GcMAF for XMRV--Gc protein-derived macrophage activating factor--anyone taking it?
- Thread starter Sushi
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Hi Citybag
I still have not recovered from Gcmaf although stopping a year ago. I also know several other patients that are doing worse after Gcmaf. Several are suffering from colitis, some have gotten other infections or autoimmune diseases triggered...
I still have not recovered from Gcmaf although stopping a year ago. I also know several other patients that are doing worse after Gcmaf. Several are suffering from colitis, some have gotten other infections or autoimmune diseases triggered...
globalpilot
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It's funny you mention this now because just yesterday I was reading about how activated macrophages can trigger demyelination. THis isn't where I read it (can't find that now) but this says the same thing. http://www.hindawi.com/crim/pathology/2011/514613/
I also read in a paper I have here by Yamamoto http://www.transonc.com/pdf/manuscript/v01i02/neo08106.pdf
on prostate cancer that 100ng GCMAF increases macrophage production of superoxide 15 fold within 3.5 hours. Superoxide is a potent oxidant and that is a very significant increase. It is also the chemical they are speaking about in the first article causing demyelination. I was able to determine based on the data in Yamamoto's report that my MAF is operating at about 60% so I surely don't need an increase of 15 fold.
This is why I am considering a very low dose ... to fix an underactivation without going into an overactivation. I guess these symptoms others are experiencing outline where they have problems but I sure hope it's not too late for the symptoms to reverse.
I also read in a paper I have here by Yamamoto http://www.transonc.com/pdf/manuscript/v01i02/neo08106.pdf
on prostate cancer that 100ng GCMAF increases macrophage production of superoxide 15 fold within 3.5 hours. Superoxide is a potent oxidant and that is a very significant increase. It is also the chemical they are speaking about in the first article causing demyelination. I was able to determine based on the data in Yamamoto's report that my MAF is operating at about 60% so I surely don't need an increase of 15 fold.
This is why I am considering a very low dose ... to fix an underactivation without going into an overactivation. I guess these symptoms others are experiencing outline where they have problems but I sure hope it's not too late for the symptoms to reverse.
Some things de Meirleir said at Enlander's Mt. Sinai conf (if I got it right). Intestinal bacteria produce nagalase, as well as HIV and cancer cells. Sickest have much higher levels of LPS polysaccharides from intestinal bacteria. LPS leads to NO (ONOO). Gcmaf and LPS use competing mechanisms to activate macrophages so gcmaf diminishes effects of LPS.
68 of 108 patients had noticeable improvement. 44 of that 68 had diminished fatigue. Theoretically can cause autoimmune disease. 0 of the 108 developed autoimmune disease. If someone has high TGF beta, IL-6 or high ANA or thyroid temporarily exclude from gcmaf. In HIV IRIS occurs where immune system has been heavily damaged. 20-30% of ME patients had IRIS, with low t cells or activated T cells. Look at cytokines, c4a, t cells (CD23, HLA DR+) They are finding IRIS to be related to coinfections. Do broad screening, fungal, viral bacteria parasites. Find missed pathogens. 7 had babesia.
68 of 108 patients had noticeable improvement. 44 of that 68 had diminished fatigue. Theoretically can cause autoimmune disease. 0 of the 108 developed autoimmune disease. If someone has high TGF beta, IL-6 or high ANA or thyroid temporarily exclude from gcmaf. In HIV IRIS occurs where immune system has been heavily damaged. 20-30% of ME patients had IRIS, with low t cells or activated T cells. Look at cytokines, c4a, t cells (CD23, HLA DR+) They are finding IRIS to be related to coinfections. Do broad screening, fungal, viral bacteria parasites. Find missed pathogens. 7 had babesia.
hi everyone
it is been a while since i have been here.
i was on gc maf from dec 2010 till may 2011.
I had so many side-effects and felt worse and worse, so i had to stop.
i followed this thread everyday but since may i couldnt do it anymore.
I had the worsed summer of my life!!! it was hell!!
i dont have the energy to read al this again but have a couple of questions.
Do a lot of doctors now work with gc maf?? I am a patient of KDM
Do these doctors also test your nagalase levels??
Are there many people who feel a lot better with gc maf?
And my last question: Can you fight against hhv6 with gc maf or is that impossible??
I hope you can answer my questions, thanks very mych
it is been a while since i have been here.
i was on gc maf from dec 2010 till may 2011.
I had so many side-effects and felt worse and worse, so i had to stop.
i followed this thread everyday but since may i couldnt do it anymore.
I had the worsed summer of my life!!! it was hell!!
i dont have the energy to read al this again but have a couple of questions.
Do a lot of doctors now work with gc maf?? I am a patient of KDM
Do these doctors also test your nagalase levels??
Are there many people who feel a lot better with gc maf?
And my last question: Can you fight against hhv6 with gc maf or is that impossible??
I hope you can answer my questions, thanks very mych
froufox
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Hi Nabo so sorry to hear you've been so sick, do you come into any of these - someone who has high TGF beta, IL-6 or high ANA or thyroid?? looks like these people won't respond well to Gcmafaccording to this report from KdM. Hope things get better for you soon.
Hi, all.
I'm reposting this response to Sushi from another thread, so people here will be able to read it. It's my summary of Dr. de Meirleir's talk on GcMAF at the meeting convened by Dr. Enlander yesterday at the Icahn Institute of the Mt. Sinai Medical Center in New York City:
Hi, Sushi.
I asked Dr. de Meirleir about the effect of GcMAF on NK number and function. He replied that he does not have information on that yet. I'm not sure I understood him exactly, but I think he meant that he has the data but has not analyzed it yet.
In his talk, he offered four possibilities for what could be causing the nagalase elevation in ME/CFS patients: retroviruses, herpes viruses, intestinal bacteria, and HERVs (human endogenous retroviruses).
Dr. Enlander told me that he had split a sample into three, sent them to the lab, and received three different results. I don't know how different, but apparently different enough that it has caused him to question the reliability of the test. On the other hand, Dr. de Meirleir reported that in 395 patients, the average nagalase level in his practice has been 1.72 nmol/min/mg, while controls have been less than 0.69 (the range of controls is 0.35 to 0.68). Dr. de Meirleir also quoted Dr. Cheney as reporting that in his practice, thepatients average 3.0, with a range of 0.8 to 6.7. He said Dr. Cheney has also reported that he finds the nagalase level in his patients to vary inversely with their Karnovsky scale value.
Dr. de Meirleir also reported that he has found that if he divides his patients into two groups, having higher and lower nagalase values, he does not find that those with the higher nagalase have a lower VO2max than those with lower nagalase values.
He did make the point that some intestinal bacteria do produce nagalase.
He said that in a Norwegian study it had been found that when comparing seriously ill, bedridden patients with a low Karnovksy number to a less-ill group with a Karnofsy number of 60 to 70, it was found that LPS [lipopolysaccharide, from the cell walls of gram-negative bacteria, also called endotoxin] was higher in the bedridden patients. He attributed this to altered intestinal flora and more severe leaky gut syndrome in these patients.
He explained that both GcMAF and LPS are able to activate macrophages. However, they do it by different mechanisms. When it is done by LPS, it leads to elevated nitric oxide, interference with MRP2, and loss of control of redox status. I think he said that CCD14 was also elevated in this case. He said that these two processes compete and are mutually exclusive. The affinity for GcMAF is higher, and it does not involve release of IL-1 and TNF-alpha. What he called "bad" activation of macrophages by LPS is inhibited by activation with GcMAF.
He emphasized how small the amount of GcMAF is that is injected in the patients (100 nanograms in 1 milliliter of physiological serum).
The dosages have ranged between 25 and 100 nanograms per week. Three-quarters of his patients have had the full dosage.
The duration of treatment of his patients at this time is 5 to 40 weeks, with an average of 15 weeks.
He reported that 68 out of 100 are improved, and the symptoms improve essentially across the board.
There has been a suggestion by others that GcMAF might promote autoimmunity. He has not found this in his cases, but he does exclude patients from this treatment who have elevated TGF-beta, IL-6, or high ANA or thyroid antibodies, to be on the safe side.
He also talked about IRIS (immune reconstitution inflammatory syndrome). This occurs in HIV patients who have been treated with GcMAF, and he attributed it to a heavily damaged immune system and the presence of infections with other pathogens in addition to HIV in these patients. It occurs when there is a repopulation of T cells. I think he said that 20-30% of his patients develop IRIS. In view of this, he tests his patients for coinfections, and he also monitors cytokines, C4a, and activated T cells. It is important to start with a low dose of GcMAF in patients who have the characteristics that would make them susceptible to developing IRIS.
He said he doesn't have much data yet on the behavior of nagalase under GcMAF treatment, and hopes to have more next week, but at the present he could report that in 15 out of 18 patients for whom he has data, nagalase dropped from an average of 2.50 to an average of 1.87.
I think that is pretty much what he said, except for basic introductory info about GcMAF, which I know you already know. The video of the meeting will be posted soon by Peter Cairns, son of "PatientAdvocate", who videoed the meeting, so you will be able to check to see if I got the details right.
Best regards,
Rich
I'm reposting this response to Sushi from another thread, so people here will be able to read it. It's my summary of Dr. de Meirleir's talk on GcMAF at the meeting convened by Dr. Enlander yesterday at the Icahn Institute of the Mt. Sinai Medical Center in New York City:
Hi, Sushi.
I asked Dr. de Meirleir about the effect of GcMAF on NK number and function. He replied that he does not have information on that yet. I'm not sure I understood him exactly, but I think he meant that he has the data but has not analyzed it yet.
In his talk, he offered four possibilities for what could be causing the nagalase elevation in ME/CFS patients: retroviruses, herpes viruses, intestinal bacteria, and HERVs (human endogenous retroviruses).
Dr. Enlander told me that he had split a sample into three, sent them to the lab, and received three different results. I don't know how different, but apparently different enough that it has caused him to question the reliability of the test. On the other hand, Dr. de Meirleir reported that in 395 patients, the average nagalase level in his practice has been 1.72 nmol/min/mg, while controls have been less than 0.69 (the range of controls is 0.35 to 0.68). Dr. de Meirleir also quoted Dr. Cheney as reporting that in his practice, thepatients average 3.0, with a range of 0.8 to 6.7. He said Dr. Cheney has also reported that he finds the nagalase level in his patients to vary inversely with their Karnovsky scale value.
Dr. de Meirleir also reported that he has found that if he divides his patients into two groups, having higher and lower nagalase values, he does not find that those with the higher nagalase have a lower VO2max than those with lower nagalase values.
He did make the point that some intestinal bacteria do produce nagalase.
He said that in a Norwegian study it had been found that when comparing seriously ill, bedridden patients with a low Karnovksy number to a less-ill group with a Karnofsy number of 60 to 70, it was found that LPS [lipopolysaccharide, from the cell walls of gram-negative bacteria, also called endotoxin] was higher in the bedridden patients. He attributed this to altered intestinal flora and more severe leaky gut syndrome in these patients.
He explained that both GcMAF and LPS are able to activate macrophages. However, they do it by different mechanisms. When it is done by LPS, it leads to elevated nitric oxide, interference with MRP2, and loss of control of redox status. I think he said that CCD14 was also elevated in this case. He said that these two processes compete and are mutually exclusive. The affinity for GcMAF is higher, and it does not involve release of IL-1 and TNF-alpha. What he called "bad" activation of macrophages by LPS is inhibited by activation with GcMAF.
He emphasized how small the amount of GcMAF is that is injected in the patients (100 nanograms in 1 milliliter of physiological serum).
The dosages have ranged between 25 and 100 nanograms per week. Three-quarters of his patients have had the full dosage.
The duration of treatment of his patients at this time is 5 to 40 weeks, with an average of 15 weeks.
He reported that 68 out of 100 are improved, and the symptoms improve essentially across the board.
There has been a suggestion by others that GcMAF might promote autoimmunity. He has not found this in his cases, but he does exclude patients from this treatment who have elevated TGF-beta, IL-6, or high ANA or thyroid antibodies, to be on the safe side.
He also talked about IRIS (immune reconstitution inflammatory syndrome). This occurs in HIV patients who have been treated with GcMAF, and he attributed it to a heavily damaged immune system and the presence of infections with other pathogens in addition to HIV in these patients. It occurs when there is a repopulation of T cells. I think he said that 20-30% of his patients develop IRIS. In view of this, he tests his patients for coinfections, and he also monitors cytokines, C4a, and activated T cells. It is important to start with a low dose of GcMAF in patients who have the characteristics that would make them susceptible to developing IRIS.
He said he doesn't have much data yet on the behavior of nagalase under GcMAF treatment, and hopes to have more next week, but at the present he could report that in 15 out of 18 patients for whom he has data, nagalase dropped from an average of 2.50 to an average of 1.87.
I think that is pretty much what he said, except for basic introductory info about GcMAF, which I know you already know. The video of the meeting will be posted soon by Peter Cairns, son of "PatientAdvocate", who videoed the meeting, so you will be able to check to see if I got the details right.
Best regards,
Rich
Lou
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Or MAF 878? Thanks,
Hi, ukxmrv and Lou.
Dr. Enlander mentioned MAF 314, in particular its high cost. He is working with a company on Long Island that is developing MAF 878. He plans to test it, and I got the impression that it is intended to be less expensive than MAF 314 currently costs patients.
Best regards,
Rich
Dr. Enlander mentioned MAF 314, in particular its high cost. He is working with a company on Long Island that is developing MAF 878. He plans to test it, and I got the impression that it is intended to be less expensive than MAF 314 currently costs patients.
Best regards,
Rich
thanks for responding.
I do have high IL 6 and some others IL 10 also.
So i cant tollerate gc maf???
mojoey
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I'm glad KDM is focusing now on the autoimmune element now, although I think he could've very well replaced autoimmune with "overreactivity" and made the same point. We've all seen through our crowdsourcing document that high baseline c4a does not result in a pleasant outcome with gcmaf, so why is he not paying more attention to this?
Maybe because no one really knows what c4a represents, but using that to measure probability of an ugly response could save a lot of time and money. I've never had high TGF-b1, il-6, positive ANA, or thyroid. However, I did have c4a of 28,000 at one point and if i had taken gcmaf at that point, I'm sure the results would've been downright disastrous.
Peterson said some time ago that he didn't want to use gcmaf because it caused autoimmune issues. He has been right about more things than any ME/CFS doctor I know. He recently said he thinks the crux of ME/CFS is still the NK cells. This is something I've always strongly believed, and I'm still waiting for someone to publish gcmaf's effect on NK cells.
Maybe because no one really knows what c4a represents, but using that to measure probability of an ugly response could save a lot of time and money. I've never had high TGF-b1, il-6, positive ANA, or thyroid. However, I did have c4a of 28,000 at one point and if i had taken gcmaf at that point, I'm sure the results would've been downright disastrous.
Peterson said some time ago that he didn't want to use gcmaf because it caused autoimmune issues. He has been right about more things than any ME/CFS doctor I know. He recently said he thinks the crux of ME/CFS is still the NK cells. This is something I've always strongly believed, and I'm still waiting for someone to publish gcmaf's effect on NK cells.
mojoey thanks so much for that info, I haven't tried Gcmaf as I've been too ill to get back to Belgium, I had high c4a on testing so maybe it worked out better for me not taking it??? I think after this trial period KdM should now be more able to say which patients would benefit, than giving it as a blanket treatment, as its obvious it isn't the treatment for everyone.
jenbooks
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Hi Rich, thanks for that good summary.
Seems to me the at risk folks might benefit from the Kane protocol (the LPS really mess with the cell membrane) and a fecal transplant, before trying GcMAF.
Seems to me the at risk folks might benefit from the Kane protocol (the LPS really mess with the cell membrane) and a fecal transplant, before trying GcMAF.
thanks for info.
My c4a was also very high.
and my TGF-b1 and il-6 where also to high. (now even higher then before gc maf)
So gc maf is very bad for me????? I never should have taken it from KDM ??
Sushi
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I sent my sample to them about 2 weeks later than you so I guess I will still have to wait. Frustrating, as according to their estimates I should have had it 2 weeks ago and I had to cancel a phone consult with my doc as it wasn't in yet.
Sushi