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Has anybody seen this lecture by DR. Kenny De Meirlier at Mt Sinai in NY on 11/2011 ?

Xandoff;250622 said:
Grettings and salutions!
I just found this video of Dr. De Meirleir and I it is very informative. My Doctor just had my blood sent out to Belgium for the Nagalase teast on March 7, 2012 and for my vitamin D levels. I am XMRV positive and just came off 14 months of Valcyte which did help. I have also just titrated my LDN from 1.5 to 3.0 mg with great results.

GcMAF Treatment for ME/CFS
Six presentations were given at the Mt. Sinai ME/CFS Research and Treatment Center conference on Sunday November 20, 2011. Here is a lecture delivered by Dr. Kenny De Meirleir, who practices medicine in Brussels. Dr. De Meirleir has worked with ME/CFS patients for many years and is seen as one of the foremost ME/CFS Clinician/Researchers. Dr. De Meirleir spoke for a half-hour on the compassionate use of GcMAF in this patient population. Dr. De Meirleir will be associated with this new ME/CFS Center at Mt. Sinai- as a clinical consultant.

The video and audio was made by Peter and Nicholas Cairns.



Correct me if I am wrong, but is KDM saying that while Nagalase might not have high ME specificity, it has 97% sensitivity? He also claims it is correlated with severity, and Cheney says the same. These are also correlated with LPS.

These are the main points I took from the presentation:

LPS is high in CFS and highly immunogenic. Even in moderate patients it is fairly high. This implies altered gut biota and increased permiability.

GcMAF is the cleaved form of a vitamin D binding protein Gc.

Vitamin D receptor polymorphisms appear to be associated with patient response to treatment.There are high and low responders based on these polymorphisms. These are used to calibrate initial GcMAF dosage.

Osteoporosis is extremely common.

GcMAF and LPS activate macrophages using different mechanisms.

Soluble CD14 (sCD14) is increased, not just LPS.

LPS stimulation of macrophages leads to increased nitric oxide and peroxynitrite, cholestasis, MRP2 interference and decreased redox control (Alex: related to oxidative stress).

Cholestasis is bile defect resulting in reduced paristalsis, decreased bial and so reduced digestion.

Data on multiple resistance protein 2, not discussed in the presentation, is to be published soon. (Alex: This protein is also linked to bile and digestion.)

GcMAF is stronger than LPS at activating macrophages and at lower concentrations without the LPS side effects.

GcMAF stimulation competes with LPS due to higher affinity, and results in phagocytosis without IL-1 and TNFa.

So competitive inhibition of LPS activation occurs.

Patients use syringe self administration after an initial clinical IV. Dosage initially depends on VDR responder status.

Risk: Risk of increased autoimmunity. No cases of this in 108 patients (and more not analyzed yet).

Exclusions: Patients with increased TGFb, IL6 and high titres ANA or thyroid antibodies, are excluded until more is understood.

Too much GcMAF can induce IRIS if immune system is already heavily damaged. This may be due to high levels of co-infections. (Alex: The implication is that co-infections may need to be treated first.)

20-30% of patients with ME/CFS on GcMAF have IRIS. It must be monitored for.

Prevention of IRIS: broad screening for infection. Now start GcMAF at a low dose, and increase slowly. Example: babesia was found in 7 patients with IRIS.

Result of treating with GcMAF: for most the Nagalase level decreased but the number studied so far is still too small.

Most had improved sleep, fatigue, pain, digestive problems, payback. Some improved on neurocognitive measures and OI.

Further reading (my list): CD14

CD14 is a human receptor for detecting LPS. The soluble form is derived from it.

Of particular interest is CD14 levels do NOT decline fast after the infection is treated. They are persistent.

We are reported to have an extremely high incidence of chronic lymphocytic leukemia. CLL is induced by increased cell survival rates. Elevated CD14 can do this. So one reason we might be at risk of CLL is the elevation of CD14 from elevated LPS.

Human CD14 is abundant in liver hepatocytes and in monocytes (including macrophages). Much of the soluble CD14 may be produced from the liver. This makes sense because the blood from the gut passes through the liver first, and the gut bacteria are the primary source of LPS.

So CD14 can be used as a surrogate marker for LPS but it is more persistent.


Significant Elevation of Serum Soluble CD14 Levels in Patients with Brucellosis


Soluble CD14 Mediates Lipopolysaccharide-Induced Intercellular Adhesion Molecule 1 Expression in Cultured Human Gingival Fibroblasts

(This paper was however focussed on the mouth.)


Soluble CD14 is a novel monocyte-derived survival factor for chronic lymphocytic leukemia cells, which is induced by CLL cells in vitro, and present at abnormally high levels in vivo


Hepatocytes Contribute to Soluble CD14 Production, and CD14 Expression Is Differentially Regulated in Hepatocytes and Monocytes

(This was a mouse study using transgenic human CD14.)
Cort;bt6872 said:
Does anyone know where to get video's of the other lectures?

Thank you all for this, and I too would like to see the other lectures.
Thanks Persimmon for the links. I am also looking for Rich's presentation and I cannot seem to locate it. If anyone has a link, please post here. The conference will be more complete this way.
Best wishes, Helene

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