Might Cerebral Insulin Activity be Part of ME?

[Wishful]

I noticed an article about changes in glucose metabolism in the brains of Alzheimer's victims ( https://www.nature.com/articles/s41591-020-0815-6 ) That led me to find https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237995/ , which as about how insulin regulates some brain functions. Cerebral insulin affects food intake, which some member here have problems with. Cerebral insulin also affects cognitive function, which I think most of us have trouble with. Insulin transport into the brain is via astrocytes, whose function may be affected by ME (chronic immuoactivation).

I'm not claiming that this is the root cause of ME, or anything like that. I just thought it was a suspicious possible link, which might explain some symptoms for some PWME. Maybe someone more knowledgeable will think about it.

Another thing I noticed in the latter link was this:

"In multiple studies and several species (including humans), CSF has been used as a surrogate for brain ISF. Recent findings, however (vide infra), underscore that the composition of CSF measured in the cerebral ventricles or the subarachnoid space of the cisterna magna or lumbar spine is quite different from brain ISF. "

This makes studying ME's cerebral fluids even more challenging. Any findings from CSF samples, positive or negative, may be meaningless for what's going on in specific parts of the brain. I think ME involves glial cells, and the finding above means that working with CSF samples isn't enough. Testing ISF is probably more expensive too.


Just stuff to think about.

 

[roller]

yes, the brain doesnt make sugars/insulin.

so the sugars in the brain must come from the body.
if its too high in the brain, then it must be too high somewhere the body, too?
but its not, for what i understand.

did they find out, where this sugar/high insulin in the brain comes from?

 

[Wishful]

It seems that the insulin enters the brain through astrocytes. That's why I wonder whether it's affected by whatever effects ME has on the immune system.

I just checked; several PWME have tried intranasal insulin with little if any effects, so it's probably not a significant part of ME in general. It still might be an issue for some people.

 

[Hip]

I tried intranasal insulin 15 IU daily a few years back, but did not notice much.

The only thing it did was reduce appetite.

 

[Pearshaped]

I know a of a german researcher who is convinced that in ME glucose can not be used efficiently,for whatever reason.
Our brain is starving,like in Alzheimers.
He suggests a snack with carbs and fat before bedtime to enhance sleep quality. worked for me a bit for a while.

 

[Hopeful2021]

I know a of a german researcher who is convinced that in ME glucose can not be used efficiently,for whatever reason.
Our brain is starving,like in Alzheimers.
He suggests a snack with carbs and fat before bedtime to enhance sleep quality. worked for me a bit for a while.

Hello
Do you know the research of Dr Stephen Cunnane? He has data about how ketones help the person with Alzheimer's brain. 3.0-5.0mmol is ideas.
I'm new to this forum and not sure how to post a link.
I'm keto adapted 4 years approx and saw great improvements for my brain.
When exogenous ketone esters (not the salt mixes) but esters became commercially available in the USA, I tried them and they helped me greatly especially during severe episodes when I could not talk (just stutter briefly) nor walk more than an off balanced shuffle. Mainly a shuffle, dragging one leg.
So indeed there's stuff one can do to help the brain.
I also love Hyperbariac oxygen. I'll be doing two sessions next week just for maintenance.
But recently I added iv glutathione to the end of my IV NAD and that's helped my brain even more.
Looking forward to learning more. I'm very interested in hearing about your experience esp with regards to the brain.
Thank you.

 

[Hopeful2021]

I tried intranasal insulin 15 IU daily a few years back, but did not notice much.

The only thing it did was reduce appetite.

I have a chemist friend who had brain trauma and finds intranasal insulin very very helpful. I prefer to stay in ketosis .... but it is definitely very good to know test it exists and is an option.
so far, I like how a high level of ketones gives my brain a good source of fuel.
Do you recall why you stopped taking the intranasal insulin?

 

[suevu]

I noticed an article about changes in glucose metabolism in the brains of Alzheimer's victims ( https://www.nature.com/articles/s41591-020-0815-6 ) That led me to find https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237995/ , which as about how insulin regulates some brain functions. Cerebral insulin affects food intake, which some member here have problems with. Cerebral insulin also affects cognitive function, which I think most of us have trouble with. Insulin transport into the brain is via astrocytes, whose function may be affected by ME (chronic immuoactivation).

I'm not claiming that this is the root cause of ME, or anything like that. I just thought it was a suspicious possible link, which might explain some symptoms for some PWME. Maybe someone more knowledgeable will think about it.

Another thing I noticed in the latter link was this:

"In multiple studies and several species (including humans), CSF has been used as a surrogate for brain ISF. Recent findings, however (vide infra), underscore that the composition of CSF measured in the cerebral ventricles or the subarachnoid space of the cisterna magna or lumbar spine is quite different from brain ISF. "

This makes studying ME's cerebral fluids even more challenging. Any findings from CSF samples, positive or negative, may be meaningless for what's going on in specific parts of the brain. I think ME involves glial cells, and the finding above means that working with CSF samples isn't enough. Testing ISF is probably more expensive too.


Just stuff to think about.

I am constantly hungry.

 

[bertiedog]

He suggests a snack with carbs and fat before bedtime to enhance sleep quality. worked for me a bit for a while.

I always have a small snack at 10 pm of a no sugar oatcake with 6g carbs and a touch of butter and some natural peanut butter. Usually I will also eat a couple of cashews. When I tried not eating before going to bed I couldn't get to sleep possibly because I have my main meal around 6 pm which is much lower carb, just a small portion of meat or fish with vegetables followed by some berries from the garden and a little yoghurt.

Definitely I have issues with blood sugar and my brain and muscles need my blood sugar to be around 6 for me to be able to do anything physically. I do have a very large number of SNPs that indicate a high risk for diabetes type 2 but I haven't progressed to that thankfully probably because around 19 years ago I change to a fairly low carb diet and have stuck with it.

My problem isn't helped by having to take Prednisolone 6.5 mg daily due to adrenal insufficiency but I had huge blood sugar issues for probably 20 years prior to taking the steroid so it definitely isn't just an issue because of the steroid. I wasn't able to get any stability with my blood sugar and suffered with horrendous hypoglycaemia which gradually got worse and worse. At least now I can guarantee it won't drop like a stone leaving me shaking, sweating with incapacitating panic attacks that used to feel life threatening and completely ruined my life.

Pam

 

[bertiedog]

My experience with ketosis was a disaster and my blood sugar actually went up and would stay there. I don't thing ketosis for anything length of time is a good idea for anybody with weak adrenals btw.

Pam

 

[pattismith]

I know a of a german researcher who is convinced that in ME glucose can not be used efficiently,for whatever reason.
Our brain is starving,like in Alzheimers.
He suggests a snack with carbs and fat before bedtime to enhance sleep quality. worked for me a bit for a while.

In this AD study , they tend to think that Mitochondria-related energy failure may precede glycolysis-related hypometabolism in brain regions....

interesting!


In vivo mitochondrial and glycolytic impairments in patients with Alzheimer disease

Tatsuhiro Terada 1, Tomokazu Obi 1, Tomoyasu Bunai 1, Takashi Matsudaira 1, Etsuji Yoshikawa 1, Ichiro Ando 1, Masami Futatsubashi 1, Hideo Tsukada 1, Yasuomi Ouchi 2
2020 Mar 5.

Abstract

Objective: In vivo glycolysis-related glucose metabolism and electron transport chain-related mitochondrial activity may be different regionally in the brains of patients with Alzheimer disease (AD).

To test this hypothesis regarding AD pathophysiology, we measured the availability of mitochondrial complex-I (MC-I) with the novel PET probe [18F]2-tert- butyl-4-chloro-5-2H- pyridazin-3-one ([18F]BCPP-EF), which binds to MC-I, and compared [18F]BCPP-EF uptake with 18F-fluorodeoxyglucose ([18F]FDG) uptake in the living AD brain.

Methods: First, the total distribution volume (VT) of [18F]BCPP-EF from 10 normal controls (NCs) was quantified using arterial blood samples and then tested to observe whether VT could substitute for the standard uptake value relative to the global count (SUVRg). Eighteen NCs and 14 different NCs underwent PET with [18F]BCPP-EF or [18F]FDG, respectively. Second, 32 patients with AD were scanned semiquantitatively with double PET tracers. Interparticipant and intraparticipant comparisons of the levels of MC-I activity ([18F]BCPP-EF) and glucose metabolism ([18F]FDG) were performed.

Results: The [18F]BCPP-EF VT was positively correlated with the [18F]BCPP-EF SUVRg, indicating that the use of the SUVRg was sufficient for semiquantitative evaluation.
The [18F]BCPP-EF SUVRg, but not the [18F]FDG SUVRg, was significantly lower in the parahippocampus in patients with AD, highlighting the prominence of oxidative metabolic failure in the medial temporal cortex. Robust positive correlations between the [18F]BCPP-EF SUVRg and [18F]FDG SUVRg were observed in several brain regions, except the parahippocampus, in early-stage AD.

Conclusions: Mitochondrial dysfunction in the parahippocampus was shown in early-stage AD.

Mitochondria-related energy failure may precede glycolysis-related hypometabolism in regions with pathologically confirmed early neurodegeneration in AD.