Learner1
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Folks, the reality is something like this (courtesy of Sigma Aldrich):
Preliminary result of furthered improvement obviously leading to health
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Learner1
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That's not what the data says....
"We confirm reports of altered plasma levels of choline, carnitine and complex lipid metabolites and demonstrate that patients with ME/CFS and IBS have increased plasma levels of ceramide."
https://www.nature.com/articles/s41598-018-28477-9
"Metabolomics showed that chronic fatigue syndrome is a highly concerted hypometabolic response to environmental stress that traces to mitochondria and was similar to the classically studied developmental state of dauer. This discovery opens a fresh path for the rational development of new therapeutics and identifies metabolomics as a powerful tool to identify the chemical differences that contribute to health and disease...
...Eighty percent of the diagnostic metabolites were decreased, consistent with a hypometabolic syndrome. Pathway abnormalities included sphingolipid, phospholipid, purine, cholesterol, microbiome, pyrroline-5-carboxylate, riboflavin, branch chain amino acid, peroxisomal, and mitochondrial metabolism."
https://www.pnas.org/content/113/37/e5472
"The most intriguing finding concerns acyl cholines, belonging to the fatty acid metabolism sub-pathway of lipids, for which all compounds are consistently reduced in two distinct ME/CFS patient cohorts.'
https://www.mdpi.com/2218-1989/10/1/34
"Recent studies by Naviaux et al. (2016) demonstrated abnormalities in energy metabolism that affected mitochondrial function in patients with ME/CFS. Oxidative stress markers have been reported as abnormal in ME/CFS with finding showing reduced antioxidants levels and increased markers of oxidative damage (Maes et al. 2011; Kennedy et al. 2005). The proinflammatory cytokines produced during chronic inflammation in ME/CFS was found to trigger the production of reactive oxygen species linking the chronic inflammatory response to oxidative stress (Morris & Maes 2014). Toxic exposures, metabolic abnormalities, and nutritional deficiencies decrease antioxidative capacities in the body and may contribute to the severity of the health status in patients with ME/CFS (Vecchiet et al., 2003)."
https://www.nova.edu/academic-affai...ioxidant-capacity-toxic-exposures-me-cfs.html
gbells
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Ceramides are apoptosis signalers and oxidation is revved up in apoptosis too. You are looking at aborted apoptosis.
sunshine44
The only way out, is through.
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I completely agree that something is happening with absorption and deficiencies in quite a few of us. I think you are onto something. I am bedridden 4 years now and playing with transdermal delivery because i cannot tolerate oraldelivery and have been abandoned by healthcare system.....there seems to be an order and a 'listening within' of when to up doses etc. Although i show deficiencies of many vitamins on bloodwork, i do not think bloodwork is yet sensitive enough to see how its getting in some of our cells etc. I appreciate this thread.
percyval577
nucleus caudatus et al
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Figuring out what the disturbance is, though I don´t thing that it´s an infection.
In my case I suspect that a high driven Mn-action in the immune-system is the reason, though it might be wrong. Also one might think on the possibility that the immune-system impacts geometrical actions, which the last posts have been about.
I again agree. All the tendencies which have been more or less consistently found will hardly account for the disease. Its much more likely that they are downstream-effects.
I agree also in the detail, that cell turnover appears more and more as one crucial candidate, in which respect ever it may be.
percyval577
nucleus caudatus et al
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Thank you. And very interesting observation - thank you again!
andyguitar
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This was one that I found particularly interesting.
percyval577
nucleus caudatus et al
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To me the most sense theoretically makes, that the dopamine system is skewed, being in a wrong architecture.
And practically it will not adjust itself from stuff in normal foods: It would not help sufficiently to change the shape. Etiologicalwise would an any possible impact disturb the architecture, and it would be not too simple to rebuilt it. There may well be predispositions of any kind, but this unimportant anyway.
The following scheme might be my chart to readjust the system slowly, maybe over a year min??
Every stuff can become a bottleneck.
Again: all together won´t do the thing, for some reason, mathmatically to be described.
I want to say that I had and still can have bad effects from I-A): a normal dose of an neuroleptic (antipsychotic) was once worst decision ever I have made, long lasting effects. I now take pretty small amounts of luteoline and never without tyrosine. I add VitC [normal dose] as well which though again takes away Dopamine, making NE.
Zhang et al 2010 on luteolin
II-A): the first three have actions on nitric oxide. (VitC therefore is part with two actions).
As said above, I think II is on geometrical actions, and only small and in tendency single doses will help to rebuild a structure along the geometrical macrostructures basalganglia and thalamus.
Avoidances may be important
1. other stuff: caffeine, alcohol etc.
2. e.g. in my case B6 is bad and already in food Mn must be done carefully.
E.g my case: Mn is ambivalent when taken together with Zn and TYR.
There is a Mn/Zn exporter. Here also the Vitamin D receptor is needed to encode the transporter, so in my case VitD is another option to eat higher Mn containing food, and possibly to have the good effects from Mn even for the rebuilt.
Hope its clear enough. Last theoretical question: Is it the casue and other findings are downstream or will it only be downstream itself (though with longer lasting influence). My guess is on the first possibility.
And practically it will not adjust itself from stuff in normal foods: It would not help sufficiently to change the shape. Etiologicalwise would an any possible impact disturb the architecture, and it would be not too simple to rebuilt it. There may well be predispositions of any kind, but this unimportant anyway.
The following scheme might be my chart to readjust the system slowly, maybe over a year min??
Every stuff can become a bottleneck.
Again: all together won´t do the thing, for some reason, mathmatically to be described.
I want to say that I had and still can have bad effects from I-A): a normal dose of an neuroleptic (antipsychotic) was once worst decision ever I have made, long lasting effects. I now take pretty small amounts of luteoline and never without tyrosine. I add VitC [normal dose] as well which though again takes away Dopamine, making NE.
Zhang et al 2010 on luteolin
II-A): the first three have actions on nitric oxide. (VitC therefore is part with two actions).
As said above, I think II is on geometrical actions, and only small and in tendency single doses will help to rebuild a structure along the geometrical macrostructures basalganglia and thalamus.
Avoidances may be important
1. other stuff: caffeine, alcohol etc.
2. e.g. in my case B6 is bad and already in food Mn must be done carefully.
E.g my case: Mn is ambivalent when taken together with Zn and TYR.
There is a Mn/Zn exporter. Here also the Vitamin D receptor is needed to encode the transporter, so in my case VitD is another option to eat higher Mn containing food, and possibly to have the good effects from Mn even for the rebuilt.
Hope its clear enough. Last theoretical question: Is it the casue and other findings are downstream or will it only be downstream itself (though with longer lasting influence). My guess is on the first possibility.
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percyval577
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The idea to take TYR together with my avoidance/restriction Mn does not prevail, it might though be good once a week or so.
Also bad in my case is to diminish dopamine action (luteolin), it might be good maybe once a month?? I probabaly will skipp it completely after my bad experience with a neuroleptic.
However:
to take TYR together with food seems to be very good, not too fast though. In this manner, I reason, the each specific stuff from food would induce nerve actions prone for each specific stuff and then the additional TYR would replenish the dopamine pool in these cells.
This goes conform with the observation that application of small dose single stuff has helped me but not all stuff together: In single application in small dosage. the TYR physiologically around would replenish the dopamine pool in these cells. But in combo the TYR physiological around would be insufficient quantity-wise and therefore serve further chaos.
This is in accordance with the common observation that stuff works for some time but then looses its effect: In the first time there would be enough dopamine in the cells to induce a good action. but is not supported over longer time because the physiological surrounding TYR is insufficient, quantity-wise.
Another pro is, that this can explain the wide concrete range of symptoms, as dopamine is simply to short here or there, depending on genetics and history. The common in ME/CFS would be the dynamics of impact/impacts.
Also bad in my case is to diminish dopamine action (luteolin), it might be good maybe once a month?? I probabaly will skipp it completely after my bad experience with a neuroleptic.
However:
to take TYR together with food seems to be very good, not too fast though. In this manner, I reason, the each specific stuff from food would induce nerve actions prone for each specific stuff and then the additional TYR would replenish the dopamine pool in these cells.
This goes conform with the observation that application of small dose single stuff has helped me but not all stuff together: In single application in small dosage. the TYR physiologically around would replenish the dopamine pool in these cells. But in combo the TYR physiological around would be insufficient quantity-wise and therefore serve further chaos.
This is in accordance with the common observation that stuff works for some time but then looses its effect: In the first time there would be enough dopamine in the cells to induce a good action. but is not supported over longer time because the physiological surrounding TYR is insufficient, quantity-wise.
Another pro is, that this can explain the wide concrete range of symptoms, as dopamine is simply to short here or there, depending on genetics and history. The common in ME/CFS would be the dynamics of impact/impacts.
percyval577
nucleus caudatus et al
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Slowly the following scheme has arisen over the last year and since summer 2018:
Application changes a bit over the course of time, as far as I can see from the hindsight.
Schemewise though it's from A to C and from 1 to 3 in different possibilities.
At least recently I found best always to begin with a 3.
Eg in zigzag with B two times incremented.
or one column from 1. to 3, or the whole thing not in zigzag.
Zigzag might be best.
I know for certain, that at begin 1. was more important than 3, now its 3, and 1. has probabaly fallen away.
Column C is relatively new and for now more important than column A.
Most decicive might be column B!! And now enough B3:
Then two years ago I had very good effects from inhibitory molecules, which stopped after four months. Now its back again, but seldom enough, maybe two each second day. I 'll see.
This might work in an ongoing manner only with a
occasionally taken.
Theoretical approach is given above, in a prelaminary manner.
[B3 has been shown to work on mitochondria in the nucleus accumbens,
TRP seems to me to work on the frontal part of the nucleus caudatus (here acetate diminshes actions!)]
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percyval577
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The approach has developed probably almost to its final state.
all in small amounts in water, but often over the day
roughly columns up and/or from left to right
last two columns so far interchangeable
last column consists of inhibitory stuff, being carefully as might be bad then
first line stands extra but most often convenient after line two
but Zn in more normal amounts only somethimes or transdermal
first three columns I can tak at least now alltogether, very easy then, but even smaler amounts.
(thereby B2 lowest, and so on, needs to be checked out after having gotten a feeling)
then sometimes inhibitory stuff.
for the ratio B3/TRP see also above, now best 12 : 1 dosages = 198 : 250 mg (for a week or so)
Cl in MgCl.
The Bad History: passiv smoking and alcohol in food + Mn from ticks (4 years old - I remember the impact)
Probalby already born with something (a very little anomaly in the ribbs may hint to it).
Then infectious event might have given the rest, but my EBV has a Mn-action as well.
It seems it's now a matter of being patient and doing it adroitly. Approach has taken four years to come to this here.
Theory
massive deregulation in the basalganglia + thalamus
crucially in the caudatus when the synaptical firing will not come from the smal end to the front and into the accumbens
the stuff should be used by the brain for communication (the possibility of the deregulation) Such a communication has been shown for nitric oxide, only difference thats a gas, so what
all in small amounts in water, but often over the day
roughly columns up and/or from left to right
last two columns so far interchangeable
last column consists of inhibitory stuff, being carefully as might be bad then
first line stands extra but most often convenient after line two
but Zn in more normal amounts only somethimes or transdermal
first three columns I can tak at least now alltogether, very easy then, but even smaler amounts.
(thereby B2 lowest, and so on, needs to be checked out after having gotten a feeling)
then sometimes inhibitory stuff.
for the ratio B3/TRP see also above, now best 12 : 1 dosages = 198 : 250 mg (for a week or so)
Cl in MgCl.
The Bad History: passiv smoking and alcohol in food + Mn from ticks (4 years old - I remember the impact)
Probalby already born with something (a very little anomaly in the ribbs may hint to it).
Then infectious event might have given the rest, but my EBV has a Mn-action as well.
It seems it's now a matter of being patient and doing it adroitly. Approach has taken four years to come to this here.
Theory
massive deregulation in the basalganglia + thalamus
crucially in the caudatus when the synaptical firing will not come from the smal end to the front and into the accumbens
the stuff should be used by the brain for communication (the possibility of the deregulation) Such a communication has been shown for nitric oxide, only difference thats a gas, so what
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percyval577
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This application actually works now relatively very good. I guess it must realy be small amounts: just as much, that good action would be served, but not that much, that also bad actions from the past would be served.
In general ca. with selling dosages as a normal:
B2 < B1 < B7
LYS < B5 > BCAA
Its a 12th of a B2 normal dosage, a quarter of a B1 normal dosage, a half of a B7 normal dosage;
LYS a bit from a capsula, B5 a little bit more from a capsula, BCAA realy a bit only
into 0.75 L water.
It feels as the BCAA's would serve the circumdirection of the funnel of the caudatus, so have no inherent direction to the front.
Anothe question is, how many other needed stuff may not be included in this specific list. The more, the longer it will take. But a fast success will not be possibly anyway, according to this approach.
percyval577
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A slight but important change:
BCAA are the entrance, and B3 / TRP close a round (not as convenient as the entrance)
So, one strong influence woud be missing, probably an amino acid.
BCAA are the entrance, and B3 / TRP close a round (not as convenient as the entrance)
So, one strong influence woud be missing, probably an amino acid.
percyval577
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To my surprice tyrosin fits in here. Indeed strong.
TYR was my first longer lasting and good influece, but later it got aut of work and then had a bad effect. Last year it worked for some time again and then turned bad. It probabaly came back because of the intake of iron, which I lately had good effects from (not earlier, maybe because the supps came with VitC)
As having said, I think that the all the stuff works on geometrical directions of nerve cell firing. Although the effect can change over the course of time, the following interpretation stays possibel in how it feels (with basiccally desireable foreward projection vs undisereable backward projection). For the nucleus accumbens the effect of B3 has been shown.
Now, there are two parts of the pallidus:
globus pallidus medialis
globus pallidus lateralis
So, there could be an additional row, maybe with methionin with one of the parts, as I suspect from earlier good influence (MET though might serve aging, as deprivation delays aging). This would be somehow interesting as MET is the first step in builing up proteins, even in the cases, where it is removed later, and here it would work in the innerst part (gp medialis).
percyval577
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Posting it mainly for myself here:
Methionine_production-a_critical_review
review basal ganglia pmc/articles/PMC7020857/
The review on the basal ganglia shows mainly that not that much insight has been achieved
The review on MET mentions some interesting MET related diseases.
MET and BCAA's seem to corner stones in my disease.
I had two times a pronounced bad effect from taking them together (very low dosage).
But each with some other stuff each may be key indeed.
Methionine_production-a_critical_review
review basal ganglia pmc/articles/PMC7020857/
The review on the basal ganglia shows mainly that not that much insight has been achieved
The review on MET mentions some interesting MET related diseases.
MET and BCAA's seem to corner stones in my disease.
I had two times a pronounced bad effect from taking them together (very low dosage).
But each with some other stuff each may be key indeed.
percyval577
nucleus caudatus et al
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It turns out that I should take actually none of the molecules/atoms together, as it caused noese blooding which was initianally induced by a single intake of a D2 antagonist. Nevertheless there is a relationship to BCAA and MET.
Then I tried VitA, the last to try, with some strong but ambivalent effect. https://en.wikipedia.org/wiki/Vitamin_A It seems to act on the whole of the nevers in quastion, wheras the other ones seem to have specific regions where they act predominantly.
Apart from a D2 agonist I probabaly won't have any more idea. It probaaly will take 2 years minimum as far as I would estimate, nevertheless it workds, hopefully to full remission.
Then I tried VitA, the last to try, with some strong but ambivalent effect. https://en.wikipedia.org/wiki/Vitamin_A It seems to act on the whole of the nevers in quastion, wheras the other ones seem to have specific regions where they act predominantly.
Apart from a D2 agonist I probabaly won't have any more idea. It probaaly will take 2 years minimum as far as I would estimate, nevertheless it workds, hopefully to full remission.
percyval577
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the new stage then is (all only in sips, modul 2 in the order roughly as given)
modul 1
B3 + D + orange oil (simply in eg orange juice, I guess a D2 agonist)
modul 2
pre : B3
main: lysin --- tyrosin --- BCAA
side: B2 ------B1 --------B7
the bottleneck seems to be the accumbens (so alcohol in food during cildhood)
the line B2-1-7 holds already for years, but is least imnportant. modul 1 is completely new.
modul 1
B3 + D + orange oil (simply in eg orange juice, I guess a D2 agonist)
modul 2
pre : B3
main: lysin --- tyrosin --- BCAA
side: B2 ------B1 --------B7
the bottleneck seems to be the accumbens (so alcohol in food during cildhood)
the line B2-1-7 holds already for years, but is least imnportant. modul 1 is completely new.
percyval577
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the inhibitory line is now with also B3 (accumbens) and newly B5 (shown to be elevated in ME/CFS)
B12 -------TAUR--------VitC
there is also a role for K(+), Cl(-) and Mg, which stays uncetain for now.
B12 -------TAUR--------VitC
there is also a role for K(+), Cl(-) and Mg, which stays uncetain for now.
percyval577
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I finally will get it then ... It has simplyfied in a manner:
1a. [B3 >> B9] = [B7 < B1 > B6 > B9] > [B12] ................... 1b. [B3 >> B9] + [KCl (occasionally)]
2. [B3 >> B9] +[Ni - - -]
3a. [B3 >> B9] = [BCAA > TYR > LYS] > [TAU > VitC] ......... 3b. [B3 >> B9] + [MgCL (more seldom)]
Extra. B3 after eating (good brand here: Kal, taking a quarter pill = 62.5 mg) and B9 10-40 minutes later, here a sixth or even a eigth of a standart pill, maybe 0.8mg, can be very strong.
When taking slow amounts in Water (fast resorption), the different mixures must not be taken together, importantly.
Good is taking it in Breakfast Nut Creme (containing manganese) (slow resorption), here the different mixures can be taken together, can be strong.
VitD can nalso be taken in the creme, I use an extra one so far, will see. In coffee I ever put some VitD in form of a fraction of a tablet.
Note that B5 is lacking now, it has been reported to be high in ME/CFS. It might be, that it fits in in 3a.
I think this will be the final knowlwedge here, after six years working on the approach. I hope for 6-18 months.
Agmatine might be heplful, though it has been roprted to be produced by heliobacter pyori in high amounts and maybe causing the typical ulcerus, so not a good idea to take probably.
3a is still a bit unclear, maybe splitting it up.
1a. [B3 >> B9] = [B7 < B1 > B6 > B9] > [B12] ................... 1b. [B3 >> B9] + [KCl (occasionally)]
2. [B3 >> B9] +[Ni - - -]
3a. [B3 >> B9] = [BCAA > TYR > LYS] > [TAU > VitC] ......... 3b. [B3 >> B9] + [MgCL (more seldom)]
Extra. B3 after eating (good brand here: Kal, taking a quarter pill = 62.5 mg) and B9 10-40 minutes later, here a sixth or even a eigth of a standart pill, maybe 0.8mg, can be very strong.
When taking slow amounts in Water (fast resorption), the different mixures must not be taken together, importantly.
Good is taking it in Breakfast Nut Creme (containing manganese) (slow resorption), here the different mixures can be taken together, can be strong.
VitD can nalso be taken in the creme, I use an extra one so far, will see. In coffee I ever put some VitD in form of a fraction of a tablet.
Note that B5 is lacking now, it has been reported to be high in ME/CFS. It might be, that it fits in in 3a.
I think this will be the final knowlwedge here, after six years working on the approach. I hope for 6-18 months.
Agmatine might be heplful, though it has been roprted to be produced by heliobacter pyori in high amounts and maybe causing the typical ulcerus, so not a good idea to take probably.
3a is still a bit unclear, maybe splitting it up.
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