I see your logic in the Faroese angle. a perfectly reasoned argument!
I appreciate your assessment of how the lack of parasites has changed or bodies and can see the point; of course it has to have caused some consequences.
I do not buy the idea though. If I understnad the larger implication and big picture it is that the parasites, who naturally engender some tolerance of their parasitic selves, allow some of that tolerance to wash over to tolerance of self antigens. Without the parasite, the immune system is on overdrive and mistakenly attacks "self".
But here is one of my heros speaking on MS Behan and Chaudhuri Pathogenesis of MS revisited foundHERE
exemplified by several investigators, Guseo and Jellinger
found in a detailed study of 19 cases of MS with a short
clinical course (the mean of less than one year) a significant
number of these patients had no perivascular infiltrate
in the CNS.53 The absence of lymphocyte cuffing in
patients with acute MS is not the exception and is said
to occur in one-third of all cases.36 Lymphocytes are a
normal occurrence in the perivascular spaces. Similar
infiltrates, in fact exceeding that found in MS, may occur
in a wide variety of pathological conditions including
trauma, infarcts, tumour and following infections. Most
investigators who have looked for lymphocytes in contact
with the myelin sheaths and oligodendroglia found that
‘the number of lymphocytes that leave the perivascular
compartment and enter the parenchyma is very small,
both in absolute numbers and relative to the number of
There are multiple reports of detailed and sophisticated
It's a long paper there is a large amout of data about MS lesions that support the idea it as degenerative without there being any immune system involved in the damage, parasite primed or not.
Here is nother key piece from Barnett and Prineas (John Prineas is a dystel prize winning MS researcher most of what we know about MS lesions came from his pathology lab)
Pathology of the newly forming lesion in RRMS
Such “acute” lesions generally are described
as actively demyelinating lesions in which myelin
phagocytes directly engage normal-appearing myelin
sheaths in the presence of infiltrating T cells. Because
similar changes are observed in some forms of experimental
allergic encephalomyelitis (EAE), this has encouraged
the view that tissue destruction in MS is the
result of a T-cell–mediated cellular immune response directed
against myelin. This study describes the clinical
and pathological findings in a young patient with relapsing
and remitting MS who died within 24 hours of the
onset of a new symptomatic brainstem lesion. In view of
the unusual findings, we reviewed tissue obtained at autopsy
from other patients with rapidly deteriorating MS.
Nine lesions were found that were essentially identical to
the fatal brainstem lesion in the first case. The earliest
structural change shared by all 10 lesions was extensive
oligodendrocyte apoptosis in tissue exhibiting early microglial
activation but few or no infiltrating lymphocytes
or myelin phagocytes. This is unlike any current laboratory
model of the disease, in particular, experimental allergic
encephalomyelitis, which raises the possibility of
some novel disease process underlying lesion formation
in relapsing and remitting MS.
That's an older paper at '04, but Barnett has continued to write along the lines of "its not autoimmune...." and has a lot of papers on that thought. Prineas is semi retired at this point.
If I misunderstand then let me know but essentially the hygiene hypothesis requires the immune system to do the damage does it not? so if I accept the work of these workers and others writing along these lines, the lack of parasites has little to do with MS as they are pointing out it is degenerative not immune related?
Nonetheless, good article with interesting points. Extinct parasites! man, never thought of that!