Yes. Thank you, Bob.
I have no science background so, I am at a disadvantage at analyzing such things. I do not understand though why these findings (i.e. nk cell function, cytokine profiles, viral loads, neurological deficits) are not assessed as possible biomarkers for the disease. The draft starts out in stating that there are no biomarkers, yet there possibly are. We just need larger scale studies to prove it. The same goes for treatments. Rituximab and Ampligen might be treatments, we just need larger scale studies to prove it.
That's what this report is critically stating. The research is not there:
Do patients just skim over and pull out what they want or do they actually read the entire document. There is no mention of Fuduka in this document.
They mention CBT/GET, depression as ancillary to ME/CFS. Every major disease has depression, anxiety etc. Is MS, Cancer a psychosomatic disorder because they include CBT/GET, and other alternative modalities to deal with pain? Will MS, Cancer become a psychiatric disease becasue they use some psychological and alternative tools to manage coping with these diseases? No
They ruled this is not a psychiatric, psychological, psycho-somatic disease...period. How many times does this have to be copy and pasted over and over again before everyone realizes they cannot then treat patients with these modalities as a primary treatment protocol when they have identified it as a biological disease? They stated as such in this report.
They are stating that the methodology of the research model is lacking. Why do some patients respond to Valcyte and others do not? Does anyone know? Why do some get better on Famvir and others do not? Why do some patients get better on antiviral medication and others do not? Why do some patients improve on Immune Modulators and others do not? Why do some respond to Rituximab and others do not? Why do some relapse and other do not? Why do some
improve on antibiotics and other do not? What about enteroviruses or the Stanford fMRI find on reduced brain matter?
They want to know the answer to these questions.
To date, clinical research and trials the lack of inclusion of the homebound, rural residents, and a research focus on men. Minorities also are rarely represented in studies, so there are no data to confirm whether minorities have a higher or lower risk and treatments. Is this not correct?
Someone mention no PEM
Fatigue has been the defining focus of recent research,
but many other symptoms need to explored, primarily neurocognitive deficit (“brain fog”), post-exertion malaise, and pain. Most ME/CFS studies focus on adults, excluding children with similar symptoms.
We noted unproven. Clinical studies have focused on predominantly Caucasian, middle-aged women.
Is this not true? Representative, ethnically diverse samples across the lifespan are lacking. Investigations of natural history and familial linkages may
identify genetic predispositions and lead to early identification and primary prevention
. Some on the forum have mentioned how their children developed ME/CFS. Is their a genetic component or predisposition in a subset?
Carefully designed and adequately powered studies defining the spectrum of ME/CFS in urban and rural communities are lacking, limiting their applicability to an increasingly diverse society. Specifically, it is critical to include patients with limited access to clinical services (e.g., non-ambulatory patients).
Is this not true? Did not members of the patient community complain that researchers need to include patients who are bed ridden and housebound patients, the sickest of the sick, because they could not particpate in trials.
The symptoms patients consider clinically meaningful are not in the scientific literature; this discordance must be rectified. Is this not true? We know the psych model is included in scientific literature. Are we not upset that as a patient community PEM, is not included?
Some mention the lack of natural killer cell dysfunction is not mentioned. Read below.
An integrated, systems-level approach should be followed to understand how immunologic, neurologic, and metagenomic factors may contribute to ME/CFS. Immunologic mechanisms of ME/CFS and pathways associated with disease progression must be defined and characterized (e.g.,
defining cytokine profiles involved in pathogenesis; studying inflammation; and comprehending the basis for natural killer cell dysfunction observed in many patients with ME/CFS).
These also should be longitudinal studies to explore the possibility of a progressive immune exhaustion or dysfunction in ME/CFS.
There are tremendous opportunities on which we have not yet capitalized to learn across disciplines and from other diseases such as Gulf War Syndrome, Lyme disease, fibromyalgia, multiple sclerosis, and Parkinson’s disease, to determine commonalities and differences.
What they are saying is that the research model is lacking in many areas to determine the size, scope and severity of this disease across the entire population involving all of the above metrics including the ones not mentioned in this post but were included in the report
. The research that has been completed to date has not been robust enough, too small in number, too exclusionary for the sickest and is limited as to gender, ethnic and age specificity...Good Grief!
