High reading

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This topic contains 6 replies, has 3 voices, and was last updated by  Dan52 2 years, 7 months ago.

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    a friend had prostate cancer started DCA 4 months ago his PSA reading when he started DCA treatment was 88 after 4 months treatment with DCA only ( no chemotherapy or radiation) his PAS reading went up to 211 it was shock for everyone does anyone have explanation ?


    Hi hopeful11,

    It would help to know at what clinical stage your friend was diagnosed and when, also where the tumors are — bone, soft tissue, bladder or other organs. What was his PSA at Dx and what was his Gleason score?

    What treatments aside from DCA has your friend tried? You do not mention Triple Hormonal Blockade, (CHB) which is front-line standare of care. If he has not yet used hormonal blockade he should see his urologist or oncologist right away and ask about CHB. This therapy may reduce his PSA reading from 211 to 0.05 (ideally), and he then could coast for a couple of years

    Chemotherapy will not extend survival time for prostate cancer patients, it is used for pain relief only. Sometimes radiation is utilized with curative intent and sometimes for palliative purposes.


    … continued (hit "send" too soon.)

    No two people respond to DCA in the same way, and some do not respond at all. Some patients report better results using a companion treatment, or adjunct. Caffeine is one example. But finding the right adjunct is a hit-or-miss proposition and cancer patients cannot afford to make a mis-step.

    I'm a Stage IV prostate cancer patient myself, and failed all the front-line treatments my oncologist could offer (we found the cancer too late). At that point I had nothing to lose so I started DCA, 15mg/kg. I saw excellent results in 30 days and the cancer was in remission at 60 days. But I was one of the lucky ones and I would never recommend "alternative" therapies in place of those we know to work for most people. Given the rise in PSA score you report after 4 months, I'm guessing DCA will not help your friend. He should see an oncologist and put the brakes on this thing. From your brief report, hormonal blockade may be his best option.

    Best wishes to your friend,




    Hi Mito,

    could you please inform if you had also prostate nodules. Last Nov my PSA was 2.3

    *but* free/total PSA ratio was 0.06 (ok should be > 0.15). I started DCA (10 mg/kg/day) last Jan and now PSA is 0.88 with free/total = 0.12. Next weeks I'll have my first prostate nodule biopsy and right now I don't know if it contains cancer cells. 





    Just to confirm Mito's words "some do not respond at all": "We hypothesized that DCA may have differential effects on hypoxic versus normoxic colorectal cancer cells, and

    found that while some cell lines are refractory to DCA’s effects, most colorectal cancer cells examined actually displayed enhanced survival under hypoxic conditions in

    the presence of DCA. Consistent with this, DCA treated xenografts showed no anti-tumor effect but instead there was enhanced growth of treated tumors. Our findings suggest

    that DCA may have differential effects on cancer cell survival depending on the regional microenvironment within treated tumors, which may complicate its usefulness

    as an adjuvant anti-cancer therapy." (Sodium dichloroacetate (DCA) reduces apoptosis in colorectal tumor hypoxia, http://www.sciencedirect.com/science/article/pii/S030438351000251X ).

    "Thus, although DCA inhibits growth of a variety of cancer cells, the effect and the underlying mechanisms seem to be cell-type dependent. A likely explanation for these differential effects could be the difference in expression of the PDK isoenzymes in the cancer cells examined. Dichloroacetate is a non-specific inhibitor of PDK (Whitehouse and Randle, 1973), and has a different Ki for each of the four PDK isoenzymes (Bowker-Kinley et al, 1998). In addition, the four PDK isoenzymes are known to be differentially expressed in various tissues. Thus, there is a need to develop inhibitors to the individual PDK isoenzymes that should allow cancer cell-type-specific metabolic manipulation."

    (Dichloroacetate induces apoptosis and cell-cycle arrest in colorectal cancer cells. , http://www.nature.com/bjc/journal/v102/n12/full/6605701a.html )





    Hi Mito , hi Dan

    Thx a lot for all ur valuable info to be honest I don’t have the full details of my friend’s case but I’ll ask him to register here and give us more details about his case




    To underline the importance of research about cancer metabolism, that involves also the DCA, I add a link to James D. Watson (Nobel Prize) article on  NYT:  "we may have to turn our main research focus away from decoding the genetic instructions behind cancer and toward understanding the chemical reactions within cancer cells." (http://www.nytimes.com/2009/08/06/opinion/06watson.html?pagewanted=all) and to Science (http://sciencecareers.sciencemag.org/career_magazine/previous_issues/articles/2011_03_25/science.opms.r1100102) .


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