@Tally - I'm baffled by what you're driving at...
By your logic each one of us has different illness.
Yes, I believe we do. But we share the same symptoms, and many of the same metabolomic abnormalities and comorbidities from a wide variety of triggers.
Yes, of course there are differences, but the main question is, are those differences important for the underlying pathophysiology and ultimately for the treatment and cure.
Yes they are. Though I fit every criteria in most schemas of ME/CFS diagnostics, except pain, and have many metabolic abnormalities and comorbidities, my triggers were not typical of most patients.
- I had a long history of allergies, viruses, bronchitis and sinus infections, each made my doctors suspect immunodeficiency, maybe due to genetics
- Prior to getting ME/CFS I was diagnosed and treated for stage 3 uterine/ovarian cancer, which baffled my oncologist, as I was 10 years too young with BMI too low - I'd been in the best shape of my life. Treatment put me into menopause instantly during surgery, a great shock to my immune system and paclitaxel and carboplatin damaged my mitochondrial membranes.
- I acted as health advocate for my sister during the last 4 years of her short life, flying to Nevada, California, and Washington to help her get treatment, while she became a manic skeleton and kept walking out of hospitals - she was so crazy and uncooperative that the hospital requested we gain legal guardianship to transfer her across state lines to Stanford, but she died of a massive heart attack in the ICU beforehand. By this point, my adrenals crashed, and I had full blown ME/CFS and the next year was the worst I ever was.
- In addition to having celiac genes and some quirky methylation SNPs which make my family prone to storing toxins better than most, like the proverbial "canary in the coal mine" - 4/5 of my immediate family has toxin related diseases, other SNPs have been very pertinent as well.
- PEMT, Phosphatidylethanolamine N-Methyltransferase, is an enzyme responsible for the conversion of phosphatidylethanolamine (PE) into phosphatidylcholine (PC) in the liver. PC is a key component of the flexible cell membranes which surround every cell in our body. If it isn't working properly, it can be difficult to repair damaged membanes, which can be leaky - gut, BBB, and/or mitochondrial membranes.
- HFE - heriditary hemochromatosis, which can help to damage mitochondrial membranes and damage or shut down all organs
- SOD2 - lessens the superoxide mutase made to about 17% of normal, so that it can't defang the massive superoxide radicals coming out of my mitochondria. Instead, these superoxides combine with NO to become peroxynitrites, which damage the same membranes.
- Factor 2 - a genetic clotting factor variant which gives me thick blood, in top of what the researchers have been finding
- I had an estrogen driven cancer, and so, though I need hormones to optimize my function, they must be thoughtfully prescribed, managed, and adjusted so as not to promote future hormone driven cancers.
- There are several more pieces to this complex puzzle, but delving in to figure the roots out and customizing a treatment plan around my idiosyncracies is the secret to my success so far.
So, I do not believe that everyone should follow my exact protocol - they likely don't share my exact set of problems. But, though I've shared some of my uniqueness to make a point here, I do recognize that I may benefit from current ME/CFS research, particularly as many of my lab results, symptoms, and health history do match the researchers findings.
But there's a fallacy in everyone's searching for the Holy Grail - there is no magic bullet that can cure us. After my lengthy experiences in the health world trying both heavy duty conventional and natural treatments and common and exotic tests, I have a great respect for the complicated hairball this thing is.
Yes, I believe if traps are found and corrected, suramin or Ampligen or IVIG or Rituximab or 10 pass ozone are used and guts are cleansed of SIBO, Candida, worms, and other nasties and the gut wall and BBB become more stable and less leaky, that we should all have hope for a cure. But it will be a multi-step approach, not a magic pill.
99% of research on ME/CFS is being done on moderately ill because they can get to research centers and severely iĺl never rejected that research as not pertaining to them. One research is done on severely ill and suddenly it's "us vs. them" (I won't even start on how blurry the lines are between groups mildly, moderately and severely affected, and how all severe patients didn't start as severe, and how some mild patients will become severe and some severe will become mild......)
Part of this is a limitation in grants for research funding. And I do see the irony of patients moving back and forth between categories. I do think any stuff that is done gives us new morsels of info to chew on - its just maddeningly slow to get anything usable in a clinical setting...so, for now, we must make our best guesses from what we read and from what our symptoms, labs, and genes say.
I've tried to enroll in several studies so far to be told:
- I'm too old
- I'm post menopause
- I didn't have a well-documented viral illness triggering this
- I have POTS and MCAS and food allergies. I can't take many drugs, like Celebrex which has corn or milk in all versions and can't be compounded.
- I'm steadily improving (still pretty sick, but not sick enough to qualify)
- I'm 7-2500 miles from all US test sites, and the University of Washington has its head firmly in the sand and refuses to acknowledge this disease.
- Most studies are done on men and research done in women is not published in most medical journals.
- Doctors gaslight female patients.
I think there could be something to be learned about my case that would help science by volunteering.
On the other hand, I read every study I can with caution. Should I take advice from the conclusion, or were the patients too different from me for some reason that the theory might not work for me. One example is following a thread here on rapamycin and stimulating mTOR to increase it. So as a cancer survivor, I balked as overstimulation of mTOR PROMOTES cancer, something not wise for me.
This is incredibly complex. The analogy I have in my mind is of putting together one of those 1000 piece puzzles on the dining table, one that's missing 350 pieces. So, it sits there, week after week, while family members come by adding 1-3 pieces at a time while the comprehensive picture slowly evolves.
None of us know what that picture in the puzzle looks like today. And though we are making good progress, we are still missing those other 350 pieces. Do we borrow from other medical puzzles we've encountered along the way) Did someone find some under the sofa cushions, lost along the way? Or do new ones need to be colored and cut out of raw materials to fit?
We are far from a comprehensive overview of this disease with definitions of the varying subsets. So, it is counterproductive to treat us as cookie cutter widgets, or as a single subset of the whole. But, as studies are done, they should note which subsets they are choosing to look at, just as Ron Davis' colleague told me that I'll be looked at as a part of the cancer subset as they study the sample gave her.
And, I'm disappointed in the NIH criteria. I'd love to do it but don't qualify. Seems like hardly anyone else does either. Wonder if they might rethink that sometime soon...
