Geplaatst: 22 nov 2011, 15:11
Dit is een verslag van een lezing van dml van afgelopen 20nov over gf maf.
. 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. T
here 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.
. 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. T
here 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.
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