The 12th Invest in ME Research Conference June, 2017, Part 2
MEMum presents the second article in a series of three about the recent 12th Invest In ME International Conference (IIMEC12) in London.
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Chi et al: Metabolic mechanism of a polysaccharide from Schisandra chinensis to relieve CFS

Discussion in 'Latest ME/CFS Research' started by mango, Aug 24, 2016.

  1. mango

    mango Senior Member

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    Metabolic mechanism of a polysaccharide from Schisandra chinensis to relieve chronic fatigue syndrome

    Chi A1, Zhang Y2, Kang Y2, Shen Z2.

    Author information
    1 Laboratory of Nutrition and Hygiene, Shaanxi Normal University, Xi'an 710119, China.
    2 Laboratory of Nutrition and Hygiene, Shaanxi Normal University, Xi'an 710119, China.

    Int J Biol Macromol. 2016 Aug 18. pii: S0141-8130(16)31224-7. doi: 10.1016/j.ijbiomac.2016.08.042.

    Abstract
    Schisandra chinensis fruits are a famous traditional Chinese medicine to treat all kinds of fatigue. This study aimed to investigate the therapeutic effect and metabolic mechanism of a polysaccharide (SCP) from Schisandra chinensis fruits on chronic fatigue syndrome (CFS). SCP was isolated and the physicochemical properties were analyzed. A CFS model of rats was established and the urinary metabonomic studies were performed using gas chromatography time-of-flight mass spectrometry (GC-TOF-MS) in combination with multivariate statistical analysis. The results showed that SCP is a protein-bound polysaccharide. The amino acid composition of SCP consisted of 12 amino acids. The growth and the behaviors of the rats in the CFS model group were worse than those in the control group and improved after SCP treatment. Analysis of the GC-TOF-MS revealed that twelve metabolites were significantly changed, and six metabolites were oppositely and significantly changed after the SCP treatment. The TCA cycle metabolic pathways and the alanine, aspartate and glutamate metabolism were identified as significant metabolic pathways involved with SCP. The therapeutic mechanism of SCP against CFS was partially due to the restoration of these disturbed pathways.

    KEYWORDS: Chronic fatigue syndrome; Metabonomics; Schisandra chinensis
    http://www.ncbi.nlm.nih.gov/pubmed/27545408
     
  2. A.B.

    A.B. Senior Member

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    A rat CFS model. Sounds like total nonsense.
     
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  3. Valentijn

    Valentijn Senior Member

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    Seriously. Did the rat have PEM and OI? How were its little ratty lymph nodes doing? :rofl:

    "We made the critter act fatigued" is not a good model of ME/CFS!
     
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  4. mango

    mango Senior Member

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    Isn't that what the NIH is planning for their new study...?

    ETA: Hmm... or maybe that's something completely different?
     
    Last edited: Aug 24, 2016
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  5. thegodofpleasure

    thegodofpleasure Player in a Greek Tragedy

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    Matlock, Derbyshire, Uk
    I had a look at the full paper.
    They provide a supplementary downloadable .sml file, which supposedly describes "The protocol of CFS model"
    It doesn't work / is illegible in Quicktime player - which is supposed to be the correct app to view .sml files within.

    Unfortunately, I can't upload that type of file here. (I tried)

    This looks very fishy to me, as there is no other way of knowing what their "CFS model" actually is.
     
    Last edited: Aug 24, 2016
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  6. Marky90

    Marky90 Science breeds knowledge, opinion breeds ignorance

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    Good lord..
     
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  7. thegodofpleasure

    thegodofpleasure Player in a Greek Tragedy

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    Just found this on page 10 of the paper:

    "The animals were randomly allocated to Normal control group (10 rats) and CFS model group (20 rats). Based on previous reports [25–28], four methods (restraint-stress, forced exercise, and crowded and noisy environments) were adopted to mimic the multiple-factor pathogenesis of CFS. The rats in the CFS model group were exposed to these conditions for 4 weeks."

    FFS!

    This paper is utter garbage
     
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  8. A.B.

    A.B. Senior Member

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    You mean your CFS didn't start after being chained to a wall, repeatedly made to overexhaust yourself, in a crowded, loud prison? :rolleyes:
     
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  9. sarah darwins

    sarah darwins I told you I was ill

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    Pretty good example of one of the biggest problems we face, though, isn't it. They think they're studying ME/CFS but they're not. THey're studying the effects of constant, abnormal stress which, as one or two people here may have pointed out before, is NOT THE SAME THING.
     
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  10. sarah darwins

    sarah darwins I told you I was ill

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    Actually, mine did, but I prefer not to talk about it.
     
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  11. Valentijn

    Valentijn Senior Member

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    Where do you think I got the photo for my forum avatar? :D
     
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  12. alex3619

    alex3619 Senior Member

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    [Satire] "We painted wooden dummies to look like someone bedbound with CFS. We then tested the properties of special clothing lines. The dummies looked better when dressed with particularly swish gear."

    Rats? Using unvalidated models, even combined, is not the same thing as a real patient. Until we know what the core mechanism is, at a molecular level, such models are more likely to be completely wrong than even partially right. Even with a mechanism that is the same at the molecular level such models are notoriously unreliable. My guess is they are trying to get something that will justify a small human trial.
     
  13. TiredSam

    TiredSam The wise nematode hibernates

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    What I don't understand is why they're working so hard to cure rats and mice. How did they get to jump the queue while we humans have to wait so long?
     
  14. thegodofpleasure

    thegodofpleasure Player in a Greek Tragedy

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  15. thegodofpleasure

    thegodofpleasure Player in a Greek Tragedy

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    Do you recognise yourself in their description on P17 of their fairystory?

    3.3. Behaviour analysis
    Many animal models have been used to study CFS, including mental stimulation, forced exercise, and restraint-stress protocols [33−35]. The required time for CFS model construction is always longer than two weeks [36,37].
    CFS patients always present with behavioral symptoms such as memory deficit, inattention and disinterest in new things, and disappointment or depression in the depressive environment


    Shame they didn't tell that to all those highly motivated pesky activists, who harass the dear researchers, so diligently trying to cure them of their aberrant illness beliefs.
     
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  16. thegodofpleasure

    thegodofpleasure Player in a Greek Tragedy

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    On P20, they further convince themselves that they have created a valid mouse model and that the polysacharide treatment they administered was successful :

    In the OPLS-DA score plots, the CFS control group exhibited a tendency to deviate from the Normal control group, revealing a visible perturbation of the urine metabolic profiles in the CFS model (Fig. 6 A1). These results confirmed that the CFS model was successfully established based on the changes in endogenous metabolites at the physiological level.
    Additionally, the OPLS-DA score plots of the SCP treatment groups were completely separated with the CFS control group (Fig. 6 B1), indicating obvious therapeutic effects of SCP treatment in CFS rats.
     
  17. Sidereal

    Sidereal Senior Member

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    These are valid mouse models of depression, not CFS. I don't know of any mouse model of CFS.
     
  18. TiredSam

    TiredSam The wise nematode hibernates

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    Another bunch of crackpots pretending to do science, trying to build careers without any regard to the potential harm their flawed assumptions may cause to sufferers. There ought to be a law.
     
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  19. Ben H

    Ben H OMF Correspondent

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    The analysis technique of this is actually quite impressive.

    Its just a shame that they went beyond bat crazy in their model of 'inducing' pathogenesis of CFS, and believing it to be a valid representation. There really arnt any words, so I will just use good ol' Keanu to illustrate my reaction:

    image.jpeg


    B
     
    Last edited: Aug 24, 2016
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  20. sdmcvicar

    sdmcvicar

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    As a biochemist whose work (non-CFS related) sits at a similar interface, I find it easy to understand that reviewers of the article would be focused on the bioanalytical techniques used and data collected, and gloss over the animal model. Without understanding the etiology of the disease for at least a subset of CFS/ME patients, some researchers are going to work on trying to produce an animal model that has at least some of the pathophysiology in common with the disease, because it can be done relatively cheaply, and done now. An analogous process generated the experimental autoimmune encephalomyeletis model for multiple sclerosis, which allowed researchers to study the process of neural demyelination, even though in no way could it have been the process by which human beings developed MS.

    Unfortunately, that's a process at least 20 years out of date. We recognize now that these models are pretty useless for any kind of pharmacological intervention. The approach mentioned in @mango 's post is better, but it's completely black box, and there's no guarantee that even a humanized mouse would develop CFS/ME symptoms using this approach. In an ideal world we'd identify susceptibility factors in human patients (for example, if a specific MTHFR mutation was demonstrated to increase likelihood/severity of ME/CFS*), create a transgenic mouse with these mutations, apply a viral insult such as that seen in many acute onset patients, and see the mice develop some of the same symptoms. Unfortunately that outcome is highly unlikely, would require levels of funding not currently available for this research, and is years away from validation.

    Once again we're simply faced with the issue that chronic fatigue syndrome is a terrible name for the disease and it affects researchers thinking and approach to studying this disease, as CFS and chronic fatigue quickly become interchangeable in their minds. These rats are chronically fatigued due to the protocol, and exhibit reduced memory as a result. The authors' methods conform to established research methods for monitoring fatigue (time spent motionless in the tail suspension test) and memory (time spent searching for the platform in the Morris water maze) in rats. It's a false equivalence to CFS/ME, though. Methamphetamine and modafinil would probably have similar results in this model, but aren't effective for symptom control in the bulk of CFS/ME patients.

    My major worry about their results is simply that these kinds of animal models can be self-perpetuating, as their claims that "a rat model of CFS was established" (Conclusion paragraph 1, p. 21), and that there are seven references to rat and mouse "models of CFS" gives a pedigree for future pharmaceutical and nutraceutical studies that also want to use this model to establish "effectiveness in curing CFS". Once it's published, it can be referenced. Once referenced, it can become "the established animal model of CFS" even without validation.

    [*Note: edited to clarify that no specific MTHFR mutation has been identified to be causative for CFS/ME, as per @Valentijn 's post]
     
    Last edited: Aug 25, 2016
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