Preliminary news from Lipkin & co

[halcyon]

This is also a good point. It would have been better if the outbreak cases of ME were seperated out from the sporadic cases.

According to Ramsay and others there isn't really a discernible difference between the two in terms of clinical appearance. Separating sudden onset from insidious onset might be more interesting.

 

[msf]

Yes, I think they should do that too.

There might not be a difference in clinical appearance, but there may well be one in terms of biomarkers.

 

[msf]

You're getting world-class research, and this is not good enough for you? No one can define the perfect entry criteria at this point.

Who said it wasn´t good enough for me? I was just pointing out some possible problems with the study that apply to most of the other ME studies too, I thought that was allowed on this forum.

 

[lauluce]

I've got an important question, excuse if the answer is already in the forum: Has the microbiome discovery project study, which needed to reach approximately 1.4 million dollars already started now that it reached its funding goal, or if not, when is it going to start? Thank you!
THIS ONE:
https://twitter.com/MicrobeProject?refsrc=email

 

[Bob]

I've got an important question, excuse if the answer is already in the forum: Has the microbiome discovery project study, which needed to reach approximately 1.4 million dollars already started now that it reached its funding goal, or if not, when is it going to start? Thank you!
THIS ONE:
https://twitter.com/MicrobeProject?refsrc=email

https://twitter.com/i/web/status/685209146560495617

 

[lauluce]

https://twitter.com/i/web/status/685209146560495617

oh! I had already read that, but I misunderstood what "pressing forward" meant, english is not my primary language

 

[Bob]

oh! I had already read that, but I misunderstood what "pressing forward" meant, english is not my primary language

I see why you would misunderstand it.

 

[adreno]

Back to guessing: a metabolite, connected to fungi and the gut, looked at before but never given much attention, and capable of precipitating the symptoms of ME/CFS? I'm guessing acetaldehyde.

 

[Gijs]

I can not understand what a start with a viral or bacterial infection has to do with an intestinal problem. unless you've had an intestinal flu. Then there must be something changes that keeps the (immunological?) disease in progress. Or ME is primarily a metabolic disease. Anyway Lipkin has found something very significant. I look forward to his publication.

 

[A.B.]

I can not understand what a start with a viral or bacterial infection has to do with an intestinal problem. unless you've had an intestinal flu.

I had a colonscopy to rule out other problems. A week before the procedure I had the flu. They could still see the effects of the infection in gut tissue sample. I wouldn't have described that flu as gut flu if asked about it. The virus must have been in a lot of places.

 

[ScottTriGuy]

I had a colonscopy to rule out other problems. A week before the procedure I had the flu. They could still see the effects of the infection in gut tissue sample. I wouldn't have described that flu as gut flu if asked about it. The virus must have been in a lot of places.

Curious (as I'm having a colonoscopy in a few days), how do they know the effects they saw in your gut tissue sample was not from ME?

 

[Antares in NYC]

Back to guessing: a metabolite, connected to fungi and the gut, looked at before but never given much attention, and capable of precipitating the symptoms of ME/CFS? I'm guessing acetaldehyde.

It wouldn't surprise me, @adreno. My brainfog and cognitive issues feel like a never-ending hangover.

 

[Rick Sanchez]

It wouldn't surprise me, @adreno. My brainfog and cognitive issues feel like a never-ending hangover.

CFS does really feel like a perpetual hangover in a lot of ways.

 

[daisybell]

CFS does really feel like a perpetual hangover in a lot of ways.

This was really brought home to me on New Years Day, when the rest of the house looked and felt like I do! It's been so long since I had an actual hangover, I'd forgotten what they are like. For one day my energy was matched by others around me and it was nice for me anyway....

 

[Forbin]

Back to guessing: a metabolite, connected to fungi and the gut, looked at before but never given much attention, and capable of precipitating the symptoms of ME/CFS? I'm guessing acetaldehyde.

It may just be a coincidence, but Ian Lipkin was an author on this 2014 paper which suggested that tropospheric winds, unexpectedly carrying high amounts of candida, were concurrent with outbreaks of Kawasaki Disease in Japan.

Tropospheric winds from northeastern China carry the
etiologic agent of Kawasaki disease from its source to Japan
http://www.pnas.org/content/111/22/7952.abstract

Sampling campaigns over Japan during the KD season detected major differences in the microbiota of the tropospheric aerosols compared with ground aerosols, with the unexpected finding of the Candida species as the dominant fungus from aloft samples (54% of all fungal strains). These results, consistent with the Candida animal model for KD, provide support for the concept and feasibility of a windborne pathogen. A fungal toxin could be pursued as a possible etiologic agent of KD, consistent with an agricultural source, a short incubation time and synchronized outbreaks.

 

[Forbin]

One other guess about metabolites. It might not be a human metabolite. Mycotoxins, for instance, are metabolites produced by fungi / yeasts.

 

[cigana]

One other guess about metabolites. It might not be a human metabolite. Mycotoxins, for instance, are metabolites produced by fungi / yeasts.

I've no doubt mycotoxins play a huge role in MECFS. The suspense is killing me!

 

[acer2000]

I hope he (or someone) figures this out soon. It sucks being sick.

 

[ukxmrv]

I wonder if it will tie in with this really old research finding from Australia? Their research stopped (old memory though) when their lab burned down.

http://www.ncbi.nlm.nih.gov/pubmed/8809350

Preliminary determination of the association between symptom expression and urinary metabolites in subjects with chronic fatigue syndrome.
McGregor NR1, Dunstan RH, Zerbes M, Butt HL, Roberts TK, Klineberg IJ.
Author information
1Collaborative Pain Research Unit, University of Sydney, Australia.
Abstract
Chronic fatigue syndrome (CFS) patients have a urinary metabolite labeled CFSUM1 with increased incidence (P < 0.004) and relative abundance (P < 0.00003). The relative abundances of urinary CFSUM1 and beta-alanine were associated with alterations in metabolite excretion and symptom incidence. In 20 CFS patients and 45 non-CFS subjects, symptom/metabolite associations were investigated by assessing symptom sensitivity and specificity, and symptom indices of total symptom incidence, CFS core symptoms, cognitive, neurological, musculoskeletal, gastrointestinal, infection-related and genitourinary symptom indices, as well as a visual analogue pain scale of average pain intensity. Thirty-three symptoms had significant (P < 0.005) sensitivity and specificity in the CFS patients compared to that in the non-CFS controls. Severe fatigue was the only symptom with 100% sensitivity and specificity and CFSUM1 excretion was the primary metabolite for expression of this symptom. All nine symptom indices had elevated responses in the CFS patients (all P < 0.0000001). Multiple regression analyses indicated that all the symptom indices had significant correlations (R) with changes in the urinary excretion of metabolites (P < 0.0001). CFSUM1 and beta-alanine were the first and second metabolites correlated with the CFS core symptom index and CFSUM1 was primarily associated with infection-related and musculoskeletal indices whereas beta-alanine was primarily associated with gastrointestinal and genitourinary indices. The strong associations of CFSUM1 and beta-alanine with CFS symptom expression provide a molecular basis for developing an objective test for CFS.
PMID: 8809350 [PubMed - indexed for MEDLINE]

 

[adreno]

Clin Chim Acta. 2006 Feb;364(1-2):148-58. Epub 2005 Aug 10.
CFSUM1 and CFSUM2 in urine from patients with chronic fatigue syndrome are methodological artefacts.
Chalmers RA1, Jones MG, Goodwin CS, Amjad S.
Author information

Abstract
McGregor et al. reported increased levels of an unidentified urinary compound (CFSUM1) in patients with chronic fatigue syndrome (CFS), with reduced excretion of another unidentified compound (CFSUM2), and suggested the possibility of chemical or metabolic 'markers' for CFS. The identity of CFSUM1 as reported was erroneous and the identities of these compounds have remained unknown until now. Urine samples were obtained from 30 patients with ME/CFS, 30 age- and sex-matched healthy controls, 20 control patients with depression and 22 control patients with rheumatoid arthritis. Samples were prepared using the published methods of McGregor et al. to produce heptafluorobutyryl-isobutyl derivatives of urinary metabolites. Alternative preparations utilised isopropyl, n-butyl and trifluoroacetyl derivatives. These were separated and identified using gas chromatography-mass spectrometry. CFSUM2 was identified as being partially derivatised [isobutyl ester-mono-heptafluorobutyryl (HFB)] serine. CFSUM1 was identified as partially derivatised pyroglutamic acid, being the isobutyl ester without formation of a HFB derivative. Both CFSUM1 and CFSUM2 are artefacts of the sample preparation procedure and previously reported quantitative abnormalities of CFSUM1 and CFSUM2 in urine from patients with ME/CFS are also artefactual. Pyroglutamic acid may be of primarily dietary origin. The methods used cannot provide reliable qualitative or quantitative data on urinary metabolites. No clinical or biochemical significance can be drawn between these compounds in ME/CFS or any other clinical conditions.

PMID:16095585