haidut

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As many readers know, using baking soda to treat cancer has been labelled as "quack medicine" by many official mouthpieces of mainstream medicine, as well as by several "watchdog" groups. Here are some links "debunking" the usage of baking soda for cancer.
https://sciencebasedmedicine.org/another-cancer-tragedy-in-the-making/
https://scienceblog.cancerresearchu...the-hype-10-persistent-cancer-myths-debunked/
This must be the most sickening cancer scam I have seen for a while

Some of the claims of the baking soda proponents are not entirely accurate (e.g mechanism of action). Namely, the baking soda proponents claim that cancer tissue is highly acidic, and that this acidic environment feeds a cancer-causing fungus. As the story goes, administering baking soda alkalizes the tissues and that kills the fungus as it requires an acidic environment to grow. Strangely enough, the criticism of the "debunkers" has completely missed the real gaps in the baking soda treatment protocol and instead criticizes the portion that is actually correct - i.e. that acidity (Warburg "effect") drives cancer and baking soda corrects that pathology.

Well, the actual evidence points to the fact that cancer cells maintain a highly akaline (high pH) intracellular environment and pump out the massive amounts of lactic acid they produce outside the cell, thus producing a highly acidic (low pH) extracellular environment. Peat has mentioned this dozens (if not hundreds) of times in his articles and interviews, explaining the tumor promoting (bystander) effects of lactic acid (e.g. through VEGF/angiogenesis, hypoxia/HIF, etc) and how acidification of the tumor cells inside quickly triggers apoptosis. Cabonic anhydrase (CA) inhibitors are perhaps the most direct approach to acidifying the intracellular tumor environment, but other approaches exist such as methylene blue, niacinamide, thiamine, acetazolamide and, of course, baking soda.
https://raypeatforum.com/community/threads/niacinamide-causes-dramatic-increase-in-nad-and-fall-in-lactate.9773/
https://raypeatforum.com/community/threads/niacinamide-fully-prevents-breast-cancer-metastasis.9774/
https://raypeatforum.com/community/threads/thiamine-acts-similarly-to-dca-and-may-be-helpful-in-cancer.3895/
https://raypeatforum.com/community/threads/thiamine-treats-cancer-in-humans-its-deficiency-may-cause-cancer.21350/

But the cancer industry cannot be convinced of anything, and continues to bark idiotic imbecilities about cancer being genetic disease and metabolic therapies like baking soda being "nonsense". Parallel to the official stance on cancer, the medical establishment has been pushing a number of drugs as longevity- and health-promoters, even going as far as to say that some of those drugs prevent cancer. Perhaps the most publicized such drug is metformin - the so-called gold standard for treating diabetes type II. Such is the love affair between the medical establishment and metformin that there have even been calls to put everyone over the age of 40 on it in order to prevent every named chronic disease the medical establishment has managed to concoct in the last 100 years. Not to be outdone, Silicon Valley executives and all kinds of "busy" (read: stressed to death and highly serotonergic) professionals are popping metformin like candy in the hopes of staving off disease and even death.
Metformin in Longevity Study (MILES). - Full Text View - ClinicalTrials.gov
Silicon Valley techies are turning to a cheap diabetes drug to help them live longer

This study below comes almost 4 years after we posted on the forum about the toxic effects of metformin, confirmed by Peat in numerous interviews/emails.
https://raypeatforum.com/community/threads/metformin-is-a-mitochondrial-toxin-and-raises-lactate.3896/

It pours cold water on both the genetic claim and the "beneficial" effects of metformin (at least in regards to cancer). First, it confirms the alkaline intracellular / acidic extracellular nature of cancer and demonstrates that tumor cells overexpress CA, which breaks down CO2 thus alkalizing the inside of the cell. Simultaneously, cancer cells overproduce lactic acid due to the so-called Warburg Effect. This lactic acid is transported outside the cells resulting in a highly acidic extracellular tumor-stroma environment. Perhaps most importantly, the study demonstrates that "...Extracellular acidity is necessary and sufficient for the induction of candidate splicing events". Those candidate splicing events are what drives aggressive cancer phenotypes and even initial cancerization. Second, it demonstrates that administering baking soda orally retards tumor growth by effectively acidifying the inside of the tumor (by raising CO2 levels) and alkalizing the outside (by neutralizing lactic acid). Third, it shows that administering metformin has a cancer-promoting effect due to the ability of that drug to increase lactic acid synthesis inside ANY cell.

So, if baking soda is therapeutic for cancer then what is the protocol. The study used an oral administration of a human equivalent dosage (HED) of about 250mg/kg daily for a period of 8 weeks. This means that an oral dose of about 20g daily should be enough for most people. The reason I mention the 20g dosage is that it also happens to be the most widely used dosing regimen for enhancing performance among athletes. The performance-enhancing effect is achieved through the same mechanism with which baking soda is therapeutic for cancer - i.e. neutralizing lactic acid (lactic acid promotes muscle fatigue), and increasing CO2 (which improves tissue oxygenation and further depresses lactic acid synthesis).

There you have it folks. After decades of absolute incompetence (and possibly fraud as well), the truth is slowly coming out. Soon, it may very well turn out that your grandmother's remedies (notable members of which include aspirin and baking soda) pack more punch than the latest "advances" in medicine, even against something as serious as cancer!

Bicarbonate Increases Tumor pH and Inhibits Spontaneous Metastases
Acidification of Tumor at Stromal Boundaries Drives Transcriptome Alterations Associated with Aggressive Phenotypes. - PubMed - NCBI

"...Unlike normal cells, cancer cells can adapt to survive in low pH environments through increased glycolytic activity and expression of proton transporters that normalize intracellular pH. Acidosis-driven adaptation also triggers the emergence of aggressive tumor cell subpopulations that exhibit increased invasion, proliferation, and drug resistance (4–7). Acidosis also promotes immune escape, which maintains tumor growth (8)."

"...Transcriptome-wide studies suggest that tumor stressors such as hypoxia, nutrient starvation, and lactate acidosis can each regulate gene expression at the transcriptional and posttranscriptional levels in vitro (12–14). For instance, low extracellular pH induces increased histone deacetylation, thereby influencing the expression of certain stress responsive genes and concomitantly contributing to normalization of intracellular pH through the enhanced release of acetate anions that are co-exported with protons through monocarboxylate transporters (15, 16). However, how these changes influence transcriptome dynamics is not well understood, nor is it clear whether changes in gene expression arising from such stresses in vitro also correlate with those induced by equivalent physiologic stressors in vivo."

To confirm that pHLIP reliably labeled acidic tumor areas, we evaluated its overlap relative to two additional markers associated with low extracellular pH: expression of CA9 and of plasma membrane-localized LAMP2 (PM-LAMP2; refs. 2, 29, 30). CA9 is a major transporter that contributes to extracellular acidification through reversible hydration of carbon dioxide to bicarbonate and protons. CA9 expression significantly correlated with areas of pHLIP retention at cell membranes in both the primary tumor (Fig. 1C) and metastatic lesions (Supplementary Fig. S1D). Given the extensive overlap with, and similar patterns of CA9 expression (Fig. 1D; Supplementary Fig. S1E) relative to pHLIP positive cells in the mouse model, we used CA9 as a surrogate to label cells in acidic areas in human tumor tissues. Similar to the mouse tumors, the CA9 was enriched at tumor-stroma interfaces in human tumors (Supplementary Fig. S1F).

PM-LAMP2 indicates cellular adaptation to chronic acidosis (2, 31). PM-LAMP2 overlapped significantly with pHLIP labeled cells (Supplementary Fig. S2A) and most cells with PM-LAMP2 were proximal to the tumor–stroma interface confirming that it is acidic (Supplementary Fig. S2B). Similarly, in human IDC tumors, cells expressing CA9 significantly overlapped with cells exhibiting PM-LAMP2 (Supplementary Fig. S2C and S2D). Therefore, areas containing pHLIP labeled cells or cells expressing high levels of CA9 likely correspond to cellular areas exposed to acidic conditions in vivo.

"...To mimic increased glycolysis conditions in culture, we used metformin, a drug that inhibits the complex I of mitochondria and therefore forces excessive lactate production (44). As expected, metformin addition increased the amount of lactate in the media and acidified the media (Fig. 5C′). Metformin addition also induced the pattern of low pH-induced splicing, which were blocked by addition of HEPES (Fig. 5C). Lactate content remained increased under hypoxic or lactate acidosis conditions with or without HEPES buffering (Supplementary Fig. S5C and S5D). These results indicate that, at least for the splicing events tested, exposure to extracellular acidity is sufficient to induce the observed changes, while hypoxia-induced changes in HIF expression or increased lactate are dispensable."

"...To evaluate the pH responsiveness of the candidate splicing events in vivo, we examined the events in tumors collected from mice that received regular or bicarbonate water. As before, consumption of bicarbonate water was sufficient to reduce tumor acidity, evident by the reduction of pHLIP-localization in cells from those tumors relative to control (Fig. 7A–A′), and to reduce lung metastasis (26). In addition, the percentage of MenaINV positive cells was significantly reduced in those tumors (Fig. 7A′–A″). To examine the pH-responsive splicing candidates in vivo, tumors from control or treated mice were analyzed by qPCR analysis. Compared with the control samples, in tumors from PyMT mice that consumed bicarbonate water the inclusion ratio of the INV exon of Mena was significantly reduced. Similarly, the DOCK7 exon 23 and DLG1 exon 6 trended toward increased ratios, following the expected directionality, however, in these cases the changes were not statistically significant (Fig. 7B). The effect of buffering on pH-responsive exons was also evaluated in a xenograft model derived from MDA-MB-231 cells. In line with the findings in the MMTV-PyMT tumors, the appearance of all candidate pH-responsive splicing events was significantly attenuated in tumors collected from bicarbonate water treated group in the xenograft model (Fig. 7C). These data indicate that alteration in the extracellular acidity in vivo directly influences the expression of the pH-responsive signature."

"...We characterized the spatial characteristics of acidic tumor microenvironment using pHLIP technology, and demonstrated that tumor–stroma interfaces are acidic and that cells within the acidic front are invasive and proliferative. We found that exposure to low extracellular pH in vitro modulates RNA metabolism, particularly RNA splicing, and identified a potential role for a family of RBPs with affinity for AU-rich motif, in the pH-induced transcriptomic signature. The low-pH signature indicated extensive changes in alternative splicing and was notably enriched for splicing of genes implicated in regulation of adhesion and cell migration. Although the global regulation of RNA splicing in response to acidosis in vivo remains to be determined, we demonstrated that a set of functionally important candidate splicing events is similarly pH responsive in vitro and in vivo. The pH-responsive splicing of Mena and CD44 was sensitive to pH-induced histone deacetylation in vitro, demonstrating a link between chromatin deacetylation and modulation of RNA splicing in response to extracellular acidity. These findings provide new molecular insight into one way in which acidosis contributes to local transcriptomic alterations that promote prometastatic phenotypes."

Consistent with its well established role in local invasion and malignant progression (7, 46), we found that acidosis is enriched adjacent to tumor–stroma interfaces in addition to areas within hypoxic cores. Acidosis in well-oxygenated areas can be caused by adaptation to increased aerobic glycolysis or oxidative phosphorylation (1, 47). LDHA expression was indeed enriched within a subset of acidic cellular areas at the tumor–stroma interfaces (3, 32). Acidic regions, however, were not restricted to sites of increased glycolysis marked by LDHA, indicating that acidosis may also be induced by other means such as protons generated through oxidative phosphorylation. Prolonged exposure to extracellular acidification shifts cancer cell metabolic reprogramming towards reactive oxygen species homeostasis and therefore promotes proliferation and aggressive phenotypes under harsh conditions. An example of such mechanism is mediated through a balance between histone deacetylation, mitochondrial hyper acetylation, and increased fatty acid oxidation (16). Consistently, we observed that cells within low pH areas express high levels of HDAC and Ki-67 in vivo. Our results build upon previous reports on the correlation of extracellular acidity and local growth (7) and improve our understanding of the distribution of the acidic microenvironment relative to hallmarks of tumor progression.

The inclusion of exon 19 of CD44 generates a short isoform of CD44 with a truncated cytoplasmic tail. Its expression in vitro is upregulated in multidrug-resistant MCF-7/Adr cells, and also affects cell invasion through the Ras/MAPK signaling pathway (37). Here we demonstrate both in vivo and in vitro that acidosis is necessary and sufficient to drive the expression of these isoforms in both mouse and human tumors. These examples indicate that acidic microenvironment induces the expression of isoforms of genes associated with malignancy; however, it remains to be established if acidosis in vivo induces a global transcriptomic rewiring that influences splicing similar to the phenomenon observed in vitro.

Together, our results lead us to propose that acidosis, an intrinsic feature of the microenvironment, is enriched at the tumor invasive fronts and triggers adaptive changes in gene expression and splicing that are potentially controlled through a specific set of RBPs and downstream of pH-induced chromatin modifications. Our study provides new insights into how acidosis contributes to alterations underlying malignant progression. Understanding how acidosis evokes transcriptomic changes that confer aggressive tumor phenotypes will provide therapeutically valuable insight.
 
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tankasnowgod

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As many reader know, using baking soda to treat cancer has been labelled as "quack medicine" by many official mouthpieces of mainstream medicine, as well as by several "watchdog" groups. Here are some links "debunking" the usage of baking soda for cancer.
https://sciencebasedmedicine.org/another-cancer-tragedy-in-the-making/
https://scienceblog.cancerresearchu...the-hype-10-persistent-cancer-myths-debunked/
This must be the most sickening cancer scam I have seen for a while

One thing I've noticed about those "debunking" sites is that they only debunk strawman arguments, if they even attempt to "debunk" anything at all. Nor do they ever cite or quote studies that show that radiation or chemotherapy are effective treatments. And I don't know why people don't challenge their doctors for more proof, since the only "treatment" appears to be hitting the cancer patient with insanely potent carcinogens. Then "the debunkers" mock the idea that industries would ever push dangerous ineffective treatments simply for tens or hundreds of billions of dollars. Because, apparently, no human or organization would POSSIBLY engage in unscrupulous behavior due to greed.

The quote from that Edzard Ernst site sums up their laziness perfectly-

"There are far too many falsehoods in this text (and most of them are too obvious) for me to even begin to correct them."

There are so many errors and they are so obvious that I can't even find one!
 

haidut

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One thing I've noticed about those "debunking" sites is that they only debunk strawman arguments, if they even attempt to "debunk" anything at all. Nor do they ever cite or quote studies that show that radiation or chemotherapy are effective treatments. And I don't know why people don't challenge their doctors for more proof, since the only "treatment" appears to be hitting the cancer patient with insanely potent carcinogens. Then "the debunkers" mock the idea that industries would ever push dangerous ineffective treatments simply for tens or hundreds of billions of dollars. Because, apparently, no human or organization would POSSIBLY engage in unscrupulous behavior due to greed.

The quote from that Edzard Ernst site sums up their laziness perfectly-

"There are far too many falsehoods in this text (and most of them are too obvious) for me to even begin to correct them."

There are so many errors and they are so obvious that I can't even find one!

Very aptly said. I am beginning to suspect that in most industries these days "complexity" is surrogate/euphemism for fraud. If it is good and working then it should be simply explainable. If all that we hear is "trust me, it is too complex to explain" then it's obvious what is being sold.
 
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@haidut, very good information!!!
Do you think it's a good idea to inject bicarbonate directly into the tumor [as Dr. Simoncini does]?
And perhaps it isa interesting idea to use bicarbonate´s enema [rectally] to more directly impact a prostate tumor?
 

haidut

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@haidut, very good information!!!
Do you think it's a good idea to inject bicarbonate directly into the tumor [as Dr. Simoncini does]?
And perhaps it isa interesting idea to use bicarbonate´s enema [rectally] to more directly impact a prostate tumor?

I think it would have a stronger effect but the benefits must be weighed against the invasiveness. It is not so easy/safe to inject baking soda into say brain, liver, pancreas, etc. For hard to access cancers, acetazolamide, thiamine, methylene blue, etc would be preferable IMO.
 
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I think it would have a stronger effect but the benefits must be weighed against the invasiveness. It is not so easy/safe to inject baking soda into say brain, liver, pancreas, etc. For hard to access cancers, acetazolamide, thiamine, methylene blue, etc would be preferable IMO.
Yes, @haidut , you are all right. I don ´t think in injection. I thought more on enema. I´m thinking on thiamine but I don´t find the dose.
I saw a video with you [Stress, estrogen, endotoxins], very very good. And many times I got the products of idealabs. You do a very important work, my friend.
 

jondoeuk

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I think it would have a stronger effect but the benefits must be weighed against the invasiveness. It is not so easy/safe to inject baking soda into say brain, liver, pancreas, etc. For hard to access cancers, acetazolamide, thiamine, methylene blue, etc would be preferable IMO.

Tullio Simoncini was expelled from the Italian Medical Association and in 2006 was tried and found guilty of fraud and manslaughter Archivio Corriere della Sera Last year he received another jail sentence for manslaughter Doc gets 5 yrs for treating cancer - English
 

Tansia

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There is another study about NADH:NAD+ imbalance and metformin if you're interested: An engineered enzyme that targets circulating lactate to alleviate intracellular NADH:NAD+ imbalance
“We next tested ABP-LOXCAT in a model of drug-induced acute mitochondrial dysfunction using metformin, a mitochondrial complex I inhibitor2 (…) Intraperitoneal (i.p.) injection of 300 mg kg−1 of metformin elevated the blood lactate:pyruvate ratio by 1.5-fold(P = 0.0003) in 1 h (Fig. 4d). ABP-LOXCAT treatment lowered the ratio by 59% (P < 0.0001)..”
 

Ledo

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"...Unlike normal cells, cancer cells can adapt to survive in low pH environments through increased glycolytic activity and expression of proton transporters that normalize intracellular pH. Acidosis-driven adaptation also triggers the emergence of aggressive tumor cell subpopulations that exhibit increased invasion, proliferation, and drug resistance (4–7). Acidosis also promotes immune escape, which maintains tumor growth (8)."
Isn't this quote implying something dangerous with Cabonic anhydrase (CA) inhibitors like thiamine, MB, forcing the extracellur PH from latic acid driven acidodis outside the cell to higher PH, more acidic, inside the cell which presumably causes apoptosis of the cancer cell?

Isn't this forcing the cancer cell to adapt and as they put it- " triggers the emergence of aggressive tumor cell subpopulations that exhibit increased invasion, proliferation, and drug resistance (4–7). Acidosis also promotes immune escape, which maintains tumor growth"

They seem to say elsewhere gene expression can cause this breakout into metastasis? I don't know if I'm reading this right. The writing and word style is on the complex side. Thanks.

Edit: I just realized Thiamine and the like are not CA inhibtors, that is a class of drug, but still may have the same effect
 
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Tansia

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I can k
Isn't this quote implying something dangerous with Cabonic anhydrase (CA) inhibitors like thiamine, MB, forcing the extracellur PH from latic acid driven acidodis outside the cell to higher PH, more acidic, inside the cell which presumably causes apoptosis of the cancer cell?

Isn't this forcing the cancer cell to adapt and as they put it- " triggers the emergence of aggressive tumor cell subpopulations that exhibit increased invasion, proliferation, and drug resistance (4–7). Acidosis also promotes immune escape, which maintains tumor growth"

They seem to say elsewhere gene expression can cause this breakout into metastasis? I don't know if I'm reading this right. The writing and word style is on the complex side. Thanks.

I'm pretty certain that if MB and B1 drives cancer cell apoptosis that's pretty good thing? Why would you think it may be dangerous?
 

Ledo

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I'm pretty certain that if MB and B1 drives cancer cell apoptosis that's pretty good thing? Why would you think it may be dangerous?


Most of the portions of the studies Haidut quoted did infer possible benefit. However the quote I highlighted suggests the cancer cell may also adapt to inter cellular PH change from alkaline to acidic which yes of course would be the ideal by committing apoptosis, but instead doing the following:

" triggers the emergence of aggressive tumor cell subpopulations that exhibit increased invasion, proliferation, and drug resistance (4–7). Acidosis also promotes immune escape, which maintains tumor growth"

If this is possible, it is kind of shocking and dangerous I think.
Maybe you could go to first post and see if you read it that way. I selected from a few paragraphs down
 

Ledo

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For context of the highlighted quote, please page down about 10 paragraphs in Haidut's original post #1
 
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Consider the lack of sodium and it’s effect on stress hormones, and the benefits of baking soda compared to table salt, and clearly this makes that “grandmother remedy” extremely powerful

thanks for the reminder
 

Tansia

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Most of the portions of the studies Haidut quoted did infer possible benefit. However the quote I highlighted suggests the cancer cell may also adapt to inter cellular PH change from alkaline to acidic which yes of course would be the ideal by committing apoptosis, but instead doing the following:

" triggers the emergence of aggressive tumor cell subpopulations that exhibit increased invasion, proliferation, and drug resistance (4–7). Acidosis also promotes immune escape, which maintains tumor growth"

If this is possible, it is kind of shocking and dangerous I think.
Maybe you could go to first post and see if you read it that way. I selected from a few paragraphs down

Ok @Ledo now I understand what you mean. I had a look on the original papers and it looks like when they talk about "acidity" they mean microenvironmental acidity, so I understand that's outside of the cancer cell. If that's the case both haiduts quotes make sense?
 

Ledo

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Ok @Ledo now I understand what you mean. I had a look on the original papers and it looks like when they talk about "acidity" they mean microenvironmental acidity, so I understand that's outside of the cancer cell. If that's the case both haiduts quotes make sense?

Yes that is called extra-cellular due to lactic acid flushed from inside the cancer cell to the outside which then lowers PH inside making it more alkaline inside the cancer cell. Then the (CA) inhibition or thiamine type agents can therapeutically lower that inter cellular (cancer cell) PH hopefully killing the cell. All good so far.

Unfortunately the paper springs the fact the cancer cell can adapt, mentions some tools it uses, to spring or bust out the sub population of some cancer cells when it sees the acid level going up inside. This would not be good! It sounds like tumor metastasis.

Thanks for checking that Tansia. @haidut
 

Tansia

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Had a look on other references and they all talk about tumour cells adapting to external acidic environment and that adaptation seem to be associated with drug resistance and radio-resistance- 'A low extracellular pH also contributes to drug resistance both in-vitro and in-vivo. The acid-outside pH gradient generated between intra- and extracellular space affects the distribution and uptake of select weak base chemotherapeutic drugs resulting in physiological drug resistance 2427. Tumors cells adapted to low pHe in-vitro harbor p53 mutations and have elevated activity of p-glycoprotein both of which can contribute to drug resistance 2830. In addition, chronically adapted low pHe cells are radio-insensitive in-vitro 31." The same paper says the same as Haidut: 'Sodium bicarbonate significantly increases extracellular pH of tumors in-vivo'.
About tumour cells adaptation to low pHe: 'Because acidity may cause p53-dependent apoptosis, selection of p53-mutant cells may occur 30. This loss of apoptotic potential and other adaptive changes are likely repair driven by microenvironment-induced genomic instability and inhibition of DNA repair .'
I understand that if cancer cell becomes acidic it undergoes p53-apoptosis (which is great!) but some cells will survive that low pHe by acquiring mutant p53 which will block cancer cell apoptosis and will drive genomic instability and will lead to highly resistant mutant that will promote mestastasis.
 

jzeno

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I don't know how to reconcile Dr. Gerson's thoughts on salt and everything I read on here. He says it will cause cancer and yet here we have evidence that baking soda may treat cancer. I can't make heads or tails of it.
 

Ledo

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Had a look on other references and they all talk about tumour cells adapting to external acidic environment and that adaptation seem to be associated with drug resistance and radio-resistance- 'A low extracellular pH also contributes to drug resistance both in-vitro and in-vivo. The acid-outside pH gradient generated between intra- and extracellular space affects the distribution and uptake of select weak base chemotherapeutic drugs resulting in physiological drug resistance 2427. Tumors cells adapted to low pHe in-vitro harbor p53 mutations and have elevated activity of p-glycoprotein both of which can contribute to drug resistance 2830. In addition, chronically adapted low pHe cells are radio-insensitive in-vitro 31." The same paper says the same as Haidut: 'Sodium bicarbonate significantly increases extracellular pH of tumors in-vivo'.
About tumour cells adaptation to low pHe: 'Because acidity may cause p53-dependent apoptosis, selection of p53-mutant cells may occur 30. This loss of apoptotic potential and other adaptive changes are likely repair driven by microenvironment-induced genomic instability and inhibition of DNA repair .'
I understand that if cancer cell becomes acidic it undergoes p53-apoptosis (which is great!) but some cells will survive that low pHe by acquiring mutant p53 which will block cancer cell apoptosis and will drive genomic instability and will lead to highly resistant mutant that will promote mestastasis.
I guess that is it then. Bad news really because how can one confidently do anything that challenges PH outside and inside a cancer cell in the hopes of killing the cell when that course of action may cause the cancer cell to adapt and the cancer become more virulent?
 

Ledo

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I don't know how to reconcile Dr. Gerson's thoughts on salt and everything I read on here. He says it will cause cancer and yet here we have evidence that baking soda may treat cancer. I can't make heads or tails of it.
Another good point in light of this discussion.

What is strange is that we are talking about this. Surely if this were common knowledge @haidut would have known about it but come on, this seems pretty simple really. Billions dollars of cancer research going on for decades and no deep understanding of this? Something is not right. Will any oncologist say "of course, that has always been the problem, welcome to my world" ?
 
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