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12-22-2006, 07:50 AM
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#1
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Senior Member
Join Date: Apr 2006
Posts: 543
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New research supporting pH control as possible help in cancer treatment
I think the medical community most believe acidity is a consequence rather than a cause of cancer. But here is a piece of recent research on the possible influence of pH:
http://biology.plosjournals.org/arch....0050010-S.pdf
Manipulating Cellular pH Suggests Novel Anticancer Therapy
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01-27-2007, 12:27 AM
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#2
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Senior Member
Join Date: Apr 2006
Posts: 543
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Lactic acid resulting from glycolysis in cancer cells:a possible cause of metastasis
The following extract from an article on the recently released research paper on DCA, the potential anticancer drug ( http://www.depmed.ualberta.ca/dca/) provides another possible explanation on the apparent role of acidity in cancer proliferation (a consequence of glycolysis rather than a cause of cancer initiation):
http://www.depmed.ualberta.ca/dca/newscientist.pdf
New Scientist 20Jan 2007
DCA attacks a unique feature of cancer cells: the fact that they make their energy throughout the main body of the cell, rather than in distinct organelles called mitochondria. This process, called glycolysis, is inefficient and uses up vast amounts of sugar. Until now it had been assumed that cancer cells used glycolysis because their mitochondria were irreparably damaged. However, Michelakis's experiments prove this is not the case, because DCA reawakened the mitochondria in cancer cells. The cells then withered and died (Cancer Cell, DOI: 10.1016/j. ccr.2006.10.020).
Michelakis suggests that the switch to glycolysis as an energy source occurs when cells in the middle of an abnormal but benign lump don't get enough oxygen for their mitochondria to work properly (see Diagram). In orderto survive, they switch off their mitochondria and start producing energy through glycolysis.
Crucially, though, mitochondria do another job in cells: they activate apoptosis, the process by which abnormal cells self-destruct. When cells switch mitochondria off, they become "immortal", outliving other cells in the tumour and so becoming dominant. Once reawakened by DCA, mitochondria reactivate apoptosis and order the abnormal cells to die."The results are intriguing because they point to a critical role that mitochondria play: they impart a unique trait to cancer cells that can be exploited for cancer therapy," says Dario Altieri, director of the University of Massachusetts Cancer Center in Worcester.
The phenomenon might also explain how secondary cancers form. Glycolysis generates lactic acid, which can break down the collagen matrix holding cells together. This means abnormal cells can be released and float to other parts of the body, where they seed new tumours.
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01-27-2007, 05:37 AM
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#3
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Senior Member
Join Date: Jan 2007
Location: UK
Posts: 617
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good stuff
Thanks for that. It helps as I have been wondering that now that my chemo has finished what else I could do diet wise to help staying in remission. Alkalising your body and alkaline diet seems worth a shot now... Although I have also been thinking that since glycolysis uses sugar I should be trying to maintain a low gi diet to avoid sugar rush and increased insulin and therefore include protein in the diet (fish but that is acid). Some people have also mentioned about "starving off" the cancer, not sure what they mean..
Will miss my carbs and treats..
Best wishes
Karina
__________________
35 y/o
June 06: BC stage I
Grade 3; ER/PR neg
Her-2+++; lumpectomies
Aug 06: Stage IV
liver mets: 6 tumours
July 06 to Jan 07: 2*FEC+6*Taxotere; 3*TACE; LITT
March 07- Sept 07: Vaccination trial (phase 2, peptide based) at the UW (Seattle).
Herceptin since 2006
NED til Oct 09
Recurrence Oct 2009: to internal mammary gland since October 2009 missed on Oct and March 2010 scan.. palpable nodes in May 2010 when I realised..
Nov 2011:7 mets to lungs progressing fast failed hercp/tykerb/xeloda combo..
superior vena cava blocked: stent but face remains puffy
April 2012: Teresa Trial, randomised to TDM1
Nov 2012 progressing on TDM1
Dec 2012 blockage of my airways by tumours, obliteration of these blocking tumours breathing better but hoping for more- at mo too many tumours to count in the lungs and nodes.
Dec 2012 Starting new trial S-222611 phase 1b dual egfr her2+ inhibitor.
'Under no circumstances should you lose hope..' Dalai Lama
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01-27-2007, 08:38 AM
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#4
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Senior Member
Join Date: Apr 2006
Posts: 543
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Karina,
If it was beyond doubt that DCA is safe, it would be the ideal drug to try as an alkalizing agent in fighting cancer since it has been used to treat acidosis. And I dearly hope, whatever the mode of action of DCA is, that the rat experiments at the University of Alberta will be translated into safe human treatments.
But at this time, reading about some of the past preclinical (on dogs) & clinical trials (on patients with acidosis) is rather scary. Permanent neurological damage (including paralysis) & deaths were frequent at doses in the 50mg/kg or more range.
The Alberta tests were done at higher doses, & they do not report side effects as bad as this. So may be they have found a way to minimize them.
Or perhaps the victims of acidosis & dogs are particularly vulnerable to the side effects of DCA. An other possibility is that these past experiments were chronic relatively long term treatments & side effects reflected the cummulative impact. If DCA works quickly in the case of cancer, then side
effects may not reach untolerable levels.
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01-27-2007, 10:49 AM
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#5
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Senior Member
Join Date: Jan 2007
Location: UK
Posts: 617
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Thanks Hebla, I did not realise that DCA was used to treat acidosis, that is very interesting indeed and I can understand now why you have put these papers (DCA & cell pH) in the same post. I must definitly get more knowledgeable on this.. In the meantime it sounds like alkalising my diet is the way forward..Is it what you do, if I may ask?
__________________
35 y/o
June 06: BC stage I
Grade 3; ER/PR neg
Her-2+++; lumpectomies
Aug 06: Stage IV
liver mets: 6 tumours
July 06 to Jan 07: 2*FEC+6*Taxotere; 3*TACE; LITT
March 07- Sept 07: Vaccination trial (phase 2, peptide based) at the UW (Seattle).
Herceptin since 2006
NED til Oct 09
Recurrence Oct 2009: to internal mammary gland since October 2009 missed on Oct and March 2010 scan.. palpable nodes in May 2010 when I realised..
Nov 2011:7 mets to lungs progressing fast failed hercp/tykerb/xeloda combo..
superior vena cava blocked: stent but face remains puffy
April 2012: Teresa Trial, randomised to TDM1
Nov 2012 progressing on TDM1
Dec 2012 blockage of my airways by tumours, obliteration of these blocking tumours breathing better but hoping for more- at mo too many tumours to count in the lungs and nodes.
Dec 2012 Starting new trial S-222611 phase 1b dual egfr her2+ inhibitor.
'Under no circumstances should you lose hope..' Dalai Lama
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01-27-2007, 03:36 PM
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#6
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Senior Member
Join Date: Mar 2006
Posts: 1,843
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Heblaj01 - another very thought provoking and informative post which I need time to assimilate. Thank you for your work.
Mitochondria have a key relationship with fats which are "burnt" to make energy. If you think of the mitochondria as the boiler room in a steam ship...
Complicated and highly simplistic but maybe if you put the wrong fuel in the burner the exhaust products are more damaging to the "environment" than the average, the "grate" clogs up, mitochonria stop working and the surrounding environement is damaged.
Fats and the mitochonria and the mitochondrial membanes is a fascinating enormous difficult to comprehend topic if you are wandering on the web.
RB
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01-27-2007, 03:41 PM
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#7
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Senior Member
Join Date: Mar 2006
Posts: 1,843
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Karina
If you are looking at risk reduction factors you might like to look at the posts on omega three and six.
Some trials have come up with risk reduction factors as high as seventy percent.
You can search clicking on the search button above and entering search terms omega three, DHA, etc.
There is quite a lot in this link but there is some thought provoking material.
http://www.her2support.org/vbulletin...ght=greek+diet
RB
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