• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

High-dose intravenous Vitamin C effective against Epstein-Barr-Virus?

Daffodil

Senior Member
Messages
5,875
High dose intravenous vitamin C has been used for decades, and I have not heard about any ill effects from it. SO it is probably safe, but I found it concerning that it has these cytotoxic effects. I wonder how well IV C has been formally researched for safety.
I think high dose vitamin C has the potential to cause kidney problems but generally, it is pretty safe.

One doctor I know uses it for cancer. I met the daughter of one of his patients who lived 8 years on vitamin C IV's even though he was terminal. He died only because he stopped or lessened the frequency of his Vitamin C IV's

I think this doctor does a 20 g push and does the rest (80g?) by infusion...this raises blood levels of the C

There are tons of people who have used it for CFS and as an antiviral

I would not bother trying to make liposomal vitamin C at home...I dont think you would get the particle size small enough and the taste is really really gross, too. Was a waste of time and money for me.
 

pattismith

Senior Member
Messages
3,930

Hip

Senior Member
Messages
17,824
High-dose Intravenous Vitamin C as a Successful Treatment of Viral Infections

(This is from a clinic that sells high-dose VC treatments, so I take everything they say with a grain of salt)

https://riordanclinic.org/2014/02/h...s-a-successful-treatment-of-viral-infections/

The Riordan Clinic are the same people who published the study that you linked to in the first post (click on author information). The study data comes from the clinic's own database. The study says:
Among people in our database who were treated at the clinic with intravenous vitamin C (7.5 g to 50 g infusions) for various illness, we found 178 patients who showed elevated levels of EBV IgG (range 25 to 211 AU) and forty who showed elevated levels of EBV VCA IgM (range 25 to 140 AU). These subjects, all being treated between 1997 and 2006, formed the basis of our study. Most of these patients (110 subjects) had a diagnosis of chronic fatigue syndrome, with the rest being diagnosed as having mononucleosis, fatigue, or EBV infection.


They say:
The average EBV EA IgG level before treatment was 80±55 (SD) AU, while the average after treatment was 46±43 (SD) AU. This was an average improvement of roughly forty percent,


But there may be a slight flaw in the study, which you can see in this paragraph:
Analysing these data further, we broke down patients into two groups: patients who did not receive IVC treatment and patients who received five or more treatments. Figure 2 shows how EBV EA IgG levels changed with time of treatment for patients in these two groups.

The flaw is that the allocation of the group who received the IV vitamin C and the group who did not receive treatment may not be random, which it needs to be for a proper randomized controlled trial.

The authors do not mention the reasons why patients were given IV vitamin C treatment or not given this treatment, but for example, if doctors at the clinic decided on who gets treatment on the basis of symptom severity, then the two groups will not be randomly chosen groups.



It is interesting that the authors found higher EBV antibody levels in patients with lower blood vitamin C levels:
We also found evidence that EBV antibody expression correlates with plasma ascorbic acid concentrations. Figure 4 shows the inverse relationships between plasma ascorbic acid levels (pre-treatment) and EBV EA IgG and VCA IgM. The trend is for subjects with high plasma ascorbic acid levels to have lower EBV antigen loads; this is particularly true for VCA IgM.

So that suggests that taking oral vitamin C possibly might help reduce Epstein-Barr virus infection.

They also they found higher EBV antibody levels in patients with lower blood vitamin D levels:
Finally, we analysed the other values of clinical tests for these patients (vitamins and minerals) to find other variables that correlate with EBV antibodies. Thus far, we have found that vitamin D concentration correlates with EBV EA IgG antibody levels (Figure 6).

So that suggests that taking oral vitamin D possibly might help reduce Epstein-Barr virus infection.
 

Wonkmonk

Senior Member
Messages
1,006
Location
Germany
They also they found higher EBV antibody levels in patients with lower blood vitamin D levels:

There seems to be some evidence for this in peer reviewed journals as well:

http://journals.sagepub.com/doi/abs/10.1177/1352458516654310

From a personal experience, I can definitely say that high Vitamin D makes me much worse. Tried it 3 times and each time the same thing. But I think it's perhaps not the Vitamin D per se, but the higher calcium absorption, because calcium supplements also make me much worse.

I think calcium is an activator for some cytokines, so if Dr Montoya is right and elevated cytokines play a role, then this could make sense.
 
Messages
28
I think calcium is an activator for some cytokines, so if Dr Montoya is right and elevated cytokines play a role, then this could make sense.
@Wonkmonk is there any evidence for that? I'm asking because that would be interesting as Vit D also makes me worse (but if my Vit D levels are higher e. g. sun exposure I'm feeling better). I never had problems with IV Vit C or oral.
 
Last edited:

Wonkmonk

Senior Member
Messages
1,006
Location
Germany
@mari_gold There are dozens of studies that describe the links between calcium and immune response. Too many to post all the links, but easy to find in google, just use the search terms calcium + immune system and calcium + cytokines.

Vitamin D makes me worse, also when it is naturally from sunlight.
 

Wonkmonk

Senior Member
Messages
1,006
Location
Germany
By the way, I did my first infusion this morning (7.5g). No negative events. I think I feel a bit better, but as of now, I assume this is a placebo effect and not real or permanent. I am also on a very slow upward trend since doing the antibiotics, so it might be unrelated to the Vitamin C.

I plan to do a 2nd course of antibiotics starting tomorrow. I'm not sure yet if I'm going to continue Vitamin C parallel or do finish the antibiotics first.
 

Wonkmonk

Senior Member
Messages
1,006
Location
Germany
From Wikipedia (in fairness, this might be bogus, but it sounds interesting):

"Humans and other species that do not synthesize vitamin C carry a mutated and ineffective form of the enzyme L-gulonolactone oxidase, the fourth and last step in the ascorbate-producing machinery. In the anthropoids lineage, this mutation likely occurred 40 to 25 million years ago. The three surviving enzymes continue to produce the precursors to vitamin C, but the process is incomplete and the body then disassembles them.

In the 1960s, the Nobel-Prize-winning chemist Linus Pauling, after contact[20]with Irwin Stone, began actively promoting vitamin C as a means to greatly improve human health and resistance to disease. His book How to Live Longer and Feel Better was a bestseller and advocated taking more than 10 grams per day orally, thus approaching the amounts released by the liver directly into the circulation in other mammals: an adult goat, a typical example of a vitamin-C-producing animal, will manufacture more than 13,000 mg of vitamin C per day in normal health and much more when stressed."

https://en.wikipedia.org/wiki/Vitamin_C_megadosage#Relative_deficiency_hypothesis
 
Messages
28
By the way, I did my first infusion this morning (7.5g). No negative events. I think I feel a bit better, but as of now, I assume this is a placebo effect and not real or permanent. I am also on a very slow upward trend since doing the antibiotics, so it might be unrelated to the Vitamin C.
As for me it took 24 hours to notice any effect of IV Vit C and it lastet for 3-4 days. I'm excited how this is going to work out for you @Wonkmonk!
Did you apply the infusion yourself or did you go to your GP?
 

Hip

Senior Member
Messages
17,824
an adult goat, a typical example of a vitamin-C-producing animal, will manufacture more than 13,000 mg of vitamin C per day in normal health and much more when stressed

If that amount of vitamin C is required each day, I wonder why humans have difficulty absorbing high doses of vitamin C orally. In know in my case, if I start going about around 12 grams a day of ascorbic acid (taken in 3 divided doses of 4 grams), then I get bowel flushing (diarrhea).

The bowel flushing might be related to the cytotoxic of ascorbic acid on epithelial cells: the study I mentioned earlier found that the CC50 (the concentration that kills 50% of the epithelial cells after 24 hours) was around 2 mM = 350 μg/ml = 350 mg/liter.

So 350 mg of ascorbic acid per liter is the CC50 concentration that is toxic to epithelial cells (which line the bowels). So perhaps that's why when you take high doses like say 5 grams of vitamin C orally, you get bowel flushing, to protect the bowel from the toxic effects of high dose vitamin C.



"The recommended daily dose of vitamin C for humans is just one mg/kg, while goats, for example, produce the vitamin at a striking rate of 200 mg/kg each day."

https://www.sciencedaily.com/releases/2008/03/080320120726.htm

That article also states:
Unlike the more than 4,000 other species of mammals who manufacture vitamin C, and lots of it, the red blood cells of the handful of vitamin C-defective species are specially equipped to suck up the vitamin's oxidized form, so-called L-dehydroascorbic acid (DHA), the researchers report in the March21st issue of Cell, a publication of Cell Press.

Once inside the blood cells, that DHA--which is immediately transformed back into ascorbic acid (a.k.a. vitamin C)--can be efficiently carried through the bloodstream to the rest of the body, the researchers suggest.
In essence, the red cells of animals that can't make vitamin C recycle what little they've got.

So it seems that although humans cannot make vitamin C, we have evolved a way to recycle vitamin C in our red blood cells.
 

Learner1

Senior Member
Messages
6,305
Location
Pacific Northwest
Having seen hundreds of IV C infusions and had over 100 myself, and seen how it had helped people and dug into how it works, here are a few things I've learned;
  • @Hip You are correct. There's a maximum of how much oral can get through your intestines and into your bloodstream, according to Mark Levine at NIH. See attached.
  • The Blood Brain Barrier is not some brick brick wall that can't be passed. Its actually more permeable in many people, including sick people and those with leaky guts, which is most of us. Vitamin C has been successfully used to treat brain cancers, supporting the idea it gets through the BBB into the brain.
  • Kidneys should be monitored, but I haven't heard of any issues in the clinics I've been in in the past 5 years.
  • The one gotcha for high dose vitamin C is in people with a defective G6PD gene. In these patients, it can be fatal, so the first step my doctors do is to test for that gene.
 

Attachments

  • Oral vs IV C.pdf
    267 KB · Views: 23

pamojja

Senior Member
Messages
2,384
Location
Austria

Result of that Oral vs IV C.pdf:

RESULTSWhen 1.25 g of vitamin C was given intravenously,
plasma concentrations were significantly higher than when
the vitamin was given orally (P 0.001 by repeated-mea
sures ANOVA) (Figure 1). In addition, plasma concentra
tions were significantly higher over all doses (P 0.001 by
repeated-measures ANOVA) with intravenous compared
with oral administration (Figure 1, inset). At the highest
dose of 1.25 g, mean peak values from intravenous admin
istration were 6.6-fold higher than mean peak values from
oral administration. When all doses were considered, peak
plasma vitamin C concentrations increased with increasing
intravenous doses, whereas peak plasma vitamin C concen
trations seemed to plateau with increasing oral doses. Urine
vitamin C concentrations were higher for the same dose
given intravenously compared with that administered by
the oral route. At the highest dose of 1.25 g, peak urine
concentrations from intravenous administration were ap
proximately 3.5 times higher than from oral administration
(data not shown).

The 3-compartment vitamin C pharmacokinetic
model that we developed predicted that a single oral dose
of 3 g, the maximum tolerated single dose, produced a
peak plasma concentration of 206 mol/L (Figure 2, top).
Peak predicted concentration after a single 1.25-g oral dose
was slightly lower at 187 mol/L. For 200 mg, an amount
obtained from vitamin C–rich foods, peak predicted con
centration was approximately 90 mol/L. Plasma concen
trations for all of these amounts returned to steady-state
values, approximately 70 to 85 mol/L, after 24 hours.
With 3 g given orally every 4 hours, the maximum tolera
ble (6), peak predicted plasma concentration was approxi
mately 220 mol/L (Figure 2, top). By contrast, after in
travenous administration, predicted peak plasma vitamin C
concentrations were approximately 1760 mol/L for 3 g,
2870 mol/L for 5 g, 5580 mol/L for 10 g, 13 350mol/L for 50 g, and 15 380 mol/L for 100 g (Figure 2,bottom). Doses of 60 g given intravenously are used for
cancer treatment by complementary and alternative medi
cine practitioners (2). Predicted peak urine vitamin C con
centrations were as much as 140-fold higher after intrave
nous administration compared with oral administration
(data not shown).

Compare that extrapolation from serum levels of 1.25g to this other study which measured actual serum levels from up to 20g orally:

Journal of the New Zealand Medical Association, 23-August-2002, Vol 115 No 1160

Glycohaemoglobin and ascorbic acid

Copplestone et al1 (http://www.nzma.org....al/115-1157/25/) identified misleading glycohaemoglobin (GHb) results due to a haemoglobin variant (Hb D Punjab) and listed a number of other possible causes for such false results (ie, haemolytic anaemia, uraemia, lead poisoning, alcoholism, high-dose salicylates and hereditary persistence of foetal haemoglobin).

We have observed a significant "false" lowering of GHb in animals and humans supplementing ascorbic acid (AA) at multigram levels. Mice receiving ~7.5 mg/d (equivalent to > 10 g/day in a 70 kg human) exhibited no decrease in plasma glucose, but a 23% reduction in GHb.2 In humans, supplementation of AA for several months did not lower fasting plasma glucose.3,4 We studied 139 consecutive consenting non-diabetic patients in an oncology clinic. The patients had been encouraged as part of their treatment to supplement AA. Self-reported daily intake varied from 0 to 20 g/day. The plasma AA levels ranged from 11.4 to 517 µmol/L and correlated well with the reported intake. Regression analysis of their GHb and plasma AA values showed a statistically significant inverse association (eg, each 30 µmol/L increase in plasma AA concentration resulted in a decrease of 0.1 in GHb).

A 1 g oral dose of AA can raise plasma AA to 130 µmol/L within an hour and such doses at intervals of about two hours throughout the day can maintain ~230 µmol AA/L.5 Similar levels could also be achieved by use of sustained-release AA tablets. This AA concentration would induce an approximate 0.7 depression in GHb. The GHb assay used in our study, affinity chromatography, is not affected by the presence of AA.3 Thus, unlike the case with Hb D Punjab, our results were not caused by analytical method artifact. More likely, the decreased GHb associated with AA supplementation appears related to an in vivo inhibition of glycation by the elevated plasma AA levels, and not a decrease in average plasma glucose.3 If this is true, the effect has implications not only for interpretation of GHb but also for human ageing, in which glycation of proteins plays a prominent role in age-related degenerative changes.

A misleading GHb lowering of the magnitude we observed can be clinically significant. Current recommendations for diabetics suggest that GHb be maintained at 7, a level that is associated with acceptable control and decreased risk of complications; when GHb exceeds 8, re-evaluation of treatment is necessary.6 Moreover, relatively small increases in average blood sugar (ie, GHb) can accompany adverse reproductive effects. A difference in mean maternal GHb of 0.8 was found for women giving birth to infants without or with congenital malformations.7 In either of these circumstances, an underestimation of GHb could obscure the need for more aggressive intervention.

Vitamin usage is common in New Zealand and after multivitamins, AA is the most often consumed supplement.8 Moreover, diabetics are encouraged to supplement antioxidants, including AA. Thus, it seems prudent for primary care health providers to inquire regarding the AA intake of patients, especially diabetics, when using GHb for diagnosis or treatment monitoring.

Cheryl A Krone
Senior Research Scientist
John TA Ely
Director
Applied Research Institute
PO Box 1925
Palmerston North

References:

Copplestone S, Mackay R, Brennan S. Normal glycated haemoglobin in a patient with poorly controlled diabetes mellitus and haemoglobin D Punjab: implications for assessment of control. NZ Med J 2002;115(1157). URL: http://www.nzma.org....al/115-1157/25/
Krone CA, Ely JTA. Vitamin C and glycohemoglobin revisited. Clin Chem 2001;47(1):148.
Davie SJ, Gould BJ, Yudkin JS. Effect of vitamin C on glycosylation of proteins. Diabetes 1992;41(2):167–73.
Paolisso G, Balbi V, Bolpe C, et al. Metabolic benefits deriving from chronic vitamin C supplementation in aged non-insulin dependent diabetics. J Am Coll Nutr 1995; 14(4):387–392.
Lewin S. Vitamin C: Its Molecular Biology and Medical Potential. New York: Academic Press; 1976.
Kenealey T, Braatvedt G, Scragg R. Screening for type 2 diabetes in non-pregnant adults in New Zealand: practice recommendations. NZ Med J 2002;115(1152):194–6.
Rosenn B, Miodovnik M, Dignan PS, et al. Minor congenital malformation in infants of insulin-dependent diabetic women: association with poor glycemic control. Obstet Gynecol 1990;76:745–9.
Allen T, Thomson WM, Emmerton LM, Poulton R. Nutritional supplement use among 26-year-olds. N Z Med J 2000;113(1113):274–7.

(emphasis added by me) With IVs these peaks are reached for a few hours per IV, with oral 20 g/d up to 517 µmol/L would be steady state.

I only get bowel issues above 50 g/d of ascorbic acid. Have been taking about 23 g/d orally for the last 9 years. With many benefits.
 

Wonkmonk

Senior Member
Messages
1,006
Location
Germany
If that amount of vitamin C is required each day, I wonder why humans have difficulty absorbing high doses of vitamin C orally.

This is a great question. One may also ask why we can only absorb a few µg of Vitamin B12 per meal and just 1-3% of higher doses, even with severe deficiency and very low intake. It may be the case that the way the gut works, there is a level above which further absorption of Vitamin C is not possible.

I only get bowel issues above 50 g/d of ascorbic acid. Have been taking about 23 g/d orally for the last 9 years. With many benefits.

You take it all orally, correct?
 

Wonkmonk

Senior Member
Messages
1,006
Location
Germany
Had the second VC infusion 2 hours ago, with the double dose (15g). Felt a bit dizzy this time, but no adverse reactions otherwise so far.

I think I am feeling a bit better after the infusions, but I don't feel a substantial effect so far.

I think I am going to continue, just ordered a 20-dose package from a internet pharmacy. As long as there are no negative effects, I want to up the dose gradually, perhaps until 50 or 75 grams. Let's see how it goes.
 

pattismith

Senior Member
Messages
3,930
@Wonkmonk ,

I can see the Pascorbin product exists in two forms, ampoules or bottle; Would you tell me which one you use?
Do you dilute it? How long does it take for the infusion?

Instructions from the site:

5 ml ampoule:
Slowly inject 5 ml a day intravenously, up to 50 ml injection solution in addition to the infusion.

50 ml injection bottle:
For peripheral-venous short infusion dilute 50 ml PASCORBIN with 100 ml of isotonic saline solution and slowly infuse.