Medical Researches
Moderately Effective
Based on 25 Researches
We explored the effects of folate, a form of vitamin B, on heart problems associated with TANGO2-deficiency disorder (TDD). This genetic condition can lead to dangerous heart rhythms that don’t respond well to standard treatments. To dive deeper into this issue, we established patient-derived heart cells, known as iPSC-CMs, to mimic the heart abnormalities seen in TDD.
In our observations, we found that high doses of folate almost completely eliminated arrhythmias in these heart cells. Interestingly, our clinical observations revealed that TDD patients taking multivitamins, particularly those high in B vitamins, experienced a significant reduction in cardiac crises. This suggests that folate may play a critical role in protecting against these life-threatening heart issues.
Our findings not only highlight the potential of folate as an effective treatment but also emphasize the importance of considering dietary supplements in managing cardiac risks in patients with TDD. Thus, we believe that boosting folate intake could offer a valuable strategy to enhance heart health in those affected by this disorder.
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Vitamin B6 shows heart health promiseProtective effects of pyridoxine, amlodipine, and their combination in a vasopressin-induced angina model in rats.
Limited relevance to heart disease
We explored the effects of vitamin B6 (pyridoxine) on heart health, specifically looking at its protective qualities against angina provoked by vasopressin in a rat model. Vasopressin was administered to observe its impact on heart function, which included elevated stress on the heart indicated by changes on the electrocardiogram and increased cardiac enzymes.
The study found that when we gave rats pyridoxine in varying doses, it effectively reduced the ST elevation and heart rate changes caused by vasopressin. Notably, higher doses of pyridoxine (7 mg/kg) showed significant protective effects, outperforming both amlodipine and isosorbide. In addition, we observed that pyridoxine at these doses helped prevent cardiac tissue damage and improved heart structure.
Interestingly, while combining pyridoxine with amlodipine led to a trend of increased adverse cardiovascular events, the results underscored the potential of vitamin B6 in enhancing heart health. It appears vitamin B6 may work by improving certain functions in the body that support heart health, such as better blood vessel function and reduced levels of harmful substances.
Overall, our findings suggest that vitamin B6 could serve as a promising agent in preventing coronary heart disease, but more research is necessary to fully explore its benefits and practical applications in humans.
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We explored the effects of vitamin B6 (VB6) on heart recovery after an acute myocardial infarction (AMI). The study aimed to determine if VB6 could promote angiogenesis, the process of new blood vessel formation, which is crucial for healing the heart after such an event.
To investigate this, we looked at the ability of VB6 to enhance cell migration and tube formation in human umbilical vein endothelial cells, which are key players in the formation of blood vessels. Our results showed that VB6 not only encouraged these processes but also increased the phosphorylation of AMPK, a protein that plays a vital role in cellular energy regulation.
Importantly, these beneficial effects of VB6 on cell behavior were found to depend on AMPK activation. When we used specific inhibitors to block AMPK, the positive changes from VB6 were no longer observed. Additionally, in an animal model, long-term supplementing with VB6 led to significant improvements in heart function, more new blood vessel growth, and reduced inflammation markers in mice after AMI.
In summary, our findings suggest that vitamin B6 could be an effective support for heart recovery due to its role in promoting angiogenesis through AMPK activation following heart attacks. Given that VB6 shows promise in limiting ischemic heart injury, it could be a valuable addition to existing heart disease treatments.
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Vitamin B-6 aids heart healthVitamin B-6 Prevents Heart Failure with Preserved Ejection Fraction Through Downstream of Kinase 3 in a Mouse Model.
Relevant but dietary factors involved
We examined how vitamin B-6 might play a role in preventing heart failure with preserved ejection fraction (HFpEF), a condition that often results from changes in heart-related immune cells called macrophages. Our research was based on a mouse model that mimicked HFpEF through a high-fat diet paired with a specific supplement. By monitoring heart function using various imaging techniques, as well as examining heart tissue for changes, we gathered important insights into vitamin B-6's potential benefits.
We found that when vitamin B-6 was added to the diet of mice prone to HFpEF, it significantly improved several heart failure symptoms. There were notable enhancements in heart function, reducing pressure in the heart and allowing for better exercise capacity. However, we made a crucial discovery: the positive effects of vitamin B-6 were diminished when we examined mice lacking a specific protein called DOK3. This suggests that DOK3 is key to vitamin B-6’s success in mitigating heart failure symptoms.
Essentially, our findings indicate that vitamin B-6 might lower the risk of heart failure by halting harmful changes in cardiac macrophages thanks to its ability to boost DOK3 signaling. This research offers exciting possibilities for a new therapeutic approach aimed at improving heart health and managing HFpEF effectively.
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We focused on how pyridoxamine, a form of vitamin B6, impacts heart health during treatment with doxorubicin, a common cancer drug. In an experimental setup with Sprague Dawley rats, we observed that those receiving doxorubicin experienced a decrease in heart function, specifically a reduced left ventricular ejection fraction, and an increase in heart volume.
Notably, when we added pyridoxamine to the treatment, these harmful effects were significantly lessened. The rats that took pyridoxamine alongside doxorubicin maintained better heart function compared to those who only received doxorubicin. This suggests that pyridoxamine acts as a protective agent for the heart, countering some of the negative impacts caused by doxorubicin.
However, we also investigated how doxorubicin and pyridoxamine affected breast cancer cells in the lab. While doxorubicin effectively reduced cancer cell viability and increased cell death, pyridoxamine didn’t change these outcomes. This indicates that while pyridoxamine can preserve heart health during chemotherapy, it doesn’t interfere with the cancer-fighting effects of doxorubicin.
Overall, this research highlights pyridoxamine's promising role as a cardioprotectant during cancer treatment, allowing for heart preservation without diminishing the effectiveness of anticancer therapies.
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User Reviews
Heart health improvements
Finding this supplement was a revelation; it combines active folic acid and B12 in a sublingual form, helping absorption and potentially lowering heart disease risks. I noticed a lift in mood and energy shortly after taking it. The slight chemical sweet taste is the only downside for me.
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I switched to this more affordable complex to lower my homocysteine. It’s vital for preventing heart disease, and I'm pleased with the results—my homocysteine dropped significantly, and it’s particularly important for women trying to conceive.
Protection against disease
I take Jarrow Formulas each morning to regulate my homocysteine, as high levels can damage my arteries and increase heart disease risk. Complementing it with Omega-3 seems effective for my overall heart health.
After taking this supplement, my cholesterol levels improved significantly. It’s integral to managing heart disease risk alongside dietary changes and exercise.
This supplement lowers homocysteine, a marker for heart disease, particularly when taken with Jarrow TMG. My levels normalised within two months. I take one tablet after a meal but avoid coffee or tea around that time. It’s important for overall health.