Natural Medicine Talk - Blogs

Introduction - sodium bicarbonate for use with cancer

jfh — Tue, 31 Aug 2010 03:09:00 GMT

I'm an amateur on a health quest, and want to share what I learn on my path.

I am trying to determine the value of sodium bicarbonate (baking soda) when one has cancer. I really want to know if the pH environment, alkaline or acid, has any effect on the curing, slowing, progression of cancer, or at least metastasis of existing cancer. Is low pH (acid) and high pH (alkaline -or base) to a cancer cell similar to hot and cold to humans? Is there something more than pH that affects the cell growth?

Apparently, cancer is caused by mutation of cells due to several toxic events, such as virus, fungus, chemical, and probably others that I haven't discovered yet.

I want to know why this oral sodium bicarbonate prostate cancer protocol works. http://phkillscancer.com/protocol

Humans are not rats or test tubes or petri dishes, yet that, so far, has been the most info that I've found. So, I'll take whatever I can get to help answer my questions.

Manipulating a high acid or high alkaline environment is not a good thing. The body does it better. The body will immediately try to adjust itself back to its narrow pH range. Different parts of the body have their own pH range, and the immune system will expect that to be maintained. Many pathogens, including most bacteria, thrive in an alkaline environment. That is why so many areas of our body are acidic such as the stomach and skin. The acids are part of the body's defense mechanism against pathogens. Look at Helicobacter pylori bacteria, which causes stomach ulcers and cancer. It can be killed by the acidic environment of the stomach, so to protect itself the bacteria releases alkaline ammonia to neutralize the stomach acid. The fact is that the body has a number of systems to regulate its pH. This includes breathing. When the blood starts becoming too acidic, the breathing rate increases to blow off carbon dioxide reducing the acidity. If we go too alkaline, the breathing decreases to retain more carbon dioxide increasing carbonic acid levels. Let the body do its work. It has a number of systems to use for this manipulation.

From Bill Sardi, refuting the Warburg Effect (acid/alkaline therapy):

But it wasn’t just conventional medicine that got side-tracked by Warburg’s discovery. In "the Warburg Effect," tumor cells expel lactic acid as a by-product, and this later became known as the alkalinity-acidity theory of cancer promoted by many pseudo-scientists. This spawned a number of books that mistakenly advocated an alkaline diet would cure or prevent cancer. Actually, cancer cells are a bit more acid immediately outside their boundaries than inside due to the expelling of lactic acid.

The pursuit of a state of alkalinity appears to be nonsensical. Not only does the absence of acidity in the gastric tract and bladder establish an environment that is conducive to tumor growth, the control of blood pH (alkalinity/acidity) is automatically controlled in a neutral pH range (7.2–7.4). The diet has little influence over the pH of the blood.

In 1987 an experiment was conducted where the effects of alkalinity or acidity were examined in bladder cancer. Animals were fed a diet that was somewhat acidic, mildly alkaline or more alkaline. Bladder tumors occurred in 39% of the acidic group, 65% of the alkaline group and 71% of the more alkaline group.

Many alternative medical practitioners inexplicably recommend acid-forming supplements (Lactobacillus acidophilus) for cancer patients, yet they contrarily suggest an alkaline diet. An experiment conducted in 1980 showed that the provision of acid-forming bacteria (Lactobacillus acidophilus) reduced chemically-induced colon cancer in animals from 77% to 40%. Enough said about misdirection since Warburg’s discovery.
http://www.lewrockwell.com/sardi/sardi141.html

Technically, the cesium chloride does not directly kill the cancer cells. What is does is allow the immune system to kill the cancer cells. When you see a statment that cesium chloride does not kill cancer cells, that is technically correct.

Cesium has been proven to get into cancer cells, when other nutrients cannot.

Makes the cancer cells alkaline (Note: the BLOOD is NOT made alkaline, only the inside of the cancer cells)
http://www.cancertutor.com/Cancer/Alkaline.html

Sodium bicarbonate is an alkaline pH. It has a high pH of around 8. Normal blood pH is about 7.4. Normal urine pH is 6.0. Normal silive pH ranges from 6.0 to 7.4.

The kidneys alone produce about two hundred and fifty grams (about half a pound) of bicarbonate
per day in an attempt to neutralize acid in the body.
The kidneys monitor and control the acidity or "acid-base" (pH) balance of the blood. If the blood is too acidic, the kidney makes bicarbonate to restore the bloods pH balance. If the blood is too alkaline, then the kidney excretes bicarbonate into the urine to restore the balance

Pasted from <http://www.imva.info/news/sodium-bic...y-disease.html>

This blog will continue as I find information on sodium bicarbonate in relation to cancer. The post, at the bottom of all the posts, is a continuing summary, in case you don't want to go through all of the posts yet.

Definitions

jfh — Tue, 31 Aug 2010 02:11:00 GMT

Definitions.
I'm just an amateur, so I don't understand much in these medical journals. So, I need definitions. I'll add to these a I go.

apoptosis (ˌ�pəpˈtəʊsɪs)
biology Also called: programmed cell death the programmed death of some of an organism's cells as part of its natural growth and development

in vivo
[in vee-voh]
(of biological processes or experiments) occurring or carried out in the living organism

in vitro[in vee-troh]
(of a biological process) made to occur in a laboratory vessel or other controlled experimental environment rather than within a living organism or natural setting.

NaHCO(3) Sodium bicarbonate

Extracellular outside the cell.

Intracellular inside the cell.

Summary so far

jfh — Tue, 31 Aug 2010 01:30:00 GMT

I have decided to put this ongoing summary near the top, so you don't have to wade through my confirmation postings. I will try to keep up with it, each time I post.

The body maintains the intracellular cell's pH by using transport proteins located on the cell membrane and intracellular vesicles. The sodium bicarbonate co-transport is only one of these mechanisms.
The function of these proteins is closely linked to several hormone blood levels, systemic acid-base status, protein diet content as well as other factors. It has been recently demonstrated that the pHi (pH inside the cell) may be involved in numerous aspects of cell function, such as metabolism, apoptosis, malignancy and it is implicated in the pathogenesis of particular forms of renal stones (Dent's disease). Now, the question is, "Does the extracellular environment affect the inside?"

The environment, surrounding the tumor cells, which are normally acid, can be made alkaline with use of sodium chloride. The outside, of the tumor and its cells, is normally acid. The inside is in the neutral-to-alkaline range of pH. This outside environment keeps weak 'base' drugs from working properly. These drugs need to move the cell's inside to a higher pH (alkaline). It has been demonstrated that this environmental change can occur with tumour alkalinization following chronic ad libitum (oral, injection, IV) administration of NaHCO3 (sodium bicarbonate). All of this can enhance the use of chemotherapy.

The external pH of solid tumors is acidic as a consequence of increased metabolism of glucose and poor perfusion. Acid pH has been shown to stimulate tumor cell invasion and metastasis in vitro and in cells before tail vein injection in vivo. Oral NaHCO(3) selectively increased the pH of tumors and reduced the formation of spontaneous metastases in mouse models of metastatic breast cancer.
The weakness of this treatment regimen is that it was shown to significantly increase the extracellular pH, but not the intracellular pH. Bicarbonate treatment had mixed results, inhibiting the formation of metastases from PC3M prostate cancer cells, but not those of B16 melanoma. Seems so selective. Low pH was shown to increase the release of active cathepsin B. This is not a good thing. See my notes in my post, Bicarbonate inhibits spontaneous metastases. This is a plus for sodium bicarbonate treatment.

Proceed with caution. Enough of it can neutralize stomach acid, leading to unhealthy conditions. Of course, that can be corrected with other supplementation. Like TMG, trimethylglycine (unacidified betaine), or other methyl donors, B vitamins (B6, B12, folate), and zinc. Even apple cider vinegar can help. NaHCO(3) significantly increased the development of gastric cancer in a rat gastric stump model. Carbonate ions, which represent a major constituent of intestinal reflux into the stomach, increase the expression of ODC (ornithine decarboxylase) and thereby enhance cell proliferation in nontransformed mucosa, and consequently elevate the risk of gastric cancer. See my post on, "Proceed with caution" The carbonate ions come from the sodium bicarbonate. That is the CO3 part of the NaHCO3. I don't trust the test, as we don't know if bicarbonate was added to the food, causing neutralization of stomach acids. This is unhealthy. Common sense is required. Take it on an empty stomach.

It has been reported that a number of lipophilic statins cause apoptosis in various cells, but it is still not clear whether intracellular acidification is involved in statin-induced apoptosis. Bicarbonate can suppress this. Accordingly, bicarbonate suppressed statin-induced apoptosis. The strategy to combine statins with bicarbonate can lead to reduction in the chance of the severe adverse events including myopathy or rhabdmyolysis (generally refers to a disintegration in the muscle fibers).

Osmotic shock or osmotic stress is a sudden change in the solute concentration around a cell, causing a rapid change in the movement of water across its cell membrane. Under conditions of high concentrations of either salts, substrates or any solute in the supernatant, water is drawn out of the cells through osmosis. This also inhibits the transport of substrates and cofactors into the cell thus “shocking” the cell. Alternatively, at low concentrations of solutes, water enters the cell in large amounts, causing it to swell and either burst or undergo apoptosis.

Liquid ionic cesium chloride works by making cancer cells highly alkaline, typically 8.0 and above, thus making them so "sick" the immune system attacks and kills them.

Cesium chloride not only kills cancer cells indirectly, it immediately stops the metastasis of the cancer; can start shrinking tumor masses within weeks; and almost always stops the pain of cancer within 24 to 48 hours, depending on what is causing the pain.

The Cesium Chloride Protocol directly targets cancer cells. Normal cells do not ingest the cesium chloride. Cesium has been proven to get into cancer cells, when other nutrients cannot. I makes the cancer cells alkaline internally. I limits the intake of glucose into the cell, starving it. I neutralizes the lactic acid. It stops the fermentation process. Sodium bicarbonate can do some of the same things, but only for the outside of the cell. Maybe the molasses is the trick to get it inside the cell.

My post, "extracellular and intracellular pH on immune function cannot be ignored", indicates that it is important not to overlook the relationship of intracellular pH, extracellular pH, and the immune system. This one is hard to summarize, so go read it. Essentially, "The lowest pH values are found in those regions where tumor cells are growing adjacent to a basement membrane, causing necrotic foci and promoting tumor invasion." Meaning that the external environment should become more alkaline in order for the immune system to fight the invasion. That is part of what we were looking for. Right? But each cancer microenvironment is unique. For example, leukemic cells have a greater intracellular alkalinity. Increasing that alkalinity, will just make them multiply quickly. In the case of leukemia, neither the cesium nor the sodium bicarbonate protocol would work.

The sodium carbonate will neutralize the stomach acid, allowing the molasses or maple syrup to pass through will little digestion. This is a good method to get them both to the cancer cells. Cancer cells require more glucose than other normal cells. I don't know what that will do for some bad pathogens, like Candida Albicans. They like the alkaline environment and love sugar too. However, this recipe may kill the Candida, by increasing their intracellular pH, by the method of osmotic shock. See my post on binding the sodium bicarbonate with molasses for the recipe.

Now, all that's left, is to determine which cancers respond to this protocol. Not all do.

intracellular pH in the regulation of cell function

jfh — Tue, 31 Aug 2010 01:15:00 GMT

The article's use of sodium bicarbonate is in reference to that which is produced by the pancreas and kidneys.
The pancreas is primarily responsible for the production of enzymes and bicarbonate necessary for normal digestion of food. Bicarbonate is so important for protecting the kidneys that even the kidneys get into the act of producing bicarbonate.

Quote:

The importance of intracellular pH in the regulation of cell function
[Article in Italian]
Capuano P, Capasso G.
Cattedra di Nefrologia, Seconda Universita' di Napoli, Napoli, Italy. gb.capasso@unina2.it
Abstract
Cell life is possible only if intracellular pH (pHi) oscillations are kept within a very narrow range. Measurement of pHi is therefore a very important parameter when examining cell and organ functions. Several methods have been used to monitor pHi; these include fluorescent dyes and pH sensitive electrodes. In addition, many instruments have been applied to the detection of pHi in living organs even at the level of single cells: NMR and confocal microscopy are just an example. Transport proteins located on the cell membrane and intracellular vesicles are responsible for maintaining the correct pHi. In renal tubular cells these include the sodium hydrogen exchanger (NHE), the sodium-dependent and independent chloride-bicarbonate exchanger (Cl--HCO3-), the sodium bicarbonate co-transport (Na+-HCO3-), the ATP-coupled proton pump (H+-ATPasi) and the ATP-dependent proton-potassium pump (H+-K+-ATPasi). All these carriers have been cloned and it is now clear that there are several isoforms with specific properties. The function of these proteins is closely linked to several hormone blood levels, systemic acid-base status, protein diet content as well as other factors. In addition, these carriers are not homogeneously distributed along the nephron and are sensitive to specific stimuli like interstitial osmolality and luminal fluid flow rate. Finally, it has been recently demonstrated that the pHi may be involved in numerous aspects of cell function, such as metabolism, apoptosis, malignancy and it is implicated in the pathogenesis of particular forms of renal stones (Dent's disease).
PMID: 12746799

Pasted from <http://www.ncbi.nlm.nih.gov/pubmed/12746799>

Cesium, also spelled Caesium, is a chemical element that has a 50% cure rate for cancer. It involves the manipulation of the intracellular pH.

How cesium works.

Technically, the cesium chloride does not directly kill the cancer cells. What is does is allow the immune system to kill the cancer cells. When you see a statement that cesium chloride does not kill cancer cells, that is technically correct.

Cesium has been proven to get into cancer cells, when other nutrients cannot.

Makes the cancer cells alkaline (Note: the BLOOD is NOT made alkaline, only the inside of the cancer cells)

http://www.cancertutor.com/Cancer/Alkaline.html

pH and chemotherapy

jfh — Tue, 31 Aug 2010 00:21:00 GMT

This article indicates that the environment, surrounding the tumor cells, which are normally acid, can be made alkaline. It does not indicate how the sodium bicarbonate gets there to do this function. I'm going to assume that it is orally.

Quote:

pH and chemotherapy
Raghunand N, Gillies RJ.
University of Arizona Health Sciences Center, Cancer Center Division, Tucson 85724-5024, USA.
Abstract
In vivo pH measurements by magnetic resonance spectroscopy reveal the presence of large regions of acidic extracellular pH in tumours, with the intracellular pH being maintained in the neutral-to-alkaline range. This acid-outside plasmalemmal pH gradient acts to exclude weak base drugs such as the anthracyclines and vinca alkaloids, a behaviour that is predicted by the decrease in octanol-water partition coefficients of mitoxantrone and doxorubicin with decreasing solution pH. This pH gradient can be reduced or eliminated in mouse models of breast cancer by systemic treatment with sodium bicarbonate. We have demonstrated tumour alkalinization following chronic ad libitum administration of NaHCO3 and acute intraperitoneal administration of NaHCO3 to tumour-bearing mice. Chronic treatment of tumour-bearing SCID mice with NaHCO3 results in an enhancement in MCF-7 tumour xenograft response to doxorubicin. Intraperitoneal administration of NaHCO3 to tumour-bearing C3H/Hen mice prior to treatment with mitoxantrone results in a greater-than 4.5-fold increase in cell-kill in the syngeneic C3H mammary tumour model. Most combination chemotherapy regimens include at least one weak base drug. Our results suggest that agents such as sodium bicarbonate, Carbicarb and the diuretic furosemide--which are known to induce metabolic alkalosis in humans--may be useful in enhancing the efficacy of these treatment regimens in humans.
PMID: 11727930

Pasted from <http://www.ncbi.nlm.nih.gov/pubmed/11727930>

Bicarbonate inhibits spontaneous metastases

jfh — Mon, 30 Aug 2010 23:26:00 GMT

Quote:

Bicarbonate increases tumor pH and inhibits spontaneous metastases.
Robey IF, Baggett BK, Kirkpatrick ND, Roe DJ, Dosescu J, Sloane BF, Hashim AI, Morse DL, Raghunand N, Gatenby RA, Gillies RJ.
Arizona Cancer Center, University of Arizona, Tucson, Arizona, USA.
Abstract
The external pH of solid tumors is acidic as a consequence of increased metabolism of glucose and poor perfusion. Acid pH has been shown to stimulate tumor cell invasion and metastasis in vitro and in cells before tail vein injection in vivo. The present study investigates whether inhibition of this tumor acidity will reduce the incidence of in vivo metastases. Here, we show that oral NaHCO(3) selectively increased the pH of tumors and reduced the formation of spontaneous metastases in mouse models of metastatic breast cancer. This treatment regimen was shown to significantly increase the extracellular pH, but not the intracellular pH, of tumors by (31)P magnetic resonance spectroscopy and the export of acid from growing tumors by fluorescence microscopy of tumors grown in window chambers. NaHCO(3) therapy also reduced the rate of lymph node involvement, yet did not affect the levels of circulating tumor cells, suggesting that reduced organ metastases were not due to increased intravasation. In contrast, NaHCO(3) therapy significantly reduced the formation of hepatic metastases following intrasplenic injection, suggesting that it did inhibit extravasation and colonization. In tail vein injections of alternative cancer models, bicarbonate had mixed results, inhibiting the formation of metastases from PC3M prostate cancer cells, but not those of B16 melanoma. Although the mechanism of this therapy is not known with certainty, low pH was shown to increase the release of active cathepsin B, an important matrix remodeling protease.
PMID: 19276390 [PubMed - indexed for MEDLINE]

Pasted from <http://www.ncbi.nlm.nih.gov/pubmed/19276390>

Sodium bicarbonate introduction sure seems selective. It does seem good for prostate cancer. That would account for the success of the protocol in my introduction.

The article indicates a release of Cathepsin B due to acid pH. Is it cause of metastasis where cancer already exists? It seems so. Does alkaline pH inhibit CatB? Never the less, CatB could be used in prognosis of metastasis.

Cathepsin B plays an essential role in the pathogenesis of fulminant hepatic failure, and the cathepsin B inhibitor CA-074me can attenuate apoptosis and liver injury.
Pasted from <http://www.wjgnet.com/1007-9327/15/1231.asp>

These following notes are a result of reading the last line of the above article.

Although the mechanism of this therapy is not known with certainty, low pH was shown to increase the release of active cathepsin B, an important matrix remodeling protease.
...
It will be very interesting to see if a peptidomimetic, a structure based drug design and/or analogue based drug design approach can be achieved to obtain therapeutically useful compounds, as this will open a window of opportunity for the treatment of disease conditions caused by active cathepsin B.
...
Cathepsin B contributes to cartilage destruction in osteoarthritis and pathological proteolysis in rheumatoid arthritis and cancer.
Pasted from <http://www.pharmainfo.net/reviews/ca...-papain-family>

Cathepsin B also stimulates angiogenesis in cancer tissues and degrades and inactivates the inhibitors of metalloproteases.
Increased expression of cathepsin B in primary cancers, and especially in preneoplastic lesions, suggests that this enzyme might have pro-apoptotic features.
Cathepsin B is thought to play a central role in intrapancreatic trypsinogen activation and the onset of pancreatitis.
Pasted from <http://www.pharmainfo.net/reviews/ca...-papain-family>

cathepsin B can take over the role of the dominant execution protease in death receptor-induced apoptosis.
Pasted from <http://jcb.rupres

Blocking cathepsin B expression with a specific inhibitor of cathepsin B suppressed apoptosis but did not affect autophagy, which suggests that cathepsin B is a molecular link between autophagy and apoptosis.
Pasted from <http://www.nature.com/cdd/journal/va...dd201028a.html>

Proceed with caution

jfh — Mon, 30 Aug 2010 21:32:00 GMT

Proceed with caution.

It appears that a long duration of taking sodium bicarbonate could cause problems. At least, in rats. I figure that it is not good to keep the stomach acids low.
But notice that they do not say whether they added the bicarbonate to the food. That would be very bad over the duration. The stomach acids would be neutralized. Must have common sense. Cautionary guidance would be that you should not take sodium bicarbonate with food. It would not digest properly. It is already present in food. The protocol suggests taking it on an empty stomach.

As a matter of fact, this pdf article says that it is safe.

There are no directly relevant studies on repeated dose exposure, however, knowledge of prior use and available literature does not indicate any adverse effects of long-term use of exposure via any route. In vitro bacterial and mammalian cell tests showed no evidence of genotoxic activity. As with other sodium salts, high doses of sodium bicarbonate promote carcinoma formation in rat urinary bladder after pre-exposure to initiator or BBN. However, when rats were only exposed to sodium bicarbonate no carcinogenic effect on the urinary bladder was found.

Based on the available information there are no indications that sodium bicarbonate has carcinogenic effects.
Sodium bicarbonate has a long history of use in foodstuff, feed and industrial processes. The bicarbonate ion is a normal constituent in vertebrates, as the principal extracellular buffer in the blood and interstitial fluid is the bicarbonate buffer system. Excess sodium and bicarbonate ions are readily excreted in the urine. It is therefore assumed that normal handling and use will not have any adverse effects. The consequences of accidental or excessive oral ingestion have been described in a number of publications. Acute oral ingestion by the patients may result in a ruptured stomach due to excessive gas development. Acute or chronic excessive oral ingestion may cause metabolic alkalosis, cyanosis and hypernatraemia. These conditions are usually reversible, and will not cause adverse effects.
http://www.inchem.org/documents/sids/sids/sodbicarb.pdf

Quote:

Dietary supplementation with carbonate increases expression of ornithine decarboxylase and proliferation in gastric mucosa in a rat model of gastric cancer.
Ehrnstr�m RA, Bjursten LM, Ljungberg O, Veress B, Haglund ME, Lindstr�m CG, Andersson T.
Division of Pathology, Department of Laboratory Medicine of Lund University, Malm� University Hospital, Malm�, Sweden. roy.ehrnstrom@med.lu.se
Abstract
Dietary factors play essential roles in gastric carcinogenesis. We recently found that dietary supplementation with NaHCO(3) significantly increased the development of gastric cancer in a rat gastric stump model. Here, we analysed nontransformed gastric mucosa for expression of the cancer-related proteins cyclooxygenase-2 (COX-2) and ornithine decarboxylase (ODC), and we examined the relationship between expression levels of those proteins and mucosal proliferation. Research has shown that COX-2 is upregulated in gastric mucosal inflammation and is strongly associated with gastrointestinal cancer. ODC is the key enzyme in polyamine synthesis and a regulator of cell proliferation. We performed gastric resections on 48 Wistar rats to induce spontaneous gastric cancer; half of these animals were given a normal diet, and the other half received a diet supplemented with NaHCO(3). Twenty-four unoperated rats served as a control group. The surgical procedure per se led to a significant rise in mucosal expression of COX-2 and an associated increase in cell proliferation. However, the COX-2 level in gastric mucosa was not further affected by dietary supplementation of carbonate. Interestingly, nontransformed gastric mucosa in the operated rats receiving a carbonate-supplemented diet showed a pronounced increase in ODC expression that was strongly correlated with a further enhanced cell proliferation. These results indicate that carbonate ions, which represent a major constituent of intestinal reflux into the stomach, increase the expression of ODC and thereby enhance cell proliferation in nontransformed mucosa, and consequently elevate the risk of gastric cancer.
PMID: 17960625 [PubMed - indexed for MEDLINE]

Pasted from <http://www.ncbi.nlm.nih.gov/pubmed/17960625>

Bicarbonate suppresses statin-induced apoptosis

jfh — Mon, 30 Aug 2010 20:50:00 GMT

Preventive effects of bicarbonate on cerivastatin-induced apoptosis.
Kobayashi M, Kaido F, Kagawa T, Itagaki S, Hirano T, Iseki K.
Department of Clinical Pharmaceutics & Therapeutics, Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita-12-jo, Nishi-6-chome, Kita-ku, Sapporo 060-0812, Japan.
Abstract
Although HMG-CoA reductase inhibitors such as statins are the most widely used cholesterol-lowering agents, there is a risk of myopathy or rhabdmyolysis occurring in patients taking these drugs. It has been reported that a number of lipophilic statins cause apoptosis in various cells, but it is still not clear whether intracellular acidification is involved in statin-induced apoptosis. There have been few studies aimed at identifying compounds that suppress statin-induced myotoxicity. In the present study, we examined the relationship between cerivastatin-induced apoptosis and intracellular acidification and the effect of bicarbonate on cerivastatin-induced apoptosis using an RD cell line as a model of in vitro skeletal muscle. Cerivastatin reduced the number of viable cells and caused dramatic morphological changes and DNA fragmentation in a concentration-dependent manner. Moreover, cerivastatin-induced apoptosis was associated with intracellular acidification and caspase-9 and -3/7 activation. On the other hand, bicarbonate suppressed cerivastatin-induced pH alteration, caspase activation, morphological change and reduction of cell viability. Accordingly, bicarbonate suppressed statin-induced apoptosis. The strategy to combine statins with bicarbonate can lead to reduction in the chance of the severe adverse events including myopathy or rhabdmyolysis.

Pasted from <http://www.ncbi.nlm.nih.gov/pubmed/17553641>

Effect of urinary pH on the progression of tumours

jfh — Sun, 29 Aug 2010 17:51:00 GMT

This article indicates that you should not try to manipulate your body into an alkaline or acid environment. At least, not for the longer duration. The duration, of this study, was 1 year. I suppose that you won't go that long with the sodium bicarbonate cancer protocol.

But notice that they added the sodium bicarbonate to the food or diet. This would neutralize and important part of the digestive system - stomach acid.

The protocol involves taking the mixture between meals on an empty stomach. You could replenish your stomach acid by taking TMG and/or 2 tablespoons of apple cider vinegar in water with your meals.

TMG, trimethylglycine (unacidified betaine), or other methyl donors, B vitamins (B6, B12, folate), and zinc are all required for the production of stomach acid. The building block, for stomach acid formation, is salt. The sodium chloride is split and the chloride forms hydrochloric acid. The sodium is converted in to sodium bicarbonate, which is a buffer for acids in the body, including stomach acid when digestion is finished.

Acidity is required for the absorption of many nutrients, especially minerals and vitamins B6, B12, and folate. Proteins cannot be broken down either without sufficient stomach acid as the protein digestive enzyme pepsin is acid dependent for function.

So, you certainly don't want to try to alter your body's pH in either direction. The body does it better, and you will defeat your immune system.

But remember, by this time, you already have cancer and need to do something about it. So, the rules change for you. Just have common sense about it.

Quote:

Effect of urinary pH on the progression of urinary bladder tumours.
Lina BA, van Garderen-Hoetmer A.
TNO Nutrition and Food Research Institute, AJ, Zeist, The Netherlands.
Abstract
Systemic alkalosis has been postulated to enhance tumorigenesis, whereas systemic acidosis has been implicated to exert a favourable influence on tumour control and regression. In the present study the urinary pH was influenced by feeding acid-forming or base-forming diets, and the effect of alkaline or acid urine on the early and late progression phase of urinary bladder carcinogenicity was investigated in male Wistar rats. Bladder lesions were initiated by N-butyl-N-(4-hydroxybutyl) nitrosamine (0.05% BBN in the drinking water during 4 weeks) and promoted by sodium bicarbonate (3.4% NaHCO3 in the diet during 15 or 25 weeks). After short- (15 week) and more long-term (25 week) promotion with NaHCO3, groups of 20 rats were fed a diet containing the acidifying salt ammonium chloride (2.1% NH4Cl) or the control diet. All surviving rats were killed after a total study duration of 52 weeks. Additional control groups were, after initiation, fed diets containing NaHCO3 and killed after 15 wk or 25 wk of promotion, or at the end of the study. In rats fed diets with added salts, water intake and the amount of urine produced were increased and the urinary density was decreased compared to rats fed control diet. During NaHCO3 feeding, urinary pH and sodium concentration were increased. During NH4Cl feeding, urinary pH was decreased and urinary chloride and calcium concentrations were increased. Initiation by BBN followed by treatment with NaHCO3 caused a high incidence of papillary/nodular hyperplasia, papillomas and carcinomas of the bladder epithelium. These lesions progressed with time or longer duration of NaHCO3 promotion. A tumour protective effect of urinary acidification by NH4Cl was not found. In fact, both acidification and prolonged alkalinization tended to aggravate the malignancy of bladder carcinomas.
PMID: 10654592

Pasted from <http://www.ncbi.nlm.nih.gov/pubmed/10654592>

Enhance chemotherapy by using sodium bicarbonate

jfh — Sun, 29 Aug 2010 17:00:00 GMT

Once again, we are reminded that "The extracellular (interstitial) pH (pHe) of solid tumours is significantly more acidic compared to normal tissues."

This article indicates that chemotherapy can be enhanced by drinking water with sodium bicarbonate added. The article is about breast cancer, but it seems that the same would be true for other forms. It would depend upon whether the drug is a weak base (alkaline). You would be improving that alkalinity with the use of sodium bicarbonate.

Quote:

Enhancement of chemotherapy by manipulation of tumour pH.
Raghunand N, He X, van Sluis R, Mahoney B, Baggett B, Taylor CW, Paine-Murrieta G, Roe D, Bhujwalla ZM, Gillies RJ.
Arizona Cancer Center, Tucson 85724-5024, USA.
Abstract
The extracellular (interstitial) pH (pHe) of solid tumours is significantly more acidic compared to normal tissues. In-vitro, low pH reduces the uptake of weakly basic chemotherapeutic drugs and, hence, reduces their cytotoxicity. This phenomenon has been postulated to contribute to a 'physiological' resistance to weakly basic drugs in vivo. Doxorubicin is a weak base chemotherapeutic agent that is commonly used in combination chemotherapy to clinically treat breast cancers. This report demonstrates that MCF-7 human breast cancer cells in vitro are more susceptible to doxorubicin toxicity at pH 7.4, compared to pH 6.8. Furthermore 31P-magnetic resonance spectroscopy (MRS) has shown that the pHe of MCF-7 human breast cancer xenografts can be effectively and significantly raised with sodium bicarbonate in drinking water. The bicarbonate-induced extracellular alkalinization leads to significant improvements in the therapeutic effectiveness of doxorubicin against MCF-7 xenografts in vivo. Although physiological resistance to weakly basic chemotherapeutics is well-documented in vitro and in theory, these data represent the first in vivo demonstration of this important phenomenon.
PMID: 10362108

Pasted from <http://www.ncbi.nlm.nih.gov/pubmed/10362108>

Osmotic shock

jfh — Sun, 29 Aug 2010 16:30:00 GMT

Osmotic shock or osmotic stress is a sudden change in the solute concentration around a cell, causing a rapid change in the movement of water across its cell membrane. Under conditions of high concentrations of either salts, substrates or any solute in the supernatant, water is drawn out of the cells through osmosis. This also inhibits the transport of substrates and cofactors into the cell thus �shocking� the cell. Alternatively, at low concentrations of solutes, water enters the cell in large amounts, causing it to swell and either burst or undergo apoptosis.

All organisms have mechanisms to respond to osmotic shock, with sensors and signal transduction networks providing information to the cell about the osmolarity of its surroundings, these signals activate responses to deal with extreme conditions. Although single-celled organisms are more vulnerable to osmotic shock, since they are directly exposed to their environment, cells in large animals such as mammals still suffer these stresses under some conditions.

Calcium acts as one of the primary regulators of osmotic stress. Intracellular calcium levels rise during hypo-osmotic and hyper-osmotic stresses. During hyper-osmotic stress extracellular albumin binds calcium.

I'm interested in this, because the sodium bicarbonate protocol, of the successful cancer cure, based upon the replacement of extracellular acid with alkaline. http://phkillscancer.com/protocol

Can such osmotic shock kill cancer cells? The way that cesium kills, is to penetrate the cancer cell and give it a more acid environment. It does not alter the extracellular acid environment. Inside the cell is already leaning toward the alkaline side. This must be a result of osmotic shock. The hypothesis is that the molasses or maple syrup "opens" the cell, so that the bicarbonate get be allowed in. Cancer, as well as good and bad bacteria, consume glucose. That must be what opens the cancer cell. Then the cell cannot respond to the osmotic stress.

Now, I'd like to find supporting documentation.

Osmotic stress critical to growth of cells

jfh — Sun, 29 Aug 2010 16:00:00 GMT

This is from a news release from UC San Diego. I'll provide a link to the PNAS.org article below.

Researchers at the University of California, San Diego (UCSD) School of Medicine have determined that a particular type of cellular stress called osmotic stress is of critical importance to cell growth and the body�s immune response against infection. The findings may have implications for autoimmune disorders, transplant rejections, and potential cancer therapies.

Published in the online edition of the Proceedings of the National Academy of Sciences (PNAS) the week of July 5, 2004, the research in mice provided the first proof that a specific transcription factor, a gene that acts as an �on-off� switch, is essential for normal cell proliferation under conditions of osmotic stress and is also necessary for the body�s immune response to invading pathogens.

Osmotic stress occurs when the concentration of molecules in solution outside of the cell is different than that inside the cell. When this happens, water flows either into or out of the cell by osmosis, thereby altering the intracellular environment. Hyperosmotic stress causes water to diffuse out of the cell, resulting in cell shrinkage, which can lead to DNA and protein damage, cell cycle arrest, and ultimately cell death. Cells compensate or adapt to osmotic stress by activating an osmotic stress response pathway that is controlled by a gene called nuclear factor of activated T cells 5 (NFAT5)/tonicity enhancer binding protein (TonEBP). This NFAT5/TonEBP protein is the only known mammalian transcription factor that is activated by hyperosmotic stress.

Steffan N. Ho, M.D., Ph.D., a UCSD assistant professor of pathology and senior author of the paper in PNAS, noted that the findings bring to light new possibilities in the development of drugs to treat autoimmune diseases, transplant rejection and cancer.

�We are particularly excited about the implications of our findings to cancer cell biology,� Ho said. �The tissue microenvironment of tumors is unique because the unregulated growth of malignant cells does not allow for the normal development of blood and lymph vessels within the tumor, which could contribute to osmotic stress. If the growth of cancer cells in the body requires a means to adapt to osmotic stress, this stress response pathway would represent an exciting new target for the identification of anticancer drugs.�

�As immunologists, we were at first rather puzzled when we found that a protein that was thought to help cells of the kidney adapt to osmotic stress was also expressed in tissues of the immune system,� Ho said. �There was no prior evidence that cells of the immune system or any other cell outside the kidney, for that matter, were exposed to significant osmotic stress in the body.�

One of the difficulties in studying the stresses that cells are exposed to within the body is the nearly impossible task of accurately recreating, in the laboratory, the complexities of a tissue with its unique microenvironment as it exists in vivo. To investigate osmotic stress, the Ho team generated mice that expressed a defective form of the NFAT5/TonEBP protein, and found that the mice had an impaired immune response; their cells were unable to grow when exposed to osmotic stress.

�We now think that the very process of cell proliferation within a tissue microenvironment exposes the cell to osmotic stress,� Ho said. �If the can can�t adapt to that osmotic stress, it won�t be able to grow. The immune system is especially dependent on this osmotic stress response because in order to successfully overcome infection by viruses or bacteria, the cells of the immune system must proliferate very rapidly.�Pasted from <http://ucsdnews.ucsd.edu/newsrel/health/07_06_Ho.asp>

Here is the link to the original PNAS article. I could not understand what the heck they are talking about. Different planet. You'll see http://www.pnas.org/content/101/29/10673.full

I'll want to look at how cesium works and how sodium bicarbonate works with this osmotic stress switch.

Cesium

jfh — Sun, 29 Aug 2010 15:30:00 GMT

Here is a disclaimer from PubMed

Clinical effects of cesium intake.
Melnikov P, Zanoni LZ.
Federal University of Mato Grosso do Sul, Campo Grande, Mato Grosso do Sul, Brazil.
Abstract
The knowledge about cesium metabolism and toxicity is sparse. Oral intake of cesium chloride has been widely promoted on the basis of the hypothesis referred to as "high pH cancer therapy", a complimentary alternative medicine method for cancer treatment. However, no properly confirmed tumor regression was reported so far in all probability because of neither theoretical nor experimental grounds for this proposal. The aim of the present review was to resume and discuss the material currently available on cesium salts and their applications in medicine. The presence of cesium in the cell does not guarantee high pH of its content, and there is no clinical evidence to support the claims that cancer cells are vulnerable to cesium. Cesium is relatively safe; signs of its mild toxicity are gastrointestinal distress, hypotension, syncope, numbness, or tingling of the lips. Nevertheless, total cesium intakes of 6 g/day have been found to produce severe hypokalemia, hypomagnesemia, prolonged QTc interval, episodes of polymorphic ventricular tachycardia, with or without torsade de pointes, and even acute heart arrest. However, full information on its acute and chronic toxicity is not sufficiently known. Health care providers should be aware of the cardiac complications, as a result of careless cesium usage as alternative medicine.
PMID: 19655100

Pasted from <http://www.ncbi.nlm.nih.gov/pubmed/19655100>

Now that that is over with:

The effect of cesium therapy on various cancers is reported. A total of 50 patients were treated over a 3 year period with CsCl. The majority of the patients have been unresponsive to previous maximal modalities of cancer treatment and were considered terminal cases. The Cs-treatment consisted of CsCl in addition to some vitamins, minerals, chelating agents and salts of selenium, potassium and magnesium. In addition, a special diet was also instituted. There was an impressive 50% recovery of various cancers, i.e., cancer of unknown primary, breast, colon, prostate, pancrease, lung, liver, lymphoma, ewing sarcoma of the pelvis and adeno-cancer of the gallbladder, by the Cs-therapy employed. There was a 26% and 24% death within the initial 2 weeks and 12 months of treatment, respectively. A consistent finding in these patients was the disappearance of pain within the initial 3 days of Cs-treatment. The small number of autopsies made showed the absence of cancer cells in most cases and the clinical impression indicates a remarkably successful outcome of treatment.
PMID: 6522427

Pasted from <http://www.ncbi.nlm.nih.gov/pubmed/6...?dopt=Abstract>

Regarding alternative therapy:

Liquid ionic cesium chloride works by making cancer cells highly alkaline, typically 8.0 and above, thus making them so "sick" the immune system attacks and kills them.

Cesium chloride not only kills cancer cells indirectly, it immediately stops the metastasis of the cancer; can start shrinking tumor masses within weeks; and almost always stops the pain of cancer within 24 to 48 hours, depending on what is causing the pain.

Technically, the cesium chloride does not directly kill the cancer cells. What is does is allow the immune system to kill the cancer cells. When you see a statement that cesium chloride does not kill cancer cells, that is technically correct.

However, it is also possible that cesium chloride reverts cancer cells into normal cells. This can happen if the cesium chloride kills the microbes inside the cancer cells (by its high alkalinity) and the cancer cells are thus able to revert into normal cells. This is actually the ideal way to cure cancer because there is far less debris for the body to get rid of.

Exactly what percentage of the cancer cells are killed by the immune system or what percentage are reverted into normal cells is unknown. This point to make is that the protocol is very effective.

"Many tests on humans have been carried out by H. Nieper in Hannover, Germany and by H. Sartori in Washington, DC as well as by a number of other physicians. On the whole, the results have been very satisfactory. It has been observed that all pains associated with cancer disappear within 12 to 24 hr, except in a very few cases where there was a morphine withdrawal problem that required a few more hours.
http://www.cancer-coverup.com/brewer/printbrewerreport.htm

With regards to the above quote, it should be noted that Dr. Sartori used very high doses of cesium chloride in his medical clinic. These doses were far too high to be used at home.

Note that it is the CANCER CELLS, not the blood serum, that rises to 8.0 pH or above. The body keeps the blood serum within a small range of pH, around 7.4.

The Cesium Chloride Protocol directly targets cancer cells. Normal cells do not injest the cesium chloride.

Cesium has been proven to get into cancer cells, when other nutrients cannot. The cesium:

1) Makes the cancer cells alkaline (Note: the BLOOD is NOT made alkaline, only the inside of the cancer cells),

2) Limits the intake of glucose into the cell (thus starving the cell and making the cell "sick" from lack of food),

3) Neutralizes the lactic acid (which is actually what causes the cell to multiply uncontrollably), and

4) Stops the fermentation process, which is a second affect of limiting the glucose.

Pasted from <http://www.cancertutor.com/Cancer/Alkaline.html>

extracellular and intracellular pH on immune function cannot be ignored

jfh — Sun, 29 Aug 2010 15:00:00 GMT

By now, I'm overwhelmed with all the articles, I've read, with "doctor-speak". It is almost as incomprehensible as Alan Greenspan's Fed-speak. It makes it difficult for someone like me to provide search criteria. I'm pleased with what I've found, and now have to really try to interpret it. These next gleanings came fromhttp://www.jleukbio.org/cgi/content/full/69/4/522
I really encourage you to read it for yourself. I tried not to take anything out of context, but it was hard, slow reading, and most of which I did not understand. I'm exited to have found this information, as it confirms what I've been looking for. I wanted to know what is involved in this relationship between intracellular pH, extracellular pH, and the immune system. The reason it is important to me, is because I had discovered that cecium and sodium bicarbonate do not directly kill the cancer cells. Instead, they weaken them to provide a path for the immune system to do its job.

In this article pHi is intracellular pH, and pHo is extracellular.

OK. Let's start. I'm going to put my comments in brackets within the article and try to make them unique. That's another reason it may be good for you to read the article. It would be without interruption.

------------

The average pH in many tumors is about 0.5 unit lower than normal
surrounding tissues. [It seems minor, just 0.5, but apparently that is very important. That is how the cancer drugs can be selective. Also, cancer tries to hide, by mimicking normal cells.] Therefore, there is a growing awareness among immunologists and oncologists of the potential modulatory role of the prevailing tumor microenvironment on immune cell function. Necrotic foci [dead cells?] are a common feature of solid tumors, probably as a result of, in part, insufficient vascularization and subsequent hypoxia. Hypoxic cells are dependent on glycolysis for their energy needs, and the production of large amounts of lactic is an inevitable consequence of such anaerobic metabolism. [Even probiotic bacteria produce lactic acid.] Lactate accumulation results in a decrease in extracellular pH, which, when combined with hypoxia, results in diminished viability of healthy and cancerous cells. In addition, a drop in pHi from 7.0 to 6.0 results in inhibition of glycolysis with concomitant inhibition of glucose consumption and lactate production [and turns the environment acid]. Therefore, a further consequence of acidic pH isenergy deprivation, and this effect is as applicable to healthy immune cells as it is to cancer cells. Extracellular pH effects are, therefore, becoming increasingly germane to studies of tumor immunology. In an attempt to simulate the three-dimensional milieu of solid tumors, Ratner investigated lymphocyte motility in neutral and acidified extracellular matrix following stimulation with interleukin (IL)-2 in three-dimensional gels. He found increased motility at pH 6.7 compared with pH 7.1, an effect that was abolished in one-dimensional gels. He concluded that the pH effect represents a modification of lymphocyte-matrix interactions and forwarded ambient pH as a microenvironmental factor that can influence lymphocyte motility within tumors. He further speculated on a stimulatory role for weakly acidic tumor microenvironments, and extremely low pH [acid] was toxic to lymphocyte activity. Conversely, a role for extracellular pH in stimulating tumor development through inhibition of immune function is emerging from other in vitro studies. Severin et al. showed diminished cytotoxic activity of human lymphokine-activated killer (LAK) cell activity in acidic pH; Loeffler et al. found a similar depression of murine natural killer (NK) cell activity with lowered pHo.
[Probiotic bacteria also produce acid externally. It is used to kill some bad pathogens. This is good, and we are not trying to kill friendly bacteria.]
...

The lowest pH values are found in those regions where tumor cells are growing adjacent to a basement membrane, causing necrotic foci and promoting tumor invasion. [This gives rise the myth that bad pathogens don't survive in an acid environment. The problem is that there are several pathogens that not only survive in acid, but become aggessive in alkaline, Candida albicans for example.]

...

Ratner proposes that manipulation of intra-tumor pH via systemic acidosis, glucose infusion, or hyperthermia might constitute a useful adjuvant to immunotherapy if lymphocytic infiltration were increased as a result. However, it must be considered that tumor pH may not necessarily decrease in a homogenous manner; low pH may be present in large tumors, and elevated pH may be found in some necrotic areas because of the depletion of glycogen stores in these areas. Also, hypoxia in combination with low-glucose concentration and acidic pHo is capable of killing tumor cells themselves, rendering obsolete the targeted immunotherapy of such cells. In view of the likelihood of variations in pH existing within and around solid tumors, there are likely to be equally heterogenous effects of pH on immune-cell function at the locus of activity, and much research remains to be done in this area. [This says that our bicarbonate protocol may not work on all forms of cancer. And cesium as well.] It should be also considered that cancer cells use glucose at far higher rates than normal cells; thus, it is possible that insufficient glucose may be available for lymphocytes and other immune cells operating within a tumor region, further compromising the overall effectiveness of the immune response. [It is very important to note that cancer cells use glucose at a higher rate than other cells. That's why the SB protocol involves molasses or syrup.] Similarly, the inadequate perfusion of diseased tissues, which are involved in a variety of other pathological conditions such as infarction and resulting necrosis, will result in similar metabolic effects on the surrounding milieu. The effectiveness of the resultant inflammatory processes is just as likely to be compromised by low extracellular pH as are populations of immune cells congregating at the site of tumors. [This paragraph indicates that it is important to bind the molasses with the sodium bicarbonate. This will get it through the stomach acids by neutralizing them. The cancer cell will have a field day with the sugar. Unfortunately opportunistic pathogens will too.]

...

Experimental evidence is emerging gradually for an inhibition of lymphocyte activity when the surrounding pH of tumors is reduced. This may constitute a very significant finding in the context of tumor immunotherapy, and further consideration by clinicians of the effects of the acidic microenvironment of tumors on immune function would appear to be warranted. [You bet. That's how we believe the sodium bicarbonate protocol should work.]

…

Evidently, the inter-relationship between extracellular and intracellular pH on immune function cannot be ignored, especially in light of the myriad findings implicating a role for the Na+/H+ exchanger prior to activation of certain immune activities. The available data strongly suggest that the Na+/H+ exchanger is a sine quanon in generating a rapid intracellular alkalinization prior to differential activation of certain immune activities [Cesium is proven to do this]. It seems reasonable to speculate on a similarly central role for the exchanger in altering pHi in the same direction as pHo. However, the mechanism by which pHi alters in response to changes in pHo warrants investigation. [Remember that Na is sodium and H is hydrogen. The Na+/H+ exchanger is primarily responsible for maintaining the balance of sodium. In this case it is responsible for making the environment alkaline. The Na+/H+ exchanger isoform 1 (NHE1) is primarily responsible for the regulation of intracellular pH (pHi) ]

Pasted from <http://www.jleukbio.org/cgi/content/full/69/4/522>

Protocol won't work for all forms of cancer

jfh — Sun, 29 Aug 2010 14:50:00 GMT

The role of intracellular pH (pHi) regulation in hematopoiesis is an area of research that has received little attention. Yet the concern for maintaining pH as an important parameter in all in vitro work is well known. By keeping the extracellular pH (pHe) constant, we assume that the cells will be able to regulate their own pHi. This is indeed the case because cells are equipped with several different exchangers to help regulate pHi and to counteract acidification either by efflux of H+ ions or influx of HCO3 ions. The Na+-dependent and -independent Cl/HCO3 exchangers and an adenosine triphosphate-dependent H+ pump are important if the cell becomes too acidic or too alkaline. Thus, whereas the Na+-linked Cl/HCO3 antiporter exchanges Na+ and HCO3 ions for Cl ions, thereby causing a increase in cytosolic pHi, the Na+-independent Cl/HCO3 exchanger reduces pHi in cells with an alkali overload. However, the primary regulator of pHi is the Na+/H+ exchanger (NHE) of which there are 6 known isoforms. [This becomes important when using the sodium bicarbonate protocol. A lot more information, about these exchangers, can be found at the web link. Of course, increasing and lowering the H, by the exchangers, increase and lower the pH.]

...

All the growth factors [interleukin-2,3 etc. from T cells] tested have been shown to increase pHi with an associated activation of cell stimulation and proliferation. For example, using the interleukin-3 (IL-3)-dependent stem-cell line, FDCP-mix, Whetton et al demonstrated that IL-3 activates the NHE and that theresultant intracellular alkalinization was a signal for proliferationof these cells. � Removal of growth factors such as IL-2 from IL-2-dependent cytotoxic T cells resulted in a decrease in pHi and the onset of apoptosis.

�

In contrast to activation of the NHE1 and the concomitant increase in pHi by various stimuli, a decrease in pHi can result in apoptosis of the cell. Several reports using different leukemic cell lines demonstrated that if the Na+/H+ exchanger was inhibited by amiloride analogs, acidification ofthe cells occurred with a concomitant induction of apoptosis. We hypothesized that cells maintaining a high rate of proliferation should exhibit a sustained increase in pHi relative to normal cells as a result of activation of the NHE1. [So, an internal alkaline environment makes the leukemic cells multiply faster.] Here we show that leukemic cell lines and primary patient leukemic samples exhibit a greater pHi than normal cells, that pHi is correlated with cell-cycle status, and that inhibition of NHE1 in patient leukemic cells results in a decrease in pHi and an increase in apoptosis. [This means that our SB protocol won't work with leukemia. Neither will cesium, since cesium makes the intracellular environment more alkaline. A chloride channel blocker might work. That is another story, which I'm not prepared to follow yet.]

Pasted from <http://bloodjournal.hematologylibrar...full/95/4/1427>