Psycho-Oncology: Discover How Stress Causes Cancer
Phase 1 of Cancer: Inescapable Shock
Phase 2 of Cancer: Adrenaline Depletion
Phase 3 of Cancer: The Cancer Fungus
Phase 4 of Cancer: Niacin Deficiency
Phase 5 of Cancer: Vitamin C Depletion
Phase 6 of Cancer: Immune Suppression
PHASE 5 OF CANCER: VITAMIN C DEPLETION
During phase 5, depleted adrenaline levels (caused by prolonged chronic stress) cause a depletion of ascorbic acid (vitamin C) in the adrenal glands. Ascorbic acid is the key ingredient used by dopamine to make noradrenaline (norepinephrine) in the adrenal glands, which is then converted to adrenaline. During prolonged chronic stress more and more adrenaline is pumped out and then depleted, meaning more and more ascorbic acid is used up in the creation of adrenaline. During chronic stress the adrenal glands also release ascorbic acid into the body to diminish the stressful impact of adrenaline [and other stress hormones] on the heart and blood pressure systems. Ascorbic acid is essential for preventing cell DNA damage caused by “oxidative stress”, converting oxygen waste product’s superoxide and hydrogen peroxide into oxygen and water within the cell mitochondria throughout the process known as Oxidative Phosphorylation. The continual loss of ascorbic acid [during prolonged chronic stress] thereby increases cell mitochondrial DNA damage and mutation, causing normal cells to mutate into cancer cells.
THE THEORY: BY GLEN RUSSELL,
PUNA WAI ORA MIND-BODY CANCER CLINIC
Ascorbic acid (vitamin C) is an essential nutrient required by the human body for survival. It is a key anti-oxidant used to breakdown superoxide and hydrogen peroxide in the mitochondria of cells, to prevent cell DNA damage and is an essential ingredient required by the adrenal glands to produce stress hormones, including norepinephrine and adrenaline. During prolonged chronic stress, ascorbic acid is used to create norepinephrine (noradrenaline) to be converted into epinephrine (adrenaline). Dopamine uses ascorbic acid and oxygen to synthesize norephinephrine via the pathway known as "dopamine β-hydroxylase" (also known as dopamine β-monooxygenase), and it is for this reason that 100 times more ascorbic acid is found in the adrenal glands than anywhere else in the body. During prolonged chronic stress, ascorbic acid is also released from the adrenal glands to protect the heart from cardiovascular disorders and arrhythmias. Yet as the condition of prolonged chronic stress continues for months and years and adrenaline levels are depleted, ascorbic acid (vitamin C) levels are also depleted as both are inextricably linked. Without an adequate supply of ascorbic acid [and other important anti-oxidants], superoxide and hydrogen peroxide are unable to be broken down into oxygen and water within the cell's mitochondria in the process known as Oxidative Phosphorylation, and normal cells are more likely to mutate into cancer cells due to cell DNA damage.
Ewan Cameron [senior consulting physician at the Vale of Leven Hospital, Scotland] and Nobel Prize Laureate for his work in Chemistry, Linus Pauling PhD were convinced ascorbic acid should be included in the treatment of cancer and undertook a four year trial to determine the effectiveness of ascorbic acid (high dose vitamin C therapy) in 2,860 cancer patients between 1978-1982. The trial [below] involved a ten-day course of intravenous sodium ascorbic acid, followed indefinitely by 10-30 grams daily of oral ascorbic acid.
Linus Pauling (left) and Ewan Cameron
Ewan Cameron, MD: “As a single-handed surgeon working in a relatively small hospital, it would have taken me a decade or more to collect a sufficient number of identical patients with an identical type of cancer, all at the same stage of their illness, to enable me to conduct a “proper” randomized double-blind clinical trial [of ascorbic acid]. We did the best we could; we conducted two controlled trials in which the survival time of groups of 100 cancer patients given supplemental ascorbate in the later stage of their illness was compared to the survival time of 1000 matched patients not given ascorbate. In the first study, the controls were selected “blind” by a young New Zealand doctor, specially employed for the purpose. I and a research assistant selected the controls for the second study. Both trials showed a definite survival advantage for the patients given ascorbate. These papers attracted world-wide media attention, and prompted a deluge of letters from cancer patients in many countries. Dr. Pauling and I wrote the book Cancer and Vitamin C in the hope of answering such questions, and lightening our mail-bags, but our effort has been unsuccessful. The letters and telephone calls continue unabated. Dan Rather of CBS network news in a recent broadcast stated that they estimated that 100,000 cancer patients in the United States were now taking vitamin C, with or without the tacit consent of their doctors. We have recently completed a four year trial involving 2,860 cancer patients attending three medium sized general hospitals in Scotland over the four year period from 1978 to 1982. This study was mainly funded by I.B.M. (United Kingdom) Ltd., who devised a computerized records system to suit our requirements. The data has been analyzed as follows: Firstly, patients who died within two weeks of first hospital attendance are excluded. Secondly, all patients who first attended the hospital less than six months before the study ended are also excluded. Finally, all patients who remain potentially cured (e.g. no known recurrence after primary curative surgery) are also excluded. This leaves 1,826 incurable cancer patients, some of whom received supplemental ascorbate (296) and the remainder (1532) who did not, effectively randomized by the date of first hospital attendance. The median survival time of the control patients, as measured from the date of first hospital attendance to the date of death (or to the end of the study, if still alive at that time), was 180 days, whereas the comparable time for the ascorbate group was 343 days. The results of this study, in much more detail, are contained in a manuscript submitted to The New England Journal of Medicine in 1984.”
Dr Mark Levine
During normal cell respiration within the mitochondria, superoxide and hydrogen peroxide (H2O2) are damaging by-products of Oxidative Phosphorylation that must be converted into oxygen and water to avoid cell damage. Ascorbic acid and the enzyme "superoxide dismutase" are the key substances used to convert these harmful substances into oxygen and water, thereby avoiding cell DNA damage and cell mutations. This is the anti-oxidant effects of ascorbic acid that occurs within normal cells to prevent cancer. Yet the body has ingeniously designed ascorbic acid to have the opposite effect inside cancer cells, where instead of it being used as an anti-oxidant to remove superoxide and hydrogen peroxide, it is being used as a pro-oxidant to create superoxide and hydrogen peroxide to cause cell death within the cancer/tumor cell. In a landmark study conducted by the National Cancer Institute / National Institutes of Health, USA, researchers (led by Dr Mark Levine) documented this pro-oxidant mechanism of ascorbic acid within tumor cell lines in mouse models and found high levels of intravenous ascorbic acid (vitamin c) significantly reduced tumor cell growth.
Dr Mark Levine of the National Institutes of Health: "Ascorbic acid is an essential nutrient commonly regarded as an anti-oxidant. In this study, we showed that ascorbate at pharmacologic concentrations was a pro oxidant, generating hydrogen-peroxide-dependent cyto-toxicity toward a variety of cancer cells in vitro without adversely affecting normal cells. To test this action in vivo, normal oral tight control was bypassed by parenteral ascorbate (intravenous) administration. Real-time microdialysis sampling in mice bearing glioblastoma [brain cancer] xenografts showed that a single pharmacologic dose of ascorbate (vitamin C) produced sustained ascorbate radical and hydrogen peroxide formation selectively within interstitial fluids of tumors but not in blood. Moreover, a regimen of daily pharmacologic ascorbate treatment significantly decreased growth rates of ovarian, pancreatic, and glioblastoma [brain] tumors established in mice. Similar pharmacologic concentrations were readily achieved in humans given ascorbate (vitamin C) intravenously. These data suggest that ascorbate as a prodrug may have benefits in cancers with poor prognosis and limited therapeutic options.
Results: Given their relative sensitivity, the efficacy of pharmacologic ascorbate administration on the growth of Ovcar5, Pan02, and 9L tumors was examined in nude mice. Treatment commenced after tumors reached a palpable size of 5-7 mm in diameter. Xenograft experiments showed that parenteral ascorbate as the only treatment significantly decreased both tumor growth and weight by 41-53% for Ovcar5 (ovarian), Pan02 (pancreas), and 9L (glioblastoma) tumors. Metastases, present in ≈30% of 9L glioblastoma controls, were absent in ascorbate-treated animals. These preclinical data provide a firm basis for advancing pharmacologic ascorbate in cancer treatment to humans. The tumor xenograft results are especially noteworthy because ascorbate (vitamin C), considered a nutrient, was used here only as a single-agent drug. Pharmacologic concentrations of ascorbate decreased tumor volumes 41-53% in diverse cancer types known for both their aggressive growth and limited treatment options.
The following studies reveal ascorbic acid (vitamin C) to be a powerful pro-oxidant and generator of hydrogen peroxide, causing cancer cell death (apoptosis).
1. In a study conducted by the National Institutes of Health, researchers found ascorbic acid (vitamin C) to be a powerful tool for generating Hydrogen Peroxide H2O2 to initiate cancer cell death. "Our goals here were to test whether ascorbate (vitamin C) killed cancer cells selectively, and if so, to determine mechanisms, using clinically relevant conditions. For five of the nine cancer cell lines, ascorbate (vitamin C) concentrations causing a 50% decrease in [cancer] cell survival were less than 5 mM, a concentration easily achievable from i.v. (intravenous) infusion. All tested normal cells were insensitive to [a higher amount of] 20 mM ascorbate. [In addition] four cancer cell lines were incubated with 5 mM ascorbate (vitamin C) or untreated media for 1 hour. Cells were diluted and plated and growth assessed after 14 days. All four untreated cell lines grew in soft agar, whereas three of four [cancer cell lines] exposed to ascorbate displayed at least 99% growth inhibition. Human lymphoma cells (JLP-119) were studied in detail to determine the effects of ascorbate on cell death. Ascorbate [thereby] induced concentration-dependent cell death, which was nearly 100% at 2 mM. Cell death was independent of metal chelators and absolutely dependent on H2O2 (hydrogen peroxide) formation. Taken together, these data indicate that ascorbate (vitamin C) at concentrations achieved only by i.v. administration may be a pro-drug for formation of H2O2 (hydrogen peroxide), and that blood can be a delivery system of the pro-drug to tissues." [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1224653/]
2. In a study conducted by the University of Massachusetts Medical Center, researchers found ascorbic acid (vitamin C) generating hydrogen peroxide H2O2 is a potent treatment for killing prostate cancer cells. "Androgen-independent (DU145) and androgen-dependent (LNCaP) human prostate cancer cell lines were both treated in vitro with vitamin C (0-10 mM). Treatment of DU145 and LNCaP (prostate cancer) cells with vitamin C resulted in a dose- and time-dependent decrease in cell viability and thymidine incorporation into DNA. Vitamin C induced these changes through the production of hydrogen peroxide (H2O2); addition of catalase (100-300 units/ml), an enzyme that degrades hydrogen peroxide, inhibited the effects of ascorbic acid. Our results suggest that ascorbic acid is a potent anticancer agent for prostate cancer cells." [http://www.ncbi.nlm.nih.gov/pubmed/9254898]
3. In a study conducted by the Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, researchers found hydrogen peroxide H2O2 generated by ascorbic acid (vitamin C) successfully kills leukemia cells. "L-Ascorbic acid (LAA) is being investigated clinically for the treatment of patients with acute myeloid leukemia (AML) based on the observed effects of LAA (ascorbic acid) on AML (acute myeloid leukemia) progenitor cells in vitro. LAA (ascorbic acid) at concentrations of 0.25-1.0 mM induced a dose- and time-dependent inhibition of proliferation in three AML (acute myeloid leukemia) cell lines and also in leukemic cells from peripheral blood specimens obtained from three patients with AML. Flow cytometric analysis showed that LAA (ascorbic acid) at concentrations of 0.25-1.0 mM could significantly induce apoptosis (cell death) in the AML (acute myeloid leukemia) cell lines. LAA (ascorbic acid) induced oxidation of glutathione to oxidized form and subsequent H2O2 (hydrogen peroxide) accumulation in a concentration-dependent manner, in parallel to induction of apoptosis (cell death). The direct role of H2O2 (hydrogen peroxide) in the induction of apoptosis (cell death) in AML (acute myeloid leukemia) cells was clearly demonstrated by the finding that catalase could completely abrogate (block) LAA-(ascorbic acid)-induced apoptosis (cell death). In conclusion, LAA (ascorbic acid) can induce apoptosis (cell death) in AML (acute myeloid leukemia) cells, and this is clearly due to H2O2 (hydrogen peroxide) which accumulates intracellularly as a result of oxidation of reduced glutathione by LAA (ascorbic acid)." [http://www.ncbi.nlm.nih.gov/pubmed/15313465]
4. In a landmark study conducted by the University of Iowa College of Medicine, researchers found hydrogen peroxide H2O2 generated by ascorbic acid (vitamin C) successfully inhibits the growth of nearly all pancreatic cancer cell lines, in vitro and in vivo. "We hypothesized that ascorbate concentrations achievable with i.v. dosing would be cytotoxic in pancreatic cancer for which the 5-year survival is <3%. Pancreatic cancer cell lines were treated with ascorbate (0, 5, or 10 mmol/L) for 1 hour, then viability and clonogenic survival were determined. Pancreatic tumor cells were delivered s.c. into the flank region of nude mice and allowed to grow at which time they were randomized to receive either ascorbate (4 g/kg) or osmotically equivalent saline (1 mol/L) i.p. for 2 weeks. There was a time- and dose-dependent increase in measured H2O2 (hydrogen peroxide) production with increased concentrations of ascorbate. Ascorbate decreased viability in all pancreatic cancer cell lines but had no effect on an immortalized pancreatic ductal epithelial cell line. Ascorbate decreased clonogenic survival of the pancreatic cancer cell lines, which was reversed by treatment of cells with savengers of H2O2. Treatment with ascorbate (vitamin C) induced a caspase-independent cell death that was associated with autophagy. In vivo, treatment with ascorbate inhibited tumor growth and prolonged survival." [http://www.ncbi.nlm.nih.gov/pubmed/20068072]
5. In a study conducted by the Program in Integrative Medicine, University of Kansas Medical Center, Missouri, researchers found hydrogen peroxide H2O2 generated by ascorbic acid (vitamin C) induced cell death in all tested cancer cell lines and significantly reduced pancreatic tumor volume in mice. "The results showed that pharmacologic AA (ascorbic acid) induced cytotoxicity (cell death) in all tested cancer cells, with IC(50) less than 4 mM, a concentration easily achievable in humans. Treatment in mouse pancreatic cancer xenografts showed that intraperitoneal AA (ascorbic acid) at 4 g/kg daily reduced tumor volume by 42%. Although all treatments (AA, GSH [glutathione], and AA+GSH) improved survival rate, AA+GSH inhibited the cytotoxic effect of AA alone and failed to provide further survival benefit. These data confirm the pro-oxidative anti-cancer mechanism of pharmacologic AA (ascorbic acid) and suggest that AA and GSH administered together provide no additional benefit compared with AA alone." [http://www.ncbi.nlm.nih.gov/pubmed/21672627]
6. In a ground-breaking study conducted by the Fukuoka Torikai Hospital and Kamioka Kozan Hospital, Japan, researchers found terminal cancer patients administered large oral doses of ascorbic acid (vitamin C) had significantly longer survival rates than those on low doses. "Clinical trials administering supplemental ascorbate (vitamin C) to terminal cancer patients were conducted at two hospitals in Japan. During the period 1973-1977 there were 99 patients with terminal cancer at the Fukuoka Torikai Hospital. The average times of survival after the date of designation as terminal were 43 days for 44 low-ascorbate patients and 246 days for 55 high-ascorbate patients. Three of the high-ascorbate patients were still alive, their average survival being 1550 days, on April 1, 1980. Similar effectiveness of ascorbate (vitamin C) was also observed at the Kamioka Kozan Hospital. There were 31 patients with terminal cancer during the period 1975-1979. The average survival times were 48 days for 19 control patients and 115 days for 6 high-ascorbate patients. One of the high-ascorbate patients was still alive, his survival being 215 days. In addition to the increase in survival times, the administration of large doses of ascorbate (vitamin C) seemed to improve the quality of life." [http://www.ncbi.nlm.nih.gov/pubmed/6811475]
7. In a joint study conducted by Nobel Prize Laureate Linus Pauling and Ewan Cameron of the Vale of Leven Hospital, Scotland, terminal cancer patients increased survival dramatically with high dose oral ascorbic acid (vitamin c). “A study has been made of the survival times of 100 terminal cancer patients who were given supplemental ascorbate, usually 10 g/day, as part of their routine management and 1000 matched controls, similar patients who had received the same treatment except for the ascorbate (vitamin c). The ascorbate-treated patients were found to have a mean survival time about 300 days greater than that of the controls. Survival times greater than 1 yr after the date of untreatability were observed for 22% of the ascorbate-treated patients and for 0.4% of the controls. The mean survival time of these 22 ascorbate-treated patients is 2.4 yr after reaching the apparently terminal stage; 8 of the ascorbate-treated patients are still alive, with a mean survival time after untreatability of 3.5 yr.” [http://www.ncbi.nlm.nih.gov/pubmed/279931]
Within the 5th Phase of Cancer the following sequence of events can be observed in the cancer patient:
Results: Given their relative sensitivity, the efficacy of pharmacologic ascorbate administration on the growth of Ovcar5, Pan02, and 9L tumors was examined in nude mice. Treatment commenced after tumors reached a palpable size of 5-7 mm in diameter. Xenograft experiments showed that parenteral ascorbate as the only treatment significantly decreased both tumor growth and weight by 41-53% for Ovcar5 (ovarian), Pan02 (pancreas), and 9L (glioblastoma) tumors. Metastases, present in ≈30% of 9L glioblastoma controls, were absent in ascorbate-treated animals. These preclinical data provide a firm basis for advancing pharmacologic ascorbate in cancer treatment to humans. The tumor xenograft results are especially noteworthy because ascorbate (vitamin C), considered a nutrient, was used here only as a single-agent drug. Pharmacologic concentrations of ascorbate decreased tumor volumes 41-53% in diverse cancer types known for both their aggressive growth and limited treatment options.
The following studies reveal ascorbic acid (vitamin C) to be a powerful pro-oxidant and generator of hydrogen peroxide, causing cancer cell death (apoptosis).
1. In a study conducted by the National Institutes of Health, researchers found ascorbic acid (vitamin C) to be a powerful tool for generating Hydrogen Peroxide H2O2 to initiate cancer cell death. "Our goals here were to test whether ascorbate (vitamin C) killed cancer cells selectively, and if so, to determine mechanisms, using clinically relevant conditions. For five of the nine cancer cell lines, ascorbate (vitamin C) concentrations causing a 50% decrease in [cancer] cell survival were less than 5 mM, a concentration easily achievable from i.v. (intravenous) infusion. All tested normal cells were insensitive to [a higher amount of] 20 mM ascorbate. [In addition] four cancer cell lines were incubated with 5 mM ascorbate (vitamin C) or untreated media for 1 hour. Cells were diluted and plated and growth assessed after 14 days. All four untreated cell lines grew in soft agar, whereas three of four [cancer cell lines] exposed to ascorbate displayed at least 99% growth inhibition. Human lymphoma cells (JLP-119) were studied in detail to determine the effects of ascorbate on cell death. Ascorbate [thereby] induced concentration-dependent cell death, which was nearly 100% at 2 mM. Cell death was independent of metal chelators and absolutely dependent on H2O2 (hydrogen peroxide) formation. Taken together, these data indicate that ascorbate (vitamin C) at concentrations achieved only by i.v. administration may be a pro-drug for formation of H2O2 (hydrogen peroxide), and that blood can be a delivery system of the pro-drug to tissues." [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1224653/]
2. In a study conducted by the University of Massachusetts Medical Center, researchers found ascorbic acid (vitamin C) generating hydrogen peroxide H2O2 is a potent treatment for killing prostate cancer cells. "Androgen-independent (DU145) and androgen-dependent (LNCaP) human prostate cancer cell lines were both treated in vitro with vitamin C (0-10 mM). Treatment of DU145 and LNCaP (prostate cancer) cells with vitamin C resulted in a dose- and time-dependent decrease in cell viability and thymidine incorporation into DNA. Vitamin C induced these changes through the production of hydrogen peroxide (H2O2); addition of catalase (100-300 units/ml), an enzyme that degrades hydrogen peroxide, inhibited the effects of ascorbic acid. Our results suggest that ascorbic acid is a potent anticancer agent for prostate cancer cells." [http://www.ncbi.nlm.nih.gov/pubmed/9254898]
3. In a study conducted by the Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, researchers found hydrogen peroxide H2O2 generated by ascorbic acid (vitamin C) successfully kills leukemia cells. "L-Ascorbic acid (LAA) is being investigated clinically for the treatment of patients with acute myeloid leukemia (AML) based on the observed effects of LAA (ascorbic acid) on AML (acute myeloid leukemia) progenitor cells in vitro. LAA (ascorbic acid) at concentrations of 0.25-1.0 mM induced a dose- and time-dependent inhibition of proliferation in three AML (acute myeloid leukemia) cell lines and also in leukemic cells from peripheral blood specimens obtained from three patients with AML. Flow cytometric analysis showed that LAA (ascorbic acid) at concentrations of 0.25-1.0 mM could significantly induce apoptosis (cell death) in the AML (acute myeloid leukemia) cell lines. LAA (ascorbic acid) induced oxidation of glutathione to oxidized form and subsequent H2O2 (hydrogen peroxide) accumulation in a concentration-dependent manner, in parallel to induction of apoptosis (cell death). The direct role of H2O2 (hydrogen peroxide) in the induction of apoptosis (cell death) in AML (acute myeloid leukemia) cells was clearly demonstrated by the finding that catalase could completely abrogate (block) LAA-(ascorbic acid)-induced apoptosis (cell death). In conclusion, LAA (ascorbic acid) can induce apoptosis (cell death) in AML (acute myeloid leukemia) cells, and this is clearly due to H2O2 (hydrogen peroxide) which accumulates intracellularly as a result of oxidation of reduced glutathione by LAA (ascorbic acid)." [http://www.ncbi.nlm.nih.gov/pubmed/15313465]
4. In a landmark study conducted by the University of Iowa College of Medicine, researchers found hydrogen peroxide H2O2 generated by ascorbic acid (vitamin C) successfully inhibits the growth of nearly all pancreatic cancer cell lines, in vitro and in vivo. "We hypothesized that ascorbate concentrations achievable with i.v. dosing would be cytotoxic in pancreatic cancer for which the 5-year survival is <3%. Pancreatic cancer cell lines were treated with ascorbate (0, 5, or 10 mmol/L) for 1 hour, then viability and clonogenic survival were determined. Pancreatic tumor cells were delivered s.c. into the flank region of nude mice and allowed to grow at which time they were randomized to receive either ascorbate (4 g/kg) or osmotically equivalent saline (1 mol/L) i.p. for 2 weeks. There was a time- and dose-dependent increase in measured H2O2 (hydrogen peroxide) production with increased concentrations of ascorbate. Ascorbate decreased viability in all pancreatic cancer cell lines but had no effect on an immortalized pancreatic ductal epithelial cell line. Ascorbate decreased clonogenic survival of the pancreatic cancer cell lines, which was reversed by treatment of cells with savengers of H2O2. Treatment with ascorbate (vitamin C) induced a caspase-independent cell death that was associated with autophagy. In vivo, treatment with ascorbate inhibited tumor growth and prolonged survival." [http://www.ncbi.nlm.nih.gov/pubmed/20068072]
5. In a study conducted by the Program in Integrative Medicine, University of Kansas Medical Center, Missouri, researchers found hydrogen peroxide H2O2 generated by ascorbic acid (vitamin C) induced cell death in all tested cancer cell lines and significantly reduced pancreatic tumor volume in mice. "The results showed that pharmacologic AA (ascorbic acid) induced cytotoxicity (cell death) in all tested cancer cells, with IC(50) less than 4 mM, a concentration easily achievable in humans. Treatment in mouse pancreatic cancer xenografts showed that intraperitoneal AA (ascorbic acid) at 4 g/kg daily reduced tumor volume by 42%. Although all treatments (AA, GSH [glutathione], and AA+GSH) improved survival rate, AA+GSH inhibited the cytotoxic effect of AA alone and failed to provide further survival benefit. These data confirm the pro-oxidative anti-cancer mechanism of pharmacologic AA (ascorbic acid) and suggest that AA and GSH administered together provide no additional benefit compared with AA alone." [http://www.ncbi.nlm.nih.gov/pubmed/21672627]
6. In a ground-breaking study conducted by the Fukuoka Torikai Hospital and Kamioka Kozan Hospital, Japan, researchers found terminal cancer patients administered large oral doses of ascorbic acid (vitamin C) had significantly longer survival rates than those on low doses. "Clinical trials administering supplemental ascorbate (vitamin C) to terminal cancer patients were conducted at two hospitals in Japan. During the period 1973-1977 there were 99 patients with terminal cancer at the Fukuoka Torikai Hospital. The average times of survival after the date of designation as terminal were 43 days for 44 low-ascorbate patients and 246 days for 55 high-ascorbate patients. Three of the high-ascorbate patients were still alive, their average survival being 1550 days, on April 1, 1980. Similar effectiveness of ascorbate (vitamin C) was also observed at the Kamioka Kozan Hospital. There were 31 patients with terminal cancer during the period 1975-1979. The average survival times were 48 days for 19 control patients and 115 days for 6 high-ascorbate patients. One of the high-ascorbate patients was still alive, his survival being 215 days. In addition to the increase in survival times, the administration of large doses of ascorbate (vitamin C) seemed to improve the quality of life." [http://www.ncbi.nlm.nih.gov/pubmed/6811475]
7. In a joint study conducted by Nobel Prize Laureate Linus Pauling and Ewan Cameron of the Vale of Leven Hospital, Scotland, terminal cancer patients increased survival dramatically with high dose oral ascorbic acid (vitamin c). “A study has been made of the survival times of 100 terminal cancer patients who were given supplemental ascorbate, usually 10 g/day, as part of their routine management and 1000 matched controls, similar patients who had received the same treatment except for the ascorbate (vitamin c). The ascorbate-treated patients were found to have a mean survival time about 300 days greater than that of the controls. Survival times greater than 1 yr after the date of untreatability were observed for 22% of the ascorbate-treated patients and for 0.4% of the controls. The mean survival time of these 22 ascorbate-treated patients is 2.4 yr after reaching the apparently terminal stage; 8 of the ascorbate-treated patients are still alive, with a mean survival time after untreatability of 3.5 yr.” [http://www.ncbi.nlm.nih.gov/pubmed/279931]
Within the 5th Phase of Cancer the following sequence of events can be observed in the cancer patient:
