Biologisch Medisch Centrum Epe        Arts Paul van Meerendonk
88 genen beinvloeden cvs/me. Deze kunnen worden gegroepeerd in 7 genen groepen.


Biologisch Medisch Centrum
Behandeling CVS/ME
ATP energie
Dr Teitelbaum
Dr Meirleir
Dr Cheney
Arts Paul van Meerendonk

ADP-ATP efficiency
Mitochondrial dysfunction
EPD Desensibilisatie
Cvs en fibromyalgie
CVS ME aantoonbaar
CVS legitiem
Research direction

Virus en DNA
Vitamine B12
Vitamine D
Zware metalen
Dr Kerr
Meetresultaten 1

Meetresultaten 2
Meetresultaten 3
Meetresultaten 4


Seven genomic subtypes of chronic fatigue syndrome/myalgic encephalomyelitis: a detailed analysis of gene networks and clinical phenotypes


Aim: Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a multisystem disease, the pathogenesis of which remains undetermined. The authors have recently reported a study of gene expression that identified differential expression of 88 human genes in patients with CFS/ME. Clustering of quantitative PCR (qPCR) data from patients with CFS/ME revealed seven distinct subtypes with distinct differences in Medical Outcomes Survey Short Form-36 scores, clinical phenotypes and severity.

Methods: In this study, for each CFS/ME subtype, those genes whose expression differed significantly from that of normal blood donors were identified, and then gene interactions, disease associations and molecular and cellular functions of those gene sets were determined. Genomic analysis was then related to clinical data for each CFS/ME subtype.

Results: Genomic analysis revealed some common (neurological, haematological, cancer) and some distinct (metabolic, endocrine, cardiovascular, immunological, inflammatory) disease associations among the subtypes. Subtypes 1, 2 and 7 were the most severe, and subtype 3 was the mildest. Clinical features of each subtype were as follows:

subtype 1 (cognitive, musculoskeletal, sleep, anxiety/depression);
subtype 2 (musculoskeletal, pain, anxiety/depression);
subtype 3 (mild);
subtype 4 (cognitive);
subtype 5 (musculoskeletal, gastrointestinal);
subtype 6 (postexertional);
subtype 7 (pain, infectious, musculoskeletal, sleep, neurological, gastrointestinal, neurocognitive, anxiety/depression).

Conclusion: It was particularly interesting that in the seven genomically derived subtypes there were distinct clinical syndromes, and that those which were most severe were also those with anxiety/depression, as would be expected in a disease with a biological basis.



CFS Genes Research

Scientists have discovered that people with chronic fatigue syndrome (CFS) have certain genes and gene activities that reduce their body’s ability to deal with physical and psychological stress.

“It really is the first credible evidence of a biological basis for chronic fatigue syndrome,” said Dr. Julie Gerberding, director of the Center for Disease Control (CDC) at a press briefing held to announce the results of the largest-ever clinical trial focusing on chronic fatigue syndrome. The research has been published in a set of 14 articles appearing in the April, 2006 issue of the scientific journal Pharmacogenomics.


The Project

The $2 million research project examined 227 people with CFS in Wichita, Kan. Volunteers spent two full days in the hospital undergoing detailed clinical evaluations which included: sleep studies, cognitive functioning measurements, autonomic nervous system evaluations, extensive blood work and genetic testing. The activity levels of 20,000 genes were assessed.

Once the data was gathered, it was turned over to multidisciplinary teams of experts in medicine, molecular biology, epidemiology, genomics, mathematics, engineering and physics to be analyzed and interpreted. Dr. William C. Reeves, principal CFS investigator at the CDC, described the results as “groundbreaking.”


The Results

At the press briefing, Dr. Reeves stated, “For the first time ever, we have documented that people with CFS have certain genes that are related to those parts of brain activity that mediate the stress response. And that they have different gene activity levels…that are related to their body’s ability to adapt to challenges and stresses that occur throughout life, such as infections, injury, trauma or various adverse events.”

Dr. Suzanne Vernon, who oversaw the project along with Dr. Reeves, added, “I think what we’ve been able to show is that CFS is very heterogeneous, it’s not just one thing, so there’s probably not just one diagnostic marker. We’ve actually demonstrated that there are probably at least four or five molecular profiles or groups of people that make up this complex of CFS.”


Why Is This Research So Important?

This study should put to rest any lingering doubts about the validity of CFS. It is a very real illness with an identifiable biologic basis. Besides confirming its validity, Reeves and Vernon agree that having a biologic basis for CFS will also help scientists and researchers identify better ways to diagnose the illness and develop more effective treatments.

Source: Center for Disease Control, Press Briefing on Chronic Fatigue Syndrome, 4/20/06

The VDR Gene

On the patient forum Phoenix Rising, there’s been discussion recently about mutations in the Vitamin D Receptor (VDR) gene predicting patient response to the experimental drug GcMAF.  GcMAF (pronounced G C “MAF”) is believed to work on HIV, cancer and, now, ME/CFS.  These diseases turn off white cells called macrophages whose job is to ingest pathogens, and GcMAF presumably turns macrophages back on. (See YouTube video at the bottom of this post for more information on GcMAF.)

Kenny de Meirleir

Belgian physician Kenny de Meirleir has been using GcMAF, coupled with an old antiviral, the injectable Nexavir (formerly called Kutapressin), on ME/CFS patients and reports that 80 percent are improving. Derived from pig liver, Kutapressin was first used as an anti-inflammatory for skin conditions.  In the 1980s, when doctors began using Kutapressin to treat ME/CFS—the drug is particularly effective against herpes viruses—it acquired the moniker “mini Ampligen.”

cfscentral gene-pool.

Video GcMaf explained