Marc Sircus: Sodium Bicarbonate (Baking Soda) and pH Medicine

[James]

Interesting that despite Sircus' claim he never responded to me or my evidence:

+Mark Sircus : "+Brian Seavers Hey Brian, that must have been my assistant responding to you who did not quite get the irony. Can you show me any of these comments from the experts...I do not get to see such criticism and I do love to comment back on them."

I am more than happy to debate you on this as I have already exposed so much of your misinformation to begin with. Let's see if you debate the facts or delete the post. Here is one of my previous responses to your dangerous misinformation:

"So much misinformation. Neither salivary or blood pH indicate blood pH. The only way you can determine blood pH is with a blood test. Salivary pH is affected by the amount of bacteria in the mouth so things such as brushing your teeth will make the saliva more alkaline. So will drinking water, thinking of certain foods, etc. Dry mouth increases acidity as alkaline saliva normally washes away acid forming bacteria in the mouth. Urinary pH is affected by hydration levels, certain supplements and medications and by bacteria in the urine. Urinary tract infections lead to highly alkaline urine as the bacteria use the enzyme urease to split urea in to highly alkaline ammonia. The alkalinity helps the bacteria, as with most pathogens, to survive.

Cancer is not much different. Cancer cells have a higher than normal alkaline internal pH. They need this alkalinity to survive and thrive. This is why they export the acidic protons in to the external matrix making the area around the tumor acidic. Studies have also shown that when healthy cells are made excessively alkaline the healthy cells morph in to cancer cells.

Chemotherapy is not always acidic. There are alkaline chemo agents as well. Their pH makes no difference though as they do not work based on altering the internal pH of the cancer cells from an alkaline pH to an acidic pH. Although this is part of the current research in to killing cancer cells. It was found that when the cancer cell's proton pumps were blocked the cancer cells become acidic killing them.

Sircus also has many other claims wrong. For example he claims that when we are acidic carbon dioxide levels decrease. Just the opposite. Carbon dioxide forms carbonic acid, so the more carbon dioxide we retain the more acid we have. And the acidity INCREASES oxygen levels as where alkalinity DECREASES oxygen levels. Acidity is required to release oxygen from hemoglobin. Carbonic acid also dilates blood vessels increasing circulation. For example, when a person hyperventilates they blow off so much carbon dioxide that they become highly alkaline. The person passes out as the blood vessels to the brain constrict pushing blood away from the brain. When the person passes out their respiration slows or halts temporarily to build carbonic acid levels back up to restore circulation.

In severe cases of alkalosis the person dies from a lack of oxygen as the alkalosis inhibits oxygen release, constricts blood vessels decreasing circulation and due to the induced spasm contractions of the lungs, which prevents the person from breathing.

Also keep in mind that the blood is maintained in an alkaline state in nearly every case. Acidosis is EXTREMELY rare and usually results from some poisonings, severe respiratory issues and even the use of sodium bicarbonate (baking soda). Sodium bicarbonate injection or ingestion can lead to carbonic acid induced acidosis as the neutralization of acids with bicarbonate leads to carbonic acid formation. If ingested the baking soda is neutralized by the stomach acid forming large amounts of sodium chloride that can lead to hyperchloremic acidosis.

Giving sodium bicarbonate to cancer patients is especially dangerous. Not only does the neutralization of stomach acid enhance nutritional deficiencies, but this also leads to decreased methylation. Decreased methylation causes and promotes cancer as well as suppresses the immune system, leads to hormone imbalances, elevates pro-cancer homocysteine, etc."

[James]

+Mark Sircus Here is another post I did when someone tried to defend your video with a research paper they clearly did not read or understand:

+Zar Doz: "+Hveragerthi This peer reviewed paper does not agree with you; PMC4303887 Published online 2014 Dec 18. Glycolysis, tumor metabolism, cancer growth and dissemination. A new pH-based etiopathogenic perspective and therapeutic approach to an old cancer question Khalid O. Alfarouk, Daniel Verduzco, Cyril Rauch, Abdel Khalig Muddathir, H. H Bashir Adil, Gamal O. Elhassan, Muntaser E. Ibrahim, Julian David Polo Orozco, Rosa Angela Cardone, Stephan J. Reshkin, and Salvador Harguindey In fact it states the exact opposite."

LOL!!! You either:

1. Did not read the study.

or

2. Did not understand the study.

What is the first sentence of the study?:

"Cancer cells acquire an unusual glycolytic behavior relative, to a large extent, to their intracellular alkaline pH (pHi). This effect is part of the metabolic alterations found in most, if not all, cancer cells to deal with unfavorable conditions, mainly hypoxia and low nutrient supply".

Note where they say intracellular ALKALINE pH. What does this mean? It means the pH inside the cancer cell is alkaline just as I said in the first place.

Again backed up later in the study where they say "a selective hallmark of they having an alkaline cytosol and an acidic extracellular microenvironment [37,51]". Again meaning an alkaline internal pH with an external acidic pH. This acidic EXTERNAL pH is the result of the rapid export of acidic hydrogen ions (protons) in to the external matrix as a means to maintain the ALKALINE INTERNAL pH the cancer cells need to survive and thrive.

In my previous response I mentioned the internal alkalinity allows the cancer cells to survive and thrive. By thrive I am referring to the alkalinity driving glycolysis of the cancer cells, which the study you mentioned also backs up. Later in the study they start talking about over expression of phosphofructokinase-1, which in turn increases glycolysis. And what do they say about phosphofructokinase-1? "Also, a slightly alkaline pHi is the optimum to maximize PFK-1 activity [52,77-80]". So as i pointed out the INTERNAL ALKALINITY of the cancer cells is driving the glycolysis of cancer cells allowing them to thrive by the over expression of phosphofructokinase-1 supported by the INTERNAL ALKALINITY of the cancer cells.

They back this up again when they state: "On one hand, it has been known for decades that an alkaline pHi even slightly above steady-state levels stimulates the activity of this key glycolytic enzyme and inhibits gluconeogenesis. Indeed, in cancer cells a high pHi situation can increase the allosteric regulation of PFK-1 more than a 100-fold and even a raise of 0.2 pH units can convert this enzyme from an inactive form to a fully active quaternary structure [5,80-83]."

Later in the study they say:

"It has also been demonstrated that protons inhibit PFK-2 [78,127] while an alkaline pHi increases its activity [128]." So here they are saying that the ALKALINITY of cancer cells increases activity of phosphofructokinase-2. The increase of phosphofructokinase-2 increases anaerobic glycolysis in cancer cells.

Next in the study you cite they say:

"PFK-2 has 4 isoenzymes: PFKFB 1, 2, 3, 4 [129,130]. PFKFB3 and 4 are correlated with cancer and their expression is higher in metastasis as compared to primary tumors [131,132]. Interestingly, Hypoxia Inducible Factor-1 alpha (HIF-1 alpha) increases transcription of PFKFB4 [133]. Altogether, these data suggest that they could potentially become important antimetastatic targets [131]."

So they are stating that the over expression of phosphofructokinase-2 due to the ALKALINITY of the cancer cells is linked to metastases (spread) of cancer cells, and therefore targeting phosphofructokinase-2 may be a way to inhibit metastases.

Then in the study you cite they say:

"Triose phosphate isomerase also shows a higher activity at alkaline pH [141]."

Triosephosphate isomerase is another promoter of glycolysis in cancer cells. And note that the ALKALINITY of cancer cells once again promotes this compound, which in turn promotes glycolysis once again.

Next in the study you cited they say:

"Once again, intracellular alkalinity is the optimum environmental condition for aldolase activity [151]."

Adolase breaks down glucose for energy production. Therefore, increased aldolase activity from the INTERNAL ALKALINITY OF CANCER CELLS increases energy production in cancer cells by allowing them to use more glucose.

Should I go on with with more quotes from the study you cited since it is backing exactly what I said in the first place?

But thanks for providing all this evidence backing what I said in the first place and proving Mark Sircus wrong. Saves me some work.

Here are some more studies for you to look in to:

Reliance of cancer cells on oxygen:

Oxygen Consumption Can Regulate the Growth of Tumors, a New Perspective on the Warburg Effect. PLoS One 2009 Sep 15;4(9):e7033

Choosing between glycolysis and oxidative phosphorylation: a tumor's dilemma? Biochim Biophys Acta 2011 Jun;1807(6):552-61

Comparison of Metabolic Pathways between Cancer Cells and Stromal Cells in Colorectal Carcinomas: a Metabolic Survival Role for Tumor-Associated Stroma. Cancer Res January 15, 2006 66;632

Akt Stimulates Aerobic Glycolysis in Cancer Cells. Cancer Res June 1, 2004 64; 3892


That cancer growth is inhibited by low oxygen levels an die in the absence of oxygen:

Oxygen consumption can regulate the growth of tumors, a new perspective on the Warburg effect. PLoS One 2009 Sep 15;4(9):e7033

Anoxia is necessary for tumor cell toxicity caused by a low-oxygen environment. Cancer Res 2005 Apr 15;65(8):3171-8

Relationship between oxygen and glucose consumption by transplanted tumors in vivo. Cancer Res 1967 Jun;27(6):1041-52


Death of cancer cells by lack of oxygen and angiogenesis stimulation to increase the growth rate of tumors by increasing oxygen levels to the tumor:

Computational models of VEGF-associated angiogenic processes in cancer. Math Med Biol 2012 Mar;29(1):85-94

Blood Flow, Oxygen Consumption, and Tissue Oxygenation of Human Breast Cancer Xenografts in Nude Rats. Cancer Res 47, 3496-3503, July 1,1987

A Mathematical Model for the Diffusion of Tumour Angiogenesis Factor into the Surrounding Host. Tissue Math Med Biol (1991) 8 (3): 191-220

The History of Tumour Angiogenesis as a Therapeutic Target. University of Toronto Medical Journal Vol 87, No 1 (2009)



The higher affinity for oxygen by cancer cells than healthy cells:

Utilization of Oxygen by Transplanted Tumors in Vivo. Cancer Res 1967;27:1020-1030

Growth-related changes of oxygen consumption rates of tumor cells grown in vitro and in vivo. J Cell Physiol 1989 Jan;138(1):183-91



Alkalinity driving cancer cell growth and malignant transformation:

Role of the Intracellular pH in the Metabolic Switch Between Oxidative Phosphorylaiton and Aerobic Glycolysis-Relavance to Cancer. Cancer 2011;2(3):WMC001716

Na+/H+ exchanger-dependent intracellular alkalinization is an early event in malignant transformation and plays an essential role in the development of subsequent transformation-associated phenotypes. FASEBJ 2000 Nov;14(14):2185-97

Tumorigenic 3T3 cells maintain an alkaline intracellular pH under physiological conditions. Proc Natl Acad Sci USA 1990 October; 87(19): 7414–7418

31P NMR analysis of intracellular pH of Swiss Mouse 3T3 cells: effects of extracellular Na+ and K+ and mitogenic stimulation. J Membr Biol 1986;94(1):55-64

Extracellular Na+ and initiation of DNA synthesis: role of intracellular pH and K+. J Cell Biol 1984 Mar;98(3):1082-9


How cancer cells maintain their internal alkalinity and evidence that blocking the proton pumps makes cancer cells acidic killing them:

Vacuolar H(+)-ATPase in Cancer Cells: Structure and Function. Atlas of Genetics and Cytogenetics in Oncology and Haematology Sept. 2011

Vacuolar H+-ATPase in human breast cancer cells with distinct metastatic potential: distribution and functional activity. Am J Physiol Cell Physiol 286: C1443–C1452, 2004

Targeting vacuolar H+-ATPases as a new strategy against cancer. Cancer Res 2007 Nov 15;67(22):10627-30

Vacuolar H(+)-ATPase signaling pathway in cancer. Curr Protein Pept Sci 2012 Mar;13(2):152-63



That cancer cells secrete lactate, not lactic acid:

Tumor metabolism of lactate: the influence and therapeutic potential for MCT and CD147 regulation. Future Oncol 2010 Jan;6(1):127-48

Enzymes involved in L-lactate metabolism in humans. Mitochondrion 2013 Sep 9. pii: S1567-7249(13)00244-4

Tumor metabolism: cancer cells give and take lactate. J Clin Invest 2008 Dec;118(12):3835-7

Mitochondrial fission induces glycolytic reprogramming in cancer-associated myofibroblasts, driving stromal lactate production, and early tumor growth. Oncotarget 2012 Aug;3(8):798-810