Vitamin C therapy is one of those weird alternative therapies, right? I mean, if vitamin C therapy killed ovarian cancer my oncologist would tell me, right? Wrong. Vitamin C therapy suffers from an education problem.
While oral vitamin C, either in foods, juices or as supplements, has a place in the nutritional debate, it does not kill cancer. Study after study has documented how and why oral vitamin C supplementation simply will not help the cancer patient. However intravenous vitamin C does kill cancer. Equally as important, as the study linked and excerpted below explains, intravenous vitamin C synergizes with chemotherapy regimens such as cisplatin and paclitaxel to both kill cancer as well as moderate the toxicity of these chemotherapy regimens.
Further, consider other evidence-based, non-toxic integrative therapies also shown to be cytotoxic to ovarian cancer such as curcumin.
I am a long-term cancer survivor and cancer coach. I have lived in complete remission from my “incurable” cancer since ’99 by living an evidence-based, non-conventional, anti-cancer lifestyle.
If you have been diagnosed with ovarian cancer please take possible short, long-term and late-stage side effects, seriously. Please think long term.
Have you been diagnosed with ovarian cancer? What stage? Please scroll down the page, post a question or comment and I will reply to you ASAP.
“Ascorbate (vitamin C) was an early, unorthodox therapy for cancer, with an outstanding safety profile and anecdotal clinical benefit. Because oral ascorbate was ineffective in two cancer clinical trials, ascorbate was abandoned by conventional oncology but continued to be used in complementary and alternative medicine.
Recent studies provide a rationale for reexamining ascorbate treatment. Because of marked pharmacokinetic differences, intravenous, but not oral, ascorbate produces millimolar concentrations both in blood and in tissues, killing cancer cells without harming normal tissues.
In the interstitial fluid surrounding tumor cells, millimolar concentrations of ascorbate exert local pro-oxidant effects by mediating hydrogen peroxide (H(2)O(2)) formation, which kills cancer cells. We investigated downstream mechanisms of ascorbate-induced cell death. Data show that millimolar ascorbate, acting as a pro-oxidant, induced DNA damage and depleted cellular adenosine triphosphate (ATP), activated the ataxia telangiectasia mutated (ATM)/adenosine monophosphate-activated protein kinase (AMPK) pathway, and resulted in mammalian target of rapamycin (mTOR) inhibition and death in ovarian cancer cells.
The combination of parenteral ascorbate with the conventional chemotherapeutic agents carboplatin and paclitaxel synergistically inhibited ovarian cancer in mouse models and reduced chemotherapy-associated toxicity in patients with ovarian cancer. On the basis of its potential benefit and minimal toxicity, examination of intravenous ascorbate in combination with standard chemotherapy is justified in larger clinical trials.”