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.