Got to admit that I've been wondering if we'd be a bit short of questions for Dr Montoya but compiling them below, and considering we have a planned limit of 30 minutes to our time with him, I'm feeling a lot better about it.
I've done a little bit of editing down, if you feel I've misinterpreted your question then let me know.
Bone Marrow
At the recent CFSAC Meeting you briefly mentioned that there may be a mechanism in the bone marrow? Can you comment on that?
T-cells
Could you elaborate on the findings that you and Mark Davis had with clonal expansion of T-cells and a possible antigen? Can you give us an idea of how big of a discovery you think this will turn out to be if validated and when will we hear more on this and if you think their will be treatments that can target this?
Drug trials
I note that you have done clinical trials in the past on Valgancyclovir (antiviral), and on low dose Methylphenidate (stimulant) with and without Mitochondrial Support.
- Do you still use either of these treatments in your clinical practice?
- Do you have further larger trials of either of these planned?
- Would you recommend either for patients to try?
- Do you have any other drug trials planned?
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Given your focus on the inflammatory nature of ME/CFS, will your research center be pursuing any drug treatment trials? If so, which ones are you considering and why would you consider these treatments as potentially beneficial?
Biomarkers and their implications:
Given that differences between ME patients and healthy controls have been found in the brain, cytokines, the microbiome, metabolites in the blood, and mitochondrial function, can you suggest which seems the most promising source of:
- a biomarker that can be used by all doctors to distinguish ME patients from other fatiguing illnesses
- a biomarker that might lead to a better understanding of the cause of ME
- a useful direction for treatment, such as classes of drugs.
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We have seen a number of small scale studies over the years looking for biomarkers including immune system studies and brain scans. There are a few bigger studies as well. Which of the results do you think may be interesting in terms of potential to show core mechanisms and hence are there any that you feel need larger replication studies.
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Some say the immune system is a little bit like a chaotic system, i.e. if you look at its function at one point in time and then on another, it might be completely different and it might not be forecast in which way. Assuming the immune system is 'chaotic': If the immune system plays a role in ME can a biomarker be found at all?
EDS/MCAS co-morbidity
Given that a large proportion of PWME appear to have the co morbid conditions of either EDS 3 (hypermobile type), or MCAS (Mast cell activation syndrome) or both, can you say if there could be a mechanism for why this is, and do you consider these patients to be a separate sub grouping?
Disease severity and severity level diagnosis
Does he have a view on the likely mechanisms for the relapsing remitting nature of the disease and the likelihood of being able to diagnose severity level via biomarkers/metabolic profiling in the future.
Commonality of disease mechanism
With millions of PWCs experiencing fundamentally the same illness do you believe there’s some common basis in the malaise or in the etiology?
Questions on research
Is me/cfs becoming more of an area of interest for students and researchers?
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What are his research plans? What should be the research priorities?
If he was given $25 million for research tomorrow how would he spend it?
Should there be a medical speciality formally responsible for ME and would this help in expanding research interest?
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Will his research on brain scans be replicated/expanded?
Although Japan and possibly one other group also did brain scans, I believe his work should be expanded and not only include healthy controls but cohorts such as MS, Lyme, ALS, Parkinson, Autism, GWI, EDS, and patients suffering from depression. I include depression patients not because I believe we will have anything in common neurologically with this group but because we have to unwind the damage done by healthcare and psychiatry believing we are mental health patients. I don't believe any group will share our specific neurologic issues and I think that needs to be established.
Impaired PDH and potential subsets
What are your thoughts on the impaired pyruvate dehydrogenase paper by Fluge/Mella?
Do you think there are subsets in ME/CFS, such as those that may or may not respond to Rituximab?
Treatments
Could he take an educated guess on when effective treatments will be found for us....
Food intolerance
Do you think there could be a link between ME/CFS and food intolerances?
About pathogens
You recently said that pathogens have not been excluded as cause of ME/CFS. My question is: what kind of pathogens do you think might be involved, and where in the body do you think the infection is, and what kind of research needs to be done to actually fill this knowledge gap?
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In 2013, in a call with the CDC, Dr. Ian Lipkin reported finding retroviruses in 85% of samples sent to him from your lab. We have not heard any follow up over the years. Has this been explored at all? Do you think retroviruses play a role in ME/CFS?
Useful tests in a clinical setting
What would be your advice to someone who fits the criteria for mild/moderate ME/CFS, is still in the first couple years, but has not identified any significant abnormalities in standard blood tests? Is there a path to a firmer diagnosis through tests or are we not there yet and it's best to simply wait and see what the research brings? How would one pursue a practically useful diagnosis? or at least not miss any important differential diagnoses?
