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CFI Spinal Fluid study from Lipkin and Hornig is out.

Gijs

Senior Member
Messages
691
''am very open to any logical argument and of course also methological critic. If all or most of the spinal fluid samples came from Daniel Paterson's patients, this is indeed selection bias and we have to talk about that. But even then, they found abnormal cytokines levels in exactly this patient group. So do you know, how many samples are from Paterson, the exact numbers? Or is this just speculation?''

This is not entirely correct. In the study they wrote that the average lenght of the illness is 7 years. The immune profile fits within the spinal fluid profile. But they didn't split the group into < 3 years and >3 years because this patiënts are longer sick did they? So when this is the case, you don't know the cytokine profile for the patiënts less then 3 years of the illness isn't it? But even if it fits it doesn' say anything about immune dysfunction.
 

Gijs

Senior Member
Messages
691
This observation comes from the statement of Lipkin and Hornig themselves they were clearly excited to have had access to the 60 cerebrospinal fluid samples from Peterson which they used.
 

lansbergen

Senior Member
Messages
2,512
This observation comes from the statement of Lipkin and Hornig themselves they were clearly excited to have had access to the 60 cerebrospinal fluid samples from Peterson which they used.

There are only 32 ME samples in the paper and one is even from before 1994
 

Gijs

Senior Member
Messages
691
There are only 32 ME samples in the paper and one is even from before 1994
Then they didn't use everthing, why? I don''t know but they are from Peterson they said. If you don't believe Lipkin/Hornig maybe you can send him or her an email so you can hear from yourself.
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
Thank you Lansbergen. All spinal fluids from CFS patiënts came from Daniel Peterson, not the control and MS patiënts. If that is the case, this study is very biased.

This is true and I would be concerned about differences in sample processing that could alter the results. I am wondering how Hornig/Lipkin attempted to control for these differences. I don't have a copy of the paper at the moment so I haven't read it.

They still put their name on the paper though, something I doubt they'd do if the results were total crap.
 

FancyMyBlood

Senior Member
Messages
189
I really wonder how the ongoing trial of anakinra (IL-1 receptor antagonist) from the Nijmegen groups fits into this. On the one hand this study shows a depressed level of IL-1, so one could hypothesize that anakinra could make PWME feel worse. On the other hand I believe Lipkin and Horning think that the immune system of PWME gets "exhausted" after a certain time period and they actually start making less cytokines. So maybe IL-1 is a culprit, but because of the ongoing production it drops after a certain amount of time?

This is way above my head though. Anyone able to tell what these results may implicate in therms of pathophysiology?
 

msf

Senior Member
Messages
3,650
Giis, I think you are right about the limitations of this study, but you seem to be ignoring the fact that the findings corroborated the findings in the much larger study, which used patients from many different doctors.
 

Sidereal

Senior Member
Messages
4,856
I really wonder how the ongoing trial of anakinra (IL-1 receptor antagonist) from the Nijmegen groups fits into this. On the one hand this study shows a depressed level of IL-1, so one could hypothesize that anakinra could make PWME feel worse. On the other hand I believe Lipkin and Horning think that the immune system of PWME gets "exhausted" after a certain time period and they actually start making less cytokines. So maybe IL-1 is a culprit, but because of the ongoing production it drops after a certain amount of time?

I was wondering about the exact same thing.
 

Simon

Senior Member
Messages
3,789
Location
Monmouth, UK
News release from Columbia
Scientists Find Clues Into Cognitive Dysfunction in Chronic Fatigue Syndrome

looks much the same as the medexpress piece

"NEW YORK (March 31, 2015)—Scientists at Columbia University’s Mailman School of Public Health have identified a unique pattern of immune molecules in the cerebrospinal fluid of people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) that provides insights into the basis for cognitive dysfunction—frequently described by patients as “brain fog”—as well as new hope for improvements in diagnosis and treatment.

In the study published in Molecular Psychiatry, Mady Hornig, MD, and colleagues used immunoassay testing methods to measure levels of 51 immune biomarkers called cytokines in the cerebrospinal fluid of 32 people with ME/CFS for an average of seven years, 40 with multiple sclerosis, and 19 non-diseased controls. The researchers found that levels of most cytokines, including the inflammatory immune molecule interleukin 1, were depressed in individuals with ME/CFS compared with the other two groups, matching what was seen in a blood study in patients who had the disease for more than three years. One cytokine—eotaxin—was elevated in the ME/CFS and MS groups, but not in the control group.

“We now know that the same changes to the immune system that we recently reported in the blood of people with ME/CFS with long-standing disease are also present in the central nervous system,” says Dr. Hornig, professor of Epidemiology and director of translational research at the Center for Infection and Immunity at the Mailman School. “These immune differences may contribute to symptoms in both the peripheral parts of the body and the brain, from muscle weakness to brain fog.”

Implications for Diagnosis and Treatment

“Diagnosis of ME/CFS is now based on clinical criteria. Our findings offer the hope of objective diagnostic tests for disease as well as the potential for therapies that correct the imbalance in cytokine levels seen in people with ME/CFS at different stages of their disease,” adds W. Ian Lipkin, MD, John Snow Professor of Epidemiology and director of the Center for Infection and Immunity.

There is precedent for use of human monoclonal antibodies that regulate the immune response in a wide range of disorders from rheumatoid arthritis to multiple sclerosis. However, the researchers note, additional work will be needed to assess the safety and efficacy of this approach.

The study was supported by a grant from the Chronic Fatigue Initiative of the Hutchins Family Foundation and the Edward P. Evans Foundation.

Additional authors include Andrew F. Schultz, Meredith L. Eddy and Xiaoyu Che at the Mailman School; C. Gunnar Gottschalk and Daniel L. Peterson at Sierra Internal Medicine in Incline Village, NV; and Konstance K. Knox at Coppe Health Care Solutions in Waukesha, WI, and Simmaron Research in Incline Village, NV.
 

Gijs

Senior Member
Messages
691
Giis, I think you are right about the limitations of this study, but you seem to be ignoring the fact that the findings corroborated the findings in the much larger study, which used patients from many different doctors.

I would like to see replication and more research of this study:
Steven E Schutzer, Thomas E Angel, Tao Liu, Athena A Schepmoes, Therese R Clauss, Joshua N Adkins, David G Camp, Bart K Holland, Jonas Bergquist, Patricia K Coyle, Richard D Smith, Brian A Fallon, Benjamin H Natelson.
Distinct Cerebrospinal Fluid Proteomes Differentiate Post-Treatment Lyme Disease from Chronic Fatigue Syndrome. PLoS ONE, 23 Feb 2011

But there will be no replication at all.
 

lansbergen

Senior Member
Messages
2,512
This observation comes from the statement of Lipkin and Hornig themselves they were clearly excited to have had access to the 60 cerebrospinal fluid samples from Peterson which they used.

If it are Petersons samples it likely are ME patients.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
But there will be no replication at all.
The second better study is on the way. Since the first study happened the technology has improved and they no longer have to mix the samples into one giant sample to test. Now they can test individual spinal fluid. This could get interesting. I think Natelson commented on this recently. Does anyone recall where?
 

Denise

Senior Member
Messages
1,095
Now they can test individual spinal fluid. This could get interesting. I think Natelson commented on this recently. Does anyone recall where?

Natelson “But now that technology has advanced, we are collecting spinal fluid from another 40 patients and 15-20 controls via a major study being funded by the National Institutes of Health, and we are able to do much smaller pooling — maybe groups of just three or four instead of 15 or more.”
http://journals.lww.com/neurotodayo...eport_Gives_a_New_Name,_New_Diagnostic.1.aspx
 

Gijs

Senior Member
Messages
691
The second better study is on the way. Since the first study happened the technology has improved and they no longer have to mix the samples into one giant sample to test. Now they can test individual spinal fluid. This could get interesting. I think Natelson commented on this recently. Does anyone recall where?
That will be great Alex!