GcMAF for XMRV--Gc protein-derived macrophage activating factor--anyone taking it?

[CindyWillis]

I heard that adding vitamin D to GCMAF could cause kidney failure from someone who did that and ended up in the emergency room. Before this happened, it was recommended by this person.

Can anyone explain this in greater detail? Or, can anyone point me somewhere (not gcmaf.eu) that actually says GcMAF needs x level of vitamin D to work?

 

[lobba123]

if vitamin d is below 30ng/ml immune system doesn t work because macrophages cant be activated, gcmaf binds to vitamn d 25oh which binds to macrophages in extremely simple words

vitamin d 25oh must be checked closely (minimum once a month) together with calcium becuase vitamin d increases absorption of calcium which are needed both for immune system to work but they all must stay within ranges.vitamin d itself makes nothing harmful it is the rise in calcium to damage kidneys, so by close monitoring you can see if there is an excess of calcium and correct that by drinking extra water, by intravenous water, by drugs that lower calcium

if you dont monitor all this you are crazy because you might have these risks, in particular kidneys might be damaged already without showing on tests because all tests for kidneys function are extremely poor sensibility and when you have a small rise of creatinine or better creatinine clearance 50% of kidneys are usually already gone

if all this is used during cancer disease calcium is even more damagerous because cancers increase and produce calcium themselves, many dye of kidney failure due to calcium increase due to cancer.

I heard that adding vitamin D to GCMAF could cause kidney failure from someone who did that and ended up in the emergency room. Before this happened, it was recommended by this person.

Can anyone explain this in greater detail? Or, can anyone point me somewhere (not gcmaf.eu) that actually says GcMAF needs x level of vitamin D to work?

 

[lobba123]

i am using vitamin d3 and gcmaf but of course i monitor calcium, phosphorus, vitamin d 25oh, creatinine every 2 weeks and creatine clearance monthly

i do these tests routinely from 2 years since i use drugs and all drugs can damage both kidneys and liver, so even before starting gcmaf i used to monitor these parameters with many others

I heard that adding vitamin D to GCMAF could cause kidney failure from someone who did that and ended up in the emergency room. Before this happened, it was recommended by this person.

Can anyone explain this in greater detail? Or, can anyone point me somewhere (not gcmaf.eu) that actually says GcMAF needs x level of vitamin D to work?

 

[lobba123]

my good example on how i deal with gcmaf therapy:
i stopped vitamin d3 supplements the 6th of june when i reached 57ng/ml and had a small rise of calicum from baseline values, calcium was well within ranges (10.1..) but from then i started sun bed or sun at the beach and made sure to drink 2liters of water

the 6th of july vit d 25oh was 58ng/ml, i keep monitoring because gcmaf can make vit d flares anyway since they were blocked by immune disfunction and who knows how the body reacts when they are unblocked...

again if you monitor closely there is no danger from calcium rise and no danager of kidneys damage but if you do not you might end with kidney damage without simptoms and forced to stop gcmaf

i am using vitamin d3 and gcmaf but of course i monitor calcium, phosphorus, vitamin d 25oh, creatinine every 2 weeks and creatine clearance monthly

i do these tests routinely from 2 years since i use drugs and all drugs can damage both kidneys and liver, so even before starting gcmaf i used to monitor these parameters with many others

 

[lobba123]

actually both gcmaf and vitamin d can cure kidneys failure and kidneys disfunction too, it is all a matter of correct monitoring if one has no knowledge at doctors level (or even better, most doctors are ignorants) he must have a doctor to monitor treatment

http://www.marcoruggiero.org/pdf/Ruggiero and Pacini Eur Nephrol.pdf
http://www.marcoruggiero.org/pdf/vancouver.pdf



how gcmaf work
http://www.marcoruggiero.org/pdf/Pacini et al. Cancer Immunol Immunother.pdf

I heard that adding vitamin D to GCMAF could cause kidney failure from someone who did that and ended up in the emergency room. Before this happened, it was recommended by this person.

Can anyone explain this in greater detail? Or, can anyone point me somewhere (not gcmaf.eu) that actually says GcMAF needs x level of vitamin D to work?

 

[mojoey]

A lot of us have been curious about this "viral reactivation" issue wth gcmaf since someone seems to have had their hhv-6 reactivated indirectly or directly by it. KDM has since told vli that it does NOT reactivate.

I just heard from a patient who was told by cheney that it does activate not only herpes viruses but xmrv through nf-kappa b, which is proinflammatory in nature. judy mikovits has said that controlllng nf kappa b is a crucial part of xmrv treatment. I'm unsure how he is arriving at this conclusion.

So now the question is: if we find an antidote to the proinflammatory effects of gcmaf, would it still help?

 

[lobba123]

other connections between vitamin d level and immune system:
http://www.pslgroup.com/dg/25e93e.htm

Presentation title: Increased Vitamin D Levels are Associated With Undetectable Viral Loads in Patients With Chronic Hepatitis B. Abstract Su1011]

Most Patients With Chronic HBV, Low Vitamin D Levels Have Detectable Viral Loads: Presented at DDW

By Ric Susman
CHICAGO -- May 12, 2011 -- About 75% of patients with chronic hepatitis B virus (HBV) infection were found to have insufficient levels of vitamin D, according to a study presented here at Digestive Disease Week (DDW) 2011.
In this outpatient population with chronic hepatitis B, vitamin D insufficiency is prevalent, reported Katherine Small, MD, Mount Sinai Medical Center, New York, New York, on May 8. Vitamin D supplementation should be studied prospectively as a therapeutic intervention to increase the likelihood of achieving and undetectable viral load.
In their retrospective database review of 417 patients with HBV, the researchers identified 51 patients who were positive for HBV surface antigen for >6 months. Of these, serum 25-hydroxyvitamin D was measured in 29.
Any patients who were being treated for hepatitis C or HIV were excluded from the potential sample pool.
Vitamin D levels were analysed according to HBV viral load by the Mann-Whitney-Wilcoxon test.
Twenty-two of the 29 patients had vitamin D levels that were considered insufficient. Of these, 3 had very low vitamin D levels (<10 ng/ml).
In the patients with undetectable viral loads (4 of 5 patients vitamin D supplementation), vitamin D levels were significantly higher than those of patients who had detectable HBV viral loads (29.1 vs 17.0 ng/ml; P =.003).

Digestive Disease Week 2011 is cosponsored by the American Association for the Study of Liver Diseases (AASLD), the American Gastroenterological Association (AGA), the American Society for Gastrointestinal Endoscopy (ASGE), and the Society for Surgery of the Alimentary Tract (SSAT).

 

[lobba123]

there are many many studies o both hbv and hcv infectionc and immune response to the virus and clearance by interferon.
all the studies link vitamin d level and cholesterol levels too to immune control/eradication of infections hbv or hcv

 

[froufox]

Thanks for this info Joey, this is what i have suspected for a while so it doesnt surprise me at all. It does make sense since we know that macrophages boost TNF@ and TNF@ is involved in a pathway that activates NFkB...I posted some info about this a few pages back on this thread....

from http://www.rmgh.net/wiki/index.php?title=Macrophages:
"Macrophages are believed to help cancer cells proliferate as well. They are attracted to oxygen-starved (hypoxic) tumour cells and promote chronic inflammation. Inflammatory compounds such as Tumor necrosis factor (TNF) released by the macrophage activates the gene switch nuclear factor-kappa B. NF-kB then enters the nucleus of a tumour cell and turns on production of proteins that stop apoptosis and promote cell proliferation and inflammation"

I assumed this was what was happening in my case because as ive posted b4 ive had major depression at times since being on gcmaf and high tnf@ causes depression, plus with all the brain inflammation ive had.

I think its definitely worth trying NFkB inhibitors and im sure if the inflammation is not too bad then these will help, but not if its way of control like it was in my case, curcumin for eg just didnt cut the mustard. The answer for me was to just cut back on the dose, take breaks and make the treatment more tolerable that way.

I was planning on asking KDM about testing for NFkB in my phone consult with him next week. I know that Dr Beiger in Germany is already testing for this as someone posted about it on a thread here. I hope that KDM will consider starting to test for this as it will obviously be a very useful thing to keep an eye on. I'll let people know what he says.

A lot of us have been curious about this "viral reactivation" issue wth gcmaf since someone seems to have had their hhv-6 reactivated indirectly or directly by it. KDM has since told vli that it does NOT reactivate.

I just heard from a patient who was told by cheney that it does activate not only herpes viruses but xmrv through nf-kappa b, which is proinflammatory in nature. judy mikovits has said that controlllng nf kappa b is a crucial part of xmrv treatment. I'm unsure how he is arriving at this conclusion.

So now the question is: if we find an antidote to the proinflammatory effects of gcmaf, would it still help?

 

[lobba123]

as regards viruses reactivation i have found where the study is from...in a previous post a said i recalled reading something about it from yamamoto studies but it is not

http://marthashave.wordpress.com/20...n-by-dr-judy-mikovits-and-annette-whittemore/
it is from the lastest studies of mikovits
When discussing Immune Modulation, Mikovits introduced a few points that were new to me. She sees great promise in the newer treatment options popping up such as GcMAF, Stem Cell Therapy and Peptide T. However she is concerned that they may activate the inactive reservoir XMRV. Meaning there could be some XMRV in our bodies that is still dormant, but activation of our immune system might bring them out. However, she didnt stop there. She mentioned that this might actually be a good thing. As ARVs are more effective in HIV since HIV replicates considerably more than XMRV, maybe one of these will get XMRV replicating so the ARV has a job to do. Another area that will surely be discussed further.

A lot of us have been curious about this "viral reactivation" issue wth gcmaf since someone seems to have had their hhv-6 reactivated indirectly or directly by it. KDM has since told vli that it does NOT reactivate.

I just heard from a patient who was told by cheney that it does activate not only herpes viruses but xmrv through nf-kappa b, which is proinflammatory in nature. judy mikovits has said that controlllng nf kappa b is a crucial part of xmrv treatment. I'm unsure how he is arriving at this conclusion.

So now the question is: if we find an antidote to the proinflammatory effects of gcmaf, would it still help?

 

[lobba123]

so as i posted earlier reactivating dormant reservoirs of viruses is not totally bad because even if dormant they are there, probably making damage anyway

 

[mojoey]

I believe what you are referring to from Dr. Mikovits is a different phenomenon. The reason why stem cells would activate a virus probably has more to do with cell division rather than inflammation. Retroviruses love cell division. Also, seeing what happened with most ME/CFS patients that got stem cells (either didn't feel better at all or felt better temporarily and relapsed) , it is quite obvious that viral replication was definitely a problem.

Whether or not viral activation is a problem when it's due to inflammation remains to be seen. Dr. Cheney was very clear that Nf Kappa B needs to be downregulated, sharing Dr. Mikovits view on this. Based on this, I would think that they do not approve of this method of stimulating activation.

There are several experimental methods being used in HIV to stimulate reservoirs out of dormancy. It should be noted that all of them involve either inserting specific gene sequences or chemotherapy. If stimulating retroviruses out of dormancy using cell replication or inflammation were a good thing, you would think that it would've already been tried with some success in HIV. However, the closest example I can think of where it has been helpful is in the combination of interferon with AZT for HTLV versus just AZT, and the analogy to interferon for ME/CFS would be ampligen (a form of interferon), which shows us that dosage is very important for this method to work (Dr. Peterson says interferon makes a lot of ME/CFS patients very sick very quickly so not all interferon is good).

as regards viruses reactivation i have found where the study is from...in a previous post a said i recalled reading something about it from yamamoto studies but it is not

http://marthashave.wordpress.com/20...n-by-dr-judy-mikovits-and-annette-whittemore/
it is from the lastest studies of mikovits
When discussing Immune Modulation, Mikovits introduced a few points that were new to me. She sees great promise in the newer treatment options popping up such as GcMAF, Stem Cell Therapy and Peptide T. However she is concerned that they may activate the inactive reservoir XMRV. Meaning there could be some XMRV in our bodies that is still dormant, but activation of our immune system might bring them out. However, she didnt stop there. She mentioned that this might actually be a good thing. As ARVs are more effective in HIV since HIV replicates considerably more than XMRV, maybe one of these will get XMRV replicating so the ARV has a job to do. Another area that will surely be discussed further.

 

[lobba123]

viral replication was definitely a problem.

this is more genral, it is not a cfs thing or xmrv thing, this reactivation happens with all working immune systems

it is not the drugs themselves, gcmaf and ampligen, that activates dormant virus replication but activation of immune system, there is no way to clear an infection for immune system if viruses are dormant inside the cells, infection will stay cronic forever because immune system can t see what's inside cells unless the virus activates and express antigens on the infected cell.this is a immune system tool to clear cronic infections

the same applied to hbv and hiv, without activating all dormant viruses inside the cells there is no point to use these drugs because the infection will be never cleared.the dormant method is the way viruses and bacteria can avoid immune system detection

lately it was found that simple sugar could reactivate dormant bacteria in cronic bacteria infection with antibiotics resistance, probably the bacteria likes the sugar very much and gets awake....antibiotics returned non resistant and infections could be cleared

the point we are using gcmaf for hiv and hbv is exactly activation of dormant viruses inside cells, both infections are cronic because of this reservoir that can be detected by immune system
i think that nagalase makes immune system disfunction so that viruses are able to stay dormant inside cells....antiviral themselves are useless on these infections becuase even if hbvdna or hivrna are not detectable in blood and liver the templates of the viruses insides cells (dormant viruses, in case of hbv cccdna) will remake all virus and keep doing very low replication virus just exaclty xmrv.
hbv in this low replicative phase is very dangerous too because it makes liver cancer.....it is called occult hbv and although replication is extremely low to be almost undetactable by pcr or totally undetactable it makes liver cancer and cirrhosis more than normal replication virus

I believe what you are referring to from Dr. Mikovits is a different phenomenon. The reason why stem cells would activate a virus probably has more to do with cell division rather than inflammation. Retroviruses love cell division. Also, seeing what happened with most ME/CFS patients that got stem cells (either didn't feel better at all or felt better temporarily and relapsed) , it is quite obvious that viral replication was definitely a problem.

Whether or not viral activation is a problem when it's due to inflammation remains to be seen. Dr. Cheney was very clear that Nf Kappa B needs to be downregulated, sharing Dr. Mikovits view on this. Based on this, I would think that they do not approve of this method of stimulating activation.

There are several experimental methods being used in HIV to stimulate reservoirs out of dormancy. It should be noted that all of them involve either inserting specific gene sequences or chemotherapy. If stimulating retroviruses out of dormancy using cell replication or inflammation were a good thing, you would think that it would've already been tried with some success in HIV. However, the closest example I can think of where it has been helpful is in the combination of interferon with AZT for HTLV versus just AZT, and the analogy to interferon for ME/CFS would be ampligen (a form of interferon), which shows us that dosage is very important for this method to work (Dr. Peterson says interferon makes a lot of ME/CFS patients very sick very quickly so not all interferon is good).

 

[Nabo]

Hi everybody,

I already got a few lab results back.

I was on gc maf from dec 2010 - may 2011
Now i am on a break.

On june 15th my blood was tested.

My c4 a serum was 8542 and is now: 8238. So no improvement.
Maybe it was even higher when i was still on gc maf in may.
My solulble cd 14 is : 7411 no improvement.

My fungus panel is improved.

I dont have any other results back yet.

I have improved since december, but it is going really slow.
but improvement is gooooooodd !!

 

[lobba123]

just published at international hiv conference in rome, IAS2011...by the way vitamin d2 does not affect kidneys or calcium but is less effective than d3

http://pag.ias2011.org/abstracts.aspx?aid=2401

Vitamin D binding protein-macrophage activating factor directly inhibits proliferation of human breast cancer cells, vimentin expression and tumour-induced angiogenesis

S. Pacini1, M. Ruggiero2

1University of Firenze, Anatomy, Histology and Forensic Medicine, Firenze, Italy, 2University of Firenze, Experimental Pathology and Oncology, Firenze, Italy




Background: The incidence of HIV infection is rising in women and even though its impact on breast cancer incidence is still under investigation, it is well assessed that patients with HIV infection present with more advanced stage and aggressive disease, and they also have poor chemotherapy tolerance. Vitamin D binding protein-macrophage activating factor (DBP-MAF) has been successfully used in immunotherapy of HIV-infected patients (J Med Virol 81:16-26, 2009). Since HIV infection and breast cancer can coexist in women, in this study we evaluated the effects of DBP-MAF on human breast cancer cell proliferation and tumour-induced angiogenesis.
Methods: DBP-MAF was obtained from www.gcmaf.eu. Assessment of MCF-7 (human breast cancer) cell proliferation was determined by Calbiochem Rapid Cell Proliferation Kit. MCF-7 cells were also studied by scanning and conventional microscopy. MCF-7-induced angiogenesis was studied in chick embryo chorionallantoic membrane (CAM) assay.
Results: DBP-MAF (0.4-40 ng/ml, incubated for 72 h) inhibited MCF-7 cell proliferation in a dose-dependent manner. Vitamin D also inhibited MCF-7 cell proliferation and the effects of vitamin D and DBP-MAF were additive. DBP-MAF-treated cells were significantly smaller and inhomogeneous as if processes of shrinkage had occurred. Cytoplasm and nucleus appeared irregular as if fragmented. Cellular debris could be observed as well as apoptotic bodies. Vimentin expression was reduced following DBP-MAF treatment. It is worth noting that increased vimentin expression is considered a hallmark of progression of breast cancer due to tumour cells losing their epithelial features and gaining mesenchymal properties. DBP-MAF inhibited MCF-7-induced neo-angiogenesis in CAM assay, another critical step in breast cancer progression.
Conclusion: These results demonstrate that DBP-MAF, in addition to stimulating macrophages, directly inhibits human breast cancer cell growth in vitro. Therefore, administration of DBP-MAF to HIV-infected women could provide the dual benefit of immunotherapy of HIV infection and prevention of breast cancer progression.

 

[Sushi]

Thanks Lobba!

Good news. Was there anything about bypassing poor VDRs?

Sushi

 

[Leonora]

Hi Nabo

Thanks for sharing. Good that you see some improvement. Just wanted to let you know that the CD14 doesn't show how leaky your gut is right now - it actually shows the situation 6 months prior to testing (so actually at the time when you started Gcmaf in Dec). If you wanna know what the CD14 is now just after you finished Gcmaf, you need to check again in 6 months..
Btw, the value is quite good I think - 7400 is not all that bad. Initially I had 30 000!

 

[lobba123]

as you know being initaly i have close contacts....they told me that vdr is the most important factor for gcmaf response and that they are doing studies on this although i dont know if they published.
they are really focused on hiv and cancer and told me that trials and experiences on hiv infected show a direct response or lack of response according to vdr

my vdr FF/Bb was the same as a woman with full blown aids from about a decade and resistant to all hiv antivirals, professor ruggiero in florence reported she imprved in just 10 weeks from aids to hiv positive healthy carrier wit cd4 rise and hivrna big drop while another one with FF/BB had less response with IRIS but slowly improved anyway.
i guess we will have more info as trials go on and i am sure KDM has the highest quantity of data since your trial has a lot of patients but also hiv and hbv might be a good place to look at since response is much faster than CFS so it is easier to correlate response/non response
http://www.marcoruggiero.org/pdf/3- Poster ICAR 2011 GcMAF [Punzi Morucci].jpg

as to bypassing:
they are very interested in the vitamin d25oh level and checking in vitro and vivo

i dont think they are looking at bypassing specifically now but are very interested in vit d 25oh levels and see response

my guess is since ff/BB has no response to eather vitamn d3 alone or gamf maybe the combo gcmaf+vitamin d3 will do something, one thing is sure with that vdr vitamin d flares will never happen unless there is a response of gcmaf, and i'd not worry about calcium because on close monitoring of d25oh is very easy to correct a calcium/vit d3 excess...of course with no good doctor and monitoring any therapy can be very dangerous, i am sure the one who had calcium rise and kidney failure had no monitoring at all

Thanks Lobba!

Good news. Was there anything about bypassing poor VDRs?

Sushi

 

[maryb]

I haven't started on Gcmaf yet, was prescribed it a while ago but not been well enough to do anything about it. Following this thread with interest re Vit D, I struggle to take this as a supplement but can tolerate a small amount of sunshine. My vit D results last October (bearing in mind this was at the end of summer) were;
Vit D3 (25 OH-) -19,6 (ug/L) Range 20,0 -43,0
1,25 Di-OH vitamin D 35,3 (pg/ml) Range 25,1 - 66,1
Am I understanding this - would I have enough Vit D at this level to work with the macrophages?
BTW thanks Leonora for the info on CD14.

 

[lobba123]

http://www.springerlink.com/content/e01lk86533400484/

from latest hiv congress, and this same thing applies to hbv and 100% xmrv too (by they way these 3 viruses share the same antiviral tenofovir too).this is why it is essential to reactivate latent viruses in order to eradicates them...

Combination antiretroviral therapy (cART) has led to a major reduction in HIV-related mortality and morbidity. However, HIV still cannot be cured. With the absence of an effective prophylactic or therapeutic vaccine, increasing numbers of infected people, emerging new toxicities secondary to cART and the need for life-long treatment, there is now a real urgency to find a cure for HIV.
There are currently multiple barriers to curing HIV. The most significant barrier is the establishment of a latent or "silent" infection in resting CD4+ T cells. In latent HIV infection, the virus is able to integrate into the host cell genome, but does not proceed to active replication. As a consequence, antiviral agents, as well as the immune system, are unable to eliminate these long-lived, latently infected cells. Reactivation of latently infected resting CD4+ T cells can then re-establish infection once cART is stopped. Other significant barriers to cure include residual viral replication in patients receiving cART, even when the virus is not detectable by conventional assays. In addition, HIV can be sequestered in anatomical reservoirs, such as the brain, gastrointestinal tract and genitourinary tract.
Achieving either a functional cure (long-term control of HIV in the absence of cART) or a sterilizing cure (elimination of all HIV-infected cells) remains a major challenge. Several studies have now demonstrated that treatment intensification appears to have little impact on latent reservoirs. Some potential and promising approaches that may reduce the latent reservoir include very early initiation of cART and the use of agents that could potentially reverse latent infection.
Agents that reverse latent infection will promote viral production; however, simultaneous administration of cART will prevent subsequent rounds of viral replication. Such drugs as histone deacetylase inhibitors, currently used and licensed for the treatment of some cancers, or activating latently infected resting cells with cytokines, such as IL-7 or prostratin, show promising results in reversing latency in vitro when used either alone or in combination. In order to move forward toward clinical trials that target eradication, there needs to be careful consideration of the risks and benefits of these approaches, agreement on the most informative endpoints for eradication studies and greater engagement of the infected community.

A lot of us have been curious about this "viral reactivation" issue wth gcmaf since someone seems to have had their hhv-6 reactivated indirectly or directly by it. KDM has since told vli that it does NOT reactivate.

I just heard from a patient who was told by cheney that it does activate not only herpes viruses but xmrv through nf-kappa b, which is proinflammatory in nature. judy mikovits has said that controlllng nf kappa b is a crucial part of xmrv treatment. I'm unsure how he is arriving at this conclusion.

So now the question is: if we find an antidote to the proinflammatory effects of gcmaf, would it still help?