Overview
SCIENTIFIC SCORE
Possibly Effective
Based on 14 Researches
7.4
USERS' SCORE
Moderately Good
Based on 2 Reviews
7.9
Supplement Facts
Serving Size: 2 Tablets
Amount Per Serving
%DV
Vitamin D3 (as Cholecalciferol)
13 mcg (500 IU)
63%
Calcium (as Calcium Citrate)
630 mg
48%
Top Medical Research Studies
9
We examined the impact of calcitriol, the active form of vitamin D, on heart attack recovery using a mouse model of myocardial infarction (MI). In our study, we treated mice that had suffered a MI with calcitriol and observed promising results.
Our findings revealed that calcitriol helped reverse negative effects on heart function and reduced cardiac remodeling after a heart attack. It also targeted the inflammatory response typically associated with MI, improving the survival of heart muscle cells and promoting their regeneration.
We discovered that calcitriol works by enhancing the activity of the Vitamin D receptor (VDR). This process not only interferes with inflammatory signals but also leads to positive changes at the genetic level, further supporting heart health after an MI. Overall, our study provides strong evidence of calcitriol's cardioprotective properties, making it a potential treatment avenue for better outcomes following a heart attack.
Our findings revealed that calcitriol helped reverse negative effects on heart function and reduced cardiac remodeling after a heart attack. It also targeted the inflammatory response typically associated with MI, improving the survival of heart muscle cells and promoting their regeneration.
We discovered that calcitriol works by enhancing the activity of the Vitamin D receptor (VDR). This process not only interferes with inflammatory signals but also leads to positive changes at the genetic level, further supporting heart health after an MI. Overall, our study provides strong evidence of calcitriol's cardioprotective properties, making it a potential treatment avenue for better outcomes following a heart attack.
Read More
9
We explored the impact of 1,25-dihydroxyvitamin D3 (VD3) on heart health, particularly after an acute myocardial infarction (AMI). To investigate this, we used male C57/BL6J mice and conducted a series of experiments, comparing those treated with VD3 to control groups.
Our findings revealed that VD3 treated mice showed significant improvement in heart function following AMI. This treatment not only enhanced cardiac function parameters but also reduced inflammation and the extent of myocardial damage. There was a notable decline in inflammatory markers and a decrease in cell apoptosis, indicated by a rise in protective proteins and a fall in those that lead to cell death.
In our in vitro studies with cardiomyocytes, we observed that VD3 boosted autophagy markers, enhancing the body’s ability to manage damaged cells. It seemed to activate key pathways involved in cell survival and repair, specifically the PI3K/AKT/mTOR pathway. However, when we inhibited this pathway with 3-methyladenine, the benefits of VD3 were reversed, indicating a direct link between autophagy promotion and the protective effects of VD3.
In summary, our research indicates that VD3 can be a valuable ally in the fight against heart damage and inflammation after a heart attack, primarily by supporting cellular repair processes.
Our findings revealed that VD3 treated mice showed significant improvement in heart function following AMI. This treatment not only enhanced cardiac function parameters but also reduced inflammation and the extent of myocardial damage. There was a notable decline in inflammatory markers and a decrease in cell apoptosis, indicated by a rise in protective proteins and a fall in those that lead to cell death.
In our in vitro studies with cardiomyocytes, we observed that VD3 boosted autophagy markers, enhancing the body’s ability to manage damaged cells. It seemed to activate key pathways involved in cell survival and repair, specifically the PI3K/AKT/mTOR pathway. However, when we inhibited this pathway with 3-methyladenine, the benefits of VD3 were reversed, indicating a direct link between autophagy promotion and the protective effects of VD3.
In summary, our research indicates that VD3 can be a valuable ally in the fight against heart damage and inflammation after a heart attack, primarily by supporting cellular repair processes.
Read More
8
We explored the impact of vitamin D levels on heart attack severity by examining 77 patients who experienced ST-elevation myocardial infarction (STEMI). A key focus was to understand how vitamin D deficiency might relate to the amount of thrombus, or blood clots, present in coronary arteries.
The findings revealed that a striking 79.22% of patients had vitamin D levels below what is considered adequate (less than 20 ng/mL). Notably, those with mild thrombus loads had higher vitamin D levels compared to those classified with severe thrombus loads, indicating a clear connection.
Furthermore, we discovered a negative correlation between vitamin D levels and the severity of thrombus. The lower the vitamin D levels, the higher the thrombus burden and the post-procedural TIMI frame count—essentially metrics that show how blood flows in the heart after treatment. This highlights that maintaining adequate vitamin D might be crucial for individuals at risk of severe heart complications.
The findings revealed that a striking 79.22% of patients had vitamin D levels below what is considered adequate (less than 20 ng/mL). Notably, those with mild thrombus loads had higher vitamin D levels compared to those classified with severe thrombus loads, indicating a clear connection.
Furthermore, we discovered a negative correlation between vitamin D levels and the severity of thrombus. The lower the vitamin D levels, the higher the thrombus burden and the post-procedural TIMI frame count—essentially metrics that show how blood flows in the heart after treatment. This highlights that maintaining adequate vitamin D might be crucial for individuals at risk of severe heart complications.
Read More
Most Useful Reviews
9.5
Heart palpitations relief
This is the only type of calcium that alleviates my heart palpitations when combined with magnesium at bedtime. I appreciate this large bottle as it lasts a long time and is reasonably priced. I intend to keep purchasing it in the future, God willing.
Read More
0
Calcium caution
While the pill quality may be adequate, there are warnings online about calcium supplements being harmful to the heart and blood vessels. It is better to consume calcium-rich foods like cottage cheese, fish, nuts, and dairy for better absorption and health benefits, especially to prevent heart attack.
Read More
Medical Researches
SCIENTIFIC SCORE
Possibly Effective
Based on 14 Researches
7.4
- All Researches
9.5
We conducted a detailed study to uncover how vitamin D3, combined with exercise, affects recovery from heart attacks. Our research involved fifty-six male rats, some of which experienced a simulated heart attack, while others served as a control group.
The rats were then divided into several groups, receiving different treatments over eight weeks. We specifically looked at how vitamin D3 and aerobic-resistance training together impacted cardiac health, focusing on the important TGF-β1/Smad signaling pathway known to contribute to heart damage.
Our findings were quite revealing. We noticed that the combinations of vitamin D3 and exercise training significantly improved heart function. Specifically, those receiving both treatments showed higher heart ejection fractions and lower levels of TGF-β1 and collagen proteins, indicating less cardiac fibrosis. In contrast, the groups that only received one treatment did not show the same level of improvement.
This suggests that while vitamin D3 on its own was not studied in isolation, its combination with exercise led to better outcomes in heart attack recovery. Overall, these results indicate a promising role for vitamin D3 alongside exercise in supporting heart health after a heart attack.
The rats were then divided into several groups, receiving different treatments over eight weeks. We specifically looked at how vitamin D3 and aerobic-resistance training together impacted cardiac health, focusing on the important TGF-β1/Smad signaling pathway known to contribute to heart damage.
Our findings were quite revealing. We noticed that the combinations of vitamin D3 and exercise training significantly improved heart function. Specifically, those receiving both treatments showed higher heart ejection fractions and lower levels of TGF-β1 and collagen proteins, indicating less cardiac fibrosis. In contrast, the groups that only received one treatment did not show the same level of improvement.
This suggests that while vitamin D3 on its own was not studied in isolation, its combination with exercise led to better outcomes in heart attack recovery. Overall, these results indicate a promising role for vitamin D3 alongside exercise in supporting heart health after a heart attack.
Read More
9
We examined the impact of calcitriol, the active form of vitamin D, on heart attack recovery using a mouse model of myocardial infarction (MI). In our study, we treated mice that had suffered a MI with calcitriol and observed promising results.
Our findings revealed that calcitriol helped reverse negative effects on heart function and reduced cardiac remodeling after a heart attack. It also targeted the inflammatory response typically associated with MI, improving the survival of heart muscle cells and promoting their regeneration.
We discovered that calcitriol works by enhancing the activity of the Vitamin D receptor (VDR). This process not only interferes with inflammatory signals but also leads to positive changes at the genetic level, further supporting heart health after an MI. Overall, our study provides strong evidence of calcitriol's cardioprotective properties, making it a potential treatment avenue for better outcomes following a heart attack.
Our findings revealed that calcitriol helped reverse negative effects on heart function and reduced cardiac remodeling after a heart attack. It also targeted the inflammatory response typically associated with MI, improving the survival of heart muscle cells and promoting their regeneration.
We discovered that calcitriol works by enhancing the activity of the Vitamin D receptor (VDR). This process not only interferes with inflammatory signals but also leads to positive changes at the genetic level, further supporting heart health after an MI. Overall, our study provides strong evidence of calcitriol's cardioprotective properties, making it a potential treatment avenue for better outcomes following a heart attack.
Read More
9
We explored the effects of vitamin D3 on heart injury caused by ischemia/reperfusion (I/R), a common scenario during heart attacks. Using a laboratory model that mimicked this condition, we discovered that I/R treatment significantly harmed heart cells, leading to cell death and increased oxidative stress.
We observed that I/R conditions prompted an increase in mitochondrial fission and mitophagy—mechanisms that can worsen heart injury. However, when we introduced vitamin D3, it appeared to counteract these detrimental effects. Specifically, vitamin D3 decreased cell death and reduced harmful mitochondrial changes, suggesting a protective role for this vitamin.
In live mice undergoing I/R, we confirmed that vitamin D3 treatment effectively reduced not only apoptosis (cell death) but also the adverse changes in mitochondrial function and structure. Overall, our findings indicate that vitamin D3 could be an important ally in safeguarding the heart during a heart attack by maintaining the integrity of mitochondrial function.
We observed that I/R conditions prompted an increase in mitochondrial fission and mitophagy—mechanisms that can worsen heart injury. However, when we introduced vitamin D3, it appeared to counteract these detrimental effects. Specifically, vitamin D3 decreased cell death and reduced harmful mitochondrial changes, suggesting a protective role for this vitamin.
In live mice undergoing I/R, we confirmed that vitamin D3 treatment effectively reduced not only apoptosis (cell death) but also the adverse changes in mitochondrial function and structure. Overall, our findings indicate that vitamin D3 could be an important ally in safeguarding the heart during a heart attack by maintaining the integrity of mitochondrial function.
Read More
9
We explored the impact of 1,25-dihydroxyvitamin D3 (VD3) on heart health, particularly after an acute myocardial infarction (AMI). To investigate this, we used male C57/BL6J mice and conducted a series of experiments, comparing those treated with VD3 to control groups.
Our findings revealed that VD3 treated mice showed significant improvement in heart function following AMI. This treatment not only enhanced cardiac function parameters but also reduced inflammation and the extent of myocardial damage. There was a notable decline in inflammatory markers and a decrease in cell apoptosis, indicated by a rise in protective proteins and a fall in those that lead to cell death.
In our in vitro studies with cardiomyocytes, we observed that VD3 boosted autophagy markers, enhancing the body’s ability to manage damaged cells. It seemed to activate key pathways involved in cell survival and repair, specifically the PI3K/AKT/mTOR pathway. However, when we inhibited this pathway with 3-methyladenine, the benefits of VD3 were reversed, indicating a direct link between autophagy promotion and the protective effects of VD3.
In summary, our research indicates that VD3 can be a valuable ally in the fight against heart damage and inflammation after a heart attack, primarily by supporting cellular repair processes.
Our findings revealed that VD3 treated mice showed significant improvement in heart function following AMI. This treatment not only enhanced cardiac function parameters but also reduced inflammation and the extent of myocardial damage. There was a notable decline in inflammatory markers and a decrease in cell apoptosis, indicated by a rise in protective proteins and a fall in those that lead to cell death.
In our in vitro studies with cardiomyocytes, we observed that VD3 boosted autophagy markers, enhancing the body’s ability to manage damaged cells. It seemed to activate key pathways involved in cell survival and repair, specifically the PI3K/AKT/mTOR pathway. However, when we inhibited this pathway with 3-methyladenine, the benefits of VD3 were reversed, indicating a direct link between autophagy promotion and the protective effects of VD3.
In summary, our research indicates that VD3 can be a valuable ally in the fight against heart damage and inflammation after a heart attack, primarily by supporting cellular repair processes.
Read More
9
We explored how calcium signaling influences heart cell proliferation, particularly after injuries like heart attacks. Our study centered on the L-Type Calcium Channel (LTCC) and how its inhibition might help heart cells regenerate. Remarkably, when we inhibited LTCC—either through pharmacological means or by enhancing the activity of an inherent inhibitor called RRAD—we observed significant boosts in heart cell activity.
This process appears connected to calcineurin activity, a key player in cell signaling. By carefully manipulating these pathways, we managed to not only provoke heart cell growth in lab settings but also improve heart function and reduce scar tissue in live animal models post-heart attack.
Through our findings, we highlight the potential for new calcium-related treatments that could significantly benefit patients with heart injury, paving the way for exciting advancements in regenerative medicine. By understanding this intricate relationship between calcium signaling and heart cell growth, we open doors for innovative therapies that could transform recovery strategies in cardiovascular care.
This process appears connected to calcineurin activity, a key player in cell signaling. By carefully manipulating these pathways, we managed to not only provoke heart cell growth in lab settings but also improve heart function and reduce scar tissue in live animal models post-heart attack.
Through our findings, we highlight the potential for new calcium-related treatments that could significantly benefit patients with heart injury, paving the way for exciting advancements in regenerative medicine. By understanding this intricate relationship between calcium signaling and heart cell growth, we open doors for innovative therapies that could transform recovery strategies in cardiovascular care.
Read More
User Reviews
USERS' SCORE
Moderately Good
Based on 2 Reviews
7.9
- All Reviews
- Positive Reviews
- Negative Reviews
9.5
Heart palpitations relief
This is the only type of calcium that alleviates my heart palpitations when combined with magnesium at bedtime. I appreciate this large bottle as it lasts a long time and is reasonably priced. I intend to keep purchasing it in the future, God willing.
Read More
0
Calcium caution
While the pill quality may be adequate, there are warnings online about calcium supplements being harmful to the heart and blood vessels. It is better to consume calcium-rich foods like cottage cheese, fish, nuts, and dairy for better absorption and health benefits, especially to prevent heart attack.
Read More
Frequently Asked Questions
No FAQs are available for this product and symptom.
References
- Olędzki S, Siennicka A, Maciejewska-Markiewicz D, Stachowska E, Jakubiak N, et al. Calcitriol Concentration in the Early Phase of Myocardial Infarction and Its Relation to Left Ventricular Ejection Fraction. Metabolites. 2024;14. doi:10.3390/metabo14120686
- Ogata S, Manson JE, Kang JH, Buring JE, Lee IM, et al. Marine n-3 Fatty Acids and Prevention of Cardiovascular Disease: A Novel Analysis of the VITAL Trial Using Win Ratio and Hierarchical Composite Outcomes. Nutrients. 2023;15. doi:10.3390/nu15194235
- Thompson B, Waterhouse M, English DR, McLeod DS, Armstrong BK, et al. Vitamin D supplementation and major cardiovascular events: D-Health randomised controlled trial. BMJ. 2023;381:e075230. doi:10.1136/bmj-2023-075230
- Bassuk SS, Manson JE. Marine omega-3 fatty acid supplementation and prevention of cardiovascular disease: update on the randomized trial evidence. Cardiovasc Res. 2023;119:1297. doi:10.1093/cvr/cvac172
- Uguz B, Oztas S, Zengin I, Topal D, Tiryakioglu SK, et al. Relationship between vitamin D deficiency and thrombus load in patients with ST-elevation myocardial infarction. Eur Rev Med Pharmacol Sci. 2022;26:7015. doi:10.26355/eurrev_202210_29885
- Yang S, Wang C, Ruan C, Chen M, Cao R, et al. Novel Insights into the Cardioprotective Effects of Calcitriol in Myocardial Infarction. Cells. 2022;11. doi:10.3390/cells11101676
- Şen Ö, Şen SB, Topuz AN, Topuz M. Vitamin D level predicts angiographic no-reflow phenomenon after percutaneous coronary intervention in patients with ST segment elevation myocardial infarction. Biomark Med. 2021;15:1357. doi:10.2217/bmm-2020-0689
- Mehdipoor M, Damirchi A, Razavi Tousi SMT, Babaei P. Concurrent vitamin D supplementation and exercise training improve cardiac fibrosis via TGF-β/Smad signaling in myocardial infarction model of rats. J Physiol Biochem. 2021;77:75. doi:10.1007/s13105-020-00778-6
- Lee TL, Lee MH, Chen YC, Lee YC, Lai TC, et al. Vitamin D Attenuates Ischemia/Reperfusion-Induced Cardiac Injury by Reducing Mitochondrial Fission and Mitophagy. Front Pharmacol. 2020;11:604700. doi:10.3389/fphar.2020.604700
- Wei YX, Dong SM, Wang YY, Zhang P, Sun MY, et al. Autophagy participates in the protection role of 1,25-dihydroxyvitamin D3 in acute myocardial infarction via PI3K/AKT/mTOR pathway. Cell Biol Int. 2021;45:394. doi:10.1002/cbin.11495
- Akkuş O, Topuz M, Öz F, Harbalıoğlu H, Koca H, et al. Impact of 25(OH)D3 on spontaneous reperfusion and SYNTAX score in patients with ST-elevation myocardial infarction. Turk Kardiyol Dern Ars. 2018;46:268. doi:10.5543/tkda.2018.49393
- Le TYL, Ogawa M, Kizana E, Gunton JE, Chong JJH. Vitamin D Improves Cardiac Function After Myocardial Infarction Through Modulation of Resident Cardiac Progenitor Cells. Heart Lung Circ. 2018;27:967. doi:10.1016/j.hlc.2018.01.006
- Şen Ö, Topuz M, Acele A, Akkuş O, Baykan AO, et al. The influence of plasma 25-(OH) vitamin D levels in acute ST elevation myocardial infarction. Cardiol J. 2017;24:677. doi:10.5603/CJ.a2017.0066
- Devilée LAC, Salama ABM, Miller JM, Reid JD, Ou Q, et al. Pharmacological or genetic inhibition of LTCC promotes cardiomyocyte proliferation through inhibition of calcineurin activity. NPJ Regen Med. 2025;10:1. doi:10.1038/s41536-025-00389-z
