Australian researchers show that CFS is linked to a faulty cell receptor in immune cells

[keenly]

'The breakthrough came after researchers from Griffith University identified that patients with CFS/ME were far more likely to have single nucleotide polymorphisms - DNA typos - in the genetic code for certain cell receptor.

This cell receptor is known as transient receptor potential melastatin 3 (TRPM3), and in healthy cells it plays a crucial role - transferring calcium from outside the cell to the inside, where it helps regulate gene expression and protein production.'

http://www.sciencealert.com/one-of-...t-chronic-fatigue-syndrome-just-got-destroyed

 

[Alvin2]

Fascinating though i am not convinced (yet).
I thought Ron Davis already concluded this condition is not genetic, though of course that is subject to reanalysis.


Also why does it emerge suddenly, that could be evidence either way though, genetic until triggered. Why do some people recover, the rate is low but does happen, though we cant be sure they actually have ME/CFS.

The need for more research is clearly indicated.

 

[Manganus]

A search on the forum gives the hint that we have some threads on this.

(I've not read them yet.)
http://forums.phoenixrising.me/index.php?search/43655534/&q=TRPM3&o=date&c[node]=15

...like this thread, which seems to be the earliest(?)

 

[keenly]

Fascinating though i am not convinced (yet).
I thought Ron Davis already concluded this condition is not genetic, though of course that is subject to reanalysis.


Also why does it emerge suddenly, that could be evidence either way though, genetic until triggered. Why do some people recover, the rate is low but does happen, though we cant be sure they actually have ME/CFS.

The need for more research is clearly indicated.

I do not believe it is genetic.
I do know calcium efflux is a major part of CFS. The reason you are always deficient is that intracellular
magnesium needs ATP dependent membrane pumps to keep magnesium levels inside the cell normal. In a low energy state, magnesium leaks out of the cell and thence into the urine. In addition, calcium signaling ions cannot be pumped out of the cell which is potentially catastrophic to energy production and calcium balance. Low magnesium levels inside CNS cells make it impossible to sleep well and will cause sensory overload and anxiety disorders as well as seizures in the worst cases.

 

[lansbergen]

I do not believe it is genetic.

It could be. They say the receptors get upregulated with all kind of stressors.

 

[lansbergen]

Also why does it emerge suddenly,

A certain stressor.

 

[keenly]

It could be. They say the receptors get upregulated with all kind of stressors.

Okay partially genetic, but with a stressor to set it off?

 

[lansbergen]

Okay partially genetic, but with a stressor to set it off?

Could be

 

[keenly]

A search on the forum gives the hint that we have some threads on this.

(I've not read them yet.)
http://forums.phoenixrising.me/index.php?search/43655534/&q=TRPM3&o=date&c[node]=15

...like this thread, which seems to be the earliest(?)

Yes you are right, sorry.

 

[Skippa]

Calcium uptake seems to raise its head a fair bit...

 

[Alvin2]

I do not believe it is genetic.
I do know calcium efflux is a major part of CFS. The reason you are always deficient is that intracellular
magnesium needs ATP dependent membrane pumps to keep magnesium levels inside the cell normal.

How do we know this?

Low magnesium levels inside CNS cells make it impossible to sleep well and will cause sensory overload and anxiety disorders as well as seizures in the worst cases.

I'm not at all convinced of this, interestingly acetylcholine affects sleep in ways not at all researched, i have personal experience with this as well as other not journal published experience. This also jibes with the pyruvate dehydrogenase block theory. That said the whole picture is not yet available so like the magnesium statement its hard to say if what i am proposing is the actual mechanism, part of it, downstream or even related at all.

A certain stressor.

Probably, what is the billion dollar question

 

[alicec]

A search on the forum gives the hint that we have some threads on this.

'The breakthrough came after researchers from Griffith University identified that patients with CFS/ME were far more likely to have single nucleotide polymorphisms - DNA typos - in the genetic code for certain cell receptor.

There has already been considerable discussion on PR about this and other studies from this group, as the search results show.

The claim that there is a genetic basis to some of their observations has no substance. It is based on a very small (too small for statistical significance) study using inadequate statistics, discussed here. When the appropriate statistics were used by the authors themselves, the so-called differences disappeared.

That second study is discussed here.

 

[keenly]

There has already been considerable discussion on PR about this and other studies from this group, as the search results show.

The claim that there is a genetic basis to some of their observations has no substance. It is based on a very small (too small for statistical significance) study using inadequate statistics, discussed here. When the appropriate statistics were used by the authors themselves, the so-called differences disappeared.

That second study is discussed here.

I know. I have already acknowledged this.

 

[pattismith]

Fascinating though i am not convinced (yet).
I thought Ron Davis already concluded this condition is not genetic, though of course that is subject to reanalysis.
.

This conditions is not genetic means that you can't find one gene mutation that could match to the disease....
But most diseases are related to genes/epigenetic that predispose people to suffer from it.

One snp that gives an increased risk for a disease by 3 or 6 doesn't make it a genetic condition,
it is not a fatality, and recovering is still possible.