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Baking Soda And Prostate Cancer

Discussion in 'Pharmaceutical Drugs' started by gilson d dantas, Dec 10, 2018.

  1. gilson d dantas

    gilson d dantas Member

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    Does anybody knows how many teaspoon of sodium bicarbonate one person with prostate cancer may use every day? I´m using two teaspoon, but I think it is very little. But I don´t know the risks of a overdosis.
     
  2. Amazoniac

    Amazoniac Member

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    Gilson!!

    Baking Soda (pg. 66 has a suspicious discussion on amounts)
     
  3. OP
    gilson d dantas

    gilson d dantas Member

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    In the book of Sircus the dosis is: "Sodium bicarbonate can be used orally in doses of 1/2 tsp in 4 oz of water every two hours for pain relief as well as gastrointestinal upset, not to exceed 7 doses per day". And he says, no more than "Three 1/2 teaspoons if you are over 60 years. Do not use the maximum dosage for more than 2 weeks".
    Do you agree with that?
     
  4. ecstatichamster

    ecstatichamster Member

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    I think so. The risk is milk alkali syndrome. I’m not sure all of the conditions that can lead to it but high baking soda consumption creates the risk.
     
  5. OP
    gilson d dantas

    gilson d dantas Member

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    Thank you my friend
     
  6. Elephanto

    Elephanto Member

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    Make sure to drink enough water (slightly warm if cold is stressing). I eat pretty salty and tend to underestimate my hydratation needs. I think this would prevent most of the potential damage with either salt or baking soda, especially toward kidneys. It also dillutes it when you take it and salt is under-estimated as a gut irritant. I think the main mechanism is that when too much is concentrated in one spot (such as eating too much salt in a single meal) it can be corrosive enough to create holes in the intestinal barrier. Although this may only concern salt and not baking soda.

    High-Salt Diet Induces IL-17-Dependent Gut Inflammation and Exacerbates Colitis in Mice

    Coincidentally, this reminds me that IL-17 is involved in prostate cancer (and probably mpb).
    Interleukin-17 promotes prostate cancer via MMP7-induced epithelial-to-mesenchymal transition. - PubMed - NCBI

    Zinc inhibits IL-17 :
    Zinc suppresses Th17 development via inhibition of STAT3 activation. - PubMed - NCBI
     
  7. OP
    gilson d dantas

    gilson d dantas Member

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    Elephanto, what means "mpb"?
    I get zinc in shrimp and fishes from the sea, I think.
    And I don´t undestand why to use very little baking soda: "Three 1/2 teaspoons if you are over 60 years". It´s true that the dose must be so low, as say M Sircus???
    And it is a good idea to use salt diluted.
     
  8. Amazoniac

    Amazoniac Member

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    Gilson, it's better not to rely on those arbitrary figures..
    How Measuring My Urine pH Got Me to Love Working Out Again - Chris Masterjohn
     
  9. ecstatichamster

    ecstatichamster Member

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    Milk-Alkali Syndrome

    Despite extensive clinical experience, scant data are available on the pathogenesis of MAS. Throughout the years, several contributing factors have been proposed, including loss of gastric juice, preexisting renal disease, insufficient chloride intake, hemorrhage, anemia, impaired liver function, and warm weather.16,26-31

    Ingestion of excessive quantities of calcium and absorbable alkali is a prerequisite for establishing the diagnosis. What constitutes “excessive” is unclear but generally indicates at least 4 to 5 g of calcium carbonate daily.32,33

    However, ingesting large amounts of alkali and calcium alone does not result in alkalosis and hypercalcemia, respectively. McGee et al34 administered 1.3 to 2.0 g of a mixture of calcium carbonate and magnesium oxide hourly from 7 am to 9 pm for 8 days to 17 individuals with healthy kidneys. No significant changes in serum bicarbonate levels were observed.

    The authors speculated that hypochloremia and dehydration were key factors in the development of alkalosis.35 In the first reports of toxicity due to the Sippy program, Hardt and Rivers5 noted a definite correlation between the incidence of alkalosis and the presence of kidney disease. Subsequent reports confirmed that preexisting renal disease seemed to be a predisposing factor.20,26,27,36 However, it is widely recognized that MAS can develop without renal impairment.37

    Furthermore, even in patients with impaired renal function, large amounts of absorbable alkali do not lead to alkalosis in most individuals.14,38,39 Some authors found no preexisting kidney disease in most of their patients with MAS.1,15 Underlying renal disease does not seem to be a prerequisite but rather a contributing factor in the pathogenesis of MAS.

    For hypercalcemia to develop, calcium intake must be excessive, but inability to excrete the excess calcium is also an essential part of the process. Because the skeletal system does not have unlimited calcium buffer capacity, tight regulation of calcium absorption from the small intestine and excretion by the kidneys are paramount to maintain serum calcium levels. Individual variations in the buffering capacity of bone may also have a role in the susceptibility to development of hypercalcemia.40

    The role of vitamin D and PTH in MAS is unclear. Limited data suggest that 1,25-dihydroxyvitamin D (1,25-OH vitamin D; also known as calcitriol) and PTH levels are suppressed in MAS.19,41-43 However, the extent of suppression varies, and calcitriol levels may remain well within the reference range.44 Increased intake of calcium results in decreased 25-hydroxylation of vitamin D by the kidneys, which leads to a marked decrease of fractional calcium absorption in the small intestine. Besides this active regulated mechanism, nonsaturable passive diffusion occurs. Individual variability of calcium absorption varies widely. In certain individuals, high urinary calcium excretion indicative of high intestinal absorption persists despite continuous calcium ingestion and suppressed 1,25-OH vitamin D levels.4
     
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