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Despite adhering to a strict regime of 3 x 6 days a week of infusions plus twice weekly for another 3 months, and a near raw vegan diet with juicing, and a small fortune in supplements, the tumour grew.
(I did, however, feel generally well during that period so maybe it did some good.)
I’ve been thinking about why IV C didn’t work for me, and I’ve come up with the following possibilities:
1. Vitamin C was used as a monotherapy
The two women whom I know who had success using IV C were also using Vitamin B17 (laetrile) and DMSO intravenously. Unfortunately both are illegal in the UK, although you can buy Vitamin B17 tablets from kind people who have bought it from trips to the US. And I was for a short time taking B17 tablets, but oral medication is not the same as an infusion.
I did ask the doctor why he only used IV C and not other therapies and he said that he was following the lead of the Riordan Institute in the US, and wanted to keep things simple.
2. The dose of Vitamin C was not at an optimum level to be effective
People process Vitamin C at different rates. For IV C to be effective, it has to be in the bloodstream within a certain range (see below).
In the US, doctors who use IV C test for plasma levels of Vitamin C. There is a strict protocol for this test – the blood sample has to be taken immediately after the infusion from the opposite arm to the infusion arm. The sample has to be diluted (1:20) and then frozen. The lab has has to be informed that the sample has been diluted as this is not standard practice. The sample must be promptly processed and shipped frozen; delays reduce the reported level of vitamin C, and since they are really quite high they fall rapidly.
Unfortunately, to the best of my knowledge, the clinics in the UK that offer IV C do not test for plasma levels. This is scandalous – I feel they are missing a trick here.
Steve, a very well-informed genius friend of mine has done a lot of research into IV C and sent me the protocol that is used by Dr Jeanne Drisko of Kansas University. Dr. Drisko is an M.D. and director of the Program for Integrative Medicine at the University of Kansas Medical Center.
Dr Drisko used IV C as an adjunct to patients who were undergoing chemotherapy. She has these guidelines on plasma levels:
“Once the plasma ascorbate level reaches 350 to 450 mg/dl [on 75g] then the patient may remain on the dose for 2 to 3 times per week. If the plasma level has not reached the appropriate plasma level on 75g, then dose escalation to 100g for 2 doses is undertaken with repeat of the plama ascorbate level.”
What this seems to me to say is that if the patient’s plasma levels of Vitamin C are not within the optimum range of 350 to 450mg/dl (at 75g) then the dose has to be increased t0 100g. So what this implies is that there is an optimum level for IV C to be effective.
Dr Jeanne Drisko’s protocol for IV C is attached (Drisko protocol (1)).
3. My tumour cells were not sensitive to the Vitamin C
This is not the case, there was some level of sensitivity (35%) to the Vitamin C which was confirmed by the RGCC Chemosensitivity test. Maybe 35% isn’t sensitive enough. Furthermore, the RGCC test is performed on the circulating tumour cells, and not a tissue sample. CTCs may react in a different way to an actual tissue sample.
4. Vitamin C may not work if there is a high level of MDR resistance
Multi Drug Resistance (MDR1) is a form of protein expression. A high level means that cancer cells have efficient protein pumps that are able to pump out chemo agents before it can do damage. It may indicate resistance in the cancer cells to chemotherapy and this may include IV C which in high doses acts like chemo.
MDR1 levels are included in the RGCC chemosensitivity test, and also as a separate test from Neuro Lab.
Here is an article on MDR proteins and their role in drug transportation.
5. Vitamin C only works if the tumour has low levels of HIF-1
According to research carried out by the University of Otago in 2010 into endometrial cancer:
“It investigated whether the cancer cells had low vitamin C levels and whether this correlated with tumour aggressiveness and resistance to chemotherapy. Associate Professor Vissers and her colleagues found tumours were less able to accumulate vitamin C compared with normal healthy tissue, and that this related to the ability of the tumour to survive and grow.
Tumours with low vitamin C levels had more of a protein called HIF-1 which allows them to thrive in conditions of stress.
The findings are significant as they show, for the first time, a direct relationship between HIF-1 and vitamin C levels in tumours and suggest it would be beneficial for people with cancer cells to have more vitamin C. This could help limit the rate of tumour growth, increase the responsiveness to chemotherapy and may prevent the formation of solid tumours.”
I don’t see how it could be beneficial for people with cancer cells to have more vitamin C pumped into them if the tumours have high levels of HIF-1 which means that Vitamin C will have less impact on a tumour. Surely it would be better to find a way of blocking HIF-1’s action?
Here is the original abstract from Cancer Research journal:
6. Vitamin C only works if the tumour has been debulked, and its best action is as a preventative
It’s true that if there’s a certain level of tumour load, the immune system has difficulty breaking it down. I think I read somewhere that a certain integrative doctor advises all breast cancer patients to have their tumours removed before doing IV C. But my thoughts then were: how will I know that the IV C is working if I remove the tumour?
7. What about using liposomal Vitamin C?
Liposomal Vitamin C is the de rigeur oral form of Vitamin C for all cancer patients (at least in the UK) because according to lab tests, it’s the most bio-available form of Vitamin C (compared to non-liposomal brands). It is also the most expensive brand, costing about £30 for a pack of 30 x 1g sachets.
Claims are made that it can replicate the serum levels of intravenous Vitamin C. That’s why cancer patients will take 10-15 sachets per day, that’s supposedly 10g to 15g.
And that’s what I thought. I bought into the liposomal claim, and at one stage was on 10 sachets a day. I must have spent a fortune on liposomal Vitamin C.
“So you have these liposomal vitamin C’s and these other vitamin C’s that say, “Oh we have increased uptake and it’s almost like getting an IV, or it’s like getting an IV.” But in actuality they’re still in the micromolar range.”
Micromolar is not the same as grams! Granted that the tests were done on lab animals, nevertheless it makes me question the claims that the company that makes liposomal makes.
Dr Drisko does put her patients on oral Vitamin C, but as she explains, this is still not the same as being on IV C, because it is not affecting the cancer by the hydrogen peroxide route.
“We do have them on a good quality vitamin C product but it’s still a vitamin. It’s still doing vitamin jobs. It’s not doing the production of hydrogen peroxide in the extracellular space. That does not occur. We’ve shown that in multiple animal models. It’s not occurring. So oral vitamin C is not IV vitamin C.”
I hate to burst bubbles, but I don’t like having my expectations raised and dashed, and the way liposomal Vitamin C had been sold to me has been on the claim that it’s as good as IV C. Uh-uh – it may be more bioavailable but it is not IV C. I am not saying “don’t take liposomal Vitamin C”, but what I’m saying is, it’s not the same as IV C. It may work a different way, through supporting the immune system or hyaluronidase activity.
8. The blood supply to the tumour was inadequate
This theory was proposed to me by Dr Siebenhuner, who runs Praxis Siebenhuner, an integrative clinic in Frankfurt. It actually makes sense – if the blood supply to the tumour is not adequate, then the Vitamin C cannot reach the tumour in sufficient levels. There is a way of finding out what the blood supply to the breast tumour is like, and that is through ultrasound – Dr Siebenhuner had one in his practice and was trained to use it.
9. Cancer cells that are hypoxic (poorly-oxygenated) are harder to kill
Here’s what I’ve just come across on the Oasis of Hope clinic’s website on Coping with Tumour Hypoxia:
“One way to make chemotherapy more effective is to insure that cancer cells are adequately oxygenated. Because tumors tend to have haphazard blood supplies, some parts of tumors tend to receive relatively little blood flow, and are thus poorly oxygenated (hypoxic). For reasons that are not yet entirely clear, hypoxic cancer cells are often harder to kill with chemotherapy. So we use several strategies for improving the oxygenation of tumors. “
So, perhaps my tumour was hypoxic which made it less susceptible to high dose IV C. Unfortunately, the British clinic I went to for IV C did not have any diagnostics or even a strategy for improving the oxygenation to the tumour. In fact, I don’t know of any British clinic that does the IV C protocol as stringently as Mexico’s Oasis of Hope clinic. If you are reading this and thinking of doing IV C in the UK and you have £10,000 to spare, please go to Mexico and get it done properly there. At least you will get some results.
10. ??? (mystery reason why intravenous Vitamin C didn’t work)
This wasn’t a post to diss intravenous Vitamin C – it’s used by a lot of integrative doctors and there have been studies on its efficacy.
What we need to bear in mind is that cancer is a multi-factorial disease, and everyone’s tumour cells are different. For breast cancer, there are gene tests like Mammaprint which tests for 70 gene expressions of tumour samples. But that’s only the tip of the iceberg. There is so much out there we don’t know about cancer. We’re like a person in a dark room trying to locate the light switch using a walking stick. What works for one person may not work for another.
Here is an article from the BBC website (published on 16 Nov 2013) which talks about how cancer patients can have different cancer types in their tumours!
So it’s a case of managing expectations – by all means try high dose intravenous Vitamin C if you believe in it or are desperate for options, but don’t get attached to the outcome.
11. Some recent research on Vitamin C and cancer
Here is some information on how Vitamin C can help in curbing the growth of cancer cells and decreasing the resistance of cancer cells to chemotherapy. This is based on research carried out by the University of Otago (New Zealand). As this research was carried out in 2010, there may be more up-to-date developments since and I will post when I have more updates:
New research from the University of Otago, Christchurch, shows that vitamin C can help curb the growth of cancer cells.
The study, led by Associate Professor Margreet Vissers of the University’s Free Radical Research Group, is the first real evidence of a connection between vitamin C and tumour growth.
Associate Professor Vissers says “Our results offer a promising and simple intervention to help in our fight against cancer, at the level of both prevention and cure”.
The article is in the latest edition of the prestigious Cancer Research journal.
The role of vitamin C in cancer treatment has been the subject of debate for years, with many anecdotal accounts of the beneficial role of vitamin C in both the prevention and treatment of cancer.
Previous research by Associate Professor Vissers has demonstrated the vitamin’s importance in maintaining cell health and hinted at its potential for limiting diseases such as cancer.
Her latest study looked at whether vitamin C levels were lowered in patients with endometrial tumours.
It investigated whether the cancer cells had low vitamin C levels and whether this correlated with tumour aggressiveness and resistance to chemotherapy. Associate Professor Vissers and her colleagues found tumours were less able to accumulate vitamin C compared with normal healthy tissue, and that this related to the ability of the tumour to survive and grow.
Tumours with low vitamin C levels had more of a protein called HIF-1 which allows them to thrive in conditions of stress.
The findings are significant as they show, for the first time, a direct relationship between HIF-1 and vitamin C levels in tumours and suggest it would be beneficial for people with cancer cells to have more vitamin C. This could help limit the rate of tumour growth, increase the responsiveness to chemotherapy and may prevent the formation of solid tumours.
Activation of the transcription factor hypoxia-inducible factor (HIF)-1 allows solid tumors to thrive under conditions of metabolic stress. Because HIF-1 is switched off by hydroxylation reactions that require ascorbate, inadequate intracellular ascorbate levels could contribute to HIF-1 overactivation. In this study, we investigated whether the ascorbate content of human endometrial tumors [known to be driven by HIF-1 and vascular endothelial growth factor (VEGF)] influenced HIF-1 activity and tumor pathology. We measured protein levels of HIF-1α and three downstream gene products [glucose transporter 1 (GLUT-1), Bcl-2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3), and VEGF], as well as the ascorbate content of tumor and patient-matched normal endometrial tissue samples. HIF-1α and its downstream gene products were upregulated in tumor tissue, with the highest levels being present in high-grade tumors. High-grade tumors also had reduced capacity to accumulate ascorbate compared with normal tissue; however, all grades contained tumors with low ascorbate content. Tumors with the highest HIF-1α protein content were ascorbate deficient. Low ascorbate levels were also associated with elevated VEGF, GLUT-1, and BNIP3 protein levels and with increased tumor size, and there was a significant association between low tissue ascorbate levels and increased activation of the HIF-1 pathway (P = 0.007). In contrast, tumors with high ascorbate levels had lesser levels of HIF-1 activation. This study shows for the first time a likely in vivo relationship between ascorbate and HIF-1, with low tumor tissue ascorbate levels being associated with high HIF-1 activation and tumor growth. Cancer Res; 70(14); 5749–58. ©2010 AACR.