
- Li Y, Shu J, Tan P, Dong X, Zhang M, et al. Genetic variants in folate metabolism-related genes, serum folate and hepatocellular carcinoma survival: the Guangdong Liver Cancer Cohort study. Br J Nutr. 2024;132:1411. 10.1017/S0007114524001776
- Xu W, Wang Y, Cui S, Zheng Q, Lin Y, et al. Methylcobalamin protects against liver failure via engaging gasdermin E. Nat Commun. 2025;16:1233. 10.1038/s41467-024-54826-6
- Abu-Zahab ZA, Qureshi H, Adham GM, Elzefzafy WM, Zalam SS, et al. Frequency of comorbid diseases with high serum Vitamin B12 levels in patients attending King Salman Medical City (KSAMC), at Madinah. Int J Health Sci (Qassim). 2025;19:15.
- Espina S, Casas-Deza D, Bernal-Monterde V, Royo-Esteban A, GarcÃa-Sobreviela MP, et al. Unraveling the Association of Liver Steatosis and Fibrosis with Vitamin B12: A Cross-Sectional Study. Metabolites. 2024;14. 10.3390/metabo14110618
- Roy A, Trigun SK. The restoration of hippocampal nerve de-myelination by methylcobalamin relates with the enzymatic regulation of homocysteine level in a rat model of moderate grade hepatic encephalopathy. J Biochem Mol Toxicol. 2024;38:e23695. 10.1002/jbt.23695
- Pai SL, Torp KD, Insignares VC, DeMaria S, Giordano CR, et al. Use of hydroxocobalamin to treat intraoperative vasoplegic syndrome refractory to vasopressors and methylene blue during liver transplantation. Clin Transplant. 2024;38:e15271. 10.1111/ctr.15271
- Liu K, Chen Y, Chen J, Chen W, Sun X, et al. Genetically determined circulating micronutrients and the risk of nonalcoholic fatty liver disease. Sci Rep. 2024;14:1105. 10.1038/s41598-024-51609-3
- Boachie J, Zammit V, Saravanan P, Adaikalakoteswari A. Metformin Inefficiency to Lower Lipids in Vitamin B12 Deficient HepG2 Cells Is Alleviated via Adiponectin-AMPK Axis. Nutrients. 2023;15. 10.3390/nu15245046
- Oula JO, Mose JM, Waiganjo NN, Chepukosi KW, Mitalo NS, et al. Vitamin B12 blocked Trypanosoma brucei rhodesiense-driven disruption of the blood brain barrier, and normalized nitric oxide and malondialdehyde levels in a mouse model. Parasitol Int. 2023;96:102775. 10.1016/j.parint.2023.102775
- Ujianti I, Sianipar IR, Prijanti AR, Hasan I, Arozal W, et al. Effect of Roselle Flower Extract ( Linn.) on Reducing Steatosis and Steatohepatitis in Vitamin B12 Deficiency Rat Model. Medicina (Kaunas). 2023;59. 10.3390/medicina59061044
- Ahmed Mohammed R, Fadheel QJ. Hepatoprotective Effect of Vitamin B12 in Acetaminophen Induce Hepatotoxicity in Male Rats. Arch Razi Inst. 2023;78:419. 10.22092/ARI.2022.359353.2408
