5/16/2025
Last update
5/16/2025
Reviewed By
Reviewed By
Overview
SCIENTIFIC SCORE
Possibly Effective
Based on 16 Researches
7.7
USERS' SCORE
Good
Based on 1 Review
8.4
Supplement Facts
Serving Size: 1 Capsule
Amount Per Serving
%DV
Vitamin D3 (as cholecalciferol)
125 mcg
625%
Vitamin K activity from:Vitamin K1 (as phytonadione)Vitamin K2 (as menaquinone-4)Vitamin K2 (as trans menaquinone-7)
2,100 mcg1,000 mcg1,000 mcg100 mcg
1,750%
Iodine [from Sea-Iodine™ Complex Blend (organic kelp and bladderwrack extracts, potassium iodide)]
1,000 mcg
667%
Top Medical Research Studies
9
We explored the potential benefits of vitamin D3 (specifically, 1,25-vitamin D3) for protecting the brain during events such as strokes caused by impaired blood flow, known as cerebral ischemia-reperfusion injury (CIRI). In this study, rats received vitamin D3 supplementation for a week before undergoing a procedure that mimicked a stroke. The results were striking; those treated with vitamin D3 showed significant improvements in neurological function, with reduced areas of brain damage and more surviving neurons.
We also tested the effects of vitamin D3 on rat cortical neurons in a laboratory setting, specifically observing its influence on cell survival during oxygen-glucose deprivation and reoxygenation (a model for stroke). The vitamin D3 treatment not only improved cell viability but also appeared to reduce cell death and inflammation. Our analyses revealed that vitamin D3 boosts important protective proteins in the brain, which help combat oxidative stress and inhibit pathways linked to inflammatory cell death.
Overall, our findings strongly suggest that vitamin D3 could be a valuable resource in stroke management by protecting neurons through its antioxidant actions and reduction of harmful inflammation.
We also tested the effects of vitamin D3 on rat cortical neurons in a laboratory setting, specifically observing its influence on cell survival during oxygen-glucose deprivation and reoxygenation (a model for stroke). The vitamin D3 treatment not only improved cell viability but also appeared to reduce cell death and inflammation. Our analyses revealed that vitamin D3 boosts important protective proteins in the brain, which help combat oxidative stress and inhibit pathways linked to inflammatory cell death.
Overall, our findings strongly suggest that vitamin D3 could be a valuable resource in stroke management by protecting neurons through its antioxidant actions and reduction of harmful inflammation.
Read More
9
We investigated the impact of 1α,25-dihydroxyvitamin D3, commonly known as vitamin D3, on stroke recovery, particularly focusing on its effects on brain function after cerebral ischemia-reperfusion injury. Using a model called middle cerebral artery occlusion (MCAO), we aimed to understand how vitamin D3 influences mitochondrial health and signaling pathways crucial for brain recovery.
Our findings revealed that vitamin D3 effectively reduced the size of brain damage and improved neurological function in rats. We noted significant changes in various metrics, including a decrease in markers associated with cell death. Specifically, vitamin D3 activated important signaling pathways—AMPK, AKT, and GSK-3β—essential for promoting brain health post-stroke.
Furthermore, vitamin D3 enhanced the expression of factors that support blood vessel growth and decrease oxidative stress, both vital for neuronal protection. Some blocking effects of pyridoxal-5-phosphate suggested that vitamin D3 acts through specific receptors to achieve these protective benefits. This research highlights vitamin D3 as a promising treatment direction for stroke rehabilitation by regulating mitochondrial metabolism and promoting neuronal survival.
Our findings revealed that vitamin D3 effectively reduced the size of brain damage and improved neurological function in rats. We noted significant changes in various metrics, including a decrease in markers associated with cell death. Specifically, vitamin D3 activated important signaling pathways—AMPK, AKT, and GSK-3β—essential for promoting brain health post-stroke.
Furthermore, vitamin D3 enhanced the expression of factors that support blood vessel growth and decrease oxidative stress, both vital for neuronal protection. Some blocking effects of pyridoxal-5-phosphate suggested that vitamin D3 acts through specific receptors to achieve these protective benefits. This research highlights vitamin D3 as a promising treatment direction for stroke rehabilitation by regulating mitochondrial metabolism and promoting neuronal survival.
Read More
9
We investigated how vitamin D3, specifically 1α,25-dihydroxyvitamin D3, affects outcomes after a stroke in rats through a carefully designed study using a model of middle cerebral artery occlusion (MCAO). Our goal was to understand its role in boosting recovery, especially regarding neuroprotection and the growth of new blood vessels.
During our experiments, we measured the size of brain injury and blood flow around damaged areas. We found that rats treated with vitamin D3 experienced significantly smaller brain injuries and improved blood circulation compared to those that did not receive this treatment.
We also noted an increase in key proteins involved in the body's healing processes, which are crucial for promoting the growth of new blood vessels in the brain. These findings suggest that vitamin D3 activates pathways that lead to better recovery following a stroke.
In essence, vitamin D3 appears to support brain repair by enhancing circulation and influencing important growth factors. This exciting research indicates that vitamin D3 could be a potential new treatment avenue for stroke, highlighting the need for further studies in humans.
During our experiments, we measured the size of brain injury and blood flow around damaged areas. We found that rats treated with vitamin D3 experienced significantly smaller brain injuries and improved blood circulation compared to those that did not receive this treatment.
We also noted an increase in key proteins involved in the body's healing processes, which are crucial for promoting the growth of new blood vessels in the brain. These findings suggest that vitamin D3 activates pathways that lead to better recovery following a stroke.
In essence, vitamin D3 appears to support brain repair by enhancing circulation and influencing important growth factors. This exciting research indicates that vitamin D3 could be a potential new treatment avenue for stroke, highlighting the need for further studies in humans.
Read More
Most Useful Reviews
7.5
Great for eyesight
2 people found this helpful
Excellent for eye health. It has significantly improved my husband’s eyesight after he suffered a stroke in his eye.
Read More
Medical Researches
SCIENTIFIC SCORE
Possibly Effective
Based on 16 Researches
7.7
- All Researches
9
We explored the potential benefits of vitamin D3 (specifically, 1,25-vitamin D3) for protecting the brain during events such as strokes caused by impaired blood flow, known as cerebral ischemia-reperfusion injury (CIRI). In this study, rats received vitamin D3 supplementation for a week before undergoing a procedure that mimicked a stroke. The results were striking; those treated with vitamin D3 showed significant improvements in neurological function, with reduced areas of brain damage and more surviving neurons.
We also tested the effects of vitamin D3 on rat cortical neurons in a laboratory setting, specifically observing its influence on cell survival during oxygen-glucose deprivation and reoxygenation (a model for stroke). The vitamin D3 treatment not only improved cell viability but also appeared to reduce cell death and inflammation. Our analyses revealed that vitamin D3 boosts important protective proteins in the brain, which help combat oxidative stress and inhibit pathways linked to inflammatory cell death.
Overall, our findings strongly suggest that vitamin D3 could be a valuable resource in stroke management by protecting neurons through its antioxidant actions and reduction of harmful inflammation.
We also tested the effects of vitamin D3 on rat cortical neurons in a laboratory setting, specifically observing its influence on cell survival during oxygen-glucose deprivation and reoxygenation (a model for stroke). The vitamin D3 treatment not only improved cell viability but also appeared to reduce cell death and inflammation. Our analyses revealed that vitamin D3 boosts important protective proteins in the brain, which help combat oxidative stress and inhibit pathways linked to inflammatory cell death.
Overall, our findings strongly suggest that vitamin D3 could be a valuable resource in stroke management by protecting neurons through its antioxidant actions and reduction of harmful inflammation.
Read More
9
We investigated the impact of 1α,25-dihydroxyvitamin D3, commonly known as vitamin D3, on stroke recovery, particularly focusing on its effects on brain function after cerebral ischemia-reperfusion injury. Using a model called middle cerebral artery occlusion (MCAO), we aimed to understand how vitamin D3 influences mitochondrial health and signaling pathways crucial for brain recovery.
Our findings revealed that vitamin D3 effectively reduced the size of brain damage and improved neurological function in rats. We noted significant changes in various metrics, including a decrease in markers associated with cell death. Specifically, vitamin D3 activated important signaling pathways—AMPK, AKT, and GSK-3β—essential for promoting brain health post-stroke.
Furthermore, vitamin D3 enhanced the expression of factors that support blood vessel growth and decrease oxidative stress, both vital for neuronal protection. Some blocking effects of pyridoxal-5-phosphate suggested that vitamin D3 acts through specific receptors to achieve these protective benefits. This research highlights vitamin D3 as a promising treatment direction for stroke rehabilitation by regulating mitochondrial metabolism and promoting neuronal survival.
Our findings revealed that vitamin D3 effectively reduced the size of brain damage and improved neurological function in rats. We noted significant changes in various metrics, including a decrease in markers associated with cell death. Specifically, vitamin D3 activated important signaling pathways—AMPK, AKT, and GSK-3β—essential for promoting brain health post-stroke.
Furthermore, vitamin D3 enhanced the expression of factors that support blood vessel growth and decrease oxidative stress, both vital for neuronal protection. Some blocking effects of pyridoxal-5-phosphate suggested that vitamin D3 acts through specific receptors to achieve these protective benefits. This research highlights vitamin D3 as a promising treatment direction for stroke rehabilitation by regulating mitochondrial metabolism and promoting neuronal survival.
Read More
9
We investigated how vitamin D3, specifically 1α,25-dihydroxyvitamin D3, affects outcomes after a stroke in rats through a carefully designed study using a model of middle cerebral artery occlusion (MCAO). Our goal was to understand its role in boosting recovery, especially regarding neuroprotection and the growth of new blood vessels.
During our experiments, we measured the size of brain injury and blood flow around damaged areas. We found that rats treated with vitamin D3 experienced significantly smaller brain injuries and improved blood circulation compared to those that did not receive this treatment.
We also noted an increase in key proteins involved in the body's healing processes, which are crucial for promoting the growth of new blood vessels in the brain. These findings suggest that vitamin D3 activates pathways that lead to better recovery following a stroke.
In essence, vitamin D3 appears to support brain repair by enhancing circulation and influencing important growth factors. This exciting research indicates that vitamin D3 could be a potential new treatment avenue for stroke, highlighting the need for further studies in humans.
During our experiments, we measured the size of brain injury and blood flow around damaged areas. We found that rats treated with vitamin D3 experienced significantly smaller brain injuries and improved blood circulation compared to those that did not receive this treatment.
We also noted an increase in key proteins involved in the body's healing processes, which are crucial for promoting the growth of new blood vessels in the brain. These findings suggest that vitamin D3 activates pathways that lead to better recovery following a stroke.
In essence, vitamin D3 appears to support brain repair by enhancing circulation and influencing important growth factors. This exciting research indicates that vitamin D3 could be a potential new treatment avenue for stroke, highlighting the need for further studies in humans.
Read More
9
Calcitriol shows neuroprotective effects
We aimed to explore the effects of calcitriol, a form of vitamin D3, on brain injury following a stroke in rat models. The study involved inducing ischemia, a condition where blood supply to the brain is reduced, and then allowing reperfusion, where blood flow is restored. Prior to this, we administered calcitriol to the rats for seven days to see if it could provide neuroprotective benefits during this process.
Our findings revealed that calcitriol does indeed offer protection to the brain against injury caused by ischemia and reperfusion. We observed that it seems to work by reducing oxidative stress—harmful effects caused by free radicals—and activating a crucial cellular pathway known as the Nrf2/HO-1 pathway. This is significant because the activation of this pathway can help combat the damage caused by reduced blood flow and subsequent restoration.
Notably, our study utilized several tests to measure the extent of brain injury and the effectiveness of the treatment, including examining the behavioral deficits in the rats and the size of stroke-induced brain lesions. Through our research, we highlight how the interaction between calcitriol and a cellular protein might be pivotal in enhancing the brain's resilience against such injuries—a promising finding that could encourage further studies in human applications.
Our findings revealed that calcitriol does indeed offer protection to the brain against injury caused by ischemia and reperfusion. We observed that it seems to work by reducing oxidative stress—harmful effects caused by free radicals—and activating a crucial cellular pathway known as the Nrf2/HO-1 pathway. This is significant because the activation of this pathway can help combat the damage caused by reduced blood flow and subsequent restoration.
Notably, our study utilized several tests to measure the extent of brain injury and the effectiveness of the treatment, including examining the behavioral deficits in the rats and the size of stroke-induced brain lesions. Through our research, we highlight how the interaction between calcitriol and a cellular protein might be pivotal in enhancing the brain's resilience against such injuries—a promising finding that could encourage further studies in human applications.
Read More
8
We explored the impact of vitamin D3, also known as calcitriol, on outcomes following intracerebral hemorrhage (ICH), especially in individuals with vitamin D deficiency (VDD). Previous observations suggested that VDD might worsen clinical outcomes for stroke patients, prompting our research into whether acute vitamin D supplementation could make a significant difference.
Using mice models, we induced ICH in both vitamin D deficient and sufficient subjects. By assessing factors like the size of the hematomas and levels of hemorrhage, we aimed to understand how VDD might influence post-stroke survival and neurofunctional recovery.
Our findings revealed that mice experiencing VDD faced higher mortality rates and more significant motor deficits compared to their vitamin D sufficient counterparts after ICH. Additionally, their blood-brain barrier (BBB) appeared more disrupted, leading to worse overall outcomes. However, the silver lining came with acute vitamin D treatment, which showed promising results for improving those affected by VDD after stroke.
Overall, this research gives us valuable insights into how vitamin D3 could potentially help mitigate the adverse effects of VDD in stroke situations, emphasizing the importance of addressing vitamin deficiencies in stroke recovery.
Using mice models, we induced ICH in both vitamin D deficient and sufficient subjects. By assessing factors like the size of the hematomas and levels of hemorrhage, we aimed to understand how VDD might influence post-stroke survival and neurofunctional recovery.
Our findings revealed that mice experiencing VDD faced higher mortality rates and more significant motor deficits compared to their vitamin D sufficient counterparts after ICH. Additionally, their blood-brain barrier (BBB) appeared more disrupted, leading to worse overall outcomes. However, the silver lining came with acute vitamin D treatment, which showed promising results for improving those affected by VDD after stroke.
Overall, this research gives us valuable insights into how vitamin D3 could potentially help mitigate the adverse effects of VDD in stroke situations, emphasizing the importance of addressing vitamin deficiencies in stroke recovery.
Read More
User Reviews
USERS' SCORE
Good
Based on 1 Review
8.4
- All Reviews
- Positive Reviews
- Negative Reviews
7.5
Great for eyesight
2 people found this helpful
Excellent for eye health. It has significantly improved my husband’s eyesight after he suffered a stroke in his eye.
Read More
Frequently Asked Questions
No FAQs are available for this product and symptom.
References
- Chan AA, Lam TL, Liu J, Ng AC, Zhang C, et al. Acute calcitriol treatment mitigates vitamin D deficiency-associated mortality after intracerebral haemorrhage. Neurosci Lett. 2024;838:137922. 10.1016/j.neulet.2024.137922
- Song T, Li J, Xia Y, Hou S, Zhang X, et al. 1,25-D3 ameliorates ischemic brain injury by alleviating endoplasmic reticulum stress and ferroptosis: Involvement of vitamin D receptor and p53 signaling. Cell Signal. 2024;122:111331. 10.1016/j.cellsig.2024.111331
- Zhang SY, Yuan B, Luo WJ, Zhu LG, Zhang YJ, et al. Electro-scalp acupuncture regulates the expression of CYP27a1/b1, CYP24a and related inflammatory cytokines in ischemic cortex of rats with middle cerebral artery occlusion. Zhen Ci Yan Jiu. 2024;49:463. 10.13702/j.1000-0607.20221351
- Kouchek M, Shojaei S, Amniati S, Ghaffari M, Salarian S, et al. Effect of High-dose Vitamin D on IL-1β Blood Level in Patients with Moderate Stroke: A Randomized Clinical Trial. Anesth Pain Med. 2023;13:e138810. 10.5812/aapm-138810
- Qiao J, Ma H, Chen M, Bai J. Vitamin D alleviates neuronal injury in cerebral ischemia-reperfusion via enhancing the Nrf2/HO-1 antioxidant pathway to counteract NLRP3-mediated pyroptosis. J Neuropathol Exp Neurol. 2023;82:722. 10.1093/jnen/nlad047
- Vergatti A, Abate V, Zarrella AF, Manganelli F, Tozza S, et al. 25-Hydroxy-Vitamin D and Risk of Recurrent Stroke: A Dose Response Meta-Analysis. Nutrients. 2023;15. 10.3390/nu15030512
- Tajalli-Nezhad S, Mohammadi S, Atlasi MA, Kheiran M, Moghadam SE, et al. Calcitriol modulate post-ischemic TLR signaling pathway in ischemic stroke patients. J Neuroimmunol. 2023;375:578013. 10.1016/j.jneuroim.2022.578013
- Lasoń W, Jantas D, Leśkiewicz M, Regulska M, Basta-Kaim A. Vitamin D3 and Ischemic Stroke: A Narrative Review. Antioxidants (Basel). 2022;11. 10.3390/antiox11112120
- Li Y, Li X, Xu S, Zhao Y, Pang M, et al. 1,25-D3 attenuates cerebral ischemia injury by regulating mitochondrial metabolism the AMPK/AKT/GSK3β pathway. Front Aging Neurosci. 2022;14:1015453. 10.3389/fnagi.2022.1015453
- Eghbali BB, Ramezani S, Alavi CE, Ghayeghran AR, Herfeh SS, et al. The association of 25 (OH) D3 serum level with ischemic cerebrovascular accident risk, severity and outcome in Iranian population. Am J Hum Biol. 2022;34:e23810. 10.1002/ajhb.23810
- Li G, Li L, Adachi JD, Wang R, Ye Z, et al. Relationship between Serum 25-Hydroxyvitamin D Level and Risk of Recurrent Stroke. Nutrients. 2022;14. 10.3390/nu14091908
- Zhang Y, Mu Y, Ding H, Du B, Zhou M, et al. 1α,25-Dihydroxyvitamin D3 Promotes Angiogenesis After Cerebral Ischemia Injury in Rats by Upregulating the TGF-β/Smad2/3 Signaling Pathway. Front Cardiovasc Med. 2022;9:769717. 10.3389/fcvm.2022.769717
- Vahidinia Z, Khassafi N, Tameh AA, Karimian M, Zare-Dehghanani Z, et al. Calcitriol Ameliorates Brain Injury in the Rat Model of Cerebral Ischemia-Reperfusion Through Nrf2/HO-1 Signalling Axis: An in Silico and in Vivo Study. J Stroke Cerebrovasc Dis. 2022;31:106331. 10.1016/j.jstrokecerebrovasdis.2022.106331
- Khassafi N, Zahraei Z, Vahidinia Z, Karimian M, Azami Tameh A. Calcitriol Pretreatment Attenuates Glutamate Neurotoxicity by Regulating NMDAR and CYP46A1 Gene Expression in Rats Subjected to Transient Middle Cerebral Artery Occlusion. J Neuropathol Exp Neurol. 2022;81:252. 10.1093/jnen/nlac011
- Hesami O, Iranshahi S, Shahamati SZ, Sistanizd M, Pourheidar E, et al. The Evaluation of the Neuroprotective Effect of a Single High-Dose Vitamin D in Patients with Moderate Ischemic Stroke. Stroke Res Treat. 2022;2022:8955660. 10.1155/2022/8955660
- Wang L, Zhao XM, Wang FY, Wu JC, Wang Y. Effect of Vitamin D Supplementation on the Prognosis of Post-stroke Fatigue: A Retrospective Cohort Study. Front Neurol. 2021;12:690969. 10.3389/fneur.2021.690969
