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haidut

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Yet another study linking chronic stress to cancer growth. I posted several threads in the past demonstrating the negative effects epinephrine and lipolysis on cancer cell growth and how administering a beta blocker can inhibit the growth of tumors.
Stress (adrenaline, Noradrenaline) As The Main Driver Of Cancer Metastases

The new study below corroborates these findings and adds yet more evidence that lactate is also intimately involved in cancer growth, and it is the epinephrine elevated by chronic stress that leads to increased lactate which then activates cancer stem cells. Perhaps more importantly, it shows that approaches such as chemotherapy, radiation and surgery are likely pointless because it is cancer stem cells that can seed new tumor growth after treatment and the "kill, poison, burn" approach not only does not address the stem cells but likely also fuels their growth due to the additional stress imposed. Finally, as the study shows, the very act of cancer diagnosis may be fueling its growth through the stress and depression this diagnosis causes.
And just as Linus Pauling demonstrated more than 5o years ago, vitamin C may be able to halt this process. I wonder if one day vitamin C is approved as cancer treatment if the people who ruined the later part of Pauling's life by relentlessly labeling his vitamin C treatment a fraud will face any consequences...One may only wish.

Mouse Study: Chronic Stress Fuels Cancer, Vitamin C May be Potential Therapy

"...In a new study of chronically stressed mice, University of Illinois researchers demonstrated the effects of chronic stress on cancer stem cell growth, a novel twist on previous research that did not specifically focus on these self-perpetuating cells. This first time discovery, published in the Journal of Clinical Investigation, shows the role of epinephrine in promoting breast cancer. The finding suggests that when women experience chronic stress and depression accompanying a diagnosis, they may inadvertently fuel additional breast cancer cell growth. “You can kill all the cells you want in a tumor, but if the stem cells, or mother cells, are not killed, then the tumor is going to grow and metastasize. This is one of the first studies to link chronic stress specifically with the growth of breast cancer stem cells,” said Dr. Keith Kelley, emeritus professor in the Department of Animal Sciences and the College of Medicine at the University of Illinois."

"...In the study, researchers induced chronic stress in mice, by placing them in small enclosures that limited their movement. All the mice were stressed for a week before being inoculated with either human or mouse breast cancer cells. After inoculation, the mice were split into two groups: controls, which were moved into large cages; and stressed, which stayed in the small enclosures for an additional 30 days. Confirming the researchers’ expectations, the mice experiencing chronic stress showed behavioral changes consistent with anxiety and depression. They also had bigger, faster-growing tumors and more cancer stem cells than mice in control conditions."

"...First, epinephrine levels were significantly elevated in mice that experienced stress for the duration of the experiment. Second, in stressed mice that received treatments to inactivate the ADRB2 receptor for epinephrine, tumors were significantly smaller and fewer stem cells were found. “When most people think of stress, they think it’s cortisol that’s suppressing the immune system. The amazing thing is cortisol was actually lower after a month of stress,” Kelley said. Once epinephrine binds to one of its two receptors, ADRB2, it elevates levels of an enzyme called lactate dehydrogenase. In normal situations, this enzyme delivers quick energy to muscles in a fight-or-flight situation and produces lactate as a byproduct. But cancer cells need lactate for energy. With excessive amounts of lactate dehydrogenase in chronically stressed individuals, cancer-causing genes are activated and cancer cells proliferate."

"...Importantly, and consistent with findings in mice, patients with high serum epinephrine had significantly lower overall survival and disease-free survival compared to patients with low epinephrine levels. In a final test, the researchers grew breast cancer cells in the lab and introduced a wide variety of FDA-approved cancer drugs. Several treatments, including vitamin C, suppressed lactate dehydrogenase production. When vitamin C was injected into stressed mice, tumors shrank. Scientists have suspected Vitamin C’s cancer-fighting potential for decades, and several clinical trials have demonstrated positive results. This study contributes a new understanding of the vitamin’s action in biochemical pathways relevant to chronically stressed breast cancer patients. “Taken together, these findings show that vitamin C might be a novel and effective therapeutic agent for targeting cancer in patients undergoing chronic stress,” Liu said."
 

Mauritio

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This study is also mentioned by the authors, and specifically mentions the death of cancer cells by inhibiting glycolysis ,as far as I can see:
Vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH. - PubMed - NCBI

More than half of human colorectal cancers (CRCs) carry either KRAS or BRAF mutations and are often refractory to approved targeted therapies. We found that cultured human CRC cells harboring KRAS or BRAF mutations are selectively killed when exposed to high levels of vitamin C. This effect is due to increased uptake of the oxidized form of vitamin C, dehydroascorbate (DHA), via the GLUT1 glucose transporter. Increased DHA uptake causes oxidative stress as intracellular DHA is reduced to vitamin C, depleting glutathione. Thus, reactive oxygen species accumulate and inactivate glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Inhibition of GAPDH in highly glycolytic KRAS or BRAF mutant cells leads to an energetic crisis and cell death not seen in KRAS and BRAF wild-type cells. High-dose vitamin C impairs tumor growth in Apc/Kras(G12D) mutant mice. These results provide a mechanistic rationale for exploring the therapeutic use of vitamin C for CRCs with KRAS or BRAF mutations.
 
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Whats the dose for vit C?
 

tallglass13

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is there a supplement of Vit C that is superior? is Ascorbic Acid all we need? Has Ray every stated what Vit C supplement is the safest?
 

lampofred

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is there a supplement of Vit C that is superior? is Ascorbic Acid all we need? Has Ray every stated what Vit C supplement is the safest?

Dr. Peat discourages all synthetic Vit C, says even milk and meat have lots of Vit C (if you don't drink OJ)
 

schultz

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Dr. Peat discourages all synthetic Vit C, says even milk and meat have lots of Vit C (if you don't drink OJ)

As dehydroascorbic acid according to Ray, if people are wondering. It wouldn't be on food labels.
 

tankasnowgod

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is there a supplement of Vit C that is superior? is Ascorbic Acid all we need? Has Ray every stated what Vit C supplement is the safest?

If you look at guys like Linus Pauling, Ewan Cameron, Abram Hoffer and Robert Cathcart, they were all using plain Ascorbic Acid, or Sodium Ascorbate.
 

haidut

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Can someone make sense of that data and extract the used dosage out of that ? It is listed on page 24 .
Also they tested 200 other chemicals , that might be worth looking into as well...

JCI - Stress-induced epinephrine enhances lactate dehydrogenase A and promotes breast cancer stem-like cells

The study is really convoluted and in fact they say they used vitamin C in an in vivo model (mouse) - loo at figure 7. However, neither the main study not the supplemental information list vitamin C dose used on the mice. They only list in vitro concentrations and in that experiment vitamin C had dose-dependent effects starting at around 100uM/L (achievable with about 500mg vitamin C) and becoming very strong at 2mM/L. Concentrations above 500 uM/L are probably only achievable by injection though as oral doses in the grams range will just cause loose stool and get mostly excreted.
Btw, the more important thing to observe is that the increased lactate and the effects of vitamin C are downstream from epinephrine. So, it makes sense to target epinephrine first and prevent the rise in lactate. This exactly the approach mention in those 2 threads I mention at the beginning of the post and this study used that same approach and administered propranolol (beta blocker) to the mice and that also had tumor blocking effects.
If one decides to go the vitamin C route then you can get dehydroascorbic acid easily and cheaply by using either taking regular vitamin C combined with MB, or make a solution of dissolved vitamin C and add MB to it so that MB oxidizes the ascorbic acid and turns it into DHA. I mentioned this approach in another thread on DHA and the advantage is that if make the solution with vitamin C + MB, and leave it exposed to open air after a few days the MB will get re-oxidized back to blue color and then you consume the liquid you will have two oxidizing agents - the DHA and the newly reoxidized MB, which will likely have a much more potent effects as both MB and DHA inhibit LDH and lactate formation. The reason DHA is more effective is that cancer cells take it up by the same mechanism (GLUT4/5) as glucose and are really hungry for it. So, when they overdose on an oxidizing agent like DHA they quickly die. Adding MB makes that process even more effective.
@schultz @tankasnowgod @lampofred @tallglass13
 

haidut

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EpineNon? LactaBan?

Salt is pretty powerful anti-epinephrine agent and Oxidal/Energin/Lapodin/Pyrucet are all LactaBans :):
 

lampofred

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And hypoventilation by increasing CO2 decreases both adrenaline and lactate. It seems like stress/overthinking is the cause of all diseases and a calm mind/CO2 is the cure for all diseases.

Interesting how CO2 is demonized as an toxic pollutant.
 

Logan-

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I mentioned this approach in another thread on DHA

The role of adding vitamin K3 is to oxidize the vitamin C more readily once in the organism as a result of the powerful oxidizing effect of the K3 (menadione). The same effects can be achieved much more safely with a combination of vitamin C and any other vitamin K, emodin or methylene blue (MB). In fact, using MB would be better because inside the organism the reduced/colorless MB will oxidize again and will continue to support respiration on top of the benefit the oxidized vitamin C will have. Using vitamin K3 (menadione) will likely only provide the benefit of oxidized vitamin C but without continued redox effects that MB can provide.
 

chimdp

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The study is really convoluted and in fact they say they used vitamin C in an in vivo model (mouse) - loo at figure 7. However, neither the main study not the supplemental information list vitamin C dose used on the mice. They only list in vitro concentrations and in that experiment vitamin C had dose-dependent effects starting at around 100uM/L (achievable with about 500mg vitamin C) and becoming very strong at 2mM/L. Concentrations above 500 uM/L are probably only achievable by injection though as oral doses in the grams range will just cause loose stool and get mostly excreted.
Btw, the more important thing to observe is that the increased lactate and the effects of vitamin C are downstream from epinephrine. So, it makes sense to target epinephrine first and prevent the rise in lactate. This exactly the approach mention in those 2 threads I mention at the beginning of the post and this study used that same approach and administered propranolol (beta blocker) to the mice and that also had tumor blocking effects.
If one decides to go the vitamin C route then you can get dehydroascorbic acid easily and cheaply by using either taking regular vitamin C combined with MB, or make a solution of dissolved vitamin C and add MB to it so that MB oxidizes the ascorbic acid and turns it into DHA. I mentioned this approach in another thread on DHA and the advantage is that if make the solution with vitamin C + MB, and leave it exposed to open air after a few days the MB will get re-oxidized back to blue color and then you consume the liquid you will have two oxidizing agents - the DHA and the newly reoxidized MB, which will likely have a much more potent effects as both MB and DHA inhibit LDH and lactate formation. The reason DHA is more effective is that cancer cells take it up by the same mechanism (GLUT4/5) as glucose and are really hungry for it. So, when they overdose on an oxidizing agent like DHA they quickly die. Adding MB makes that process even more effective.
@schultz @tankasnowgod @lampofred @tallglass13

@haidut Thanks for this. I seem to have a bad reaction to MB, possibly serotonin related, where I get anxiety, since of dread, lack of clear or sharp thinking. How much Vitamin C to MB do you recommend mixing to make sure all the MB reacts with the Vit C? Also, does it need to be straight ascorbic acid or will it work with the buffered ascorbate powder (it's a mix of Sodium, Magnesium, Potassium, and Zinc Ascorbate)?
 

Makrosky

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@haidut Thanks for this. I seem to have a bad reaction to MB, possibly serotonin related, where I get anxiety, since of dread, lack of clear or sharp thinking. How much Vitamin C to MB do you recommend mixing to make sure all the MB reacts with the Vit C? Also, does it need to be straight ascorbic acid or will it work with the buffered ascorbate powder (it's a mix of Sodium, Magnesium, Potassium, and Zinc Ascorbate)?
Have you considered that the bad effects from MB could be an increased metabolism without adequate substrate to sustain it?
 
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Have you considered that the bad effects from MB could be an increased metabolism without adequate substrate to sustain it?

Speaking from my experience, MB makes me feel off too. I feel irritable and jumpy when I take too high of a dose. I dont get these effects with other quinones like Panquinone, Pau D'Arco or Lapodin (Emodin).

Could be increased metabolism making him feel that way, also could be the serotonergic qualities.
 

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