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SCIENTIFIC SCORE
Possibly Effective
Based on 16 Researches
7.4
USERS' SCORE
Good
Based on 4 Reviews
8.6
Supplement Facts
Serving Size: 1 Vegetarian Capsule
Amount Per Serving
%DV
Folate (as L-5-Methyltetrahydrofolate calcium salt)
680 mcg°
170%
Vitamin B12 (as methylcobalamin)
300 mcg
12,500%
Top Medical Research Studies
9
Folate treatment aids liver fat reduction
DNA hypermethylation-induced suppression of ALKBH5 is required for folic acid to alleviate hepatic lipid deposition by enhancing autophagy in an ATG12-dependent manner.
Direct focus on NAFLD treatment
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
Methylcobalamin aids liver health
Methylcobalamin protects against liver failure via engaging gasdermin E.
Significant findings on liver disease
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
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.
Study shows significant benefit
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
9.5
Dizziness relief
With Ménière's disease, I sometimes experience dizziness. After my doctor prescribed folic acid and B12, I found this product at IHER. I've repurchased several bottles as it seems to alleviate my dizziness. If my symptoms persist, I will continue buying it.
Read More
8.8
Liver support success
I took this supplement to support my liver, which needs B12 intake twice a week. Initially, I consumed 10 capsules daily for 10 days, then reduced it to twice weekly. My liver is grateful, as confirmed by ultrasound and blood tests for ALAT and ASAT. All is well with my health!
Read More
8.8
Gut health improvement
Suffering from rheumatoid arthritis, I often experience leaky gut. These supplements have been recommended by my practitioner and help reset my gut during my elimination diet. They make reintroducing foods easier and have no unpleasant tastes. The dosage is perfect, and I appreciate the size options available.
Read More
Medical Researches
SCIENTIFIC SCORE
Possibly Effective
Based on 16 Researches
7.4
9
Folate treatment aids liver fat reduction
DNA hypermethylation-induced suppression of ALKBH5 is required for folic acid to alleviate hepatic lipid deposition by enhancing autophagy in an ATG12-dependent manner.
Direct focus on NAFLD treatment
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
Methylcobalamin aids liver health
Methylcobalamin protects against liver failure via engaging gasdermin E.
Significant findings on liver disease
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
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.
Study shows significant benefit
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
Vitamin B12 mitigates liver toxicity
Hepatoprotective Effect of Vitamin B12 in Acetaminophen Induce Hepatotoxicity in Male Rats.
Findings support vitamin B12 use
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
Folate influences liver cancer survival
Genetic variants in folate metabolism-related genes, serum folate and hepatocellular carcinoma survival: the Guangdong Liver Cancer Cohort study.
Directly examines folate impact
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 4 Reviews
8.6
9.5
Dizziness relief
With Ménière's disease, I sometimes experience dizziness. After my doctor prescribed folic acid and B12, I found this product at IHER. I've repurchased several bottles as it seems to alleviate my dizziness. If my symptoms persist, I will continue buying it.
8.8
Liver support success
I took this supplement to support my liver, which needs B12 intake twice a week. Initially, I consumed 10 capsules daily for 10 days, then reduced it to twice weekly. My liver is grateful, as confirmed by ultrasound and blood tests for ALAT and ASAT. All is well with my health!
8.8
Gut health improvement
Suffering from rheumatoid arthritis, I often experience leaky gut. These supplements have been recommended by my practitioner and help reset my gut during my elimination diet. They make reintroducing foods easier and have no unpleasant tastes. The dosage is perfect, and I appreciate the size options available.
Read More
8.8
Liver cleanse support
I highly recommend this prophylactic product to support liver disease within my body cleansing routine. I've noticed clearer skin and improved stool. I plan to repeat this course biannually and will be purchasing it for my husband as well.
