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Our findings revealed that a concerning 79.22% of participants showed vitamin D deficiency, with those having milder thrombus loads possessing significantly higher vitamin D levels compared to those with severe thrombus loads. Moreover, as we assessed the severity of coronary artery condition, we noted that patients with higher thrombus burden also had markedly greater scores of atherosclerosis.
Importantly, we found clear negative correlations between vitamin D levels and measures of thrombus burden. Lower vitamin D levels aligned with higher TIMI frame counts—meaning more extensive vascular obstruction—suggesting that vitamin D might play a role in blood clot formation.
Overall, we determined that low 25(OH)D3 levels could be an independent predictor of high coronary artery thrombus load in STEMI patients. These findings highlight the potential significance of monitoring and perhaps addressing vitamin D levels in this vulnerable group.
These patients were randomly divided into two groups—one receiving a single dose of 300,000 IU of vitamin D3 and the other group serving as a control. Over the course of four weeks, we measured the levels of vitamin D, P-selectin, and hs-CRP to assess any changes resulting from the treatment.
While we noticed a significant decline in both P-selectin and hs-CRP in those who received vitamin D3, the overall reductions were not substantial enough to indicate a major benefit. In comparison, only hs-CRP decreased significantly in the control group. Therefore, we conclude that, based on our findings, high-dose vitamin D3 does not show a strong impact on lowering P-selectin levels or hs-CRP in patients with VTE.
Our findings revealed that klotho-deficient platelets exhibited significantly reduced responses to activation, indicating that they might not form clots effectively. Specifically, we observed that calcium signaling pathways, essential for platelet activation and aggregation, were notably inhibited in these mice. The investigation utilized multiple methods, including measuring calcium levels and evaluating platelet function through various biochemical and cellular techniques.
Interestingly, when klotho-deficient mice were given a low-vitamin D diet, we discovered that their platelet function improved, suggesting a direct link between vitamin D3 levels and platelet activity. The reduced activity was associated with decreased expression of critical signaling proteins involved in calcium entry, which vitamin D3 helps regulate. Overall, our study presents evidence that vitamin D3 deficiency due to klotho absence may hinder proper blood clotting mechanisms.
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Our findings revealed that klotho-deficient platelets exhibited significantly reduced responses to activation, indicating that they might not form clots effectively. Specifically, we observed that calcium signaling pathways, essential for platelet activation and aggregation, were notably inhibited in these mice. The investigation utilized multiple methods, including measuring calcium levels and evaluating platelet function through various biochemical and cellular techniques.
Interestingly, when klotho-deficient mice were given a low-vitamin D diet, we discovered that their platelet function improved, suggesting a direct link between vitamin D3 levels and platelet activity. The reduced activity was associated with decreased expression of critical signaling proteins involved in calcium entry, which vitamin D3 helps regulate. Overall, our study presents evidence that vitamin D3 deficiency due to klotho absence may hinder proper blood clotting mechanisms.
Our findings revealed that 96 of these recipients experienced a first episode of VTE. We noticed a significant difference in rates of blood clots among those who received calcitriol alongside angiotensin-converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARBs). In fact, recipients on the combination therapy had a markedly lower rate of VTE, showing a promising 60% reduction in risk.
However, it is important to note that the isolated effect of vitamin D3 without other treatments wasn't fully determined in this study. While calcitriol showed favorable outcomes when used with blood pressure medications, further research could help clarify its individual impact on clot prevention. Overall, this research highlights the importance of collaborative strategies in managing thrombotic complications for transplant patients.
Through our experiments, we discovered that vitamin D3 helped reduce platelet aggregation triggered by the spike protein. We noticed that it inhibited certain signaling pathways inside platelets, thereby curbing their ability to clump together. Even when the spike protein was introduced, vitamin D3 managed to lessen the platelet response significantly.
Interestingly, our findings suggest that vitamin D3 works by modulating a specific integrin signaling pathway, known as integrin αIIbβ3 outside-in signaling. We observed that this process involved key proteins that play a role in platelet function. Combining vitamin D3 with a Src family kinase inhibitor showed no added benefits, indicating that vitamin D3's effects might be closely tied to these signaling pathways.
Overall, our study indicates that vitamin D3 has a beneficial role in mitigating the heightened platelet activity associated with the spike protein, offering insights into its potential use as a treatment option during COVID-19.
Our findings revealed that a concerning 79.22% of participants showed vitamin D deficiency, with those having milder thrombus loads possessing significantly higher vitamin D levels compared to those with severe thrombus loads. Moreover, as we assessed the severity of coronary artery condition, we noted that patients with higher thrombus burden also had markedly greater scores of atherosclerosis.
Importantly, we found clear negative correlations between vitamin D levels and measures of thrombus burden. Lower vitamin D levels aligned with higher TIMI frame counts—meaning more extensive vascular obstruction—suggesting that vitamin D might play a role in blood clot formation.
Overall, we determined that low 25(OH)D3 levels could be an independent predictor of high coronary artery thrombus load in STEMI patients. These findings highlight the potential significance of monitoring and perhaps addressing vitamin D levels in this vulnerable group.
The study we reviewed highlighted how VDRs might adjust the activity of various factors that influence thrombogenicity, which is the tendency to form clots. Specifically, a clinical trial indicated that calcitriol might help reduce thrombotic events related to cancer. It was noted that mice lacking VDR showed higher thrombogenic activity, indicating that VDR plays a significant role in blood clot regulation.
Overall, we found promising insights regarding the potential usefulness of VDR activators like vitamin D3 in thrombosis treatment. However, while the findings are encouraging, it's important to recognize that these results are tied to specific contexts, such as oncology-related scenarios.
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Frequently Asked Questions
A blood clot is a mass of blood that changes from a liquid to a gel, effectively forming a plug that can stop bleeding. This natural process, known as coagulation, is critical for preventing excessive blood loss when you sustain an injury. Blood clots can occur in various areas of the body, typically at the site of a wound, but they can also form within blood vessels without an obvious injury, which may lead to serious health complications.
While blood clots are essential for healing, they can pose significant health risks if they form inappropriately. For example, a deep vein thrombosis (DVT) occurs when a clot forms in a deep vein, usually in the legs, and can travel to the lungs, causing a life-threatening condition called a pulmonary embolism. Risk factors for blood clots include prolonged immobility, certain medical conditions, and the use of specific medications, among others. It’s important to recognize the symptoms of abnormal clotting, such as swelling, pain, and redness in the affected area, and seek medical attention if they occur.
Vitamin D3 K2 is a supplement that combines two vital nutrients: vitamin D3 (cholecalciferol) and vitamin K2 (menaquinone). Vitamin D3 is crucial for maintaining healthy bones and immune function, as it helps the body absorb calcium, which is essential for bone strength. It can be obtained through sunlight exposure, certain foods, and supplements. On the other hand, vitamin K2 plays a significant role in directing calcium to the bones and teeth while preventing it from depositing in the arteries and soft tissues, thus promoting cardiovascular health and overall well-being.
The synergy between vitamin D3 and K2 is particularly important because they work together to ensure that calcium is utilized effectively in the body. While vitamin D3 boosts calcium absorption, vitamin K2 ensures that this calcium is deposited properly in the bones rather than accumulating in the arteries. This combination is believed to support bone density, cardiovascular health, and overall vitality. Many health professionals recommend considering a D3 and K2 supplement, especially for individuals who may be at risk of deficiency or those who live in areas with limited sunlight exposure. Always consult a healthcare provider before starting any new supplement regimen.
Based on user reviews, individuals taking vitamin K2 for blood clot-related issues often notice results within a few weeks of starting the supplement. Users have reported positive effects on circulation and reduced bruising, suggesting that regular use of K2 can aid in managing blood clotting and strengthen blood vessels ((Read Review); (Read Review)). However, the timeline for experiencing these benefits may vary among users, as some needed to adjust their intake or type of K2 to achieve optimal results due to differing forms of the vitamin impacting effectiveness ((Read Review)).
Research on the relationship between vitamin D and blood clots has shown mixed results, although several studies suggest that vitamin D may play a role in modulating clotting activity. For instance, a study indicated that vitamin D3 reduced platelet aggregation triggered by the SARS-CoV-2 spike protein, presenting potential benefits in mitigating elevated blood clotting risks associated with COVID-19 [1]. Furthermore, another research highlighted that low vitamin D levels correlated with increased thrombus formation in heart attack patients, suggesting that addressing vitamin D deficiency could be beneficial for this demographic [2].
However, not all findings demonstrate a clear protective effect. For instance, high doses of vitamin D3 did not significantly improve markers of thrombosis in patients with venous thromboembolism, and a study focused on postmenopausal women found no overall reduction in the risk of blood clots when supplemented with calcium and vitamin D [3][4]. While some studies, such as one involving kidney transplant recipients, showed reduced rates of blood clots when vitamin D was used in combination with other medications, the isolated effects of vitamin D require further investigation to draw definitive conclusions [7]. Overall, while there are promising insights into vitamin D's potential role in blood clot management, further research is necessary to establish clear recommendations.
Users have reported varied improvements in symptoms upon taking vitamin K2 supplements, particularly concerning blood vessel health and circulation. Several individuals noted a significant reduction in bruising, suggesting that vitamin K2 can enhance blood clotting management and strengthen blood vessel integrity ((Read Review), (Read Review)) . These experiences indicate that K2 might not only improve circulation but also support overall vascular health when included as part of a balanced supplement regimen.
Based on user reviews, combining vitamin K2 with other supplements can significantly impact blood clot management, but users urge caution in selecting the right form of K2. Some individuals reported that the MK-7 form was preferable for those with blood-related issues, as the MK-4 form may thin the blood too much, potentially leading to complications such as blood clots (Read Review). Additionally, others noted the importance of being aware of personal health conditions, as K2 is involved in blood clotting processes, and its use should be monitored for individuals with thick blood or hypertension (Read Review).
Users highlighted experiences of enhanced vascular health when supplementing with vitamin K2 alongside vitamin D3 and calcium (Read Review). However, a critical note is that those unaware of K2's blood-thickening properties faced issues, emphasizing the need for careful consideration of supplements (Read Review). Therefore, while many users advocate for a combination of these supplements to support overall circulatory and vascular health, they stress the necessity of form selection and personal health assessment.
Based on user reviews, there are varied insights regarding the appropriate dosage of Vitamin D3 K2 for managing blood clots. One user highlighted a combination of 100 mcg of K2 along with 1000 IU of Vitamin D3 as a budget-friendly option, but also warned that the K2 form was not the effective MK-4, suggesting that users should instead consider the MK-7 form of K2 for better results and lower risk of blood thinning issues (Read Review). Additionally, another user noted their experience where taking K2 led to the formation of blood clots, underlining the importance of cautious supplement selection, particularly for those with blood coagulation issues (Read Review).
Through our experiments, we discovered that vitamin D3 helped reduce platelet aggregation triggered by the spike protein. We noticed that it inhibited certain signaling pathways inside platelets, thereby curbing their ability to clump together. Even when the spike protein was introduced, vitamin D3 managed to lessen the platelet response significantly.
Interestingly, our findings suggest that vitamin D3 works by modulating a specific integrin signaling pathway, known as integrin αIIbβ3 outside-in signaling. We observed that this process involved key proteins that play a role in platelet function. Combining vitamin D3 with a Src family kinase inhibitor showed no added benefits, indicating that vitamin D3's effects might be closely tied to these signaling pathways.
Overall, our study indicates that vitamin D3 has a beneficial role in mitigating the heightened platelet activity associated with the spike protein, offering insights into its potential use as a treatment option during COVID-19.
Our findings revealed that a concerning 79.22% of participants showed vitamin D deficiency, with those having milder thrombus loads possessing significantly higher vitamin D levels compared to those with severe thrombus loads. Moreover, as we assessed the severity of coronary artery condition, we noted that patients with higher thrombus burden also had markedly greater scores of atherosclerosis.
Importantly, we found clear negative correlations between vitamin D levels and measures of thrombus burden. Lower vitamin D levels aligned with higher TIMI frame counts—meaning more extensive vascular obstruction—suggesting that vitamin D might play a role in blood clot formation.
Overall, we determined that low 25(OH)D3 levels could be an independent predictor of high coronary artery thrombus load in STEMI patients. These findings highlight the potential significance of monitoring and perhaps addressing vitamin D levels in this vulnerable group.
We divided the patients into two groups: one received a high dose of vitamin D—50,000 IU weekly for eight weeks followed by less frequent doses—while the control group did not receive any vitamin D. After one and three months, we measured levels of two key biomarkers related to blood clotting: P-selectin and hs-CRP.
We discovered that there was no significant decrease in either biomarker in both groups over the study period. This suggests that treating vitamin D deficiency doesn’t meaningfully impact these specific markers of thrombosis in patients with clotting issues.
However, we did find something interesting. Those who received vitamin D treatment appeared to manage their anticoagulant therapy with warfarin more effectively, using lower doses of the medication. While our initial hypothesis about vitamin D’s direct effect on blood clot markers didn’t hold, this potential interaction with warfarin is intriguing and warrants further investigation in larger studies to better understand the relationship between vitamin D and blood clotting.
Our analysis looked closely at the rates of VTE between those taking the supplements and those on the placebo. We found that there was no significant difference in the overall incidence of VTE between the two groups—320 events in the supplement group versus 348 in the placebo group. This translates to a hazard ratio of 0.92, suggesting that the combined supplementation did not lower the risk of blood clots for these generally healthy women.
Interestingly, while the overall risk didn’t change, we observed a noticeable reduction in the risk of idiopathic VTE (where there’s no clear cause) among women who took calcium and vitamin D3, with 40 events compared to 65 in the placebo group. This finding may call for deeper investigation, as it hints at a potential benefit that could be worth exploring further.
To sum up, regular supplementation with calcium and vitamin D3 does not seem to reduce the overall risk of blood clots in postmenopausal women. However, our observation of a lower risk for idiopathic blood clots in the treatment group offers a glimmer of hope for future studies on this topic.
Our findings revealed that 96 of these recipients experienced a first episode of VTE. We noticed a significant difference in rates of blood clots among those who received calcitriol alongside angiotensin-converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARBs). In fact, recipients on the combination therapy had a markedly lower rate of VTE, showing a promising 60% reduction in risk.
However, it is important to note that the isolated effect of vitamin D3 without other treatments wasn't fully determined in this study. While calcitriol showed favorable outcomes when used with blood pressure medications, further research could help clarify its individual impact on clot prevention. Overall, this research highlights the importance of collaborative strategies in managing thrombotic complications for transplant patients.
References
- Wang R, Tian Z, Wang C, Zhang B, Zhu M, et al. 1,25-Dihydroxyvitamin D3 attenuates platelet aggregation potentiated by SARS-CoV-2 spike protein via inhibiting integrin αIIbβ3 outside-in signaling. Cell Biochem Funct. 2024;42:e4039. doi:10.1002/cbf.4039
- 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
- Hejazi ME, Modarresi-Ghazani F, Hamishehkar H, Mesgari-Abbasi M, Dousti S, et al. The Effect of Treatment of Vitamin D Deficiency on the Level of P-Selectin and hs-CRP in Patients With Thromboembolism: A Pilot Randomized Clinical Trial. J Clin Pharmacol. 2017;57:40. doi:10.1002/jcph.774
- Blondon M, Rodabough RJ, Budrys N, Johnson KC, Berger JS, et al. The effect of calcium plus vitamin D supplementation on the risk of venous thromboembolism. From the Women's Health Initiative Randomized Controlled Trial. Thromb Haemost. 2015;113:999. doi:10.1160/TH14-05-0478
- Gholami K, Talasaz AH, Entezari-Maleki T, Salarifar M, Hadjibabaie M, et al. The Effect of High-Dose Vitamin D3 on Soluble P-Selectin and hs-CRP Level in Patients With Venous Thromboembolism: A Randomized Clinical Trial. Clin Appl Thromb Hemost. 2016;22:483. doi:10.1177/1076029614568715
- Borst O, Münzer P, Schmid E, Schmidt EM, Russo A, et al. 1,25(OH)2 vitamin D3-dependent inhibition of platelet Ca2+ signaling and thrombus formation in klotho-deficient mice. FASEB J. 2014;28:2108. doi:10.1096/fj.13-239277
- Moscarelli L, Zanazzi M, Bertoni E, Caroti L, Rosso G, et al. Renin angiotensin system blockade and activated vitamin D as a means of preventing deep vein thrombosis in renal transplant recipients. Clin Nephrol. 2011;75:440.
- Jorde R, Sneve M, Torjesen P, Figenschau Y, Hansen JB. Parameters of the thrombogram are associated with serum 25-hydroxyvitamin D levels at baseline, but not affected during supplementation with vitamin D. Thromb Res. 2010;125:e210. doi:10.1016/j.thromres.2009.12.011
- Wu-Wong JR. Are vitamin D receptor activators useful for the treatment of thrombosis?. Curr Opin Investig Drugs. 2009;10:919.
