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excrement experiment

voner

Senior Member
Messages
592
there's a article in the New Yorker magazine out this week about fecal transplantation. I found the part about Larry Smarr and his exploration of his microbiota in his gut to be pretty interesting.

I also found this FDA spokesman's statement justifying the unusual exception to their standard drug development protocol to be one to keep in mind whenever the FDA is considering treatments for ME/CFS, etc.

"there are often few or no other treatment options for these patients."

at the present time there's no pay wall, so everyone can read this article:

http://www.newyorker.com/magazine/2014/12/01/excrement-experiment
 

voner

Senior Member
Messages
592
as a follow-up to my previous post, I thought many people might be interested in this abstract?/poster from the 2014 IACFSME conference. (which has been posted on Phoenix rising forms before)....

Altered Gut Microbiome in ME/CFS Patients in Comparison to Healthy Controls
Maureen R. Hanson1
, Ludovic Giloteaux1, Julia K. Goodrich2, Susan M. Levine1,3, and Ruth E. Ley1,2
1 Cornell University, Dept. of Molecular Biology and Genetics, Ithaca NY, 2 Cornell University, Dept. of Microbiology, Ithaca NY, 3 Private Practice, New York City

Objectives. As well as the symptoms of fatigue, pain, malaise, immune dysfunction and exercise intolerance, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is associated with a variety of gastrointestinal complaints. In order to investigate the possible basis of this comorbid condition, we undertook a study to determine whether the gut microbiome in a ME/CFS population from the New York City area differs from healthy individuals.

Methods. We characterized the gut microbiota of a cohort of 48 patients with ME/CFS and 36 healthy controls from the New York City region by sequencing amplicons of the V4 region of 16S rRNA genes using the Illumina platform. Of the ME/CFS subjects, average age was 50.6 ± 13.3, 38 were female and 10 were male, while of the controls, average age was 46.5 ± 9.7, 29 were female, 7 were male. All patients fulfilled the Fukuda criteria for diagnosis of CFS. Levels of markers of inflammation, i.e. lipopolysaccharide (LPS), soluble CD14 (sCD14) and lactoferrin (LF) levels were also determined in plasma samples using standard assays.

Results. We obtained an average of 140,000 (± 86,000) high quality reads per sample. In both cases and controls, the most represented phyla were Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria. Comparisons between cases and controls indicated a shift of diversity in the patient cohort. Statistical analysis revealed significant differences between groups, i.e. a reduction in members of the Bacteroidetes and an increase in members of the Firmicutes in the patient population, also reported in Crohn’s disease and acute ulcerative colitis. Specific species, including reduction of butyrate-producer Roseburia faecis (p = 0.001, q = 0.03) and increase of Ruminococcus spp. (p < 0.001, q = 0.004), were detected in subjects with ME/CFS. The amounts of LPS, sCD14 and LF in plasma in our cohort were not statistically different from controls and fell within normal ranges. Our data do not corroborate prior reports of significantly higher levels of Lactonifactor, Alistipes and Enterococci in the feces of patients.

Conclusion. Subjects with ME/CFS in our cohort have a shift in overall microbial composition in comparison to healthy donors, a finding also characteristic of patients with inflammatory bowel disease. Our analyses highlight the contrast between the distribution of anti-inflammatory species, such as Roseburia species, which are more prevalent in healthy individuals, and potentially pro-inflammatory Ruminococcaceae, which are associated with irritable bowel syndrome and found to be more frequent in ME/CFS cases. Despite the differences in gut microbiome, three inflammatory markers did not differ between patients and controls in plasma. Whether deliberate manipulation of the composition of the gut microbiome in ME/CFS patients may ameliorate symptoms in some patients remains to be investigated.

Maureen R. Hanson, Ph.D., Liberty Hyde Bailey Professor, Dept. of Molecular Biology and Genetics, Biotechnology Bldg., Ithaca, NY 14853 USA, mrh5@cornell.edu

comments?
 

snowathlete

Senior Member
Messages
5,374
Location
UK
Given the title I was expecting something about PACE or somesuch. :D

Something I don't understand fully is what makes the reads "high quality" as apposed to other reads they may have got. Anyone know?

I'm always interested in comparing my own results with such studies, though often, as in this case, my results don't match. I had high Roseburia and very low Ruminococcus. The gut biome is complicated and ultimately this is just one slice of data. I suspect that we will only find meaningful answers when we look at all organisms in the gut, not just bacteria but fungi and viruses and so on, and we need studies with greater numbers of patients involved who meet stricter criteria than Fukuda. We're very lucky to have Prof Lipkin keen to do such a good study for us. We just need to help make it happen.
 

aimossy

Senior Member
Messages
1,106
@voner Thank you for putting this up, the New Yorker article is a very entertaining and interesting read...
Maureen Hanson's paper is very interesting as well. Hoping it will be published soon and really hope the Columbia research eventually gets funded and done.

Hanson's paper
"a reduction in members of the Bacteroidetes and an increase in members of the Firmicutes in the patient population, also reported in Crohn’s disease and acute ulcerative colitis."

It is all so interesting and so important and hoping they collect a bucket load of data in the Columbia research so they can start sorting out which findings would be meaningful.