Discussion in 'Other Health News and Research' started by natasa778, Jan 28, 2014.
full article incl interview with Mason
Dec 2013 letter to the editor re the HAART trial
Randomized controlled trial: Pilot study of highly active
antiretroviral therapy for patients with primary biliary cirrhosis.
Available at: http://clinicaltrials.gov/ct2/show/NCT01614405
Has the study still not been published?
Wow! Very impressive study!
The two following quotes are remarkable:
This study has interesting implications for ME/CFS, the autoimmune reactions after decreased immune function, and the viral connection to mitochondrial issues.
When it's all said and done, I am convinced there will find a pathogen at the heart of ME/CFS, likely a difficult enterovirus or even retrovirus. Too bad there's no funding for research on this illness.
For those in the know, could the same techniques like 'representational difference analysis’ be used for ME/CFS? Could samples of spinal fluid, or stomach tissues, be used to confirm a pathogen with these techniques?
Paging @Hip , @alex3619 , @heapsreal , @MeSci
few bits and pieces on PBC:
... It was previously thought to be a rare disease, but more recent studies have shown that it may affect up to 1 in 3–4,000 people; the sex ratio is at least 9:1 (female to male).
It is predominantly seen in middle-aged women. Typical symptoms are fatigue, pruritus (itchy skin), and abdominal pain...
Fatigue, pruritus, and Sjögren's syndrome are more common in women than men, but other signs and symptoms do not differ in the two sexes. PBC is associated with a large variety of other diseases, like arthropathy, CREST syndrome, autoimmune thyroiditis, and so on, which in addition will or will not produce symptoms.
... Most of the patients (>90%) seem to have anti-mitochondrial antibodies (AMAs) against pyruvate dehydrogenase complex (PDC-E2), an enzyme complex that is found in the mitochondria.
Primary biliary cirrhosis is considerably more common in those with gluten sensitive enteropathy than the normal population. In some cases of disease protein expression may cause an immune tolerance failure, as might be the case with gp210 and p62, nuclear pore proteins...
... This research revealed parts of the IL12 signaling cascade, particularly IL12A and IL12RB2 polymorphisms, to be important in the etiology of the disease in addition to the HLA region.
... In 2003 it was reported that an environmental Gram negative alphabacterium — Novosphingobium aromaticivorans was strongly associated with this disease. Subsequent reports appear to have confirmed this finding suggesting an aetiological role for this organism. The mechanism appears to be a cross reaction between the proteins of the bacterium and the mitochondrial proteins of the liver cells. The gene encoding CD101 may also play a role in host susceptibility to this disease.
This all seems very familiar and similar to research in another field of medicine that we're very familiar with. There doesn't seem to be quite such a backlash against these researchers though.
One of the many similarities to ME. I've only recently discovered that retroviruses respond to human sex hormones. (This seemingly exceptionally relevant fact was kept quiet during the XMRV debates. Well, I don't remember it being highlighted anyway.)
Lipkin has quietly mentioned that he has found a retrovirus in his unpublished study of ME patients. And the Paptotka paper (recombination of XMRV1 & XMRV2 in the 22RV1 cell line) has been debunked by its own authors.
But I'm off-topic and it's probably best to keep XMRV discussions on the XMRV threads.
If i temember correctly, PBC is an illness that Prof Newton in Newcastle, England has studied and she has noted similarities with some symptoms experienced by those with PBC and ME CFS.
This just chaps my rear end. So PBC affects "up to 1 in 3-4,000 people", yet it gets the right research and the results to unlock it.
Even by the government's conservative estimates, ME-CFS affects about 1 in 300 Americans, and we get jack.
(PS: I strongly believe the true numbers for ME-CFS must be greater, if cases like myself are common. I spent 14 long years bouncing from doctor to clueless doctor without a diagnosis. I bet there are scores of people trapped in that cycle.)
One of the issues I raised in a thread on enteroviruses, is that most of the pathogens implicated so far in ME have similar lifecycles and tissue tropism (where they like to live), and have been in the human population for a very long time. It is likely they have co-evolved. I wonder if that co-evolution has led to systems of pathogens causing immune dysfunction to create the perfect host, at least perfect for them. If so then looking for the pathogen will be futile, and we will continue to find evidence of multiple pathogens.
Sadly there is more to pbc that sounds very familiar
illness experience of women affected by primary biliary cirrhosis
Natasa778 thank you for starting this thread which has so many interesting finds that make me and many others here on PR salivating and fuming at the same time.
Snowathlete is absolutely right in saying that Prof. Julia Newton in Newcastle has been researching and studying PBC and most importantly seeing many similarities in more than symptoms with ME/Cfs; I think that she'll be participating at this year Invest in ME conference in London.
Sad and funny how many of this important researches in other autoimmune diseases have evident links to ME/Cfs. I don't want to hijack the thread so I stop here .
Pathogens will try anything to win the war.
Yes pathogens (bacteria, viruses and protozoa such as Toxoplasma Gondii) in order to survive and enhance their transmission manipulate their hosts by subverting cell signaling and many other pathways.
It's a fact that many scientists and medical doctors don't keep in mind or just plainly ignore ...
Dr. Andrew Mason's research deserves to be closely followed. There is a very interesting article about his idea of "Challenging the idea of Autoimmunity" on the web site of Alberta Innovates - Health Solutions. Not only is he brilliant but he persevere in translating into clinical studies this paradigm shift about the concept of autoimmunity! Not many clinician/researchers are bold enough and probably independent and influential enough to do that!
The fact that he is in Canada might be an advantage .
Now if I'd only be able to upload the file, I'd be a very happy PWME ...
Please cope with my PR poster rookie skills and the classic late afternoon brain mush
Yes, that is the article.
Of pertaining interest is the book by Noel R. Rose, Y. Shoenfeld and Nancy Agmon Levin titled: Infection and Autoimmunity, you can find it on Google books.
The introduction makes it very clear that autoimmune diseases are due to our bodies responding to infectious agents, in all of them there is inflammation, sometimes systemic, other times specific to an organ.
The logical step is helping the immune system respond to the infectious agent/s attack by modulating it, by enhancing its capabilities and not suppressing it like it's still done as a first line of attack in SLE, MS etc.
Noel R. Rose will be speaking on March 21 at the IACFSME in San Francisco. He is the director of the Center for Autoimmune Disease Research at Johns Hopkins University School of Medicine.
Thats what I do.
I think you bring an important point. Oftentimes I feel that the pathogen(s) at the heart of ME/CFS evolved to indeed debilitate the immune system and perpetuate their survival.
I also have the theory that whatever pathogen did this to us (be it viral or bacterial), may be common among the general population, but only be able to "take over" our immune system under very specific circumstances. For instance, genetic predisposition, situations where the immune system is at its weakest. This would explain the fact that most of us became ill under duress (in my case, I was going through some major stressful situations and then I got a major flu/mono-like illness; I know that my own immune system always tended to weaken when I'm stressed).
This would also explain why researchers like Dr. Lipkin didn't find statistical differences between CFS patients and the control group when he looked for pathogens. In his still unpublished study, he mentioned he found traces of retroviruses, but he also found them in the control group.
Could it be that this retrovirus/enterovirus/pathogen is more common than we think, but it takes a very specific set of circumstances for it to take over the human body?
Just food for thought.
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