Video: "Mutations in Energy and Autoimmune Genes Cooperate to Cause ME/CFS" with Alan Light, PhD

perrier

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Just a thought: if this theory were really true, wouldn't it mean that CFS/ME is an ancient disease. And that would mean that world literature would have to be filled with descriptions of situations which resemble severe cfs/me which we are now familiar with. And yet, do we have such descriptions? I'm not sure. Or then it could also mean that there is now something new in our environment which is waking up these genes. Worrisome all this, worrisome in the extreme; difficult evening with this talk.
 

wigglethemouse

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Maybe the identity of those genes can help us identify the environmental triggers, or the perpetuating factors?

Since some healthy people had the mutations, and not all CFS people had them, there's obviously more going on...
If you haven't already seen it this thread and eBook by @BeautifulDay has a similar theory that mutations in mtDNA lower the threshold for disease entry. What Alan Light has done is tie Mitochndrial/energy related variants with immune variants and shows those together occur at double the rate in patients compared to controls, which seems significant to me.

Thread : https://forums.phoenixrising.me/index.php?threads/my-e-book-“tracing-chronic-fatigue-syndrome-to-mtdna”-will-be-free-wednesday-and-thursday-on-amazon.62359/

Interesting to think how this could tie in with the IDO metabolic trap. Does the trap keep the immune system active perpetuating the disease. Alan Light alludes to the bodies immune damping system not working in patients after initial trigger has gone, and the IDO trap could possibly do this.
 
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knackers323

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Yes I’d say the genes predispose us but as pointed out, seems odd that only recently that the illness has appeared.

Anyone know if this is also true for the autoimmune illnesses, Are they a relatively new thing?

My guess is they probably are, due to modern life and the pollutants we are exposed to through diet and environment.
The gut biome probably has a decent sized role to play in this.

Autoimmune or not, at least for myself, the immune system is definitely involved.

I can take things that alter the immune system and inflammation and feel much better within hours.
But it only improves me so far and/or stops working
 

Belbyr

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This speech makes all the sense in the world. This lines up with Dr Phair/Davis metabolic trap theory and it also lines up with Dr Klimas's group in Florida with her GWS and CFS research.

I remember all of them saying there is a genetic predisposition amongst the community, and the genetic predisposition is quite common... not rare at all. This seems to be present in Dr Light's control groups.

We might not be able to do anything about the genetic predisposition at the moment, although I am sure with technology, gene modification will be common in about 5-10 years. I now totally believe that the OMF group and the Klimas computational biologics group are on the right path.

I think it's possible to flip us back into a healthy state, because we were obviously healthy prior and there are a lot of controls that are healthy with our same genetic issue. Klimas has actually already done this in a computational, cell, and mouse model. We need to get these folks funded.
 

bertiedog

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Well I have spent ages methodically going through all the SNPs mentioned only to find no data for me on the vast majority that I looked up using Livewello and Promethease. The only homozygous SNPs were on the DISC1 so not terribly encouraging at the moment, although the Light's basic hypothesis is interesting.

Pam
 

Richard7

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@knackers323
1) montoya said in one of his presentations that autoimmunity has gone up in populations that have survived many waves of infectious diseases. We have to exist in a balance between autoimmunity and infection, waves of Infectious diseases are an evolutionary pressure that favours those with aggressive immune systems but leaves you with a population has more issues with autoimmunity.

2) I have no idea how many people suffered from diseases like this in the past. I can see some evidence in the many novels with background characters who are chronically ill, though they are often treated as malingerers by the authors. I know someone else around here once pointed out that old cookbooks (19th and early 20th Century) used to have a section for invalids.

The real question is what sort of evidence would we expect to see if say 1 or 2% of the population had ME or FM or MS or something of the sort, if the state was small and not interested in providing healthcare, monitoring public health, or providing for the poor.

There may be something in church records, I know dimly that there are people who have studied the way that poor relief (if that is the right term) was managed in small communities in the 18th century and earlier (when it fell under the moral economy rather than state policy) and that in the examples I heard about the local churches where centres for organising it.

The thing is that you would have to look at the sort of evidence that comes down to us, determine whether or not it would record the existence of these sorts of illness, and then look for the evidence systematically before forming an opinion about whether these illnesses are new or not.

Otherwise we fall into something like the "medically unexplained symptoms trap", where people who are not omniscient, and ought reasonably know that, and who have not exhausted all avenues of research open to them (not even tried) opine that their inability to explain "x" is proof that it does not exist.
 

nandixon

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From Alan Light’s February 2017 talk at the Bateman Home Center, @Cort reported that all of the mitochondrial mutations found to that point were apparently somatic ones, i.e., acquired after birth:

...the Light group found at least one mitochondrial mutation not seen in healthy controls in everyone but one of the 40 ME/CFS patients… Significantly, all of the variants were acquired; i.e. none was present at birth – as the result of something in the environment the ME/CFS patients had bumped into. They were scattered throughout the complexes that make up the mitochondrial energy pathway.
https://www.healthrising.org/blog/2...ity-chronic-fatigue-syndrome-alan-light-talk/
(Emphasis in original)
(A video of Dr Light's 2017 talk is here.)


It seems a bit odd to me that the potentially damaging mutations in all 40 patients were only acquired ones, so I'm wondering if that is correct? I don't remember hearing that in the 2017 talk but maybe @Cort also talked to Dr Light.(?)

I don't think Dr Light makes any mention(?) in the current talk of what proportion of mutations were acquired versus inherited in the now larger study, although obviously they have now found inherited ones and mutations in the nuclear DNA as well.

If most of the mutations are random acquired ones then that would explain why genetic studies on ME/CFS patients have never yielded reproducible SNP findings.
 

wigglethemouse

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It seems a bit odd to me that the potentially damaging mutations in all 40 patients were only acquired ones, so I'm wondering if that is correct?
How can you tell if the mitochondrial gene variants were acquired? That implies that you had their mothers mtDNA or that RNA was different to DNA? Or am I missing something?
 

sb4

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I recently read that some mDNA actually can come from the paternal line so this could potentially muddy the results if you are comparing between siblings mitochondria.