I believe I was born to get this condition. I don't mean this in any religious/spiritual sense but in the sense that I have a genetic vulnerability to react inappropriately to drugs, inoculations, foods, viruses, parasites etc.
Why is it that in the ME outbreaks (Royal free, Lake Tahou) some people got sick and other people didn't? Surely there is a vulnerability or susceptibility to this condition?
I personally think that we would have got CFS/ME regardless of how we lived our lives and that there was very little we could have done about it except delay it for years, decades.
Again, I hope I haven't offended anyone with this thread.
I agree, however it will be subset. (ME is not one disease, due to the diagnostic criteria, it has been diluted via CFS).
I will then dilute this further myself, and only discuss slow onset severe ME in reply to you. (There are generally accepted two forms, slow onset and sudden onset). So from here on, I am discussing slow onset ME, that becomes severe and intractable. I hope that's OK.
I will then explain why I think ME in children (who become adults), isn't the same ME as in their parents (who infected them). So I'll be discussing a slow onset severe ME, as a congenital disease. In my view this is not your average ME, but 25% or less of cases. I think neuroimmune psych CFS does exist, and that's what Lipkin & Hornig are studying,hence they never find any pathogens (the reverse of ME patients who are riddled with Lyme co infections, when they get tested). So we've all got different conditions, and given the wrong diagnosis to share of CFS or CFS/ME which is probably 5+ conditions.
Sticking to your idea, here is why I agree with you (observing a slow onset severe subset) in my own personal situation as someone with a ruined life as a child now rather older than that.
The main reason:
There is apparently unpublished evidence that proves congenital transmission (not CFS). From what I can gather this will be congenital Lyme like disease, but involving
another pathogen. If correct. congenital Lyme like disease (aka slow onset ME) is not 'Lyme disease' or 'Chronic Lyme disease' (that you catch from a tick) it is something more akin to
Autism.
Naturally I don't know this, it's a unproven hypothesis for now, it may be a rumour and it's never going to be proven or even discussed, but we shall see. But I know some ME sufferers who are sick, barely make normal prion protein (PrPc) in their blood any more. What I also know, is the more severe the patient, the less normal prion (PrPC) they make. What is elusive, of course is 'evidence' of the following:
*Misfolding prion. (If PrPC is absent, then misfolding should be high). In disease, potentially massively high.
*Evidence of low PrPC in ME is not in blood, but in CSF (Spinal fluid). Blood evidence doesn't correlate with neuro.
So in terms of raw evidence, it means almost nothing, but it doesn't mean absolutely nothing it means something that needs further work.
If a certain relevant subset of ME can have the misfolding test, and test our family members (who have 'ME' light) it would then make sense why I have made the following observations that make me curious,
in this subset.
1) Some PWME will tell you,
they weren't 100% healthy before they met CDC criteria for CFS. This is important!
2) Some PWME will tell you, they can notice the first symptoms at
10 years old, or younger, but weren't 'sick'.
3) The same PWME will tell you they got full blown CFS at age 12-17 (sexual maturity). This is v.important!
4) The same PWME then split into two groups: 'slow onset', and 'sudden onset'. This is critical to remember.
Next set of observations:
5)
Fatal ME that begins in adolescence/young adulthood, observe the patients are almost always dead by late 20's early 30's - consistently. This can trick you into believing the patient only survived approx 15 years after infection. My question is, what if they were infected
in the first place, aka, a prion disease which has multi decade latency to become fatal (aka Alzheimer's disease). No evidence to prove this exists yet, and certainly not if the poor patient is deceased. Yet most survive. Survivors can be tested for any putative prions, pathogens, genes etc, but they won't if CDC keep their Fukuda CFS, hence weak fatigue criteria is immortal.
6)
Life long Severe ME also almost always begins in adolescence. They become housebound. Most, at first are very very ill. Bedridden or hospitalised. If they survive, usually 20 years later they are still very ill,
but a little less disabled. For me, this again suggests hormones are involved. (Growth hormone is a potential culprit). One thing to then think about is,
GH function in 'CFS' is never tested. In those who
are tested, they tend to have very low GH function.(IGF-1 is unreliable, use a stim test). This implies the pituitary is involved, perhaps an autoimmune attack against it.
7)
ME parents are rarely as ill as the child. Also note that it's usually
one parent infected. There are exceptions, whole families can be diagnosed, but again, always in various levels of disability.
That to me is the smoking gun. The mother is perhaps infected and gave her child the pathogen in her DNA, which explains why the child has developmental ME ('Slow Onset Life Long Severe ME) which is not the same condition (in my view) as other forms of ME or CFS at all, it's a subset. Note that slow onset ME has a much worse prognosis that sudden onset.
8) For me, this is known by the government and this is why umbilical cord is banned by the UK from mothers who develop 'CFS' during a pregnancy.
An unprecedented level of caution of pathogen spread, in a cohort alleged to be mentally ill, in need of CBT GET!!!!!
To conclude I believe the following is probable, not just possible:
Original 1950's ME is transmissible, but only to genetically linked family members. (Hence cluster outbreaks). ME is otherwise sporadic in the main. I believe these people are then carriers and can spread it as an STD, to their own children. A mitochondrial infection perhaps. These V2.0 ME patients, are far more ill, than the parents as they are born with a form of novel immunosuppression or become like this by teenage years.
Recap:
Group 1: The infected parents, (who may never become sick) or may take 50 years to get symptoms if at al (just like Alzheimers' disease).
Group 2: The infected child (who is born with latent infection and activates it during adolescence + an inflammatory cascade (infection, vaccine, acute severe stress, trauma, chemical exposure). A person who goes onto develop slow onset severe ME and never recovers as they have a DNA infection. Thus they are born to be sick.
If you then see what they did in the 1950's, the following may occur historically over time:
The kids with slow onset severe ME don't have the original 'outbreak disease', they have the congenital form, hence they are very 'different to other subsets.
This could explain why mom or dad is either asymptomatic, or CFS light,
because mom or dad wasn't born with the putative agent,they caught it, as adults who had a completed immune system (Unlike the teenagers who 'catch' ME).
