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Sunday, 1 November 2015

Should we drink that coffee or not- the dilemma.

I am wondering what was the whole worrying about caffeine and dca combination  and if it was not  to cause tumor lysis or for some other reason. Here is a link to a study showing that coffeine has some positive effect for glioblastoma. I am not advising anybody to drink just wondering myself what to advise my brother.
http://cancerres.aacrjournals.org/content/70/3/1173.long

5 comments:

  1. That mouse study does show prolonged survival in mice given high dose caffeine, although the plasma levels of caffeine in those mice were higher than what humans would get with a few cups a day.

    Nobody has yet scientifically addressed the supposed interaction between DCA and caffeine. On the one hand we have reports that caffeine increases the effects of DCA and Anders Ferry purposely drinking lots of coffee during his DCA-based therapy a few years ago. On the other hand we have reports that this could be dangerous. It is difficult to make sense of these reports unless somebody decides to study this in a scientific way. I wonder if Peter Stacpoole knows anything about this.

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  2. In this video, the woman shares her experience that she drinks black tea along with DCA:

    https://www.youtube.com/watch?v=wqij8NEltdw

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  3. Here is a lot of information about the benefits of coffeine. Moreover, the authors believe that without caffeine, DCA may not work!

    http://www.thedcasite.com/DCA_protocol/DCA_Tea_Protocol.html

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  4. The history of successful treatment for glioblastoma (DCA + caffeine):
    http://www.thedcasite.com/Glioblastoma_DCA.html

    There are also reports of risks. But as one person here said, the main risk is glioblastoma.
    We decided to make a supply of cold black tea every day and drink it with food on the days of taking the DCA.

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  5. A new study on the possible role of caffeine:
    2018 https://www.ncbi.nlm.nih.gov/pubmed/29424319

    "Caffeine represents the most used psychoactive drug in the world acting as a non-selective adenosine receptor antagonist. It exerts an anti-cancer role in glioblastoma multiforme (GBM). This neoplasia is characterized by extensive hypoxic foci triggering hypoxia-inducible factors (HIFs) expression. Among these factors, HIF-1α performs a crucial role in the induction of vascular endothelium growth factor (VEGF), a key player in angiogenesis and cell migration. In this work, we have investigated whether caffeine counteracts GBM progression by modulating hypoxic event. Our results have indicated that this psychostimulant drug significantly reduced HIF-1α and VEGF expression in GBM cells exposed to hypoxia. This effect is mediated through inhibition of PI3K/Akt and MAPK/ERK signaling pathways both implied in HIFs regulation."

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