Again I ask the same question: Is ME/CFS a genetic mutation?
Again, Warren Tate, like many other researchers, points toward "glandular fever" and "genetic susceptibility" in ME/CFS.
I have found this "genetic mutation" in some older papers, regarding ME/CFS back in 2019 and told some organizations. The still unconfirmed question is whether did Epstein-Barr virus (EBV) caused the mutation or DNA methylation.
However, for whatever reason, the genetic mutation was rejected.
Today I believe that people have a problem accepting these facts because it destroys their hope for a cure (me included).
a lovely guy who clearly knows a thing or two
but to put his comments about genetic changes and genetic risk factors in CFS in context
the genetic changes found in CFS sufferers he is referring to are epigenetic changes - ie which genes are up regulated and down regulated in CFS patients vs controls - this is not the differences in the inherited DNA of the patients - just which of their genes are switch on or off (or more on or less on by degrees).
it should be no surprise that in an illness state some genes are upregulated and some downregulated
this happens with every chronic illness we know of.
i guess the hope is these upregulated genes will point to pathways - and these pathways may give some clues to the actual cause - but these links can be circuitous and indirect - for instance, inflammation from any source will definitely upregulate many genes and down regulate others - but this does not necessarily tell us what is causing the inflammation.
this is an entirely expected and normal finding in an illness - so while certainly good logical practical work - i think just constitutes the very early steps on the path to discovery
the second genetic factor discussed was polymorphisms - or single amino acid mutations in the actual DNA of the patients vs controls - and mapping which mutations were more common in CFS sufferers - and finding some common clusters of such mutations do indeed exist.
this is actual differences in the patients DNA ( rather than transcription / epigenetics ) but again, the human genome is hyper variable in the areas that controls the immune system
it has to be that way or we would have all been wiped out millennium ago by one single pathogen or other - so we ( and pretty much every other creature on the planet ) have developed more individual variability of immune genes than just about any other area - as a safeguard for the survival of the species.
as a result whenever you look at a population with a given disease state - you will likely find such clusters of mutations in those that are effected.
this is again normal and expected
the number or degree of mutations will also be on a continuum - from none to many - with ones chances of getting CFS being associated with but not necessarily driven by (in fact never entirely driven by) genetic mutations. Simply, ones chances or probability of contracting an illness will be higher depending on the degree of mutations - but the degree of this risk - ie. does it double a persons risk if they have the full suite of mutations or multiply it by 100x ( currently unknown, i believe ).
contrary to what many prefer to believe - research on identical twins tells us that most chronic diseases have a rather low association with genetics - for instance something like 80% of an individuals risk of diabetes or heart disease is typically due to lifestyle and environmental factors and only around 20% driven by a persons individual genetics.
this means that while genetic factors may increase a persons risk of CFS by say 100% - if the lifetime risk of CFS is 0.6% - and you had all the mutations predisposing you towards it - you may then still only have a lifetime risk of 1.2% - and thus there is still plenty of room for an external root cause and therefore also an intervention that addresses that main causal factor and therefore a realistic hope of treatment or cure.
i wrote this because i think its possible to come away from that video with the idea that we are pre-ordained by our genes to get CFS and there is therefore nothing we can do about it
but i think the good professor there would agree - that we do not yet have enough research to know just how large or small a predisposing factor these genetic mutations represent - and how much other causal factors drive the overall incidence of the disease.
i think its likely that its far from a foregone conclusion based on our genes and clearly requires some other triggering and/or maintaining factors
