Review: 'Through the Shadowlands’ describes Julie Rehmeyer's ME/CFS Odyssey
I should note at the outset that this review is based on an audio version of the galleys and the epilogue from the finished work. Julie Rehmeyer sent me the final version as a PDF, but for some reason my text to voice software (Kurzweil) had issues with it. I understand that it is...
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Cortene Peptide for MECFS? "Curative"?!

Discussion in 'Latest ME/CFS Research' started by Ema, Dec 22, 2017.

  1. CFS_Kristin

    CFS_Kristin Senior Member

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  2. junkcrap50

    junkcrap50 Senior Member

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    What's the big deal if it is Urocortin II? I don't understand the significance. Has Urocortin II already been studied? Tried on CFS? What's the significance of Urocortin II and it being Cortene 38?
     
  3. Sushi

    Sushi Moderation Resource Albuquerque

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    Quoting the blog:
    I'm a bit troubled as these are not universal symptoms and in fact many of us don't fit this profile very well. While many patients have high levels of norepinephrine (I am the opposite), I think most have low cortisol--at least in the morning. And many of us have low heart rates except in the cases of POTS patients where the HR jumps in response to standing, whether or not it was low while sitting or reclined. They don't indicate "how" urine production is affected but that would be interesting to know as some of us know that our urine production is higher than normal. There has been a lot of discussion as to whether we have diabetes insipidus as part of our profile.
     
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  4. Mary

    Mary Moderator

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    Cortene posits that elevated levels of serotonin are responsible for many/most ME/CFS symptoms, and their proposed treatment is a 38-amino acid peptide. I'm wondering how, if at all, this would relate to this article: http://www.ncf-net.org/forum/Fword.htm which talks about elevated levels of tryptophan (which is needed to synthesize serotonin) causing something called "central fatigue" and how a remedy for central fatigue is BCAAs. The article also mentions a compound called BCH which is supposed to accomplish the same thing.

    Any ideas you brilliant scientists out there (which I am most definitely not!)? @Hip? Also, I saw an older post of yours recently where you tried leucine and said it didn't help you. It might be worth a try to take the full complement of BCAAs, including valine and isoleucine, as well as leucine.

    I've posted several times about BCAAs and how they cut my PEM recovery dramatically; but unfortunately they don't prevent PEM from occurring to begin with.
     
    Last edited: Mar 18, 2018
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  5. Ema

    Ema Senior Member

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    BCH is 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid.
     
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  6. neweimear

    neweimear Senior Member

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    Who is hopeful?
     
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  7. Vicki Cole

    Vicki Cole Senior Member

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    I want to be, but i am equally very scared to be... I dare not allow myself to think too much about - it is my/our finest dream to be well again. Such a gift it would be. But also devastating if i invest too much hope. It's awful how this illness makes cynics of us. Cynics with a secret hope deep inside all of us though.
    I would love to know what Ron and the omf thinks of it.
     
    neweimear likes this.
  8. Cort

    Cort Phoenix Rising Founder

    The heart rate situation is complicated - my understanding is that we have higher than normal heart rates during sleep and at rest and lower than normal heart rates during exercise (chronotropic incompetence).

    I believe Cortene believes that higher cortisol earlier in the disease lead to lower cortisol later.

    Because the initial jolt or trauma or infection or whatever may over turn into something else over time I don't know how clearly it should reflect ME/CFS. The idea that there's high cortisol early in the disease and low cortisol later has been floating around for quite some time. I don't think it's ever been tested though. It would be fascinating to find out.

    CT38 is a big experiment. It's a very interesting and totally untried hypothesis and drug. I don't have a clue how it will turn out.
     
    Last edited: Mar 19, 2018
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  9. Cort

    Cort Phoenix Rising Founder

    I think maybe cautious hope is appropriate. I keep coming back to Ron Davis's comment about how complex the body is. It's dauntingly complex and plenty of time drugs that seem like they should work don't. I think it would take a bit of luck for a new drug based on a hypothesis to works AND it's certainly possible that it will,.

    These guys do seem to be real sharp! If they think it has a good enough chance to spend a couple of years working on it full time, that's pretty good.

    There's some animal data and some human data but it's limited; the drug is not being used in humans - so we don't have data there - and it's certainly never been applied to someone with ME/CFS. I think its experimental in the true sense of the word. Crossing fingers time :)
     
    Last edited: Mar 19, 2018
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  10. Cort

    Cort Phoenix Rising Founder

    I think there are some big differences. Antidepressants can have a very wide mode of action while Cortene is much more targeted. Plus SSRI's attempt to boost serotoniin levels and CT38 seeks to reduce them. Finally the antidpressants are reuptake inhibitors while Cortene is attempting to target one receptor in the brain.

    This article does propose developing CRF1 antagonists for use in depression but also suggests that they have a different mode of action

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1525061/

    An alternative approach to antidepressant drug development targets the CRF receptor."
     
  11. Cort

    Cort Phoenix Rising Founder

    Must be another breakthrough! We could use as many as possible. I was communicating with someone about Dr. Chia. For some reason I was really surprised at how inventive he was and how willing he was to try new things. I thought that was encouraging.

    They are three LONG blogs! :)
     
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  12. Cort

    Cort Phoenix Rising Founder

    Mifepristone! We're going to hear more about that....(not from Cortene)....Sorry to be a tease but I don't know if the information is out or if the researcher is ready to have it out but we're definitely going to hear about Mifepristone. I wrote a blog on it years ago because of its natural killer cell enhancing activities. I thought it was a really interesting drug.

    https://www.healthrising.org/blog/2...al-killer-cell-drug-chronic-fatigue-syndrome/


     
    Hip likes this.
  13. Cort

    Cort Phoenix Rising Founder

    If it works well it should be speeded up. That said it will probably take far longer than any of us would want.
    I really apologize for not communicating during the delay. For some reason I didn't think of just posting something on Facebook and explain what was going on or coming on here (I just discovered this thread). I was just focused on completing the blog. Trying to get caught up...
     
    Last edited: Mar 19, 2018
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  14. Cort

    Cort Phoenix Rising Founder

    Someone asked if the trial is fully funded. It is....
     
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  15. nanonug

    nanonug Senior Member

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    So I guess "CT38 might be curative" is no hype at all, then.
     
  16. Cort

    Cort Phoenix Rising Founder

    I think the blogs clearly state that the drug is highly experimental and that we don't know what will happen and I've made that point many, many times in the comments. In fact, I've made a point of it.

    That doesn't preclude Cortene from possibly being curative if their hypothesis is correct. I don't see a disconnect between the two.

    Cortene is not saying this drug will work. They're asserting it's worth a shot.
     
  17. GodGenghis

    GodGenghis

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    @Cort , would it be correct to say that another one of the big differences between SSRI's and CT38 is that SSRI's seek to ameliorate depression by moderately increasing serotonin via blocking its reuptake, whereas CT 38 - being an CRF2 agonist - seeks to spike serotinin much higher in an effort to trip the desensitized 5HT1A auto-receptors, which are responsible for causing the CRF2 receptors to internalize, thereby turning off ME/CFS. This would explain why lower doses of CT38 cause 'ME/CFS-like' symptoms, but higher doses would theoretically turn them off.
     
    Last edited: Mar 19, 2018
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  18. Vicki Cole

    Vicki Cole Senior Member

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    It's really very exciting - I can't help but think that something will show from this...
     
  19. Sushi

    Sushi Moderation Resource Albuquerque

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    The spread among individuals makes it hard to know. I have tracked my HR closely day and night so I know what is happening and I may be an outlier (very long term ME/CFS). My HR is low during the day and about 6 beats lower at night. During exercise? Well that is complicated by the POTS response.
    Of course we were never tracking our cortisol in the early stages--at least if we have been sick for decades.
     
  20. Cort

    Cort Phoenix Rising Founder

    It should be lower at night -that's to be expected - but still higher than normal. It's the odd pattern of arousal when arousal shouldn't be there and depletion when the system should be aroused.

    Acta Paediatr. 2011 Feb;100(2):289-92. doi: 10.1111/j.1651-2227.2010.02073.x. Epub 2010 Nov 17.
    Elevated nocturnal blood pressure and heart rate in adolescent chronic fatigue syndrome.
    Hurum H1, Sulheim D, Thaulow E, Wyller VB.
    Author information

    Abstract
    AIM:
    To compare ambulatory recordings of heart rate (HR) and blood pressure in adolescents with chronic fatigue syndrome (CFS) and healthy controls. We hypothesized both HR and blood pressure to be elevated among CFS patients.

    METHODS:
    Forty-four CFS patients aged 12-18 years were recruited from our paediatric outpatient clinic. The controls were 52 healthy adolescents having similar distribution of age and gender. 24-h ambulatory blood pressure and HR were recorded using a validated, portable oscillometric device.

    RESULTS:
    At night (sleep), HR, mean arterial blood pressure and diastolic blood pressure were significantly higher in CFS patients as compared with controls (p < 0.01). During daytime, HR was significantly higher among CFS patients (p < 0.05), whereas blood pressures were equal among the two groups.

    CONCLUSIONS:
    The findings support previous experimental evidence of sympathetic predominance of cardiovascular control in adolescent CFS patients. Also, the findings prompt increased focus on cardiovascular risk assessment and suggest a possible target for therapeutic intervention.

    I actually found another study with lower heart rate during sleep (lol)
     
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