High dose Vitamin C

INTRAVENOUS HIGH-DOSE VITAMIN C IN CANCER THERAPY SANDY, UT

Vitamin C deficiency disease or scurvy brings on weakness, easy bruising, bleeding, and lethargy. Scurvy was a problem for sailors in the 16th century, where vitamin C vegetables and fruits were unavailable on long sea voyages. A published account noted that scurvy killed more sailors during the 16th, 17th, and 18th centuries than other diseases, storms, or battles. In 1747, James Line, a Scottish naval physician, proved that eating lemons and oranges prevented scurvy. Yet, it was still unknown what the properties in lemons and oranges had to do with avoiding scurvy. Two centuries later, scientists identified that the curative substance in citrus fruits was vitamin C.

Albert Szent-Gyorgi identified a six-carbon carbohydrate, hexuronic acid, as the anti-scurvy factor. Szent-Gyorgyi renamed it a-ascorbic acid, which references its anti-scurvy properties. Szent-Gyorgyi received the Nobel Prize in Physiology and Medicine in 1937.

Vitamin C has many essential functions in our body, including being an antioxidant. Therefore, it has been thought that high quantities of vitamin C or above 1 g intake per day would prevent and treat many illnesses like the common colds and heart diseases. However, using high vitamin C intake to heal diseases is still controversial.

High dose Vitamin C

Intravenous High-Dose Vitamin C in Cancer Therapy

Vitamin C deficiency disease or scurvy brings on weakness, easy bruising, bleeding, and lethargy. Scurvy was a problem for sailors in the 16th century, where vitamin C vegetables and fruits were unavailable on long sea voyages.

A published account noted that scurvy killed more sailors during the 16th, 17th, and 18th centuries than other diseases, storms, or battles.

In 1747, James Line, a Scottish naval physician, proved that eating lemons and oranges prevented scurvy. Yet, it was still unknown what the properties in lemons and oranges had to do with avoiding scurvy. Two centuries later, scientists identified that the curative substance in citrus fruits was vitamin C.

Albert Szent-Gyorgi identified a six-carbon carbohydrate, hexuronic acid, as the anti-scurvy factor. Szent-Gyorgyi renamed it a-ascorbic acid, which references its anti-scurvy properties. Szent-Gyorgyi received the Nobel Prize in Physiology and Medicine in 1937.

Vitamin C has many essential functions in our body, including being an antioxidant. Therefore, it has been thought that high quantities of vitamin C or above 1 g intake per day would prevent and treat many illnesses like the common colds and heart diseases. However, using high vitamin C intake to heal diseases is still controversial.

Vitamin C and Cancer

Clinical trials and studies found that oral vitamin C doses are not concentrated to needed levels. According to a  Mayo Clinic study, oral vitamin C doses produced peak plasma concentrations of less than 200 uM. The same dose given intravenously produces more than 25 times higher peak plasma concentrations.

Oral vitamin C concentration is controlled by different mechanisms in the body, including intestinal absorption tissue accumulation, renal reabsorption, and excretion. As a result, the utilization rate of oral vitamin C is almost nil before the vitamin C is even absorbed by cancer cells. Using intravenous vitamin C, the controls are bypassed, and concentrations of vitamin C can be achieved.

High dose Vitamin C

A clinical study revealed that ascorbate concentration could reach 25-30 mM with an infusion of 100 g of vitamin C. Plasma concentrations are maintained, and vitamin C reached cancer cells.

In 1976, a study of 100 patients with terminal cancer was treated with intravenous ascorbate. Their disease progression and survival rates were compared to 1000 control patients who did not receive vitamin C doses. Although the study was not designed in today’s protocols,  it proved that the patients treated with vitamin C improved their quality of life and increased their survival time. A follow-up study by Cameron and Pauling reported that 22% of vitamin C-treated terminal cancer patients survived for at least a year compared to only a 4% survival rate on non-treated patients.

Otto Warburg, a biochemist, found that cancer cells consumed more glucose and produced more lactate than normal cells. He called this phenomenon aerobic glycolysis or the Warburg effect. The Warburg test is still used for visualizing tumors in clinical studies by imaging the uptake of radiolabeled glucose analog and fluoro-2deoxyglucose through Positron Emission Tomography. The conclusion to these tests shows that targeting glycolysis could offer cancer patients a different strategy to treat cancer.

About half of colorectal cancers (CRCs) have activating mutations in KRAS or BRAF, and these cancers are the most stubborn to respond to targeted therapies. Studies further showed that oncogenic mutations in KRAS or BRAF follow the Warburg effect and use the glucose transporter, GLUT1. This transporter allows cancer cells to use glucose and continue growing. By targeting the metabolic liability that comes with mutant cancer’s reliance on glycolysis, studies recently proved that high dose vitamin C, given intravenously, could selectively destroy KRAS or BRAF mutant CRC cells.

GLUT1 transports glucose, and CRC cells hold KRAS or BRAF mutations. These properties increased the application of DHA using GLUT1 when treated with vitamin C. Increased DHA uptake in KRAS and BRAF cells show oxidative stress, which increased reactive oxygen species (ROS) in cells. Intracellular mutations are reduced with vitamin C at the expense of glutathione, a major antioxidant in cells. We also discovered elevated ROS activated poly (ADP-ribose) polymerase (PARP) DNA repair enzymes, and large amounts of cellular NAD+ were consumed as a cofactor.

Studies proved that high-dose vitamin C therapy reduces the number of tumors in KRAS or BRAF mutant mice compared to mice without mutations. Furthermore, these studies demonstrated that vitamin C targets KRAS or BRAF mutant tumors in mouse models of colon tumors. Picturesquely ascorbate or vitamin C becomes a “Trojan horse” because of its conversion to DHA and destructively enters cancer cells via GLUT1 to promote the generation of intracellular ROS, which ultimately kills the cancer cell.

KRAS and BRAF mutations are frequently mutated oncogenes in cancer, but they are not the only mutations that affect glucose metabolism or sensitivity toward vitamin C therapy. For example, studies have discovered that renal cancer cells (RCC) with loss of VHL (Von Hippel-Lindau), a tumor suppressor, are sensitive to ascorbate treatment compared to VHL-proficient cells.

RCC-VHL null cells have increased HIF1A transcriptional activity, which increases not only GLUT1 expression but also deregulates many other glycolytic enzymes to induce metabolic reprogramming. Additionally, cancers with increased levels of DNA damage, such as those treated with radiation or those with mutations in BRCA genes, are more reliant on DNA repair mediated by PARP. Pharmacologic vitamin C might selectively impair such cancers by depriving them of the NAD+ necessary for PARP activity.

On-Going Studies

New knowledge has spurred interest in high dosage of vitamin C for cancer and further research into the potential effectiveness of intravenous vitamin C. Case reports have begun testing high-dose vitamin C’s safety as a treatment for cancer patients in combination therapy or as a standalone drug. Many studies show improved quality of life for cancer patients by minimizing pain and protecting normal tissues from toxicity caused by chemotherapy. In addition, vitamin C shows cooperative effects when combined with standard chemotherapy and radiation.

Interestingly, a small clinical trial of high dose vitamin C suggests some positive responses, even though there is no apparent reason why cancer should respond to vitamin C. However, a  growing number of preclinical studies are proving that high-dose vitamin C will benefit cancer patients. Furthermore, these preclinical studies provide potential biomarkers that will personalize the therapeutic approach and identify the population that will likely respond to high-dose vitamin C.

Vitamin C action mechanism is becoming better defined, and vitamin C add-on therapy is becoming more cost-effective. Additionally, due to the current high financial cost of many cancer drugs, it seems rational to show the effectiveness of existing therapies by studying their clinical interactions with vitamin C.

Vitamin C and Cancer

Clinical trials and studies found that oral vitamin C doses are not concentrated to needed levels. According to a  Mayo Clinic study, oral vitamin C doses produced peak plasma concentrations of less than 200 uM. The same dose given intravenously produces more than 25 times higher peak plasma concentrations.

Oral vitamin C concentration is controlled by different mechanisms in the body, including intestinal absorption tissue accumulation, renal reabsorption, and excretion.

High dose Vitamin C

As a result, the utilization rate of oral vitamin C is almost nil before the vitamin C is even absorbed by cancer cells. Using intravenous vitamin C, the controls are bypassed, and concentrations of vitamin C can be achieved.

A clinical study revealed that ascorbate concentration could reach 25-30 mM with an infusion of 100 g of vitamin C. Plasma concentrations are maintained, and vitamin C reached cancer cells.

In 1976, a study of 100 patients with terminal cancer was treated with intravenous ascorbate. Their disease progression and survival rates were compared to 1000 control patients who did not receive vitamin C doses. Although the study was not designed in today’s protocols,  it proved that the patients treated with vitamin C improved their quality of life and increased their survival time. A follow-up study by Cameron and Pauling reported that 22% of vitamin C-treated terminal cancer patients survived for at least a year compared to only a 4% survival rate on non-treated patients.

Otto Warburg, a biochemist, found that cancer cells consumed more glucose and produced more lactate than normal cells. He called this phenomenon aerobic glycolysis or the Warburg effect. The Warburg test is still used for visualizing tumors in clinical studies by imaging the uptake of radiolabeled glucose analog and fluoro-2deoxyglucose through Positron Emission Tomography. The conclusion to these tests shows that targeting glycolysis could offer cancer patients a different strategy to treat cancer.

About half of colorectal cancers (CRCs) have activating mutations in KRAS or BRAF, and these cancers are the most stubborn to respond to targeted therapies. Studies further showed that oncogenic mutations in KRAS or BRAF follow the Warburg effect and use the glucose transporter, GLUT1. This transporter allows cancer cells to use glucose and continue growing. By targeting the metabolic liability that comes with mutant cancer’s reliance on glycolysis, studies recently proved that high dose vitamin C, given intravenously, could selectively destroy KRAS or BRAF mutant CRC cells.

GLUT1 transports glucose, and CRC cells hold KRAS or BRAF mutations. These properties increased the application of DHA using GLUT1 when treated with vitamin C. Increased DHA uptake in KRAS and BRAF cells show oxidative stress, which increased reactive oxygen species (ROS) in cells. Intracellular mutations are reduced with vitamin C at the expense of glutathione, a major antioxidant in cells. We also discovered elevated ROS activated poly (ADP-ribose) polymerase (PARP) DNA repair enzymes, and large amounts of cellular NAD+ were consumed as a cofactor.

Studies proved that high-dose vitamin C therapy reduces the number of tumors in KRAS or BRAF mutant mice compared to mice without mutations. Furthermore, these studies demonstrated that vitamin C targets KRAS or BRAF mutant tumors in mouse models of colon tumors. Picturesquely ascorbate or vitamin C becomes a “Trojan horse” because of its conversion to DHA and destructively enters cancer cells via GLUT1 to promote the generation of intracellular ROS, which ultimately kills the cancer cell.

KRAS and BRAF mutations are frequently mutated oncogenes in cancer, but they are not the only mutations that affect glucose metabolism or sensitivity toward vitamin C therapy. For example, studies have discovered that renal cancer cells (RCC) with loss of VHL (Von Hippel-Lindau), a tumor suppressor, are sensitive to ascorbate treatment compared to VHL-proficient cells.

RCC-VHL null cells have increased HIF1A transcriptional activity, which increases not only GLUT1 expression but also deregulates many other glycolytic enzymes to induce metabolic reprogramming. Additionally, cancers with increased levels of DNA damage, such as those treated with radiation or those with mutations in BRCA genes, are more reliant on DNA repair mediated by PARP. Pharmacologic vitamin C might selectively impair such cancers by depriving them of the NAD+ necessary for PARP activity.

On-Going Studies

New knowledge has spurred interest in high dosage of vitamin C for cancer and further research into the potential effectiveness of intravenous vitamin C. Case reports have begun testing high-dose vitamin C’s safety as a treatment for cancer patients in combination therapy or as a standalone drug. Many studies show improved quality of life for cancer patients by minimizing pain and protecting normal tissues from toxicity caused by chemotherapy. In addition, vitamin C shows cooperative effects when combined with standard chemotherapy and radiation.

Interestingly, a small clinical trial of high dose vitamin C suggests some positive responses, even though there is no apparent reason why cancer should respond to vitamin C. However, a  growing number of preclinical studies are proving that high-dose vitamin C will benefit cancer patients. Furthermore, these preclinical studies provide potential biomarkers that will personalize the therapeutic approach and identify the population that will likely respond to high-dose vitamin C.

Vitamin C action mechanism is becoming better defined, and vitamin C add-on therapy is becoming more cost-effective. Additionally, due to the current high financial cost of many cancer drugs, it seems rational to show the effectiveness of existing therapies by studying their clinical interactions with vitamin C.

FAQ

We all know that Vitamin C helps boost our immune system and helps increase our overall health.  As an antioxidant, it helps protect our cells from free radicals that occur within our body; and when administered at high enough doses, Vitamin C becomes an oxidant, which is good for normal cells, but not so good for the bad cells that enter our body (ie. fungus, viruses, bacteria, cancer cells).

Our body’s immune system naturally creates peroxides to combat bad cells in our body, and when our body’s immune systems are down, or not working, it is extremely beneficial to have IV High Dose Vitamin C administered.  Once administered, the Vitamin C enters directly into the blood stream and creates peroxides that the body can use to build-up our immune systems.

Many cancer chemotherapy programs use IV High Dose Vitamin C, together with their chemotherapy treatments.  They have found that there are many benefits to doing this, as Vitamin C has been shown to reduce side effects (ie. nausea, vomiting, fatigue, joint and muscle pain, loss of appetite), improve quality of life, along with improvement in other bodily functions, both physical and mental.

People suffering from cancer, and other diseases are prime candidates for High Dose Vitamin C,

However, anybody, who is sick or feels that their immune system needs a boost, or who is experiencing fatigue, some type of inflammation, or some other ailments are also good candidates.

The answer is simple. The studies required are usually sponsored by pharmaceutical companies. Vitamin C is not a drug, instead, it’s a naturally occuring nutrient that offers no monetary benefit to anyone involved.

For most people there are no real side effects; however, people with kidney disorders or those who experience kidney stones, should not be treated with high dose vitamin C.

Also, those who have G-6-PD deficiency, and hemochromatosis should not be treated.

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