IV vitamin C shown to improve quality of life measures in breast cancer patients during chemo/radiation. What this shows, is that IV vitamin C is not only safe for healthy individuals, but healthy for cancer patients.
vitamin C is powerful anti-oxidant that has implications in cardiovascular disease and cancer; but High serum levels of vitamin C are hard to maintain orally, but can be maintained via IV therapy
Just the abstract available here. Cancer is proving to be very complex--no surprise here. Antioxidant therapy can actually promote cancer progression as can tumor suppressor genes. The issue is context of the environment and the tumor in that environment.
Vitamin C is antioxidant in serum, but pro oxidant in the cancer cell. The result is a production of H2O2 and lysis of the cell.
related to
intracellular hydrogen peroxide generation
only be obtained by
intravenous administration of AA
Preferentially kills neoplastic cells
Is virtually non-toxic at any dosage
Does not suppress the immune system, unlike most chemotherapy
agents
Increases animal and human resistance to infectious agents by
enhancing lymphocyte blastogenesis, enhancing cellular immunity,
strengthening the extracellular matrix, and enhancing bactericidal
activity of neutrophils and modulation of complement protein
Strengthens the structural integrity of the extracellular matrix
which is responsible for stromal resistance to malignant invasiveness
1969, researchers at the NCI reported AA was highly toxic to Ehrlich
ascites cells in vitro
In 1977, Bram et al reported preferential AA
toxicity for several malignant melanoma cell lines, including four
human-derived lines
Noto et al reported that AA plus vitamin K3
had growth inhibiting action against three human tumor cell lines at
non-toxic levels
Metabolites of AA have also shown antitumor activity in
vitro
The AA begins to reduce cell proliferation in the tumor cell
line at the lowest concentration, 1.76 mg/dl, and is completely cytotoxic to
the cells at 7.04 mg/dl
the normal cells grew at an enhanced rate at the low dosages (1.76
and 3.52 mg/dl)
preferential toxicity of AA for tumor
cells. >95% toxicity to human endometrial adenocarcinoma and pancreatic
tumor cells (ATCC AN3-CA and MIA PaCa-2) occurred at 20 and 30 mg/dl,
respectively.
No toxicity or inhibition was demonstrated in the normal,
human skin fibroblasts (ATCC CCD 25SK) even at the highest concentration of
50 mg/dl.
the use of very high-dose intravenous AA for the treatment of
cancer was proposed as early as 1971
Cameron and Pauling have published
extensive suggestive evidence for prolonged life in terminal cancer patients
orally supplemented (with and without initial intravenous AA therapy) with
10 g/day of AA
AA, plasma levels during infusion were not monitored,
the long-term, oral dosage used in those experiments (10 g/day),
while substantial and capable of producing immunostimulatory and
extracellular matrix modulation effects, was not high enough to achieve
plasma concentrations that are generally cytotoxic to tumor cells in
culture
This low cytotoxic level of AA is exceedingly rare
5 — 40 mg/dl of AA is required in vitro to kill 100% of tumor
cells within 3 days. The 100% kill levels of 30 mg/dl for the endometrial
carcinoma cells and 40 mg/dl for the pancreatic carcinoma cells in Figure 2
are typical
normal range (95% range) of 0.39-1.13 mg/dl
1 h after beginning his first 8-h infusion of 115 g AA (Merit
Pharmaceuticals, Los Angeles, CA), the plasma AA was 3.7 mg/dl and at 5 h
was 19 mg/dl. During his fourth 8-h infusion, 8 days later, the 1 h plasma
level was 158 mg/dl and 5 h was 185 mg/dl
plasma levels of over 100 mg/dl have been maintained in 3
patients for more than 5 h using continuous intravenous infusion
In rare instances of patients with widely disseminated
and rapidly proliferating tumors, intravenous AA administration (10 — 45
g/day) precipitated widespread tumor hemorrhage and necrosis, resulting in
death
Although the outcomes were disastrous in these cases, they are
similar to the description of tumor-necrosis-factor-induced hemorrhage and
necrosis in mice (52) and seem to demonstrate the ability of AA to kill
tumor cells in vivo.
toxic effects of AA on one normal cell line were observed at 58.36 mg/dl and
the lack of side effects in patients maintaining >100 mg/dl plasma levels
Although it is very rare, tumor necrosis, hemorrhage, and subsequent
death should be the highest priority concern for the safety of intravenous
AA for cancer patients.
Klenner,
who reported no ill effects of dosages as high as 150 g intravenously over a
24-h period
Cathcart (55) who
describes no ill effects with doses of up to 200 g/d in patients with
various pathological conditions
following circumstances: renal
insufficiency, chronic hemodialysis patients, unusual forms of iron
overload, and oxalate stone formers
Screening for red cell glucose-6-phosphate
dehydrogenase deficiency, which can give rise to hemolysis of red blood
cells under oxidative stress (57), should also be performed
any cancer therapy should be started at a low dosage to ensure
that tumor hemorrhage does not occur.
patient is orally supplementing between infusions
a scorbutic rebound effect can be
avoided with oral supplementation. Because of the possibility of a rebound
effect, measurement of plasma levels during the periods between infusions
should be performed to ensure that no such effect takes place
Every effort
should be made to monitor plasma AA levels when a patient discontinues
intravenous AA therapy.
vitamin C effects decreased by hypoxia which increases HIF-1alpha. The authors propose oxygen therapy, hyperbaric, to improve and augment the cytotoxic effects of vitamin C.
pharmacological concentrations of AA can sensitize cancer cells to chemotherapy, enhancing its antineoplastic effect
synergistic effect with conventional chemotherapeutic drugs is a fact already reported, in various types of cancer, by numerous authors, namely in pancreatic (Espey et al., 2011), prostate (Gilloteaux et al., 2014), lung (Lee et al., 2017), breast (Kurbacher et al., 1996; Wu et al., 2017) and ovarian (Ma et al., 2014) cancers.
chemosensitizing effect of vitamin C has already been proven by several authors in various types of cancer
intravenous pharmacological concentrations, may not only potentiate the effects of conventional chemotherapy, but also improve the quality of life of cancer patients
AA reinforced the anti-proliferative activity of 5-FU
Combined treatment induced a reduction of 11.5% and 43% in cell viability compared with AA or Iri therapies, respectively, emphasizing the synergistic effect
cytotoxic effect occurred with treatment with Iri alone, but also this effect was further potentiated by the presence of AA.
association of AA with Oxa showed very promising results, considering that a synergistic effect was demonstrated, in almost all conditions
AA and Oxa seem to act synergistically by the activation of the intrinsic pathway of apoptosis, translated on the statistically significant increase of the ratio between BAX and BCL-2 proteins, which in turn is associated with a decrease of Δψm