A Metabolic Trap for ME/CFS?

[xrayspex]

Just a word of caution. Leucine causes release of insulin.

Another way that leucine acts as a potent anabolic agent is by spiking insulin levels. Like high-glycemic carbs, leucine increases the release of insulin from the pancreas, which helps to drive the amino into muscle cells where it can work to stimulate muscle growth.

I have diabetes. So when I took BCAA for the first time along with my insulin injection I felt sudden hunger and palpitation. I immediately checked my sugar level and it had dropped to 65. So just keep an eye on your sugar levels if you are going to use BCAA.

I tend towards hypoglycemia--would that be problematic with this too you think?

 

[xrayspex]

https://www.sciencedirect.com/science/article/pii/S1550413109000400

so how does that study make you view using BCAA as rec'd in this thread?

 

[raghav]

@xrayspex What I do is I eat my breakfast and one hour later I take the BCAA (approx. 8 grams- one full scoop). This way you can avoid sugar level plummeting. If after taking BCAA you feel giddiness or any signs of low sugar then have a snack ready. This way you can get the benefit of BCAA and also avoid going hypoglycemic.

 

[raghav]

Was browsing through the ResearchGate site on ME/CFS, update posted by Dr. Robert Phair 5 days ago

https://www.researchgate.net/project/Etiology-of-Chronic-Fatigue-Syndrome

Don't ignore common missense mutations when searching for genetic predispositions to ME/CFS
Plenty of CFS researchers are searching for rare (population allele fraction less than, say, 0.03) missense mutations that predispose an individual to falling ill with ME/CFS.

The occurrence of ME/CFS outbreaks (for example, Incline Village NV and Lyndonville NY) seems to me sufficient evidence that there are also common missense mutations (population allele fraction greater than, say, 0.15) that predispose to the disease.

This would make ME/CFS a high prevalence, low penetrance syndrome.

Do you find this argument convincing?

Can somebody interpret this ?

 

[wigglethemouse]

Good find @raghav

Was browsing through the ResearchGate site on ME/CFS, posted by Dr. Robert Phair 5 days ago

https://www.researchgate.net/project/Etiology-of-Chronic-Fatigue-Syndrome

This is similar to what Cort quoted Robert saying back in April
https://www.omf.ngo/2018/04/04/a-metabolic-trap-for-me-cfs-healthrising/

Most CFS investigators focus on rare SNVs. To me it’s just a matter of logic that predisposing genetic factors for ME/CFS must be common, not rare, in the population. Otherwise you can’t explain the many well-known CFS epidemics like Incline Village and Lyndonville. The downside of this logic is that common mutations are common! So, we still have many thousands to examine. Fortunately, we have colleagues at Stanford and at Harvard who are great at big data analytics.

I guess he is asking the scientific community if they think this argument could be real.....

 

[perrier]

Was browsing through the ResearchGate site on ME/CFS, update posted by Dr. Robert Phair 5 days ago

https://www.researchgate.net/project/Etiology-of-Chronic-Fatigue-Syndrome

Don't ignore common missense mutations when searching for genetic predispositions to ME/CFS
Plenty of CFS researchers are searching for rare (population allele fraction less than, say, 0.03) missense mutations that predispose an individual to falling ill with ME/CFS.

The occurrence of ME/CFS outbreaks (for example, Incline Village NV and Lyndonville NY) seems to me sufficient evidence that there are also common missense mutations (population allele fraction greater than, say, 0.15) that predispose to the disease.

This would make ME/CFS a high prevalence, low penetrance syndrome.

Do you find this argument convincing?

Can somebody interpret this ?

Good find Raghav indeed. Bravo and thank you. Any news about the metabolic trap trial from anyone on this site???

 

[HowToEscape?]

Was browsing through the ResearchGate site on ME/CFS, update posted by Dr. Robert Phair 5 days ago

https://www.researchgate.net/project/Etiology-of-Chronic-Fatigue-Syndrome

Don't ignore common missense mutations when searching for genetic predispositions to ME/CFS
Plenty of CFS researchers are searching for rare (population allele fraction less than, say, 0.03) missense mutations that predispose an individual to falling ill with ME/CFS.

The occurrence of ME/CFS outbreaks (for example, Incline Village NV and Lyndonville NY) seems to me sufficient evidence that there are also common missense mutations (population allele fraction greater than, say, 0.15) that predispose to the disease.

This would make ME/CFS a high prevalence, low penetrance syndrome.

Do you find this argument convincing?

Can somebody interpret this ?

I actually have no clue, but I can't resist guessing. It sounds like it means
"There's a substantial fraction of the population who have the genetic makeup which makes it possible to get this disease, but only a small number of those will actually contract it."

 

[anni66]

I actually have no clue, but I can't resist guessing. It sounds like it means
"There's a substantial fraction of the population who have the genetic makeup which makes it possible to get this disease, but only a small number of those will actually contract it."

Yes. I feel it will be the combination of mutations which will predispose people, not simply a certain one.
There will probably be a variety of potential combinations which could all lead to the same end state.

 

[frozenborderline]

Any update on this research? I know Ron Davis and his team are working as hard as they can... I'm looking for a little hope. People talked about this research maybe being done by the end of summer?

 

[ljimbo423]

Any update on this research? I know Ron Davis and his team are working as hard as they can... I'm looking for a little hope. People talked about this research maybe being done by the end of summer?

I don't think there's any additional info yet. There almost certainly will be an update though, at the OMF symposium on Sept. 29, if not before.

 

[Belbyr]

I 'expect' to hear something big at the OMF conference.

There are other research groups that have made great progress in CFS and might even have a biomarker and/or cure in hand. It's just not applied or tested yet.

ME action just sent out requests for 10,000 CFS DNA samples this past week to compare a biomarker they think they have through Dr Klimas group

 

[frozenborderline]

"A cell is a strongly integrated system and all its reactions are coupled to one another. In the normal cell the reactions are coupled in such a way that activity improves activity. Desaturation promotes further desaturation, and exercise
makes us stronger, but coupling is a two-way street, and factors which inhibit normal interactions may be coupled in such a way that they cause further inhibition. An inadequate desaturation may inhibit desaturation. This can push the cell into a vicious circle which the cell is unable to break, and Ieads it into a state of disorganization, landing it in the proliferative CY? (greek symbol didn't translate) state. If the situation is not corrected this situation may become constitutive, irreversible."

Albert Szent-Gyorgyi :
"Cancer and the Living State"
(He also basically argues that desaturation is vital to the living state, because it allows redox reactions to occur, the full piece is above my energy level to read rn but I have pdf)

 

[bthompsonjr1993]

Did anyone watch Ron's most recent video from IIME? He says that we will know whether the trap hypothesis is true in "several months to a year"

 

[frozenborderline]

A year :/



Not faulting ron at all, that's just a long time to wait when this ill

 

[shoponl]

Did anyone watch Ron's most recent video from IIME? He says that we will know whether the trap hypothesis is true in "several months to a year"

If anyone else is curious, see 44:00 in

 

[lindaso1]

I read all the speakers updates from the conference including Ron's and it seems we are still in the "figuring out the issue stage" rather than the "I think we have this figured out, let's see what works stage." I had hoped there would be some big announcement at the upcoming OMF symposium but it doesnt seem as likely now. This is A-G-O-N-I-Z-I-N-G (said very slowly). Just any small update (no specific details needed) would be so helpful for morale.

 

[JES]

If the metabolic trap hypothesis is true, and assuming it can be treated as easily as Ron claims at around 44 minutes, then that's still potentially better news than having a working theory finalized but no drug approval, or worse, needing to develop an entirely new drug somehow. Any treatment which doesn't require a 10 year long drug trial as with Rituximab is preferable.

 

[lindaso1]

@JES
Where did you hear the 44 min treatment? Was that in the lecture?

 

[anni66]

Interesting re the overlap with gene expression in autism ( particularly as suramin has been used by Naviaux)
Research in autism is looking at multiple common genetic mutations , not just a single one. It may be a similar combination.

https://www.medicalnewstoday.com/articles/amp/323035?__twitter_impression=true

 

[lindaso1]

It is interesting. I have CFS and my son has Autism & I believe its likely he may develop CFS at some point (always tired, cognitive issues, digestive issues, low immune function). We've done the 23 and me, Prometheus, self-decode & nutrihacker gene analysis & our gene mutations (rare & potentially bad ones) are very similar, while my daughters, who is fine, is not as similar to ours. An answer to CFS could potentially be a windfall for my entire family.