Breakthrough made in diagnosing CFS

Discussion in 'Fibromyalgia Main Forum' started by TigerLilea, Jan 11, 2010.

  1. TigerLilea

    TigerLilea Active Member

    Another possibility for us? Posted on ProHealth's web-site.

    BREAKING NEWS: Breakthrough made in diagnosing chronic fatigue syndrome, Japanese researchers report
    January 11, 2010

    [Note: The following press release was distributed Jan 11 via from the Japanese news site Daily Yomiuri Shimbun. We have not yet identified a journal article or other publication further detailing the study.*]

    Researchers have discovered a protein in blood that can be used to diagnose chronic fatigue syndrome, a breakthrough that could help detect the ailment during physical checkups.

    There are diagnostic criteria for chronic fatigue syndrome - a disorder involving extreme fatigue of unknown cause that continues for at least six months - that rely primarily on subjective symptoms, but there have been no objective markers such as blood tests.

    The research team led by Hiroshi Kiyama, a professor of anatomy [in the Graduate School of Medicine] at Osaka City University, examined the intermediate lobes of the pituitary glands of rats in which they induced extreme fatigue by making them exercise for five consecutive days. They found that the lobes excreted extraordinarily high amounts of a protein called alpha-MSH and that alpha-MSH levels in the animals' blood also increased.

    The neurotransmitter dopamine inhibits the secretion of alpha-MSH, but the rats' ability to produce dopamine declined as their fatigue grew.

    The group also tested the levels of alpha-MSH in the blood of 57 people diagnosed with chronic fatigue syndrome and the blood of 30 healthy people.

    The average level among the 37 people who had been diagnosed with chronic fatigue syndrome less than five years before was about 50 percent higher than in the healthy people.

    Source: Daily Yomiuri Shimbun (Japan) press release Jan 11, 2009

    * For abstracts of past reports by Hirosi Kiyama and colleagues involving alpha-MSH, see

  2. TeaBisqit

    TeaBisqit Member

    It's so good to see articles with real biomarkers.
  3. mbofov

    mbofov Active Member

    There are many others, they've just been ignored by the medical powers that be, including our bodies' response to exertion being studied at the Pacific Fatigue Lab at the University of the Pacific at Stockton, California.

    Anyways, another biomarker is good, another piece of the puzzle - thanks for posting!

  4. karynwolfe

    karynwolfe New Member

    Thanks for sharing, TigerLilea

    All I see that they've shown, is there is a test for showing how fatigued people are... Chronic fatigue is a symptom of HUNDREDS of diseases, and I'm sure they'd show the same results in things like MS and Fibromyalgia, if extraordinary fatigue is all they're testing for...? We need a test for our neuroimmune disease, not our fatigue.

    Don't want to burst any bubbles but I just don't see the point in this... Sigh!

    At least they're thinking of us?
  5. UsedtobePerkyTina

    UsedtobePerkyTina New Member

    Agreed Karyn. They found out what it looks like biologically when someone is fatigued from exercise and then tested to see if they see it in CFS patients. Well, they did. So they can measure fatigue, doesn't mean they can identify the illness we call CFS. What if someone works 12 hours a day three days in a row, then next day goes to the doctor's office?

    I wish we would hear more about the Sakudo test, which I thought was very promising.

    By the way, does anyone know how the Japanese define CFS? I read a lot about UK, US, Canadian, etc., but by what criteria do Japanese doctors diagnose CFS?

  6. karynwolfe

    karynwolfe New Member

    Well I know the Japanese call it "Low Natural Killer Syndrome"...
  7. Lono83

    Lono83 New Member

    This is another confusing CFS/ME finding. A fair number of people (myself included) have incredibly low levels of alpha-MSH - the exact opposite of the finding here.

    The test in the US for this is easy to get and should be covered by insurance. The test is MSH from LabCorp (test # 010421). A couple of additional things to note about MSH, it's incredibly important-- it assists with sleep regulation, inflammation, digestion, pain perception and a host of other things that affect people with CFS/ME & Fibro.

    Also, note that normal values for MSH are 35-81.
  8. SnooZQ

    SnooZQ New Member

    Lono, I'm wondering how you are treating the low MSH? Is it available as a medication, or is there some sort of MSH agonist available? BR>


    Dr. Schaller finds low aMSH in chronic fatigue, esp. CFS associated with mold exposure.

    With many natural body hormones, enzymes, neurotransmitters and other compounds, symptoms are experienced at levels beyond either end of normal range. For example, insulin or dopamine or gastric secretions -- having too much or too little -- either one -- makes mischief.

    But it's also possible, when there are 3rd party reports/interpretations of research, that perhaps info got mixed up.

    A direct link to the abstract on PubMed follows. If it doesn't work, it can be pulled up on G Scholar using search terms "Hiroshi Kiyama" "MSH"

    Chronic stress elicits prolonged activation of ?-MSH secretion and subsequent degeneration of melanotroph

    IMO the interpretation posted at the beginning of this thread doesn't tell the whole story. The way I read it, initially, when stressed, those lab rats did have increased aMSH related to increased melanotroph size. But as stress became chronic, the melanotrophs degenerated.

    The abstract does not specify the aMSH output from degenerated melanotrophs, but IMO it stands to reason that if aMSH output is high when melanotrophs are hyperfunctioning, then likely aMSH output crashes when the melanotrophs degenerate.

    What do you think?

    Best wishes.

    [This Message was Edited on 01/13/2010]
  9. Lono83

    Lono83 New Member

    MSH is not allowed to be prescribed in the US (I'm not sure about it's status in other countries). The biggest problem is that few pharma companies are interested in it b/c you can't patent natural-occurring neuropeptides, like MSH.

    Dr. Ritchie Shoemaker has had some luck with treating folks with low MSH, but my understanding is that instead of being able to use a targeted therapy (like prescribing MSH) the current treatments are much less direct.

    I haven't had any luck raising my MSH levels unfortunately, but I'm very interested in any possible treatments b/c I believe it would make a big difference in my health.

    The end of this article, details Dr. Shoemaker's current treatment regimen. I've heard about some people who have gotten much better following treatments like this, but I've also heard about a number of folks who have tried it and haven't really improved, but interestingly as Shoemaker mentions in this article, the people who remain ill all have low MSH and VIP (vasoactive intestinal peptide):

    Shoemaker's treatment regimen:

    "Treatment of this complex syndrome to date involves sequential (1) removal from exposure; (2) correction of toxin carriage, using VCS monitoring to assess endpoints; (3) eradication of biofilm-forming MARCoNS; (4) correction of elevated MMP9; (5) correction of ADH/osmolality; (6) correction of low VEGF; (7) correction of elevated C4a (8) reduction of elevated TGF beta-1 and (9) replacement of low VIP. Each of these steps using FDA-approved medications is available to practicing physicians. "

  10. SnooZQ

    SnooZQ New Member

    "Afamelanotide is a man-made drug being studied for use as a preventative medication for EPP sufferers. It is a synthetically produced analogue of human alpha melanocyte stimulating hormone (alpha-MSH) and is not yet available on the market."

    Afamelanotide was recruiting for Phase III Confirmatory testing as of Sept./09, for EPP -- a type of porphyria characterized by low alpha MSH.

    The fact that aMSH is low in porphyria -- which is likely vastly underdiagnosed (at least 8 diff types) -- make me wonder about those of us with CFS & "chemical sensitivity."

    Zengan is conducting alpha MSH peptide product testing for celiac disease and also for candida vaginitis.

    There is also some buzz about pharma being interested in alpha MSH for obesity issues -- but of course they will try to tweak their product to produce a patentable analogue vs. bio-identical.


    Currently available aMSH analogues are Melanotan I & II, injections to help speed suntanning. Look them up -- they aren't without side effects.

    Apparently people in the US are using the Melanotan. (It's officially available for research purposes, but various blogs describe what could only be construed as "personal research.")


    One thing I don't quite understand -- why do you say that alpha MSH isn't allowed to be Rxd in the USA? If it were available as a bio-identical, why would it not be allowed to be RXd? Other bio-identicals are. It's not an addictive controlled substance.

    I THINK WE SHOULD BESEECH THE BIG ONLINE COMPOUNDING PHARMACIES TO SEE IF THEY COULD PRODUCE A BIO-IDENTICAL. It's not the sort of thing that Big Pharma will find profitable, but bio-identicals have become the bread & butter of compounders.

    What do you think?
    [This Message was Edited on 01/13/2010]
  11. Lono83

    Lono83 New Member

    MSH has like fifteen different functions/effects. My understanding is that the MSH analogues generally only correspond to a portion (usually one portion) of the toal functions/effects. The two areas where I believe there is the most interest in MSH is in regards to metabolism (there are hopes that it might be an effective weight loss treatment) and libido. Neither of which would help CFS/ME folks that much.

    The reason pharma companies are most interested in MSH analogues is because they can patent an analogue, but if there is a demand pharma companies are willing to look into producing an analogue that is "bio-identical".

    For example, my understanding is that the vasoactive intestinal peptide (VIP) medicine Aviptadil is an analogue but performs all the same functions as VIP, which is good because VIP also does many, many different things (affects sleep, is an anti-inflammatory, has positive effects on digestion, cardiovascular functions, etc., etc.). And many folks who have low MSH, also have low VIP.
  12. richvank

    richvank New Member

    Hi, all.

    The results of this rat study in terms of alpha-MSH are opposite to what several physicians in the U.S. have found in tests on their human CFS patients. As has been noted here already, alpha-MSH has been found to decrease, rather than increase, in CFS. Dr. Ritchie Shoemaker has a very large data base of people who showed low MSH.

    I think the conclusion is that very tired normal rats are not a good model for PWCs.

    The Japanese news report on this study mentioned that there had been measurements of alpha-MSH in humans with CFS, and that it was found to be increased. This was not mentioned in the actual paper on the rat study. I think we have to wonder whether these folks actually had CFS, or whether they were just very tired, like the rats in the study.

    Best regards,

  13. Lono83

    Lono83 New Member

    Though the questions these researchers are asking don't completely track with the evidence that many CFSers have low MSH, I still think there are several encouraging things here.

    They report that in the rats they studied there was destruction of the melanotroph (where alpha-MSH is produced in the pituitary gland).

    "The present study also suggests that prolonged hyperactivation of endocrine cells could lead to disorder of secretion mechanisms and eventual degeneration."


    "Although we can not imply the function of alpha-MSH; whether it serves as an anti-fatigue or pro-fatigue hormone, further analysis would provide new function of alpha-MSH and clues for the diagnosis and treatment of both acute and chronic fatigue-associated disorders."

    I agree with Richvank that these scientists are probably not asking the "right questions" at the moment, but I am encouraged that they're interested in alpha-MSH in regards to CFS-like symptoms. There are many of us who could really benefit from some research being done in this area.

    In the scholarly paper, "Exposure to Interior Environments of Water-Damaged Buildings Causes a CFS-like Illness in Pediatric Patients: a Case/Control Study," Ritchie Shoemaker says:

    "Absence of regulation of innate immune inflammatory responses has not been evaluated systematically in CFS, but given the importance of neuropeptide regulation, levels of MSH, and possibly vasoactive intestinal polypeptide (VIP) as well may be important in revealing the mechanism of diversity of symptom development after similar illness. . ."
  14. richvank

    richvank New Member

    Hi, Lono83.

    Thanks for your comments.

    I agree that MSH is a good thing to look at.

    I saw that part about the melanotrophs dying, too. Maybe if they had gone beyond 5 days, they would have seen a drop in MSH. They reported that the rats would be dead if they ran for 7 days, though. I'm not convinced that the drop in MSH observed in PWCs is due to die-off of these cells, though.

    I'm aware of Dr. Shoemaker's work, and in fact have been in contact with him yesterday and today about the rat paper. Neither of us believes that intense acute exercise in normal, healthy rats is a good model for CFS in humans. Dr. Shoemaker has a hypothesis to explain the drop in MSH in CFS. I have another one, and we are kicking them around.

    Thanks again.

  15. Lono83

    Lono83 New Member

    I'm really glad that you and Dr. Shoemaker are both working on theories to explain persistently low MSH in many CFSers. I really hope some scientists also start doing some research in this area too. There are several researchers in Spain and Argentina, such as Elena Gonzalez-Rey and Mario Delgado, who have done some great work documenting the many important functions of alpha-MSH. But I don't know of anyone at major US research institutions who is working on this problem.

    Sharon Wardlaw at Columbia University has received some research grants to study MSH but she seems to only be interested it's possible benefits for weight loss, which wouldn't be that helpful for the CFS/ME population.

    Rich, one other thing I was wondering about. In your experience, what percent of CFSers have persistently low MSH? It's definitely not a majority, but it seems to be a significant subset.