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Nathan Goodyear

Effects of sodium ascorbate (vitamin ... [Anticancer Res. 1993 Jan-Feb] - PubMed - NCBI - 0 views

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    IV vitamin K3 shown to provide synergy with IV vitamin C in vitro study of cancer cells.
Nathan Goodyear

Tolerance and safety of vitamin E: a toxicological position report. - PubMed - NCBI - 0 views

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    Only abstract available here.  The quote that "the toxicity of vitamin E is very low" tells the story.  Always have levels evaluated to ensure need.  In this review of human studies, doses up to 3,200 IU daily "led to no consistent adverse effects".  Also consider the effects of vitamin K effects in those on vitamin E therapy.
Nathan Goodyear

Altered Deoxyribonuclease Activity in Cancer Cells and its Role in Non Toxic Adjuvant C... - 0 views

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    Combination of IV vitamin C and K3 in ratio of 100:1 shown to provide mechanism to induce cancer cell death through a process called autoschizis.
Nathan Goodyear

The association of vitamins C and K3 kills ca... [Eur J Med Chem. 2003] - PubMed - NCBI - 0 views

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    IV vitamin C and K3 show synergistic cancer cell death via autoschizis.
Nathan Goodyear

The in vitro antitumor activity of vi... [Anticancer Res. 2003 Jul-Aug] - PubMed - NCBI - 0 views

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    IV vitamin C and K3 show synergistic activity against ovarian cancer.  
Nathan Goodyear

Autoschizis: another cell death for canc... [Ital J Anat Embryol. 2001] - PubMed - NCBI - 0 views

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    The autoschizis from IV vitamin C and K3 proposed to be secondary to oxidative stress.
Nathan Goodyear

In vivo reactivation of DNases in impla... [J Histochem Cytochem. 2001] - PubMed - NCBI - 0 views

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    IV vitamin C/K3 combination therapy reactivates DNase activity in mouse model of prostate cancer.
Nathan Goodyear

Non-toxic potentiation of cancer chemotherapy b... [Int J Cancer. 1987] - PubMed - NCBI - 0 views

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    IV vitamin C and K3 induces cancer cell death through production of H2O2 in catalase deficient cancer cells.  Pretreament shown to potentiate traditional chemotherapy.
Nathan Goodyear

High dose vitamin K3 infusion in advanced hepatocellular carcinoma - Sarin - 2006 - Jou... - 0 views

  • Vitamin K has been shown to have antitumor effect
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    Vitamin K therapy and cancer 
Nathan Goodyear

Diabetes Care - 0 views

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    supplementation of Vitamin K2 in healthy men improved insulin sensitivity.  The question of whether it improves insulin sensitivity in unhealthy men and/or diabetes is not confirmed here.
Nathan Goodyear

Targeting cancer cells by an oxidant-based therapy. [Curr Mol Pharmacol. 2008] - PubMed... - 0 views

  • vitamin K3) and ascorbate (vitamin C)
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    Anti-oxidant therapy for cancer patients
Nathan Goodyear

Intravenous Ascorbate as a Tumor Cytotoxic Chemotherapeutic Agent - 0 views

  • There is a 10 — 100-fold greater content of catalase in normal cells than in tumor cells
  • induce hydrogen peroxide generation
  • Ascorbic acid and its salts (AA) are preferentially toxic to tumor cells in vitro (6 — 13) and in vivo
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  • 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.
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    Older study, 1995, but shows the long-standing evidence that IVC preferentially is cytotoxic to cancer cells.`
Nathan Goodyear

The Pharmacokinetics and Interactions of Ivermectin in Humans-A Mini-review - 0 views

  • This drug is extensively metabolized by human liver microsomes by cytochrome P450
  • cytochrome P-4503A4, converting the drug to at least 10 metabolites
  • its elimination half-life is around a day
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  • second rise in plasma levels (mostly occurring between 6 and 12 h after the dose) suggesting an enterohepatic recycling of the drug
  • Ivermectin is exceptionally potent, with effective dosages levels that are unusually low.
  • the optimal dose of ivermectin is 150 μg/kg, but the frequency of administration is still controversial, ranging from 150 μg/kg once to three times yearly.
  • high lipid solubility of ivermectin, this compound is widely distributed within the body.
  • To interrupt the transmission of onchocerciasis in humans, the combination of ivermectin and doxycycline is highly effective as, in infested patients, the ingestion of the anthelmintic (200 μg/kg, single dose) and the antibacterial (100 mg/kg, daily for 6 weeks)
  • ivermectin interactions with another concurrently administered drugs can occur.
  • This issue becames important, as combination chemotherapy is being used with increasing frequency as resistance to antiparasitic agents is becoming more widespread.
  • haematomatous swellings
  • prothrombin times were significantly above baseline by one week to one month after drug ingestion, suggesting an antagonist effect against vitamin K
  • bleeding disorders were not found in 15,000 patients treated with ivermectin (150 μg/kg)
  • prolonged prothrombin ratios were observed in 148 subjects given ivermectin orally. Although no patients suffered bleeding complications, factor II and VII levels were reduced in most of them, suggesting interference with vitamin K metabolism
  • Ivermectin has a minimal effect on coagulation and concern about mass treatment for this reason appears to be unjustified
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    Review of Ivermectin as an anti-parasitic.
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