How does GcMaf work?

Sushi

Moderation Resource Albuquerque
Messages
19,953
Location
Albuquerque
I need a very short yet effective explanation of how gcmaf works and I seem to remember reading on this site a very concise and succinct explanation, given by the late great Rich Van K, but I can't now find it, can anyone point me in the right direction please? The gcmaf DN website is suitably vague and other websites such as http://www.nagalasebloodtest.com/more-information-concerning-nagalase.html is too complicated for what I need. Thankyou

This may be too simple! But...GcMAF activates macrophages.

Macrophages function in both non-specific defense (innate immunity) as well as help initiate specific defense mechanisms (adaptive immunity) of vertebrate animals. http://en.wikipedia.org/wiki/Macrophage

In some patients the natural ability to activate macrophages is blocked by high levels of nagalase or, macrophages are being activated by high levels of LPS (Lipopolysaccharides)--which has a negative effect.

Activation of macrophages by bacterial Lipopolysaccharide (LPS)induces transcription of genes that encode for proinflammatory regulators of the immune response. http://www.pnas.org/content/93/7/2774.full.pdf

Injecting macrophage activating factor (GcMAF) bypasses this and, over time, reduces nagalase and enhances the ability of the immune system to fight pathogens. You can find more useful information at GcMAF.eu.

Best,
Sushi
 
Messages
3
This may be too simple! But...GcMAF activates macrophages.



In some patients the natural ability to activate macrophages is blocked by high levels of nagalase or, macrophages are being activated by high levels of LPS (Lipopolysaccharides)--which has a negative effect.



Injecting macrophage activating factor (GcMAF) bypasses this and, over time, reduces nagalase and enhances the ability of the immune system to fight pathogens. You can find more useful information at GcMAF.eu.

Best,
Sushi


I seemed to remember that he said something along the lines of the following:
Pathogens protect themselves from the body's defense system by producing nagalase which deactivates the gcprotein in the liver. This then cannot convert to gcmaf, which is the signalling mechanism for macrophages to attack the incoming viruses. So by giving extra gcmaf this then attacks the pathogens whose nagalase is then reduced to the point where the body can fend for itself.

I really would like to have this right as a friend who is thinking of trying it has asked me how it works and I can't find a suitable explanation for her. Am I on the right track here?
 

Sushi

Moderation Resource Albuquerque
Messages
19,953
Location
Albuquerque
I seemed to remember that he said something along the lines of the following:
Pathogens protect themselves from the body's defense system by producing nagalase which deactivates the gcprotein in the liver. This then cannot convert to gcmaf, which is the signalling mechanism for macrophages to attack the incoming viruses. So by giving extra gcmaf this then attacks the pathogens whose nagalase is then reduced to the point where the body can fend for itself.

I really would like to have this right as a friend who is thinking of trying it has asked me how it works and I can't find a suitable explanation for her. Am I on the right track here?

Yes, this is the right track. If your friend wants to try GcMAF, testing nagalase levels is somewhat predictive of how well GcMAF will work for him/her. It is also important to test things like inflammatory cytokines--especially IL 8-- and things like C4a and sCD14. If these are too high, your friend might have a hard time with GcMAF. Also, be aware that the usual dosing recommendations are suitable for cancer or HIV but are too high for most ME/CFS patients.

Starting on a fairly low dose (that is if other tests support the use of GcMAF)--say 10 - 25 ngs is safer than trying the usual dose of 100 ng, which can cause IRIS. Some find that they can tolerate more, some less.

Here is one quote from Rich where he was summarizing for me, KDM's talk on GcMAF at a 2011 Conference at Mt. Sinae:

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....

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.
Sorry, I do not have a direct link to his comments.

Sushi
 

JalapenoLuv

Senior Member
Messages
299
Location
unknown
No point reinventing the wheel. Gcmaf is replacement therapy for a molecule destroyed by an enzyme that virus's and cancers make. If the molecule isn't present immune system function decreases 40x.

Best info on it.
http://gcmaf.timsmithmd.com/book/book/2/

However, Gcmaf isn't the only player in CFS. Most CFS patients have epstein barr virus (EBV) and some will also have bartonella (mental symptoms-irritability, anxiety, depression). Both of these infections are potent immune blockers.

So if you have these infections and don't have a way to disable the immune blocking the immune system shouldn't be able to recover and the Gcmaf therapy shouldn't work. I think this might account for why some people get better and others don't. This is my experience as a CFS patient with chronic bartonella and EBV.
 
Back