Hi.
I just wanted to hear anyones thoughts, ideas and opinions really!
I watched a programme about the ‘obesity epidemic’ steadily growing in the UK and they mentioned that peoples genes for controlling hunger or fullness might be switched off due to an event or illness in childhood, possibly a stressful event even and therefore for this leads to the process of obesity. Therefore I wanted to know, is this what has happened with MS? That our ‘remyleination’ gene has been switched off or turned down which then makes us unable to repair our nerve fibres once damaged by infection and hence MS? Sorry this is probably facts I’ve missed or just assumed but not really thought about until the other day.
Any thoughts would be appreciated to stop my wandering mind!
Thanks
BFx
Hi Batfink,
MS is certainly at least partly genetic - the evidence for that is now overwhelming. However, it’s not quite as straightforward as a single gene being “on” or “off”. There are a few dozen genes so far - perhaps more to be discovered - that have been associated with MS, so there are “risky combinations”, not single bad genes.
However, not everyone with a risky combination goes on to get MS - even in identical twins, it’s unusual for both to get it - in two thirds of cases, only one does.
So that points to there being some kind of environmental trigger too: something one was exposed to, but the other not. That may very well be the kind of thing you’re talking about, which makes a gene variant that’s harmless to one person have catastrophic effects on another.
Tina
Hi, my interest here is in mutant genes. If it turns out I definitely do have HSP (hereditary spastic paraparesis) and not PPMS, then somehow I have either inherited the mutant genes or I have somehow become the starter of such genes.
Innit chuffin` complicated.?
luv Polllx