' 
SCIENTIFIC SCORE
Possibly Effective
Based on 18 Researches
7.4
USERS' SCORE
Good
Based on 1 Review
8.5
Supplement Facts
Serving Size: 1 Capsule
Amount Per Serving
%DV
Vitamin C (from culture of S. cerevisiae)
25 mg
28%
Folate (from culture of S. cerevisiae)
400 mcg DFE
100%
Vitamin B12 (as Methylcobalamin from culture of S. cerevisiae)
500 mcg
20833%
Iron (from Brown Rice Chelate)
22 mg
122%
RAW Organic Fruit & Vegetable BlendOrganic Apple (fruit), Organic Beet (root), Organic Broccoli (stalk & flower), Organic Carrot (root), Organic Spinach (leaf), Organic Tomato (fruit), Organic Strawberry (fruit), Organic Tart Cherry (fruit), Organic Blackberry (fruit), Organic Green Bell Pepper (fruit), Organic Brussels Sprout (leaf), Organic Blueberry (fruit), Organic Ginger (root), Organic Garlic (bulb), Organic Green Onion (bulb), Organic Raspberry (fruit), Organic Parsley (leaf), Organic Cauliflower (flower & stem), Organic Red Cabbage (leaf), Organic Kale (leaf), Organic Cucumber (gourd), Organic Celery (stalk), Organic Asparagus Juice (flower & stem)
310 mg
+
RAW Probiotic & Enzyme BlendLipase, Protease, Aspergillopepsin, beta-Glucanase, Cellulase, Bromelain, Phytase, Lactase, Papain, Peptidase, Pectinase, Hemicellulase, Xylanase, [Lactobacillus plantarum, Lactobacillus bulgaricus] (500 Million CFU)
60 mg
+
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
8.3
Natural iron boost
No stress on the stomach; it's 100% natural, so it doesn't harm my stomach or liver. It significantly raises my iron levels.
Read More
Medical Researches
SCIENTIFIC SCORE
Possibly Effective
Based on 18 Researches
7.4
- All Researches
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
9
Rubiadin reduces liver iron overload
Rubiadin Mediates the Upregulation of Hepatic Hepcidin and Alleviates Iron Overload via BMP6/SMAD1/5/9-Signaling Pathway.
Study highly relevant to liver disease
We explored the effects of rubiadin, a beneficial compound derived from a Chinese herb, on iron metabolism and its implications for liver disease. Recognizing the challenges posed by iron overload diseases, we aimed to discover a safe approach to manage excessive iron accumulation in the body. Through experiments involving various analyses, we observed that rubiadin significantly downregulated proteins that are typically elevated in conditions of high iron, such as transferrin receptor 1 and ferroportin 1.
Furthermore, when we administered rubiadin to mice with iron overload, it resulted in decreased serum and duodenal iron levels and an increase in hepcidin mRNA expression in the liver. This suggests that rubiadin may not only help the body regulate iron better but might also protect against the harmful effects of excess iron.
Our research also delved into the mechanisms behind these effects. We found that rubiadin-induced hepcidin expression was mediated through a specific signaling pathway involving bone morphogenetic protein 6 (BMP6) and SMAD proteins. The ability of rubiadin to enhance hepcidin levels points toward a promising natural strategy for tackling iron overload in liver diseases and could have broader implications for treating related conditions.
Furthermore, when we administered rubiadin to mice with iron overload, it resulted in decreased serum and duodenal iron levels and an increase in hepcidin mRNA expression in the liver. This suggests that rubiadin may not only help the body regulate iron better but might also protect against the harmful effects of excess iron.
Our research also delved into the mechanisms behind these effects. We found that rubiadin-induced hepcidin expression was mediated through a specific signaling pathway involving bone morphogenetic protein 6 (BMP6) and SMAD proteins. The ability of rubiadin to enhance hepcidin levels points toward a promising natural strategy for tackling iron overload in liver diseases and could have broader implications for treating related conditions.
Read More
User Reviews
USERS' SCORE
Good
Based on 1 Review
8.5
- All Reviews
- Positive Reviews
- Negative Reviews
8.3
Natural iron boost
No stress on the stomach; it's 100% natural, so it doesn't harm my stomach or liver. It significantly raises my iron levels.
