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NCF's Research Finds Chromosome Damage in Patients Diagnosed with CFS and ME

Discussion in 'General ME/CFS News' started by Ember, Feb 26, 2014.

  1. Ember

    Ember Senior Member

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    By National CFIDS Foundation
    Published: Tuesday, Feb. 25, 2014 - 9:02 am
    Read more articles by National CFIDS Foundation
  2. Ecoclimber

    Ecoclimber Senior Member

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    Mercer Island Wa
    FYI: I see no published peer review article in any medical journal concerning this breakthrough. Research findings are published in scientific and medical journals not by a patient 'advocacy' organization. Over the years and in past publications, this organization has proclaimed they found the cause for ME/CFS which later proved to be false. I could not find any research papers by Dr. Heng on Gulf War Veterans and chromsome damage. This organization is not to be confused with CFIDS of America or CAA as some people call it.

    I am beginning to have problems with organizations and researchers who make unsubstantiated claims on the cause of ME/CFS without first publishing their work in established and legitimate peer review medical and scientific research journals. It gives false hope to the patient community.

    This paper refutes chromosome damage in Gulf War Veterans.

    Mutat Res. 2013 Oct 9;757(2):132-9. doi: 10.1016/j.mrgentox.2013.07.008. Epub 2013 Aug 8.
    Long-term exposure to depleted uranium in Gulf-War veterans does not induce chromosome aberrations in peripheral blood lymphocytes.
    Bakhmutsky MV1, Squibb K, McDiarmid M, Oliver M, Tucker JD.
    Author information
    Abstract

    Depleted uranium (DU) is a high-density heavy metal that has been used in munitions since the 1991 Gulf War. DU is weakly radioactive and chemically toxic, and long-term exposure may cause adverse health effects.

    This study evaluates genotoxic effects of exposure to DU by measuring chromosome damage in peripheral blood lymphocytes with fluorescence in situ hybridization whole-chromosome painting.

    Study participants are Gulf War-I Veterans with embedded DU fragments and/or inhalation exposure due to involvement in friendly-fire incidents; they are enrolled in a long-term health surveillance program at the Baltimore Veterans Administration Medical Cente
    r.

    Blood was drawn from 35 exposed male veterans aged 39 to 62 years. Chromosomes 1, 2, and 4 were painted red and chromosomes 3, 5, and 6 were simultaneously labeled green. At least 1800 metaphase cells per subject were scored. Univariate regression analyses were performed to evaluate the effects of log(urine uranium), age at time of blood draw, log(lifetime X-rays), pack-years smoked and alcohol use, against frequencies of cells with translocated chromosomes, dicentrics, acentric fragments, color junctions and abnormal cells. No significant relationships were observed between any cytogenetic endpoint and log(urine uranium) levels, smoking, or log(lifetime X-rays). Age at the time of blood draw showed significant relationships with all endpoints except for cells with acentric fragments. Translocation frequencies in these Veterans were all well within the normal range of published values for healthy control subjects from around the world.
    These results indicate that chronic exposure to DU does not induce significant levels of chromosome damage in these Veterans.
    Last edited: Feb 26, 2014
    Cheshire, snowathlete and Firestormm like this.
  3. dasiymay

    dasiymay Senior Member

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    From Wayne State Uni website, info on Dr Heng's work including this para on CFS:

    http://pathology.med.wayne.edu/profile.php?id=45025

    In addition, we have linked elevated genome alterations to Chronic Fatigue Syndrome (CFS) patients based on 15 patients and 20 controls. We anticipate that this report will be well received by the medical community (manuscript in preparation), as in spite of decades’ of research on this illness, there is still no reliable diagnostic genetic marker for CFS. We believe that genome instability will serve as a clinical marker for CFS.
    SickOfSickness, snowathlete and Ember like this.
  4. dasiymay

    dasiymay Senior Member

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    Ember likes this.
  5. Ember

    Ember Senior Member

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    After posting this thread, I suggested that it might be moved to "General ME/CFS News," but the moderators must have decided to leave it here. Notice too "Chromosomal instability (CIN): what it is and why it is crucial to cancer evolution" by Henry H. Heng, et al.

    Edit: The thread has been moved now. (Thanks!:))
    Last edited: Feb 26, 2014
  6. dasiymay

    dasiymay Senior Member

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    http://phoenixrising.me/archives/9397

    Unstable At the Core? NCF Funds Cutting-Edge ME/CFS Gene Study

    APRIL 16, 2012

    Posted by Cort Johnson

    [​IMG]In a year of intriguing studies this is one of the more intriguing. Stress has been something of a keynote in CFS research lately and researchers now regularly employ different kinds of stress tests to provoke abnormalities in patients. But does this unusual response to stress make its way all into the DNA of our cells? The National CFIDS Foundation in collaboration with the Nancy Taylor Foundation is betting $133,000 that it does…

    It looks like it might be a good bet. Dr. Henry Heng has been evolving a uique theory of ‘genomic instability’ for over a decade. The theory proposes that random hits to the genome over time powered by cellular stress can derange chromosomes enough to cause complex disorders such as cancer.

    Genomic instability or the inability to duplicate the cells genome properly when cells replicate has been shown to contribute to a large variety of disorders including retinoblastoma, Ataxia telangiectasia, Xedorerma pigmentosum, Nijmegen Break syndrome, Werner syndrome, colon cancer, breast cancer, among many others. Cells that become damaged in this way can exhibit chromosomal

    Gulf War Syndrome Research Opens Up New Ground - A Discovery Channel project finding that five Gulf War Vets exhibited rates of chromosomal damage similar to those found in people with birth defects and cancer prompted the DOD to fund a $900,000 study. (Study results have not been published).

    Uranimum was believed to be the culprit in the Gulf War Vet findings but high rates of cellular stressors, such as oxidative stress, have been found in chronic fatigue syndrome. Viruses, vaccination, environmental stresses (radiation) are known to be able to cause genomic instability but Heng believes all kinds of cellular stressors can cause genomic instability (ie ‘pulverized chromosomes’) in right (wrong) person. Replace the word ‘war’ in the below quote with another stressful situation ‘ infection’ and you might have a nice theory of ME/CFS.

    We propose that under the extreme environment of war, some individuals’ genomes will become increasingly unstable, and war-induced genetic instability will lead to diverse disease traits that can be characterized as GWI..Dr Henry Heng”

    Chromosome ‘pulverization’ refers to a process in which part of a chromosome winds up getting broken apart and then pieced onto the tops of other chromosomes. Pulverization was previously thought due to such stressors as vaccination, defective genes or ‘environmental stresses’ (such as toxins, radiation, etc.) but Heng’s evidence suggests that ordinary cellular stresses can as well.

    Our data suggest that cell death is a highly complex process, and multiple forms of cell death result from a simple response to overwhelming stress(es)..Dr. Henry Heng

    [​IMG]
    Studies suggest that cellular stress protective factors during cell replication called heat shock proteins may be damaged in CFS.

    ME/CFS Link – Heat shock proteins ability to protect chromosomes may play a key role in the fragmentation process. Heat shock proteins help keep chromosomes intact as they become amplified during mitosis; without their protection pieces of chromosomes become detached from each other during this process.

    Heng has linked the reduction of a specific heat shock protein called HSP90 to increased chromosome fragmentation. HSP’s have been studied in ME/CFS. Two French studies (Jammes, 2011/James 2009) found reduced levels of other HSP’s after stress (aerobic exercise) in ME/CFS and a 2007 Canadian study found reduced levels of HSP 90 after exercise.

    Paradigm Changing – Heng’s genomic theory of cancer evolution, published in 2009, is potentially paradigm changing. Heng does not believe that the standard method of targeting specific genes that trigger cancers will tell the tale in cancer and other complex disorders because the cellular damage comes from more or less random hits that disable what he calls ‘genomic networks’.

    ‘Stress’ Again – Cellular stress plays a big role in this theory. Heng believes it causes the genome to start shifting about – patching pieces of chromosomes onto each other – in order to form an optimal response to it. One of the potential results of all this shifting is the formation of cells that shoot out of control; ie become cancerous, which then starts a new search stabiilty….. Heng’s finding indicating that genomic diversity increases rapidly during cancer suggests an almost herauclean effort by the genome to get it under control.

    Because the networks are disabled in some cases by one set of genes and sometimes by other sets, following specific genes is not effective. The key, Heng believes, is in identifying patterns of genome-wide instability….

    A growing body of evidence suggests that no distinguishable pattern can be discerned from single gene studies. Instead, it appears that finding a general mechanism will require us looking to the system as a whole – the genome.” Dr. Henry Heng

    Dr. Heng will be looking at the genome of chronic fatigue syndrome patients to see if their genomes have become ‘unstable’; ie, if in their efforts to fit the stresses they’ve encountered their cells have patched together a new genome. Heng’s theory is a variation at the genomic level on the idea that ME/CFS is a protective state.

    [​IMG]
    Does a changed genomic structure contribute to ME/CFS?

    Conclusion – Heng’s theory is new, the Gulf War Illness study award came just a month ago, and uranium radiation was the suggested stressor there…but it is intriguing and, in its own way, it’s similar to other efforts looking at system stability, not at the gene expression level this time, but at the genome level.

    …the true challenge is to understand the system behavior (stability or instability)…Dr. Henry

    If Heng finds genomic instability the next step might be to find what is triggering the genome to undergo such drastic changes; changes that are dramatic enough to be disabling to the patient, but may reflect an attempt at adaptation at some level.

    The number of cutting-edge studies in ME/CFS belies the poor funding the disorder gets…From the CAA’s KnowledgeBase, Biovista and epigenetics studies to the high tech CFI Lipkin-Hornig and the BSRI CAA/CDC pathogen studies to the Light/Broderick gene expression studies, ME/CFS researchers are taking advantage of the latest technology and the Heng study is another example of that. Heng is no fly-by-night researcher; with over 130 publications to his name he’s has got quite a track record. It’ll be fascinating to see what he comes up with.
    redrachel76 likes this.
  7. redrachel76

    redrachel76 Senior Member

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    Israel
    Recently someone from the NCF told me that their research found no difference between GWI patients and CFS/ME patients.
    I looked up the symptoms of GWI and they were the same as CFS.
    I then looked at some GWI forums they looked exactly like regular CFS/ME forums with many patients who had FMS and IBS too.

    It was interesting to read Cort's interpretation of this. Thanks for posting.
  8. beachlover1957

    beachlover1957

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    Here is my own take on this research for whatever it's worth:
    After doing a little digging, Dr. Heng has a preliminary publication out with regards to some of the
    initial research findings from his grant from the NCF and the NTF. After making a few phone calls,
    I understand that there are more publications coming. Here it an initial one, from Dr. Heng, with a new
    unclassified chromosomal abnormality from the NCF's own patient cohort:
    Karyotype heterogeneity and unclassified chromosomal abnormalities.
    Heng HH1, Liu G, Stevens JB, Abdallah BY, Horne SD, Ye KJ, Bremer SW, Chowdhury SK, Ye CJ.
    Cytogenet Genome Res. 2013;139(3):144-57.
    Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, Mich.
    Abstract
    In a departure from traditional gene-centric thinking with regard to cytogenetics and cytogenomics, the recently introduced genome theory calls upon a re-focusing of our attention on karyotype analyses of disease conditions. Karyotype heterogeneity has been demonstrated to be directly involved in the somatic cell evolution process which is the basis of many common and complex diseases such as cancer. To correctly use karyotype heterogeneity and apply it to monitor system instability, we need to include many seemingly unimportant non-specific chromosomal aberrations into our analysis. Traditionally, cytogenetic analysis has been focused on identifying recurrent types of abnormalities, particularly those that have been linked to specific diseases. In this perspective, drawing on the new framework of 4D-genomics, we will briefly review the importance of studying karyotype heterogeneity. We have also listed a number of overlooked chromosomal aberrations including defective mitotic figures, chromosome fragmentation as well as genome chaos. Finally, we call for the systematic discovery/characterization and classification of karyotype abnormalities in human diseases, as karyotype heterogeneity is the common factor that is essential for somatic cell evolution.

    If you want to read this, it is available here at http://www.karger.com/Article/FullText/348682

    Next, as far as depleted uranium goes, I suggest you look at all the publications from Dr. Allison Miller who is
    a researcher at the Applied Cellular Radiobiology Department Armed Forces Radiobiology Research Institute, Bethesda, MD. This group has many other publications out regarding DU:
    Genomic instability in human osteoblast cells after exposure to depleted uranium: delayed lethality and micronuclei formation.
    Miller AC, Brooks K, Stewart M, Anderson B, Shi L, McClain D, Page N.
    J Environ Radioact. 2003;64(2-3):247-59.
    Applied Cellular Radiobiology Department Armed Forces Radiobiology Research Institute, Bethesda, MD 20889-5603, USA.
    Abstract
    It is known that radiation can induce a transmissible persistent destabilization of the genome. We have established an in vitro cellular model using HOS cells to investigate whether genomic instability plays a role in depleted uranium (DU)-induced effects. Transmissible genomic instability, manifested in the progeny of cells exposed to ionizing radiation, has been characterized by de novo chromosomal aberrations, gene mutations, and an enhanced death rate. Cell lethality and micronuclei formation were measured at various times after exposure to DU, Ni, or gamma radiation. Following a prompt, concentration-dependent acute response for both endpoints, there was de novo genomic instability in progeny cells. Delayed reproductive death was observed for many generations (36 days, 30 population doublings) following exposure to DU, Ni, or gamma radiation. While DU stimulated delayed production of micronuclei up to 36 days after exposure, levels in cells exposed to gamma-radiation or Ni returned to normal after 12 days. There was also a persistent increase in micronuclei in all clones isolated from cells that had been exposed to nontoxic concentrations of DU. While clones isolated from gamma-irradiated cells (at doses equitoxic to metal exposure) generally demonstrated an increase in micronuclei, most clonal progeny of Ni-exposed cells did not. These studies demonstrate that DU exposure in vitro results in genomic instability manifested as delayed reproductive death and micronuclei formation.

    If you would like to look at a different group, then here is another one:
    Radiat Prot Dosimetry. 2003;103(3):211-9.
    Chromosome aberration analysis in peripheral lymphocytes of Gulf War and Balkans War veterans.
    Schröder H, Heimers A, Frentzel-Beyme R, Schott A, Hoffmann W.
    Center of Environmental Research and Technology (UFT), University of Bremen, Leobener Strasse, 28359 Bremen, Germany
    Abstract
    Chromosome aberrations and sister chromatid exchanges (SCEs) were determined in standard peripheral lymphocyte metaphase preparations of 13 British Gulf War veterans, two veterans of the recent war in the Balkans and one veteran of both wars. All 16 volunteers suspect exposures to depleted uranium (DU) while deployed at the two different theatres of war in 1990 and later on. The Bremen laboratory control served as a reference in this study. Compared with this control there was a statistically significant increase in the frequency of dicentric chromosomes (dic) and centric ring chromosomes (cR) in the veterans' group. indicating a previous exposure to ionising radiation. The statistically significant overdispersion of die and cR indicates non-uniform irradiation as would be expected after non-uniform exposure and/or exposure to radiation with a high linear energy transfer (LET). The frequency of SCEs was decreased when compared with the laboratory control.

    Lastly, there is a great deal of information out in peer-reviewed publications that link CFS to radiation exposure.
    Much of this was the result of scientific work and subsequent publications as the result of the Chernobyl disaster.
    Some of this can be read at http://www.ncf-net.org/radiation.htm

    For me, if the NCF or any other group worldwide has identified a "CFS subgroup", then so be it. If this subgroup
    is linked to environmental sources, so what? This research work certainly doesn't take away from any of the other possibilities that are on the scientific table regarding causation. If anything, this work helps to convey the seriousness of this damn disease.
    - Beach

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