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SCIENTIFIC SCORE
Moderately Effective
Based on 5 Researches
8.4
USERS' SCORE
Good
Based on 1 Review
8.5
Supplement Facts
Serving Size: 1 Veggie Softgel
Amount Per Serving
%DV
Coenzyme Q10 (Ubiquinone)
300 mg
†
Black Pepper Ext. (Piper nigrum)(fruit)(standardized to contain 95% Piperine)(BioPerine®)
5 mg
†
Top Medical Research Studies
9
CoQ10 reduces harmful blood clots
Coenzyme Q10 Upregulates Platelet cAMP/PKA Pathway and Attenuates Integrin αIIbβ3 Signaling and Thrombus Growth.
Direct assessment of CoQ10 effects
We explored how coenzyme Q10 (CoQ10), a natural compound found in various foods, impacts blood clotting functions. Through a well-structured study, we utilized a randomized, double-blind, placebo-controlled trial with dyslipidemic patients, alongside in vitro tests on human platelets.
Our findings demonstrated that CoQ10 effectively reduces platelet aggregation, granule secretion, platelet spreading, and clot retraction. This means that CoQ10 can help prevent excessive blood clot formation, which is crucial for cardiovascular health.
We observed that CoQ10 works mainly by enhancing a signaling pathway involving cyclic AMP (cAMP) which ultimately diminishes the signaling of integrin αIIbβ3, a key player in platelet function. In addition, the treatment showed promising results in reducing thrombus growth in an animal model, suggesting significant in vivo benefits as well.
This study highlights the potential of CoQ10 supplementation as a protective measure for individuals at risk of cardiovascular diseases by regulating platelet-related processes involved in clotting.
Our findings demonstrated that CoQ10 effectively reduces platelet aggregation, granule secretion, platelet spreading, and clot retraction. This means that CoQ10 can help prevent excessive blood clot formation, which is crucial for cardiovascular health.
We observed that CoQ10 works mainly by enhancing a signaling pathway involving cyclic AMP (cAMP) which ultimately diminishes the signaling of integrin αIIbβ3, a key player in platelet function. In addition, the treatment showed promising results in reducing thrombus growth in an animal model, suggesting significant in vivo benefits as well.
This study highlights the potential of CoQ10 supplementation as a protective measure for individuals at risk of cardiovascular diseases by regulating platelet-related processes involved in clotting.
Read More
9
CoQ10 reduces blood clot risk
Mitochondrial dysfunction in antiphospholipid syndrome: implications in the pathogenesis of the disease and effects of coenzyme Q(10) treatment.
High relevance due to study findings
We investigated how coenzyme Q(10) (CoQ(10)) affects blood clot risk in patients with antiphospholipid syndrome (APS), particularly focusing on oxidative stress and mitochondrial dysfunction. Our analysis compared 43 APS patients with 38 healthy individuals.
We observed a notable increase in prothrombotic and inflammatory indicators in the APS group. Specifically, the resurgence of oxidative stress was marked by higher peroxide production and altered mitochondrial function in their blood cells.
To explore the potential benefits of CoQ(10), we preincubated healthy monocytes with it before exposing them to dangerous IgG-antiphospholipid antibodies. Remarkably, CoQ(10) treatment reduced oxidative stress, improved mitochondrial health, and decreased the production of critical proteins associated with clotting and inflammation.
These findings suggest that CoQ(10) might help restore balance in the body's systems, reducing the risk of blood clots in individuals with APS by targeting the underlying oxidative mechanisms. Overall, our research points to the promise of CoQ(10) as a therapeutic option for APS patients facing increased blood clot risks.
We observed a notable increase in prothrombotic and inflammatory indicators in the APS group. Specifically, the resurgence of oxidative stress was marked by higher peroxide production and altered mitochondrial function in their blood cells.
To explore the potential benefits of CoQ(10), we preincubated healthy monocytes with it before exposing them to dangerous IgG-antiphospholipid antibodies. Remarkably, CoQ(10) treatment reduced oxidative stress, improved mitochondrial health, and decreased the production of critical proteins associated with clotting and inflammation.
These findings suggest that CoQ(10) might help restore balance in the body's systems, reducing the risk of blood clots in individuals with APS by targeting the underlying oxidative mechanisms. Overall, our research points to the promise of CoQ(10) as a therapeutic option for APS patients facing increased blood clot risks.
Read More
8
Ubiquinol reduces clot risk markers
Ubiquinol Effects on Antiphospholipid Syndrome Prothrombotic Profile: A Randomized, Placebo-Controlled Trial.
Directly addresses coenzyme Q10 effects
We conducted a randomized, controlled trial to explore how ubiquinol, a form of coenzyme Q10, affects markers of inflammation and blood clotting in patients with antiphospholipid syndrome (APS), a condition linked to an increased risk of blood clots.
In this study, thirty-six APS patients were assigned to receive either ubiquinol or a placebo for one month. Of these, thirty-three completed the intervention. The results showed that ubiquinol significantly raised plasma levels of coenzyme Q, which in turn improved endothelial function, a crucial factor for maintaining proper blood flow and reducing clot risk.
Notably, we observed that ubiquinol decreased the expression of certain proteins tied to blood clotting and inflammation. It also inhibited specific biochemical pathways associated with thrombosis while improving mitochondrial health within cells. This suggests a potential dual benefit: reducing inflammation and enhancing cellular health may help manage the prothrombotic profile seen in APS.
Overall, our findings indicate that ubiquinol could serve as a beneficial adjunct therapy in APS treatment, with minimal side effects and promising therapeutic potential regarding blood clot risk.
In this study, thirty-six APS patients were assigned to receive either ubiquinol or a placebo for one month. Of these, thirty-three completed the intervention. The results showed that ubiquinol significantly raised plasma levels of coenzyme Q, which in turn improved endothelial function, a crucial factor for maintaining proper blood flow and reducing clot risk.
Notably, we observed that ubiquinol decreased the expression of certain proteins tied to blood clotting and inflammation. It also inhibited specific biochemical pathways associated with thrombosis while improving mitochondrial health within cells. This suggests a potential dual benefit: reducing inflammation and enhancing cellular health may help manage the prothrombotic profile seen in APS.
Overall, our findings indicate that ubiquinol could serve as a beneficial adjunct therapy in APS treatment, with minimal side effects and promising therapeutic potential regarding blood clot risk.
Read More
Most Useful Reviews
8.8
Improved blood pressure
After taking it for two months, my blood pressure appears to have improved.
Read More
Medical Researches
SCIENTIFIC SCORE
Moderately Effective
Based on 5 Researches
8.4
9
CoQ10 reduces harmful blood clots
Coenzyme Q10 Upregulates Platelet cAMP/PKA Pathway and Attenuates Integrin αIIbβ3 Signaling and Thrombus Growth.
Direct assessment of CoQ10 effects
We explored how coenzyme Q10 (CoQ10), a natural compound found in various foods, impacts blood clotting functions. Through a well-structured study, we utilized a randomized, double-blind, placebo-controlled trial with dyslipidemic patients, alongside in vitro tests on human platelets.
Our findings demonstrated that CoQ10 effectively reduces platelet aggregation, granule secretion, platelet spreading, and clot retraction. This means that CoQ10 can help prevent excessive blood clot formation, which is crucial for cardiovascular health.
We observed that CoQ10 works mainly by enhancing a signaling pathway involving cyclic AMP (cAMP) which ultimately diminishes the signaling of integrin αIIbβ3, a key player in platelet function. In addition, the treatment showed promising results in reducing thrombus growth in an animal model, suggesting significant in vivo benefits as well.
This study highlights the potential of CoQ10 supplementation as a protective measure for individuals at risk of cardiovascular diseases by regulating platelet-related processes involved in clotting.
Our findings demonstrated that CoQ10 effectively reduces platelet aggregation, granule secretion, platelet spreading, and clot retraction. This means that CoQ10 can help prevent excessive blood clot formation, which is crucial for cardiovascular health.
We observed that CoQ10 works mainly by enhancing a signaling pathway involving cyclic AMP (cAMP) which ultimately diminishes the signaling of integrin αIIbβ3, a key player in platelet function. In addition, the treatment showed promising results in reducing thrombus growth in an animal model, suggesting significant in vivo benefits as well.
This study highlights the potential of CoQ10 supplementation as a protective measure for individuals at risk of cardiovascular diseases by regulating platelet-related processes involved in clotting.
Read More
9
CoQ10 reduces blood clot risk
Mitochondrial dysfunction in antiphospholipid syndrome: implications in the pathogenesis of the disease and effects of coenzyme Q(10) treatment.
High relevance due to study findings
We investigated how coenzyme Q(10) (CoQ(10)) affects blood clot risk in patients with antiphospholipid syndrome (APS), particularly focusing on oxidative stress and mitochondrial dysfunction. Our analysis compared 43 APS patients with 38 healthy individuals.
We observed a notable increase in prothrombotic and inflammatory indicators in the APS group. Specifically, the resurgence of oxidative stress was marked by higher peroxide production and altered mitochondrial function in their blood cells.
To explore the potential benefits of CoQ(10), we preincubated healthy monocytes with it before exposing them to dangerous IgG-antiphospholipid antibodies. Remarkably, CoQ(10) treatment reduced oxidative stress, improved mitochondrial health, and decreased the production of critical proteins associated with clotting and inflammation.
These findings suggest that CoQ(10) might help restore balance in the body's systems, reducing the risk of blood clots in individuals with APS by targeting the underlying oxidative mechanisms. Overall, our research points to the promise of CoQ(10) as a therapeutic option for APS patients facing increased blood clot risks.
We observed a notable increase in prothrombotic and inflammatory indicators in the APS group. Specifically, the resurgence of oxidative stress was marked by higher peroxide production and altered mitochondrial function in their blood cells.
To explore the potential benefits of CoQ(10), we preincubated healthy monocytes with it before exposing them to dangerous IgG-antiphospholipid antibodies. Remarkably, CoQ(10) treatment reduced oxidative stress, improved mitochondrial health, and decreased the production of critical proteins associated with clotting and inflammation.
These findings suggest that CoQ(10) might help restore balance in the body's systems, reducing the risk of blood clots in individuals with APS by targeting the underlying oxidative mechanisms. Overall, our research points to the promise of CoQ(10) as a therapeutic option for APS patients facing increased blood clot risks.
Read More
8
Ubiquinol reduces clot risk markers
Ubiquinol Effects on Antiphospholipid Syndrome Prothrombotic Profile: A Randomized, Placebo-Controlled Trial.
Directly addresses coenzyme Q10 effects
We conducted a randomized, controlled trial to explore how ubiquinol, a form of coenzyme Q10, affects markers of inflammation and blood clotting in patients with antiphospholipid syndrome (APS), a condition linked to an increased risk of blood clots.
In this study, thirty-six APS patients were assigned to receive either ubiquinol or a placebo for one month. Of these, thirty-three completed the intervention. The results showed that ubiquinol significantly raised plasma levels of coenzyme Q, which in turn improved endothelial function, a crucial factor for maintaining proper blood flow and reducing clot risk.
Notably, we observed that ubiquinol decreased the expression of certain proteins tied to blood clotting and inflammation. It also inhibited specific biochemical pathways associated with thrombosis while improving mitochondrial health within cells. This suggests a potential dual benefit: reducing inflammation and enhancing cellular health may help manage the prothrombotic profile seen in APS.
Overall, our findings indicate that ubiquinol could serve as a beneficial adjunct therapy in APS treatment, with minimal side effects and promising therapeutic potential regarding blood clot risk.
In this study, thirty-six APS patients were assigned to receive either ubiquinol or a placebo for one month. Of these, thirty-three completed the intervention. The results showed that ubiquinol significantly raised plasma levels of coenzyme Q, which in turn improved endothelial function, a crucial factor for maintaining proper blood flow and reducing clot risk.
Notably, we observed that ubiquinol decreased the expression of certain proteins tied to blood clotting and inflammation. It also inhibited specific biochemical pathways associated with thrombosis while improving mitochondrial health within cells. This suggests a potential dual benefit: reducing inflammation and enhancing cellular health may help manage the prothrombotic profile seen in APS.
Overall, our findings indicate that ubiquinol could serve as a beneficial adjunct therapy in APS treatment, with minimal side effects and promising therapeutic potential regarding blood clot risk.
Read More
8
CoQ10 improves plaque quality
Effect of coenzyme Q10 on experimental atherosclerosis and chemical composition and quality of atheroma in rabbits.
Moderate relevance to blood clotting
We conducted a study to see how coenzyme Q10 (CoQ10) treatment affects blood clotting, particularly in the context of atherosclerosis. In our controlled trial involving rabbits, we compared the effects of CoQ10 with a placebo over 24 weeks while the animals were fed a diet high in trans fatty acids.
We observed that CoQ10 administration led to significant reductions in markers of oxidative damage, such as thiobarbituric acid reactive substances and malondialdehyde. These changes suggested that CoQ10 helped lower oxidative stress without directly affecting lipid levels.
Importantly, we found that the size and quality of atheromas, or plaques, were better in the group receiving CoQ10. Atherosclerosis scores and the presence of complications like ulceration or thrombosis were also notably lower compared to the placebo group. However, while we noted improvements in plaque quality and associated factors, the effects specific to blood clotting were not directly examined in terms of statistical significance.
Overall, our findings suggest that while coenzyme Q10 might benefit atherosclerosis and enhance plaque quality, its effects specifically on blood clotting remain less clear. Further research could clarify this aspect.
We observed that CoQ10 administration led to significant reductions in markers of oxidative damage, such as thiobarbituric acid reactive substances and malondialdehyde. These changes suggested that CoQ10 helped lower oxidative stress without directly affecting lipid levels.
Importantly, we found that the size and quality of atheromas, or plaques, were better in the group receiving CoQ10. Atherosclerosis scores and the presence of complications like ulceration or thrombosis were also notably lower compared to the placebo group. However, while we noted improvements in plaque quality and associated factors, the effects specific to blood clotting were not directly examined in terms of statistical significance.
Overall, our findings suggest that while coenzyme Q10 might benefit atherosclerosis and enhance plaque quality, its effects specifically on blood clotting remain less clear. Further research could clarify this aspect.
Read More
8
CoQ10 effects on blood clotting
Could coenzyme Q10 affect hemostasis by inhibiting platelet vitronectin (CD51/CD61) receptor?
Relevant study on CoQ10's impact
We explored the effects of coenzyme Q10 (CoQ10) on blood clotting mechanisms and specifically how it influences platelets. In our study, we had 15 human participants and 10 swine who received 100 mg of CoQ10 twice a day for 20 days, alongside their regular diet. This regimen led to a remarkable three-fold increase in total serum CoQ10 levels.
During this period, we observed noteworthy declines in several important markers associated with blood clotting, including plasma fibronectin, thromboxane B2, prostacyclin, and endothelin-1. One of the most significant findings was the consistent inhibition of the vitronectin receptor on platelets throughout the treatment. This suggests that CoQ10 might directly affect how platelets function, potentially reducing the risk of dangerous blood clots.
Overall, our research outlines how dietary CoQ10 could play a role in managing blood clotting by impacting platelet behavior. These results may help explain why CoQ10 supplementation has been associated with fewer thrombotic complications in certain patients.
During this period, we observed noteworthy declines in several important markers associated with blood clotting, including plasma fibronectin, thromboxane B2, prostacyclin, and endothelin-1. One of the most significant findings was the consistent inhibition of the vitronectin receptor on platelets throughout the treatment. This suggests that CoQ10 might directly affect how platelets function, potentially reducing the risk of dangerous blood clots.
Overall, our research outlines how dietary CoQ10 could play a role in managing blood clotting by impacting platelet behavior. These results may help explain why CoQ10 supplementation has been associated with fewer thrombotic complications in certain patients.
Read More
User Reviews
USERS' SCORE
Good
Based on 1 Review
8.5
8.8
Improved blood pressure
After taking it for two months, my blood pressure appears to have improved.
