Myths and Misinformation
There are NO free trials with Gc-MAF anywhere in the world. If you have been told there are, it is probably not true. Please contact us with the details if you have been offered a free trial and we will verify the information for you.
ELN (European Laboratories of Nutrients) in Bunnik does not produce, sell or offer Gc-MAF to patients. You can get your Nagalase levels tested via them.
Although remaining a marker, Nagalase is almost obsolete when it comes to determining if Gc-MAF therapy is effective for a patient. There are other, more convenient and cheaper (insurance covered) tests that will reveal if Gc-MAF is effective rather quickly.
Nagalase levels should not be a criterium to determine if a patient qualifies for Gc-MAF treatment, overall diagnosis should be. Nagalase is elevated in most cases of severe illness. Please have your physician contact BGLI for more information.
Prices of Gc-MAF at BGLI depend on the quantity ordered. If your physician orders on your behalf and applies Gc-MAF therapy for more patients, he receives a discount which each patient should benefit from.
Some physicians say to their patients that they are ordering Gc-MAF from BGLI, while in fact they have obtained it from an unreliable source. Please contact us if you meant to order from BGLI but are unsure if your doctor uses our product.
You cannot reclaim the cost of Gc-MAF from any health insurance provider anywhere in the world. People who receive Gc-MAF via BGLI can reclaim some of the cost via their tax return; Providing your doctor wrote a prescription, you ordered and paid for the Gc-MAF yourself and you have an invoice from BGLI stating official registration information.
It is an absolute myth that Gc-MAF is safe to use for everyone without close monitoring by a physician. Patients who follow this route are taking a serious health risk, they have no way of determining if Gc-MAF therapy is effective and if something goes wrong, Gc-MAF may be banned for future use in their country.
Please prevent problems and help ensure the availability of Gc-MAF in the future; contact BGLI if you wish to use Gc-MAF in a safe and effective way.
2011 Credits
We would like to express our gratitude to dr. Paul Cheney MD, PhD for using our product GHP (GcMAF) in his study to benefit M.E. patients.
We would like to thank all of dr. Cheney's patients for collaborating in this effort.
Another milestone is set by receiving a Certificate of Analysis, for which we would like to thank the staff at European Laboratory of Nutrients at Bunnik in The Netherlands and Health Diagnostics and Research Institute in New Jersey (US).
Last but not least, thank you to all physicians and clinics working with our product and providing us with feedback for records and product development..
We appreciate all efforts by all parties involved in making GHP (GcMAF) available to patients around the world and are looking forward to our continued collaboration in the New Year.
Sincerely,
BGLI
Certificate of Analysis GHP/GcMAF
Certificate of Analysis GHP/GcMAF d.d. 28 november 2011 
Development of:
- p53 oncogen-suppressor gene-injectables
- RNAi - PCR, including optional IGFBP, GDEPT , ultimately CRAds
- Tumor marker-application, eg.; NaGa-, Cyclin D + E (variations)-, SAP2- & p53-assays
- Artemisinin & transferrin-injectables; (dihydro)artemisinin x (holo)transferrin-tagging-injectables
In production (certified activity & purity):
- Gc-MAF (vitamin D3-binding protein (Gc protein)-derived macrophage activating factor) - GHP
Available in The Netherlands and the US:
- Nagalase testing (please email us for details)
Available in Belgium:
- Vitamin D Receptor Genotyping test (VDR polymorphism) (please email us for details)
GcMAF studies presented at IACFS/ME meetings in Ottawa
December 4th, 2011, published in Public Relations at the Cheney Clinic Website: www.cheneyclinic.com/blog
GcMAF appears to be an effective therapy for well defined CFS patients
At he IACFS/ME meetings in Ottawa, Canada in September, 2011, three studies on GcMAF therapy in CFS cases were presented by Kenny DeMeirleir MD, PhD out of Belgium and by Paul R. Cheney MD, PhD out of NC. GcMAF is a partially deglycosylated vitamin-D binding protein also know as Gc protein. The functional change in the Gc protein caused by serial deglycosylation is known as GcMAF or Gc Macrophage Activating Factor. GcMAF is made naturally in the body under certain conditions of immune activation but can also be made outside the body by chemical or laboratory means and by the use of certain probiotics in a Yogurt-like mixture in your own kitchen.
GcMAF is extremely potent and will at very low concentrations activate, regulate and expand macrophages which are the central processing unit of the immune system and capable of modulating and controlling both the innate and cognate immune systems.
Three GcMAF studies presented in Ottawa showed improvement in CFS symptoms using a similar patient-centered assessment instrument. Dr. DeMeirleir, using an injectable (IV or SQ) chemically derived GcMAF given at 100 ng on a weekly basis, showed at 63% response rate (68/108) over 5-40 weeks of therapy.
Dr. Cheney used a similarly manufactured chemical GcMAF (GHP-GcMAF - BGLI) in 19 patients treated at 100 ng every 5 days over 8 weeks by SL route but he also used, in a separate study, a novel probiotic-based GcMAF given by oral daily route (MAF 314) developed by Prof’s Ruggiero and Pacini out of Florence, Italy. The SL chemical GcMAF demonstrated a response rate of 79% (15/19) over at least 8 weeks while the probiotic-based oral GcMAF (MAF 314) demonstrated a 76% (16/21) response rate over only 28 days. Given the lower numbers and shorter time frames in Dr. Cheney’s two studies, there was likely no significant difference between the three studies in terms of overall response rate in CFS patients.
However, there appeared to be differences in the chemical GcMAF response rate that depended on the patient’s vitamin-D VDR polymorphisms that was not seen in the probiotic GcMAF (MAF 314) and positive response rates were generally seen much quicker in the probiotic GcMAF (MAF 314).
There were mild to moderate side effects seen in all three studies and generally responded to dose reduction as well as other measures. GcMAF, given by a number of different routes, appears to be an effective therapy for well defined CFS patients.
Source: published in Public Relations at the Cheney Clinic Website: www.cheneyclinic.com/blog
Please visit Dr. Cheney's website for more valuable information for CFS (M.E.) patients and immunological research.
Compassionate use of GHP (GcMAF) in CFS (M.E.)
Compassionate Use Treatment of CFS with GHP (GcMAF)
Paul R. Cheney MD, PhD ~~~~ www.cheneyclinic.com
Asheville, North Carolina, US, September 2011
Introduction
GcMAF is a partially deglycosylated vitamin D binding protein (VDBP) also known as Gc protein. The functional change in the Gc protein caused by serial deglycosylation is known as GcMAF. GcMAF is extremely potent and will at very low concentrations activate, regulate and expand macrophages which are the central processing unit of the immune system and capable of modulating and controlling both the innate and cognate immune systems.
Methods
Twenty-five CFS patients meeting the 1994 CDC criteria were selected from a national referral practice and under informed consent were self-treated with a semi-synthetic GcMAF administered by sub-lingual route. Previous reports from clinicians in The Netherlands using this commercial-grade version of human GcMAF suggested significant bioactivity and promising clinical responses in CFS cases in The Netherlands. Patients were monitored for blood chemistry, CBC, active and non-active forms of vitamin D as well as Nagalase activity. VDR polymorphisms determined from restriction enzyme products of BsmI and FokI were determined and a clinical instrument for symptom assessment of the seven key CFS symptoms was used to evaluate patient response. The protocol called for administering initially low doses of GcMAF at 20 ng SL every five days for the first 30 days followed by a q 5 day ramp to 100 ng SL using 20 ng increments. The study length was scheduled for 5-6 months but is being extended on a case-by-case basis.
Results
Results are reported here for those nineteen CFS patients who have received a minimum of two months of sub-lingual GcMAF. 7/19 or 36.8% had a significant to clinically resolved response in at least two of seven critical CFS symptoms and two of those were functional cures at 80 KPS units or better. 4/19 or 21.1% failed to respond at all or even got worse over those same seven key symptoms. The remainder or 42.1% (8/19) had a mild to moderate improvement in two or more significant symptoms. A total of 78.9% (15/19) responded to chemical GcMAF. VDR polymorphism data in 17 of 19 patients are known and the balance pending. Of these 17 with known VDR results, 100% of all non-responders were either BB (50%) or Bb (50%) genotypes. On the other hand, there was only one BB in the best responding group of five or 20% and only two BB’s or 25% in the moderate responders or only three or 23% in the responding group of thirteen who were BB. The bb genotype was 39% in the response group as against 0% in the non-response group. Within the FokI VDR grouping, 25% were an ff in the non-responders as against 36% in the response group. FF appeared to be about equally distributed in all response vs. non-response groupings. In summary, the best genotype to have to avoid nonresponse was a bb. The homozygous mutation BB was uncommon (20%) in the best responders and common in the nonresponders (50%). Analysis of calcitriol levels demonstrated that there were three response patterns to GcMAF that were predictive of clinical response. All those with low to normal calcitriol to start with who then had a modest rise in calcitriol in response to GcMAF responded clinically (6/6). All those whose calcitriol was initially low to normal that did not respond at all to initial doses of GcMAF failed to respond clinically (4/4). In those with elevated initial calcitriol (>68) had a mixed response with 5 of 7 responding and 2 of 7 not responding. Initial D3 levels were variable and did not predict response nor did their response to GcMAF predict response. Nagalase activity was elevated in all study participants (average 3.4, range 1.3-6.5). 87.5% of the patients tested for XMRV were positive (14/16). In all 8 with known response data, Nagalase activity eventually declined with therapy and one patient declined to normal and is one of the recovered patients (KPS > 80).
Conclusions
GcMAF appears to be a relatively benign and generally effective treatment for CFS. Most patients, however, had early though short bouts of what appeared to be exacerbations of CFS symptoms regardless of the eventual outcome. Two patients who were deemed responders developed clinical vitamin D toxicity later in their treatment heralded by a rapid rise in calcitriol above 90 as Nagalase dropped but responded very well to GcMAF dose reduction or elimination with no lasting effect on their previously good responses. Nagalase activity generally fell early on, especially in the best responders and initial calcitriol response was especially predictive of outcome in most patients. VDR genomic data appears to also be a predictor of the relative chance of response vs. non-response to GcMAF. A bb genotype appears to support a response and especially appears to avoid a non-response. BB was relatively common (50%) in non-responders and relatively uncommon in responders (23%).
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