Overview
SCIENTIFIC SCORE
Possibly Effective
Based on 12 Researches
7.7
USERS' SCORE
Moderately Good
Based on 3 Reviews
7.7
Supplement Facts
Serving Size: 1 Vegetable Capsule
Amount Per Serving
%DV
Vitamin C
500 mg
556%
Top Medical Research Studies
8
We aimed to discover how vitamin C supplementation affects oxidative stress in individuals diagnosed with chronic gastritis. In this study, we looked at 244 Japanese patients suffering from atrophic gastritis. They were randomly assigned to receive either 50 mg or 500 mg of vitamin C every day for five years.
After analyzing the results, we found notable differences between the two groups. The high-dose group experienced a significant decrease in reactive oxygen species (ROS), suggesting that vitamin C may help reduce oxidative stress associated with chronic gastritis. In contrast, the low-dose group reported an increase in ROS levels. These findings prompt further interest in how vitamin C can protect against oxidative stress in similar conditions.
Overall, our study supports the idea that higher doses of vitamin C could have a beneficial effect on oxidative stress, particularly in those dealing with gastritis. This insight opens avenues for considering vitamin C as a potential supportive treatment for managing oxidative stress-related issues in digestive health.
After analyzing the results, we found notable differences between the two groups. The high-dose group experienced a significant decrease in reactive oxygen species (ROS), suggesting that vitamin C may help reduce oxidative stress associated with chronic gastritis. In contrast, the low-dose group reported an increase in ROS levels. These findings prompt further interest in how vitamin C can protect against oxidative stress in similar conditions.
Overall, our study supports the idea that higher doses of vitamin C could have a beneficial effect on oxidative stress, particularly in those dealing with gastritis. This insight opens avenues for considering vitamin C as a potential supportive treatment for managing oxidative stress-related issues in digestive health.
2
We explored the potential benefits of vitamin C supplementation for individuals suffering from atrophic gastritis. Conducted as a double-blind, randomized controlled trial in Japan, this study involved participants living in a region known for high rates of stomach cancer. Over five years, volunteers were assigned to receive daily doses of either 50 mg or 500 mg of vitamin C.
The results were intriguing: while those in the high-dose group had higher levels of serum vitamin C, the levels of two important inflammatory markers—C-reactive protein (CRP) and serum amyloid A (SAA)—showed no significant difference between the low- and high-dosage groups. Both biomarkers remained fairly constant, indicating that vitamin C supplementation did not effectively reduce inflammation or infection risk among these individuals with atrophic gastritis.
Overall, our findings suggest that high doses of vitamin C may not provide the hoped-for relief from inflammation in this patient group. Thus, it appears that vitamin C supplementation alone is insufficient in managing or alleviating gastritis-related inflammation.
The results were intriguing: while those in the high-dose group had higher levels of serum vitamin C, the levels of two important inflammatory markers—C-reactive protein (CRP) and serum amyloid A (SAA)—showed no significant difference between the low- and high-dosage groups. Both biomarkers remained fairly constant, indicating that vitamin C supplementation did not effectively reduce inflammation or infection risk among these individuals with atrophic gastritis.
Overall, our findings suggest that high doses of vitamin C may not provide the hoped-for relief from inflammation in this patient group. Thus, it appears that vitamin C supplementation alone is insufficient in managing or alleviating gastritis-related inflammation.
9
We investigated how vitamin C might help improve chronic atrophic gastritis (CAG), a condition characterized by gastric mucosal damage and inflammation. Our research utilized data from a well-known dataset, focusing on changes in gene expression related to CAG. Notably, we pinpointed IGFBP7 as a central gene that appeared to be strongly associated with this condition.
In our study, we treated CAG patients with vitamin C and observed significant improvements in blood parameters and the overall health of their gastric mucosa. Moreover, when we looked at gastric cells in the lab, vitamin C not only boosted cell viability but also reduced inflammation and cell death caused by a harmful compound known as MNNG. These effects included lowering the levels of inflammatory markers and apoptosis-related proteins.
Interestingly, our findings suggested that IGFBP7 plays a role in these protective effects of vitamin C. When we knocked down IGFBP7 in the lab tests, we noted changes in how vitamin C worked, suggesting a complex interaction.
Overall, our study highlights the potential of vitamin C and IGFBP7 as key players in managing chronic atrophic gastritis and enhancing gastric health, opening doors for new therapeutic approaches.
In our study, we treated CAG patients with vitamin C and observed significant improvements in blood parameters and the overall health of their gastric mucosa. Moreover, when we looked at gastric cells in the lab, vitamin C not only boosted cell viability but also reduced inflammation and cell death caused by a harmful compound known as MNNG. These effects included lowering the levels of inflammatory markers and apoptosis-related proteins.
Interestingly, our findings suggested that IGFBP7 plays a role in these protective effects of vitamin C. When we knocked down IGFBP7 in the lab tests, we noted changes in how vitamin C worked, suggesting a complex interaction.
Overall, our study highlights the potential of vitamin C and IGFBP7 as key players in managing chronic atrophic gastritis and enhancing gastric health, opening doors for new therapeutic approaches.
Most Useful Reviews
9
Highly recommended
In my opinion, Solgar offers the best vitamin C. Its quality is outstanding and truly revitalising, especially for ARVI. I have not experienced any kidney stones from it, unlike with ascorbate. This vitamin does not irritate the gastrointestinal tract. However, those with gastritis should opt for Ester-S from Solgar. I highly recommend it.
0
Gastritis aggravated
2 people found this helpful
I bought a vitamin C drink combined with collagen for better absorption. Unfortunately, I had to stop taking vitamin C as my gastritis flared up. My son is currently using it instead.
7.5
No stomach pain
Wonderful! Everything is well-packaged. I was pleasantly surprised that this vitamin C does not cause burning or stomach pain. I hope it continues to be gentle on my stomach, especially since I have pancreatitis and gastritis.
Medical Researches
SCIENTIFIC SCORE
Possibly Effective
Based on 12 Researches
7.7
- All Researches
9.5
We conducted a one-year double-blind placebo-controlled trial to explore the effects of daily supplementation on patients with gastric premalignant lesions known as intestinal metaplasia (IM). Our focus was on a specific supplement consisting of Ester-C, which includes 2100 mg of Ca-ascorbate and 340 mg of bioflavonoids, alongside other antioxidants.
The results were promising, showing a significant decrease in the activity of ornithine decarboxylase, an enzyme that can indicate abnormal cell growth. Remarkably, we observed that 11 out of 18 patients showed nearly total regression of their IM, which translates to a success rate of 61%.
While this study highlights the potential benefits of antioxidant supplementation, including vitamin C, it's essential to note that multiple components were present in the treatment. This complexity makes it challenging to pinpoint the specific effect of vitamin C alone on gastritis treatment.
The results were promising, showing a significant decrease in the activity of ornithine decarboxylase, an enzyme that can indicate abnormal cell growth. Remarkably, we observed that 11 out of 18 patients showed nearly total regression of their IM, which translates to a success rate of 61%.
While this study highlights the potential benefits of antioxidant supplementation, including vitamin C, it's essential to note that multiple components were present in the treatment. This complexity makes it challenging to pinpoint the specific effect of vitamin C alone on gastritis treatment.
9
We investigated how vitamin C might help improve chronic atrophic gastritis (CAG), a condition characterized by gastric mucosal damage and inflammation. Our research utilized data from a well-known dataset, focusing on changes in gene expression related to CAG. Notably, we pinpointed IGFBP7 as a central gene that appeared to be strongly associated with this condition.
In our study, we treated CAG patients with vitamin C and observed significant improvements in blood parameters and the overall health of their gastric mucosa. Moreover, when we looked at gastric cells in the lab, vitamin C not only boosted cell viability but also reduced inflammation and cell death caused by a harmful compound known as MNNG. These effects included lowering the levels of inflammatory markers and apoptosis-related proteins.
Interestingly, our findings suggested that IGFBP7 plays a role in these protective effects of vitamin C. When we knocked down IGFBP7 in the lab tests, we noted changes in how vitamin C worked, suggesting a complex interaction.
Overall, our study highlights the potential of vitamin C and IGFBP7 as key players in managing chronic atrophic gastritis and enhancing gastric health, opening doors for new therapeutic approaches.
In our study, we treated CAG patients with vitamin C and observed significant improvements in blood parameters and the overall health of their gastric mucosa. Moreover, when we looked at gastric cells in the lab, vitamin C not only boosted cell viability but also reduced inflammation and cell death caused by a harmful compound known as MNNG. These effects included lowering the levels of inflammatory markers and apoptosis-related proteins.
Interestingly, our findings suggested that IGFBP7 plays a role in these protective effects of vitamin C. When we knocked down IGFBP7 in the lab tests, we noted changes in how vitamin C worked, suggesting a complex interaction.
Overall, our study highlights the potential of vitamin C and IGFBP7 as key players in managing chronic atrophic gastritis and enhancing gastric health, opening doors for new therapeutic approaches.
9
We sought to understand how vitamin C affects the absorption of levothyroxine, a common medication for hypothyroidism, particularly in patients who also experience gastritis. Our study involved 31 patients, most of whom had poorly controlled hypothyroidism along with gastrointestinal issues.
Participants took levothyroxine alongside a solution that either contained or did not contain vitamin C, and we monitored their hormone levels over several months. Our findings revealed that vitamin C can actually improve levels of free T4 and T3, as well as TSH, suggesting it enhances the absorption of medication in these patients.
This is particularly significant because individuals dealing with both hypothyroidism and gastritis often struggle to maintain stable thyroid hormone levels. Our research indicates that incorporating vitamin C into their treatment regimen could serve as a beneficial strategy in managing their condition.
Participants took levothyroxine alongside a solution that either contained or did not contain vitamin C, and we monitored their hormone levels over several months. Our findings revealed that vitamin C can actually improve levels of free T4 and T3, as well as TSH, suggesting it enhances the absorption of medication in these patients.
This is particularly significant because individuals dealing with both hypothyroidism and gastritis often struggle to maintain stable thyroid hormone levels. Our research indicates that incorporating vitamin C into their treatment regimen could serve as a beneficial strategy in managing their condition.
9
We explored how vitamin C, or ascorbic acid, plays a role in the development of gastritis, specifically focusing on acute gastric mucosal lesions induced by a compound known as C48/80 in rats. In our study, we injected fasted Wistar rats with C48/80 to trigger gastric lesions, followed by varying doses of oral vitamin C.
After assessing the severity of the lesions and measuring various biochemical markers in the gastric mucosa and serum, we found that lesions appeared 0.5 hours post treatment and continued to worsen over the next 3 hours. Notably, the administration of vitamin C right after the initial treatment appeared to significantly reduce the progression of these lesions. It also helped maintain the levels of various protective substances in the gastric lining and overall health indicators.
By the end of our study, it was clear that vitamin C has a crucial protective effect in this scenario. Our results suggest that timely vitamin C administration can prevent the worsening of gastritis caused by mast cell degranulation. This adds a promising angle to the conversation about dietary vitamins in managing gastric health.
After assessing the severity of the lesions and measuring various biochemical markers in the gastric mucosa and serum, we found that lesions appeared 0.5 hours post treatment and continued to worsen over the next 3 hours. Notably, the administration of vitamin C right after the initial treatment appeared to significantly reduce the progression of these lesions. It also helped maintain the levels of various protective substances in the gastric lining and overall health indicators.
By the end of our study, it was clear that vitamin C has a crucial protective effect in this scenario. Our results suggest that timely vitamin C administration can prevent the worsening of gastritis caused by mast cell degranulation. This adds a promising angle to the conversation about dietary vitamins in managing gastric health.
8
We explored the effects of Ascorbic Acid 2-Glucoside (AA2G), a stable form of Vitamin C, on human gastric epithelial cells infected with Helicobacter pylori, a common cause of gastritis and related stomach issues. In our research, we focused on understanding how AA2G could mitigate the damage caused by this bacterium on stomach cells.
Our findings revealed that AA2G significantly reduced oxidative stress—a harmful condition triggered by H. pylori that can damage cells. We observed that treatment with AA2G led to lower levels of harmful substances, such as reactive oxygen species, known to contribute to cell damage.
Notably, AA2G also helped restore the cells' mitochondrial function, which is often impaired during H. pylori infection. This improvement included an increase in ATP levels and enhanced mitochondrial membrane potential, both essential for cell energy production and health.
Ultimately, we found that AA2G effectively reduces the apoptosis (or programmed cell death) that results from H. pylori infection, suggesting that it provides a protective effect on gastric epithelial cells. Our research supports the potential use of AA2G as a beneficial intervention for combatting the adverse effects of H. pylori infection on gastritis.
Our findings revealed that AA2G significantly reduced oxidative stress—a harmful condition triggered by H. pylori that can damage cells. We observed that treatment with AA2G led to lower levels of harmful substances, such as reactive oxygen species, known to contribute to cell damage.
Notably, AA2G also helped restore the cells' mitochondrial function, which is often impaired during H. pylori infection. This improvement included an increase in ATP levels and enhanced mitochondrial membrane potential, both essential for cell energy production and health.
Ultimately, we found that AA2G effectively reduces the apoptosis (or programmed cell death) that results from H. pylori infection, suggesting that it provides a protective effect on gastric epithelial cells. Our research supports the potential use of AA2G as a beneficial intervention for combatting the adverse effects of H. pylori infection on gastritis.
User Reviews
USERS' SCORE
Moderately Good
Based on 3 Reviews
7.7
- All Reviews
- Positive Reviews
- Negative Reviews
9
Highly recommended
In my opinion, Solgar offers the best vitamin C. Its quality is outstanding and truly revitalising, especially for ARVI. I have not experienced any kidney stones from it, unlike with ascorbate. This vitamin does not irritate the gastrointestinal tract. However, those with gastritis should opt for Ester-S from Solgar. I highly recommend it.
0
Gastritis aggravated
2 people found this helpful
I bought a vitamin C drink combined with collagen for better absorption. Unfortunately, I had to stop taking vitamin C as my gastritis flared up. My son is currently using it instead.
7.5
No stomach pain
Wonderful! Everything is well-packaged. I was pleasantly surprised that this vitamin C does not cause burning or stomach pain. I hope it continues to be gentle on my stomach, especially since I have pancreatitis and gastritis.
Frequently Asked Questions
9
Highly recommended
In my opinion, Solgar offers the best vitamin C. Its quality is outstanding and truly revitalising, especially for ARVI. I have not experienced any kidney stones from it, unlike with ascorbate. This vitamin does not irritate the gastrointestinal tract. However, those with gastritis should opt for Ester-S from Solgar. I highly recommend it.
7.5
No stomach pain
Wonderful! Everything is well-packaged. I was pleasantly surprised that this vitamin C does not cause burning or stomach pain. I hope it continues to be gentle on my stomach, especially since I have pancreatitis and gastritis.
0
Gastritis aggravated
2 people found this helpful
I bought a vitamin C drink combined with collagen for better absorption. Unfortunately, I had to stop taking vitamin C as my gastritis flared up. My son is currently using it instead.
9
We investigated how vitamin C might help improve chronic atrophic gastritis (CAG), a condition characterized by gastric mucosal damage and inflammation. Our research utilized data from a well-known dataset, focusing on changes in gene expression related to CAG. Notably, we pinpointed IGFBP7 as a central gene that appeared to be strongly associated with this condition.
In our study, we treated CAG patients with vitamin C and observed significant improvements in blood parameters and the overall health of their gastric mucosa. Moreover, when we looked at gastric cells in the lab, vitamin C not only boosted cell viability but also reduced inflammation and cell death caused by a harmful compound known as MNNG. These effects included lowering the levels of inflammatory markers and apoptosis-related proteins.
Interestingly, our findings suggested that IGFBP7 plays a role in these protective effects of vitamin C. When we knocked down IGFBP7 in the lab tests, we noted changes in how vitamin C worked, suggesting a complex interaction.
Overall, our study highlights the potential of vitamin C and IGFBP7 as key players in managing chronic atrophic gastritis and enhancing gastric health, opening doors for new therapeutic approaches.
In our study, we treated CAG patients with vitamin C and observed significant improvements in blood parameters and the overall health of their gastric mucosa. Moreover, when we looked at gastric cells in the lab, vitamin C not only boosted cell viability but also reduced inflammation and cell death caused by a harmful compound known as MNNG. These effects included lowering the levels of inflammatory markers and apoptosis-related proteins.
Interestingly, our findings suggested that IGFBP7 plays a role in these protective effects of vitamin C. When we knocked down IGFBP7 in the lab tests, we noted changes in how vitamin C worked, suggesting a complex interaction.
Overall, our study highlights the potential of vitamin C and IGFBP7 as key players in managing chronic atrophic gastritis and enhancing gastric health, opening doors for new therapeutic approaches.
8
We explored the effects of Ascorbic Acid 2-Glucoside (AA2G), a stable form of Vitamin C, on human gastric epithelial cells infected with Helicobacter pylori, a common cause of gastritis and related stomach issues. In our research, we focused on understanding how AA2G could mitigate the damage caused by this bacterium on stomach cells.
Our findings revealed that AA2G significantly reduced oxidative stress—a harmful condition triggered by H. pylori that can damage cells. We observed that treatment with AA2G led to lower levels of harmful substances, such as reactive oxygen species, known to contribute to cell damage.
Notably, AA2G also helped restore the cells' mitochondrial function, which is often impaired during H. pylori infection. This improvement included an increase in ATP levels and enhanced mitochondrial membrane potential, both essential for cell energy production and health.
Ultimately, we found that AA2G effectively reduces the apoptosis (or programmed cell death) that results from H. pylori infection, suggesting that it provides a protective effect on gastric epithelial cells. Our research supports the potential use of AA2G as a beneficial intervention for combatting the adverse effects of H. pylori infection on gastritis.
Our findings revealed that AA2G significantly reduced oxidative stress—a harmful condition triggered by H. pylori that can damage cells. We observed that treatment with AA2G led to lower levels of harmful substances, such as reactive oxygen species, known to contribute to cell damage.
Notably, AA2G also helped restore the cells' mitochondrial function, which is often impaired during H. pylori infection. This improvement included an increase in ATP levels and enhanced mitochondrial membrane potential, both essential for cell energy production and health.
Ultimately, we found that AA2G effectively reduces the apoptosis (or programmed cell death) that results from H. pylori infection, suggesting that it provides a protective effect on gastric epithelial cells. Our research supports the potential use of AA2G as a beneficial intervention for combatting the adverse effects of H. pylori infection on gastritis.
2
We explored the potential benefits of vitamin C supplementation for individuals suffering from atrophic gastritis. Conducted as a double-blind, randomized controlled trial in Japan, this study involved participants living in a region known for high rates of stomach cancer. Over five years, volunteers were assigned to receive daily doses of either 50 mg or 500 mg of vitamin C.
The results were intriguing: while those in the high-dose group had higher levels of serum vitamin C, the levels of two important inflammatory markers—C-reactive protein (CRP) and serum amyloid A (SAA)—showed no significant difference between the low- and high-dosage groups. Both biomarkers remained fairly constant, indicating that vitamin C supplementation did not effectively reduce inflammation or infection risk among these individuals with atrophic gastritis.
Overall, our findings suggest that high doses of vitamin C may not provide the hoped-for relief from inflammation in this patient group. Thus, it appears that vitamin C supplementation alone is insufficient in managing or alleviating gastritis-related inflammation.
The results were intriguing: while those in the high-dose group had higher levels of serum vitamin C, the levels of two important inflammatory markers—C-reactive protein (CRP) and serum amyloid A (SAA)—showed no significant difference between the low- and high-dosage groups. Both biomarkers remained fairly constant, indicating that vitamin C supplementation did not effectively reduce inflammation or infection risk among these individuals with atrophic gastritis.
Overall, our findings suggest that high doses of vitamin C may not provide the hoped-for relief from inflammation in this patient group. Thus, it appears that vitamin C supplementation alone is insufficient in managing or alleviating gastritis-related inflammation.
8
We aimed to understand how vitamin C, alongside vitamin E, affects inflammation in the stomach caused by Helicobacter pylori, a common bacteria linked to gastritis. In our study, patients suffering from nonulcer dyspepsia and testing positive for H. pylori were given vitamin C (500 mg) and vitamin E (200 IU) twice daily for four weeks.
After this treatment period, we collected tissue samples from different areas of the stomach to examine any changes in inflammation and vitamin levels. The results showed that vitamin C levels increased significantly in the stomach mucosa, alongside vitamin E levels.
More importantly, both the intensity of H. pylori and neutrophil activity, which indicates inflammation, decreased after supplementation. This suggests that taking these vitamins could help create a less favorable environment for the bacteria, potentially improving treatment outcomes for gastritis.
Overall, while our findings highlight the importance of vitamins C and E in reducing stomach inflammation, they also suggest that these vitamins may help improve the effectiveness of conventional treatments against H. pylori.
After this treatment period, we collected tissue samples from different areas of the stomach to examine any changes in inflammation and vitamin levels. The results showed that vitamin C levels increased significantly in the stomach mucosa, alongside vitamin E levels.
More importantly, both the intensity of H. pylori and neutrophil activity, which indicates inflammation, decreased after supplementation. This suggests that taking these vitamins could help create a less favorable environment for the bacteria, potentially improving treatment outcomes for gastritis.
Overall, while our findings highlight the importance of vitamins C and E in reducing stomach inflammation, they also suggest that these vitamins may help improve the effectiveness of conventional treatments against H. pylori.
References
- Cheng X, Gu H, Chong Y, Li F, Bei S, et al. Vitamin C Mediates IGFBP7 to Alleviate Chronic Atrophic Gastritis via the HIF-1α/VEGF Pathway. J Cell Mol Med. 2025;29:e70392. doi:10.1111/jcmm.70392
- Mei H, Tu H. Vitamin C and Infection: Current Knowledge and Future Prospects. Front Physiol. 2018;9:1103. doi:10.3389/fphys.2018.01103
- Chen X, Liu R, Liu X, Xu C, Wang X. L-ascorbic Acid-2-Glucoside inhibits Helicobacter pylori-induced apoptosis through mitochondrial pathway in Gastric Epithelial cells. Biomed Pharmacother. 2018;97:75. doi:10.1016/j.biopha.2017.10.030
- Jubiz W, Ramirez M. Effect of vitamin C on the absorption of levothyroxine in patients with hypothyroidism and gastritis. J Clin Endocrinol Metab. 2014;99:E1031. doi:10.1210/jc.2013-4360
- Ma E, Sasazuki S, Sasaki S, Tsubono Y, Okubo S, et al. Vitamin C supplementation in relation to inflammation in individuals with atrophic gastritis: a randomised controlled trial in Japan. Br J Nutr. 2013;109:1089. doi:10.1017/S0007114512002954
- Aditi A, Graham DY. Vitamin C, gastritis, and gastric disease: a historical review and update. Dig Dis Sci. 2012;57:2504. doi:10.1007/s10620-012-2203-7
- Sezikli M, Çetinkaya ZA, Güzelbulut F, Çimen B, Özcan Ö, et al. Effects of alpha tocopherol and ascorbic acid on Helicobacter pylori colonization and the severity of gastric inflammation. Helicobacter. 2012;17:127. doi:10.1111/j.1523-5378.2011.00925.x
- Kohler JE, Blass AL, Liu J, Tai K, Soybel DI. Antioxidant pre-treatment prevents omeprazole-induced toxicity in an in vitro model of infectious gastritis. Free Radic Biol Med. 2010;49:786. doi:10.1016/j.freeradbiomed.2010.05.034
- Sasazuki S, Hayashi T, Nakachi K, Sasaki S, Tsubono Y, et al. Protective effect of vitamin C on oxidative stress: a randomized controlled trial. Int J Vitam Nutr Res. 2008;78:121. doi:10.1024/0300-9831.78.3.121
- Draudin-Krylenko VA, Petukhov AB, Kuvshinov IuP, Levchuk AA, Bukin IuV. [Effect of antioxidant use in dietary therapy in patients with chronic athrofic hastritis]. Vopr Pitan. 2006;75:53.
- Rembiasz K, Budzynski A, Karcz D, Konturek PC, Konturek SJ, et al. Multifocal atrophic gastritis: pathogenesis and therapeutic implications. Eur J Gastroenterol Hepatol. 2005;17:857.
- Kamiya Y, Ohta Y, Imai Y, Arisawa T, Nakano H. A critical role of gastric mucosal ascorbic acid in the progression of acute gastric mucosal lesions induced by compound 48/80 in rats. World J Gastroenterol. 2005;11:1324.
