my low manganese diet - my success so far

percyval577

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I made up a list 28 months ago of manganese need in men. It should match up with the paper Learner1 have put. But her paper shall be better than mine.
I surched for about three weeks on that issue but could not become afraid. I asked a physcian.
Where I detected any sideeffect I put an underline.
Sometimes I eat more manganese, with fat it will get resorpt slowy, fast resorption I feel within 10-25 minutes.

  • for proline hydroxylation - (well known from lack with vit C with scorbut)
  • glycosyltransferase - (for bones, I can´t remember if for joints as well)
  • arginase - (very important on the short run in the liver because of removing poisening ammonia)
  • SOD2 = Mn-SOD - (see disscussion above with Learner1)
  • pyruvate carboxylase - (making energy out of proteins, as I had grasped it)
  • glutaminsynthetase - (for the main type of nerves, lack of coordination when eating to much non-mammal. I got the lack removed quickly by eating some carrots.)
  • for making sperms
  • for insuline - (at the end of pancreas (?) an irritational feeling, could also be one of the lots from ME/CFS that appears now in an random manner. I ate sometimes a lot of sugar)
  • for melanine
  • for prothrombine - (two times out of six I had obviously thin blood)
  • in respect of choline
al lot enzymes can alternate between manganese and magnesium,
so one might take magnesium (I do only sometimes for a couple of days). They should be found in:
  • Dobson et al. 2007
  • Au et al. 2008
  • Cabreu et al. 2010
 
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percyval577

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Big catastrophes after big mistakes at the beginning

When I firstly looked at manganese amounts in nutritation it became soon clear that the main food would roughly consist out of fruits, vegetables, meet, and yoghurt, some sugar. But no beans, nuts, bread. No tee anymore, but coffee, beware of it as well with plants, I needed to learn.
I didn´t mind to much but bought what I liked out of that list not investigated in detail. It might be enough.

The first day I felt only in another manner. The second day some good happend!!
Then for one week, I could see into eyes, fel even in love with an old woman I had now to bring about every day (she didn´t like to spent the day elsewhere). I had all a good voice. I sleep well enough since then.
Then the mistake with tea - for eight days very bad, cortex with glass on all the surface.
Then the same with three coffees with milkpowder, stupid.
Then the same with coffee with oranges (so coffee needed my stomach empty from plants, why?)
Small mistakes - six or seven walnuts, one spoon beans, but bananas did´nt any harm the first three or four weeks - popped up 22 hours after I made them, and were lasting for about 28 hours. Then conscieness wanted to clear up again (but only three times did - but what good!!) (it all was in late summer/autumn, where, as I know now, melatonine grows higher too.)

Then kidney beans with "300µg" - never again (they contain 3000µg)
I ashure, that´s horror, one might still not be able to imagine what brain can make with its energy, one would not be wanting to live longer as for about two more weeks. Torture, even geometrical torture, out of the ears cones with some little points rotating out but with backward-direction, the skull folds open neckwards, a mighty cold front is creaping high from-out the toes, the eyes squashed aside, breathing around can not happen anymore, only up and down. No sleep of course.

In october I was for three weeks completly fine, only a dark underground has stayed, but could rest there if it wanted. Half a walnut changed that state three times for two and a half days.

The next big mistake I made stirred up end of november. Looking for realy low manganese because good moments didn´t come along any longer. I bought three appels and cheese - never again I ashure (so I had to learn, milk and yoghurt as well led to high manganes uptakes, so my experience with yoghurt and only three little grapes).
Then winegums of good quality (and I was stupidly hungry), probably the spinage ones.

Then 10 months later, maybe because of autumn?, chocolate, that was for three weeks in spring at least at short run completly harmless (probably because of oxalacid), gave three weeks quit seriouse a more darkening and a more prison-feeling. Then chips gave me sudden strong depression-attacks for two weeks.


(The brain is the most complex structure in the universe we know about
And one quarter of the brain consists of immunecells.)
 
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percyval577

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During the winter I ate mostly potatoes with fat. One week without them induced no change, but in (next) summer they gave me a bad feeling.
In late summer only a few particels of almond announced their manganese at particular places in my brain (luckily this calmed down soon, I had much worse expected, knowing all over announcements).

Well, since spring/summer 2016 I could not work anymore, the first time only because I worked as a cardriver for people with dementia (to look at the traffic, to care for the people), then because of sudden seriouse particular crashes I hadn´t had before (e.g. walking some distance, and then suddenly, but being still able to talk) - while I don´t feel anymore exhausted in the whole!!! right since I´ve started (this needs to be understood as well).
 
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percyval577

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I think there are mainly two reasons why thinking passes trough a worsening when generel improvement takes place with some speed (not to slow as you would feel the effects very less, not immediatly as than all the missconceptions would fall small in comparison to realy good synapses and their probability to act/to get restrengthen).


1.
If there is realy a positive feedback Acetylcholine - Nitric oxide (I´m convinced), it will lesson, say, like so:

nucleus accumbens (=abilitiy to concentrate) with high ACh : most other regions of the brain with less ACh = ratio
(8x8=64) : (5x5=25) = 2,56
(7x7=49) : (4x4=16) = 3,0625 ........... total improvement with worse ratio not in favour for concentration.

This would explain my experience pretty well, but of course would need further investigation (math. function).

2.
The turnover in making new synapses and resolving synapses will (luckily) decrease.
But on every new state of a (luckily) total less amount of synapses
there comes the amount of new synapses that would fit the last total less amount of synpases
and therefore is to high (the faster the normalisation the more it is to high).

This will happen when a new amount of nitric oxide from the immunesystem is produced
and nitric oxide will arrive chaoticly (induced from manganese intake which I felt in this manner or from pathogenes)
and not a bit sructured as nitric oxide from the nerves.

This would explain why I am nowadays erruptive, why I cannot see well - in combination with
that these abilities should work by more space in the brain than basic feelings.


As this will happen in principle (if the nitric oxide hypothesis is true) and from every improvement
it could deserve further investigation in the symptoms section.
 
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percyval577

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When I started the quit low manganes diet I thought to be infected by borrelia
(I got tested positive one year later by an universitiy hospital, and even a second time).
Therefore my quit low and even over months very low manganese diet:
Borrelia seem to have a very big need for manganese
as they accumulate it up to a very huge amount no other cell is able to
but contain almost no iron
  • Posey and Gheradini 2000 - "Lack for a role of iron in the Lyme disease pathogen." in: Science
  • Aguirre et al. 2015 - "A Manganese-rich Enviroment Supports Superoxid Dismutase Activity in a Lyme Disease Pathogen, Borrelia Burgdorferi." in: The Journal of Biological Chemistry

After two years I got some fungi with my food and my symptoms grew higher.
Only then I thought on to hypersensitivity.
Borrelia then would be one possible cause of high manganese level in man.
When they divide in two or change shape they will release
some of their high manganese level to the bloodstream.

If this theory of hypersensitivity was not only true (I think it is)
but also would be of some weighting (here I can not judge)
then this would be great, not only for practical reason.

It could explain why this dubious disease has built up the last 60-100 years.
  • the hosts of the ticks (possibly with borrelia) have increased because their enemies have declined
  • man is consuming more milk since around 1950 which elevates manganese uptake, this should be found in: Biesalkski et al. Stuttgart 2004 -"Ernährungsmedizin." (I don´t know how much the research has grown.)
  • man is eating all the time, which would not allow proper downregulation of iNOS (steadily quit some manganese comes up)
  • taking in account that the consumption of sugar has increased as well, we could try to state: Candida will be served by sugar, and candida will also be served by manganese as it is slightly high in them, and Candida albicans in special would be served at some point (Li, Gleason et al 2015, about copper). Candida albicans was also found once to be elevated in fatique patients (Evengard 2007). So here as well might be a steady source of some manganese in man or some interdependences.
  • unknown sources of manganese from other modern changes

Further points might be:
  • it could fit easily into genetic prevalence
  • taking in account that allergic reactions (in generel) have become elevated as well, one might boldly state that these reactions have been elevated by to much manganese as well -- the evidences then would be a not only a great help for our difficult sake, but would be great in itself.
 
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percyval577

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Trying to figuer out possibilities of weightening ratios, there still is a numbering:
  1. looking for a somehow serious infection
  2. lessening any hypersensitivity of the inducible nitric oxide synthase (immunesystem)
  3. trying to lesson the symptoms (in my opinion the effect of to much nitric oxide esp. on nerves)

If there is an infection that can be found, treated, and everything is fine, there would be of course no need for 2.

If there is an infection that is steadiliy not found and not known about, or cannot be treated, it is not easy to say if 2. might be helpfull.
It could be that the nitric oxide production gets driven high over the time (unneccesary high). I find it to be quit likely.
But it should be considered of as a danger too: to less nitric oxide could diminish pathogenes DNA mechanism to less,
and therefore could be nicely good for them.
Well, my confidence would merely be that the immunesystem easily gets driven high (safety first), and then possibly to high. And animals in generel don´t live long - but it might get to high over longer lifetime, not in favour for older people of mankind.

(Trying a backwards effect 2. -> 1.)
An overacting immunesystem might be recognized as a problem, as it might bring the microbiome of the mucous membranes out of balance: here to much done, and other things will follow to fill the new gap, and are more a problem now. Here it would be all about missorganisation. The bad outcome could easily be served eating this or that.


Then there are obviously specific hypersensitivities, for example:
The moldies who like to make for the desert and feel good there,
but feel bad when some mold has arriven, that no normal person would feel.
Might it be helpfull to stand mold, that means without much manganese?
Or might it be helpfull to flight mold, without much manganese?

Here, could it be that fungi will hinder the downregulation of the nitric oxide production of the immunesystem?
Then they needed to be avoided at as much a rate as possible.
The reason should be (if true): They are not prokaryotic cells but eukaryotic ones, and could be more difficult to be detected, (but) only TLR2 (if I get it right.) 2. Only in later stage in the process of evolution they might have played a role for the multicellular organisms (but the earliest fungi so far are known to be 850.000.000 years old, the onset of multicellular organisms should be a bit later?). 3. They might be of a specific danger (maybe somehow static). 4. I would like to guess that there isn´t any/much symbiotic realtionship between man and fungi, such as there are manny ones of huge importance between man and bacteria.
 
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percyval577

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The two possibilities in generel:
Might it be helpfull to stand xy, that means with not much manganese, for lowering iNOS expression with a strength?
Or might it be helpfull to flight xy, without much manganese, because it will lower better this way?


Are there any specific bacteria, that might be used as a inducer for regauging?
They would be helpfull when they increase for some time if manganese is not high or is even low
Different infections under not much manganese would lead to different results.

Or might all bacteria do as inducers for regauging?
Same thing, but we would expect less different results.

Would a virus be a direct "source" or would it work indirectly by decoying the immunesystem and helping bacteria?
Somebody in the forum has told to feel better when he catches cold (but not any more thereafter).
So this indicates that the first possiblility might be not completly wrong.

Evaluating the huge complexitiy of immunereactions and our small knowledge
we could even imagine that there might be differences in different persons
coming from different histories of infections as well as from slightly different genetics.


One further guess along with the first possibility.

Eating ham, I felt significantly worse than eating sausages.
Well, I thought, it´s different manganese uptake (not quit logical).
A bodybuilder then brought me up to the right way of thinking:
In ham, there are more bacteria. Whereas in sausages there are very few due to sodiumnitrit.

Than I tested taurine, here and there, and now:
Taurine with sausages did not induce much good effect, if at all.
Taurine with ham did induce quit a good effect, leading to the abiliy to do something.

How on earth is it possible?
My guess would be, taurine could allow to downregulate iNOS using all the bacteria within the ham
and this leads to a quick result, that appears for the next hours.
And sausages did on their own already an effect, due to sodiumnitrit reducing bacteria,
but taurine here would allow for what is not complete due to the lack of enough bacteria.

Well, after a few months the effect dissapeared. This is a long time
considering that most drugs lose their effect within ten times (very very optimistic)
but supplements (natural, own stuff) in generel do longer and will come back to good effects.
One should but consider also that taurine is huge in the body.

This interpretation of the effect, using (1), would need to get differentiated from
that effect of taurine on the GABA system (2), which should help too.
  • (1) Redmond, Wang et al. 1998; Askwith, Zeng et al. 2012
  • (2) Caletti, Almeida et al. 2015
 
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percyval577

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Two times I experienced a significant improvement (since I have gotten sick in 2001 starting from EBV):
  1. [with a quit good mood then in 2008-2010] --since 2004 not much manganese, --ca. 2006-2008 low sugar
  2. [as described] --since aug 2015 low manganese, --since dec 2017 low sugars

Since 2008 sugar reappeared [without any negative effect].
Since May 2010 I replaced meet in favour of beans and the likes [with a strong negative effect then in Aug 2010].

The very negative effect in 2010
shows manganese as a cause,
but it is not completly clear if it would have appeared if I had not eaten sugar since some time.

The positive effect since 2015, that has still not reached its goal,
shows manganese as an influence and
shows sugar as an influence (the process seems to have fastened up, with even more difficulty to think).

Evaluation in detail therefore is not possible.
So far both interpretations are possible the infectiological one, and the immunological one:


Sugar and manganese would serve candida albicans
manganese should serve Borrelia severly
and than there might be inconvenient symbiotics.

It may seem most likely that C albicans has had his opportunity, may be with Borrelia, even inside.
But Borrelia are so slow in dividing, are found in such small amount (I didn´t surch for original sources),
that - being generous - they as a normal infection should be unimportant, despite antigenevariation and so on.
Well, they contain "two times of magnitude" more manganese than yeast - this I would recognize to be the big issue,
why they chould induce so much nitric oxide (see literature above #25 in combination with #16, #18)
why they can make so much seen damage in joints and what ever (yet here hasn´t been any further research as far as I know).

Manganese should be regarded to be able to change immunereactions, at least in respect of nitric oxide.
To small extent this might go for sugar too, so I have read somewhere but never surched for sources (having found it unimportant, and having had a need for the energy).


So the conclusion is: I would like to hope
that the modulation of the immunesystem (in respect of nitric oxide, maybe even further, who knows)
is not only likely, but would be of some bigger weighting too,
because than we could take influence on our high driven nitric oxide production
with its dysfunctional effects on nerves (especially I think), on mitochondria, on vessels (rush, pounding headaches?).

The causes for me/cfs shall be as far as I can see:
  1. A somehow serious infection (known infections, unknown infections)
  2. The immunesystem itself, even under rather normal conditions (if realy possible), with hypersensitivity
  3. A structural damage in the body e.g. thyroidal, maybe mitochondrial (in our respect)
In the second case all could be treated
(well ... I went five years the wrong direction, and now maybe five years the other)
In the cases of 1. and 3. the situation would remain more unclear
because the weighting ratio between 1. or 3. and 2. is unclear
(in regard to nitric oxide production, to which hypothesis this manganese interpretation is bound)
 
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percyval577

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If the guess I ´ve made here would be true
that high manganese, averaged over time and strength of infections,
is responsible for an overacting immunesystem in respect of nitric oxide,

it would be urgently a matter for prophylaxis to concider manganese uptake.
Not only very high but already quit high manganese levels
could be a serious danger. This danger, i.e. in view of the crucial brainwork,
might have been a restriction since old times for more manganese utilization.

Fore this danger and suggesting itself it may be a matter for research to find out
if I am guessing right (with all the research behind me, #16,#18, even #25) or not.

I ´ve talked about a strange negative treatment, to do something (manganese) less to the body.
If there could be a positive treatment, blocking some receptors
(maybe manganese detector GPP130, not to be confused with the better known Gp130)
remained to be reasurched. This positive then would be the chance to treat symptomaticly
damages in the body and infections which could not be removed (causes 3. and 1. above).
End of the 1st Conclusion
 
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percyval577

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Clusters of tasks.
(Focusing on cause 2.) - The underlying possibility of our disease
would be the tuning or finetuning of the nitric oxide production (using arginine)
of the immunesystem in respect to a healthy amount of bacteria (inducing the production anyway)
because the nerves (and vessels) are using nitric oxide as well.
(The tuning would have not prepared itself during the process of evolution for high manganese levels.)

Nitric oxide (NO) diffundates easiliy through cellmembranes being the cause of its usage.
The three well enough known nitric oxide synthases are:
  1. constitutive: NOS1 = nNOS neuronal nitric oxide synthase
  2. inducible__: NOS2 = iNOS inducible nitric oxide synthase (of the immunesystem, microglia, macrophages)
  3. constitutive: NOS3 = eNOS endothial nitric oxide synthase
An eryNOS erythema nitric oxide synthase has been guessed or shown recently.
A mtNOS mitochondrial nitric oxide synthase has been guessed or shown in the past
but its now mostly recognized as a technical aspect i.e. as the technical source of NO
(funny enough, as the possible product peroxynitrite ONOO-
that builds up from NO - and from some of the O-molecules around - likes to damage mitochondria membranes).

The purposes of the NOS´s (which build NO from arginine)
  1. nNOS - with good possibility: the mechanism of memorizing and conditioning, or - in other sight - of neuroplasticity. So the mechanism of conditioning would be ill (to condition us is mostly nonsense, if not even contraproductive, being honest).
  2. iNOS - Fighting pathogenes, slowering some DNA-mechanism there.
  3. eNOS - Helping more blood to stream around.
Guess on possible storages
The constitutive synthases should need to be long term prepared for their task
probably with quit a storage of arginine, and only getting restored from the blood.
The inducible synthase must be much more flexible, coping with quit low or even very high activity and need.
Therefore it should be served with arginine from all over the body using the bloodstream directly.


Arginine (Arg) is specially used for three tasks:
  • in the liver very importantly, removing the poisening ammonia from intake and resolving of proteins
  • for the NOS´s - including iNOS
  • wound healing -
So, if the animal is wounded, a lot af Arg would be released into the bloodstream from all over the body (I would guess according to the guess above).
It now can be picked up by more than one task-complex - wound healing and iNOS (bacteria in the wound).

-> The probability to pick up this (now necessary) molecule has arisen this way
-> in comparison to use two different molecules. So it realy makes sense. (And may have in the process of evolution).


Manganese (Mn) - Being wounded means
to make proline using Mn, and to need more thrombine having used Mn
and with some more bad luck even to heal bones using Mn,
and of course fighting bacteria, using Mn now as well, helping to indicate high activity,
and maybe even to enhence argininase (using Mn) for making more human proteins.

-> Same story of probability,
picking up this atom from the bloodstream for all tasks that hold to each other by chance.

And a big wound could - it´s speculative - switch/have switched on telomerase (which in self-ill circumstances acts in cancer or acts often in cancer, I havn´t dived much in) using Mn (some doctors think it is normaly expressed, but as far as I know it has been shown to be silent in adults - further research with more differentiated investigation might occure). This would enable the cells to divide more often or more rapidly, taking care for the ends of the DNA.
 
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percyval577

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What I wanted to say is
not only that such theory of clusters of tasks may be pretty sensible
but that in case of Mn in particular it may support (us) with a lot of coherence (for any evidence).

Though the following attempt on evolution stays fairly speculative, and does not become only quit speculative,
{neglecting for now and here different atomproperties}, it may be of some clue.


Looking at the widely used iron (Fe) and the seldom used manganese (Mn)
the question arises: Why so? - as both metals are often found in nature {saying they are potent, for keeping it simple}.

The answere would be: At an early stage of evolution the often found Mn
had become {say more by accident} used for wound healing - most important in such a world we live in.

And this healing-usage then would have limited its use
because it influenced the nerves
BECAUSE it makes sense to influence them
for SICKNESS BEHAVIOUR (to be constructed with some ease or likelihood, in the process of evolution)
when you must heal.

(and sickness behaviour can be caused within the conditioning mechanism, i.e. already logicaly! s.b.
here the ease or liklihood comes, coded then by iNOS and nNOS using the same molecule NO)

So here would have evolved a whole bunch of enzymes sticking nicely together
and other bunches not sticking so nicely together
should have died away in the process of evolution.


The medium of early evolution seawater contains (elected) today roughly (in parts per million ppm):
Cl 19000__Na 10500__Mg 1300__S 880__Ca 400__K 380__Br 65__C inorganic 28/C organic 3__

Al1.9___F1.4___Li0.1___Cu0.09___Fe0.02___Zn0.014___Mn0.01___Se0.004___

Sn0.003___Mo0.002___U0.0016___Ni0.0005___Co0.0001___Au0.000008


So, in a first step manganese would have become used for very important tasks, like iron.
Then it could have become of limited use quantitative - {actually}
due to its huge importance (healing) and then its influence on nerves (sickness behaviour = iNOS and nNOS).

Btw: If I would be such a system, and needed to look further for better equilibria in a brain then,
I would think about nickel (Ni) now [for example}, which should be in use only to small extent.
 
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percyval577

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prae.synapse __ synaptical cleft __ post.synapse

nitric oxide (NO) a) mechanism of conditioning (part of that)

For the main type of nerves (for information processing) it is commonly accepted that the best guess,
indicated by the actions of the drug AP5 on NMDAR´s (and BAPTA on Calcium)
is that these Receptors are responsible for the strengthening of the synapses (for information processing).

The ligand gated ion channels here are to be opened by
Glutamate being their main neurotransmitter.

Whereas the basic acting AMPAR´s conduct Na (+)
NMDAR´s conduct Ca (2+) from extracellular space into the cell.
NMDAR´s conduct more slowly, but stay much longer open.

Only when there has been some AMPAR action,
the NMDAR´s will open (due to more positive charge inside the cell
which will remove the NMDAR-blocking Mg (2+) outside),
meaning now that there some more important things are going on (for the animal).

Ca (2+) then - conducted by NMDAR´s - is a cause:
  1. being (a small) part of depolarization in the intracellular compartment (by its positive charge), leading eventually to firing (having caused now voltage gated channels to open rapidly one after another).
  2. inducing nNOS (it´s postsynaptical). The NO diffundates for about a second -> e.g. Glu-release preasynaptical.
  3. leading to more AMPAR´s in the postsynaptical membrane very quickly (not via gene expression).
  4. leading to more synapses (via known effects on the cytoskeleton actin)

Ever since I´ve come across this I meant that there would be a positive feedback NMDAR-NO,
getting better and better when doing things again and again,
strengthening synapses.

With 4. there is a getting better due to more synapses (according to the deeds).
But already the more AMPAR´s lead (in between) indeed
to some more open NMDAR´s or increased ones (until enough is learnt for now):
AMPAR -> NMDAR -> Ca2+ -> NO -> Glu from praesynpase -> AMPAR


More means more here (at first), because it was constructed
for nerves that learn to appercept outer enviroment how it "is",
or that learn things to do.
(Nerves that fire together are nerves that wire together).

And there could be a positive feedback with acetylcholine
which should be part of that configuration due to the diffundability of NO.
Acetylcholine is common in the brain, and might insist on his own sense as well.
Again, more means more (until to some point where NO-ACh/NMDR should decrease).
 
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percyval577

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What will happen if the amount of NO rises far enough above normality?

Isn´t it like a drawing where more and more lines will lead
no drawing anymore? Nothing goes anymore.
I would say this is feeling exhausted
or sick when more random NO occurs.

Even physically it makes sense
referring to the basic entity of our universe
some waves of energy or so that can be in order to each other
or in disorder, feeling bad and being disabled.

In the process of evolution this would be a given,
a geometrical first law for sense or unsense,
and if there is a being with both sources of NO
it can feel sick.

If there is an infection this feeling shall be helpful:
The being needs to behave calm for the purpose
i) not to be recognized by enemies, ii) to regain its strength.

Therefore:
Other beings that could have used different types of diffundable molecules
and could not feel sick would have gone.


Furtheron:
This first matter of fact should have gotten tied up -
this then would be why
all the treatments we try tend to get at some point out of work:
the brain wants the beings to feel sick.

At least this sickness feeling/behaviour (II) then wants
the being also to be tense but not to be concentrated for the purpose
iii) to be able to flight if necessary.
 
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percyval577

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As I see it now, there are two possible components in my improved treatment,

(1) a time and dose dependent special one (manganese), as described above, though other ones might be in charge as well or instead,

and (2) a nerve breakdown in the gear of the brain, as I would title the basal ganglia and the non-specific thalamus, and Mn would be only one component among many others. I started on the final steps to come, as it seems, here:

https://forums.phoenixrising.me/thr...mprovement-obviously-leading-to-health.80368/


A Mn thing is two times reported (both open access):

Nayaran et al 2020
Informatics Inference of Exercise-Induced Modulation of Brain Pathways Based on Cerebospinal Fluid Micro-RNA in [ME/CFS]


page 154:
Metabolics - Metabolomic alterations have been suggested in CFS.67,68 The list of target genes was searched in Human Metabolite Data Base (HMDB) using Metaboanalyst,69 which identified S-adenosylhomocysteine (HMDB00939), S-adenosylmethionine (HMDB01185), and manganese (HMDB01333) that participate in methane, glyoxylate, and amino acid metabolism pathways (p<0.025).

Whistler et al 2005
Exercise responsive genes measured in peripheral blood of women with chronic fatigue syndrome and matched control subjects

Figure 2: Mn-binding
 

gbells

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I want to tell about and discuss one of two components. The weighting ratio remains unclear so far.


I started my low-manganese diet in August 2015. Slowly but steadily (sometimes chaotic) my missfeelings lessend, and now I even feel good sometimes.

On the other hand my ability to think is worse, and the faster my feelings grow good the more I get shaked - sometimes without being prepared for that horror, "He is crazy." But this can be understood and (my confidence truly tells me) will not last. Sometimes I am already going to be souvereign now (but not often).

As far as I can see I will recover completly.


There might be a second component, a somehow serious infection. It would be thinkable that this component differs from person to person or from region to region, but the first component seems to be common: there are hints enough from good science. I summed them up (for the first time?).

The weighting ratio remains unclear so far.


It is common known that manganes-rich food is not necessary. In respect of low-manganese food I can tell from my experiences:
  • Meet from non-mammals do increase the need for manganese (arginase). I don´t eat them more often than once a week. Otherwise I sometimes had got problems with coordination (glutaminsynthase).
  • Milk, yoghurt and cheese do increase the manganes-uptake strongly. I only consume milk and yoghurt very very isolated (if at all). Otherwise I got to states of mind that you will not bear for some longer time.
  • No physician critisized my food. And until now I cannot detect any damage, but I do not suffer from any other sickness.

In some detail then (it´s in principle about epigenetics):
  • The direct sources of what I think is one of the mainpoints
  • What the reason for the Mn-dependency of the iNOS could be
  • The indirect sources of what I think is one of the mainpoints
I think eliminating manganese, an essential trace mineral, is a TERRIBLE idea and is going to seriously injure you.

Manganese is an essential trace element that is naturally present in many foods and available as a dietary supplement. Manganese is a cofactor for many enzymes, including manganese superoxide dismutase, arginase, and pyruvate carboxylase [1,2]. Through the action of these enzymes, manganese is involved in amino acid, cholesterol, glucose, and carbohydrate metabolism; reactive oxygen species scavenging; bone formation; reproduction; and immune response [3-7]. Manganese also plays a role in blood clotting and hemostasis in conjunction with vitamin K [5].
https://ods.od.nih.gov/factsheets/Manganese-HealthProfessional/
 

percyval577

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I think eliminating manganese, an essential trace mineral, is a TERRIBLE idea and is going to seriously injure you.
Manganese is very abandon in earth crust, its half the amount of that of iron! But the need in biological systems is surprisingly very low. The thread tried also an answer to the question Why?

@percyval577 Manganese is also used in MnSOD used to neutralize free radicals thrown off by the mitochondria.

Have you measured your manganese level?
No I haven´t, but I plan to have my bone measured. If it turns out that they are weak or breakable, I surely will blame the low manganese diet for it. But it cannot be helped, I am still quite sensitive to it. I tried to eat soy yoghurt mixed with yoghurt, and the effect turned soon bad. But I don´t think that I am deficient.


After I had eaten yoghurt with lemon, my hands changed their appearance a bit and at that time they had itchy spots. My upper front teeth got to a quarter lucide, pretty promptly, and sadly my upper jaw went a bit inside, so that I need a devise to protect my teeth during night - you see, not nice at all.

I asked the doctor, if this might have come from my low manganese diet, but she said, no. It was the third doctor answering in this manner.

An indeed more satisfying answer may well be, that the combination of citrate (with generation of NO) and calcium has induced changes in the nerves and their pattern, which would be responsible for the effects. Note also, that its normal that the teeth change position, though not to that extent, at least not as soon as you are old (I might be over 100 now), as the jaw doctor told me. A possible mechanism, as I reason, might be change of cell volume. Indeed, under certains condition, the jaw can go out again.
 
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percyval577

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The inflammatory Potential of Dietary Manganese in a Cohort of Elderly Men
Kresovich et al 2018


abstract, my paragraphs
Manganese is an essential nutrient that may play a role in the production of inflammatory biomarkers. We examined associations between estimated dietary manganese intake from food/beverages and supplements with circulating biomarkers of inflammation. We further explored whether estimated dietary manganese intake affects DNA methylation of selected genes involved in the production of these biomarkers.

We analyzed 1023 repeated measures of estimated dietary manganese intakes and circulating blood inflammatory biomarkers from 633 participants in the Normative Aging Study. Using mixed-effect linear regression models adjusted for covariates, we observed positive linear trends between estimated dietary manganese intakes and three circulating interleukin proteins.

Relative to the lowest quartile of estimated intake, concentrations of IL-1β were 46% greater (95% CI − 5, 126), IL-6 52% greater (95% CI − 9, 156). and IL-8 32% greater (95% CI 2, 71) in the highest quartiles of estimated intake. Estimated dietary manganese intake was additionally associated with changes in DNA methylation of inflammatory biomarker-producing genes. Higher estimated intake was associated with higher methylation of NF-κβ member activator NKAP (Q4 vs Q1: β = 3.32, 95% CI − 0.6, 7.3).

When stratified by regulatory function, higher manganese intake was associated with higher gene body methylation of NF-κβ member activators NKAP (Q4 vs Q1: β = 10.10, 95% CI − 0.8, 21) and NKAPP1 (Q4 vs Q1: β = 8.14, 95% CI 1.1, 15). While needed at trace amounts for various physiologic functions, our results suggest estimated dietary intakes of manganese at levels slightly above nutritional adequacy contribute to inflammatory biomarker production.
open acces​
 

percyval577

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Stephanie O`Neal works on subclinical Mn exposure, which may be interesting for low exposure and accumulation. Paragraphing and stress added for easy reading.


Subacute manganese exposure in rats is a neurochemical model for early manganese toxicity
Stephanie O´Neal et al 2015

from the abstract
However, it remains unclear if subacute, low-level Mn exposure resulted in alterations in neurotransmitter systems with concomitant behavioral deficits. The current study used high performance liquid chromatography to quantify neurotransmitter levels in rat striatum (STR), substantia nigra (SN), and hippocampus (HP).

Subacute Mn exposure via i.p. injection of 15 mg Mn/kg as MnCl2 caused significantly increased dopamine (DA) levels in the STR. The enhancement was accompanied by significantly elevated levels of the DA metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in the STR. In addition, levels of HVA were significantly increased in the SN and HP.

These data indicate that subacute, low-level Mn exposure disrupts multiple neurotransmitter systems in the rat brain which may be responsible, in part, for observed locomotor deficits.
open access​

From O´Neal´s diss 2020, abstract
https://docs.lib.purdue.edu/dissertations/AAI10106198/

Manganese (Mn) exposure is a growing public health concern as new evidence continues to show that high level exposure to this essential metal is toxic. Chiefly toxic to the central nervous system, it produces signs and symptoms resembling, but not identical to idiopathic Parkinson’s disease.

The hypothesis tested in this dissertation is that Mn accumulation in body tissues produces subclinical changes in the central nervous system altering neuronal repair mechanisms and leading to neurodegenerative damage. The studies in this dissertation evaluated the extent of these changes in the central nervous system.

Changes in the toxicokinetic properties of Mn in bone affecting the parameters of accumulation, distribution, and elimination were also identified. Importantly, the half-life of Mn in bone was estimated to be approximately 8.6 years in humans, a finding which will be essential in developing a biomonitoring system for Mn exposure.

Significant accumulation of Mn in brain and body tissues was observed along with significant metal dyshomeostasis following Mn exposure. Several brain regions had altered neurochemistry, and as a consequence, impaired motor function was observed. The subventricular zone (SVZ), one of two neurogenic niches in the adult brain, had the largest magnitude of change.

Therefore, effects of Mn exposure on cell proliferation and differentiation in this region were investigated further. The processes involved in adult neurogenesis were significantly altered following Mn exposure, particularly with regard to cell proliferation. The full extent of the consequences resulting from Mn exposure in the pathology of neurodegenerative disease remains unknown, but the results of these studies demonstrate that although Mn exposure undoubtedly leads to several changes observed early in neurodegenerative disease pathology, no overt neurodegeneration was observed.
full access​
 
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