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Vita C Infusion Mikrodermabrazja - Twoje Klucze do Promiennej Skóry
Rekindling vitamin C cancer therapy: oral vs intravenous administration
Based on studies pioneered by Mark Levine’s group at the NIH in the 2000s, the oral vitamin C doses used in the Mayo Clinic studies would have produced peak plasma concentration of less than 200 μM. In contrast, the same dose given intravenously, as used in the Pauling studies, would produce peak plasma concentrations of nearly 6 mM, more than 25 times higher. When given orally, vitamin C concentration in human plasma is tightly controlled by multiple mechanisms acting together: intestinal absorption, tissue accumulation, renal reabsorption and excretion, and potentially even the rate of utilization. However, when ascorbate is administered intravenously or intraperitoneally the tight controls are bypassed, and pharmacologic millimolar plasma concentrations of vitamin C can easily be achieved. For example, a phase I clinical study revealed that ascorbate concentrations could safely reach 25-30 mM with intravenous infusion of 100 g of vitamin C. In this study, plasma concentrations around 10 mM were sustained for at least 4 hours which, based on preclinical studies, is sufficient to kill cancer cells. Given the fact that cancer patients were only treated with vitamin C orally in the Mayo Clinic studies, the studies do not disprove high dose vitamin C’s efficacy as a cancer treatment.
More than half of colorectal cancers (CRCs) harbor activating mutations in KRAS or BRAF, yet those cancers are the most refractory to current targeted therapies. Our group and others showed that oncogenic mutations in KRAS or BRAF contribute to the Warburg effect and the addiction to glucose in part by upregulating a glucose transporter, GLUT1, that allows cancer cells to take up glucose efficiently. These data suggest a strategy for targeting KRAS or BRAF mutant cancer by exploiting the selective expression of GLUT1 and the metabolic liability that comes with increased reliance on glycolysis. Indeed, by targeting these unique features in these cancer cells, we recently showed that high dose vitamin C could selectively kill KRAS or BRAF mutant CRC cells.
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Other Ingredients
| Ingredient name | what-it-does | irr. , com. | ID-Rating |
|---|---|---|---|
| Aqua | solvent | ||
| Alumina | viscosity controlling, abrasive/scrub | ||
| Caprylic/Capric Triglyceride | emollient | ||
| Vitis Vinifera Seed Oil | antioxidant, emollient | goodie | |
| Glycerin | skin-identical ingredient, moisturizer/humectant | 0 , 0 | superstar |
| Sodium Polyacrylate | viscosity controlling | ||
| Urea | skin-identical ingredient, moisturizer/humectant | goodie | |
| Myrciaria Dubia Fruit Extract | |||
| Hippophae Rhamnoides Oil | antioxidant, emollient | goodie | |
| Helianthus Annuus Seed Oil | emollient | 0 , 0 | goodie |
| Rosmarinus Officinalis Leaf Extract | antioxidant, soothing, antimicrobial/antibacterial | goodie | |
| Glycine Soja Oil | emollient, perfuming | 0 , 3 | goodie |
| Sodium Hyaluronate | skin-identical ingredient, moisturizer/humectant | 0 , 0 | goodie |
| Panthenol | soothing, moisturizer/humectant | 0 , 0 | goodie |
| Propanediol | solvent, moisturizer/humectant | ||
| Ascorbyl Palmitate | antioxidant | 0 , 2 | icky |
| Tocopherol | antioxidant | 0 - 3 , 0 - 3 | goodie |
| Hydrogenated Vegetable Glycerides Citrate | emollient, emulsifying | ||
| Propylene Glycol | moisturizer/humectant, solvent | 0 , 0 | |
| Lecithin | emollient, emulsifying | goodie | |
| Caprylyl Glycol | moisturizer/humectant, emollient | ||
| Beta-Sitosterol | |||
| Squalene | skin-identical ingredient, antioxidant, emollient | goodie | |
| Phenoxyethanol | preservative | ||
| Lactic Acid | exfoliant, moisturizer/humectant, buffering | superstar | |
| Disodium EDTA | chelating | ||
| Citrus Limon Peel Oil | perfuming | icky | |
| Parfum | perfuming | icky | |
| Limonene | perfuming, solvent | icky | |
| Linalool | perfuming | icky | |
| Hexyl Cinnamal | perfuming | icky | |
| Citral | perfuming | icky | |
| Geraniol | perfuming | icky |
Concluding Remarks
Vitamin C as a cancer therapy has had a controversial past. What has been intriguing are small clinical trials that suggest some responses, but with no clear rationale for why cancers should respond to vitamin C or a path forward for explaining which patients are most likely to respond. Now a growing number of preclinical studies are showing how high-dose vitamin C might benefit cancer patients. Importantly, these preclinical studies provide a clear rationale and potential biomarkers that may help personalize the therapeutic approach and identify patient populations that are likely to respond to high-dose vitamin C therapy. Since the mechanisms of action of vitamin C are becoming better defined, we can propose vitamin C combinations in a more rational, hypothesis-driven manner. In addition, given the current high financial cost of new cancer drugs, it seems rational to improve the effectiveness of current therapies by studying their clinical interactions with vitamin C. In our view, the implementation of this treatment paradigm could provide benefit to many cancer patients.
This work was supported by the US National Institutes of Health (NIH) grant (R35 CA197588), Stand Up to Cancer–American Association for Cancer Research grant (SU2C-AACR-DT22-17), and the Damon Runyon Cancer Research Foundation. Lewis Cantley is a founder and member of the senior advisory boards of Agios Pharmaceuticals and Petra Pharmaceuticals, which are developing novel therapies for cancer. The Cantley laboratory also receives financial support from Petra Pharmaceuticals.
Taking RAS Research to Space
The controversial history of high-dose vitamin C in cancer treatment
Utilizing high doses of vitamin C as a cancer therapy is no exception to this controversy. Nearly 60 years ago Toronto physician William McCormick observed that cancer patients often presented with severely low levels of vitamin C in their blood and featured scurvy-like symptoms, leading him to postulate that vitamin C might protect against cancer by increasing collagen synthesis. In 1972, extending this theory, Ewan Cameron, a Scottish surgeon, hypothesized that ascorbate could suppress cancer development by inhibiting hyaluronidase, which otherwise weakens the extracellular matrix and enables cancer to metastasize. He began treating terminally ill cancer patients and published a case report of 50 patients in which some of the treated patients benefited from high dose vitamin C.
So why did the Pauling and Mayo Clinic trials have different results? There are at least two crucial differences. First, the Mayo Clinic trials abruptly stopped the ascorbate administration, switching to traditional chemotherapy, when the patient developed signs of tumor progression. Thus, the overall median time of vitamin C treatment under the Mayo Clinic trials was only 2.5 months, while the Pauling and Cameron trials treated patients for the duration of the entire study period or as long as 12 years. Secondly, the Mayo Clinic trials administered 10 g of daily ascorbate to patients only orally, while the Cameron and Pauling trials administered their vitamin C both orally and intravenously. This difference in the two dosage routes proved highly consequential.
