Electrolyte Protocol for Improved Health

[wobble]

Thanks everyone for the great info. Hoping to start this after blood/hairtest.

I was just hoping to get an opinion on whether or not this would be a reasonable replacement for the "Now Foods Amino Acid Powder"..

https://www.amazon.co.uk/BULK-POWDE...TF8&qid=1518731283&sr=1-1&keywords=EAA+powder

It seems to be a lot higher in Leucine, which isn't something I've seen mentioned here much, and lower in histidine which obviously has been. I think I've missed one of the big threads as histidine no longer seems to be getting suggested as a standalone supplement. Would the lower amount in bluk powers product be an issue?

 

[wobble]

Sorry just realised the amazon page doesn't list the ingredients. They can be seen here under the 'nutrition' tab:

Essential Amino Acids

 

[artemis]

I had to get up and throw up.

Canari, how often are you vomiting? If I'm not mistaken, I've seen you mention it a few times. WTF??? This is a serious symptom! I know nothing about anything, but I do know that if I vomited cheese, I would not eat that cheese anymore. And I think I would stop taking ANYTHING, salts included. What do you think is causing your vomiting?

 

[Helen]

Guys , we are testing this. So far I dont see it work. So just wait , no reason to rush in to any of the protocols yet

 

[bruschi11]

Guys , we are testing this. So far I dont see it work. So just wait , no reason to rush in to any of the protocols yet

It works. At least for me. But I think we gotta lay off minerals or at least I do. I think I may just use Eidon electrolytes mineral supplement instead of potassium and magnesium. I'm realizing that both potassium and magnesium doses are messing me pretty badly- I crashed pretty badly yesterday. Will likely use high potassium diet instead.

I have issues beyond pfs though so I think its going to take a bit of time to get balanced. Mercury through the roof currently.

 

[Aleksandr]

Interesting take on it, although it is Dr Wilson who Gbold thinks is crazy (I tend to agree with him after reading a lot of his stuff):

"Chlorine, a cleanser. This is a fascinating element that is found in all living tissue. Chlorine is essential for the function of cleansing the body of debris. It is also exchanged in the stomach to produce hydrochloric acid, a very necessary acid for protein digestion.
Chlorine is a member of a group of elements called the halogens. Others in this group are fluoride, iodine and bromine. The body maintains a delicate balance between all these elements. Today too much chlorine, bromine and fluoride are overwhelming the iodine and causing deficiencies in our bodies.
Deficiency of this element is non-existent, unlike all the other electrolytes. The reason is that chlorine is part of salt (NaCl). Most people eat too much, rather than too little table salt, as it is found in almost all prepared and processed food items today. Thus we do not focus on this element in terms of deficiencies.
In contrast, excessive exposure to chlorine is a severe problem. Too much table salt and chlorinated water are the main sources. Some bleached flour products are also sources. Environmental contamination of the food, water and air are constant sources of this element, which is highly toxic in these forms."

MINERALS FOR LIFE

@mattyb

 

[Helen]

In ionotropic GABAA receptors, binding of GABA molecules to their binding sites in the extracellular part of the receptor triggers opening of a chloride ion-selective pore. The increased chloride conductance drives the membrane potential towards the reversal potential of the Cl¯ ion which is about –75 mV in neurons, inhibiting the firing of new action potentials. This mechanism is responsible for the sedative effects of GABAA allosteric agonists. In addition, activation of GABA receptors lead to the so-called shunting inhibition, which reduces the excitability of the cell independent of the changes in membrane potential.

There have been numerous reports of excitatory GABAA receptors. According to the excitatory GABA theory, this phenomenon is due to increased intracellular concentration of Cl¯ ions either during development of the nervous system[10][11] or in certain cell populations.[12][13][14] After this period of development, a chloride pump is upregulated and inserted into the cell membrane, pumping Cl−ions into the extracellular space of the tissue. Further openings via GABA binding to the receptor then produce inhibitory responses. Over-excitation of this receptor induces receptor remodeling and the eventual invagination of the GABA receptor. As a result, further GABA binding becomes inhibited and inhibitory postsynaptic potentials are no longer relevan

GABA receptor - Wikipedia

So GABA can be excitatory also if too much chloride is there. LOL

@mattyb

 

[Helen]

So there is also a possibility like this for PFS

You take fin , fin kills NAPDH. This kills allo. Body adjusts by putting tons of chloride in the cell. Then you quit fin, NADPH goes up, and this causes super crazy GABA activation since there is tons of chloride in neurons?

But in that case why @TubZy is doing good on chlorides

 

[Helen]

https://www.hindawi.com/journals/np/2011/527605/

@mattyb Interesting read


Does this mean that potassium takes chloride out and sodium puts it in?

can you please read this Matty and let me know what do you think that potassium transporter depends on . On potassium levels. So is this potassium chloride ratio is what important to get chloride out and keep it low inside of the cell.

 

[Helen]

NKCC1 Chloride Importer Antagonists Attenuate Many Neurological and Psychiatric Disorders - ScienceDirect

bumetanide Is used for that
Niflumic acid

 

[Helen]

2 elements next to chloride in periodic table is Sulfur and Manganese. to Both @TubZy reacted badly. But @IHateFin seems to do well on.

 

[Helen]

WE need to keep in mind this theory also with high chloride in the cell theory stuck there. And NADPH is not allowed to go up. Since that will increases Allo and allo will modulate GABA a and gaba a will put more chloride in there.

By the way 5 htp does exactly the same thing @Ghost

 

[Helen]

And here we go on Naltrexone

GABA receptor-linked chloride channels and the behavioral effects of naltrexone in rats - ScienceDirect

It seems to effect mainly chloride channels

 

[Joshuk]

i honestly do not understand my PFS i can eat anything and everything i want and do not put weight on, i respond to no treatments. For instance i tried doing liver flushes with epsom salts drank 5 cups full nothing just like drinking warm water. i was taking 1mg armidex a day which should of crashed my estrogen did noting.... dont respond to zinc or any other amino acid betanine HCL does nothing as well .

all hormone treatments do nothing 300mg prog for 2 weeks did not feel any different its like im immune for supplements and yet i can work a full time job . kind of hilarious but worrying at the same time casue how can i fix myself if nothing helps

injecting 1000mg of test a week ( this is when i first had pfs) did not even get any benefit and my estrogen did not even budge one bit

 

[mattyb]

Cellular transduction requires a lowering in pH from extracellular compartment, to cystosol, and again to the nucleus. So in order for a cell to respond to something like a peptide hormone, by carrying it's signal from the surface to the nucleus, there needs to be a proper pH gradient because this carves out electronegative pathways for the molecules to follow along. Acidity of a molecule is determined by electronegativity and size, so chloride, being a halogen and moderate in size, is quite electronegative. And cells must maintain a certain level of electronegativity (about -60mV to -75mV). This whole pattern is disrupted in alkalosis.

In alkalosis, the negative Cl- ion is displaced by the negative HCO3- ion. In order for the cell to maintain charge, it loses chloride to take in more bicarbonate. The HCO3- creates a condition as if there was excess chloride inside the cell, by increasing the electronegativity of the cell. This causes an upregulation of the Cl- pump, which causes an efflux of chloride out of the intracellular space into the extracellular fluid, upregulating the excitatory nature of the GABA receptor and causing anxiety. This is why most people here with PFS don't report low chloride on their blood tests (and never high chloride).

Chloride is predominantly an extracellular electrolyte, but it is still in high enough concentrations inside of cells to help regulate charge.

Protein is the predominant carrier of negative charge inside the cell. But what is late stage PFS? It's a protein deficiency. So the cells have a hard time maintaining charge, and in alkalosis bicarb will take up the role of providing this charge.

This is why PFS people are responsive to pretty much nothing. Their cells are frozen in bicarb, no minerals are ionized, their signal transduction is disrupted because pH is disrupted and there are no coloumbe pathways carved out to guide signalling molecules, there's a severe lack of amino acids to carry out these functions, and chloride is being dumped out of the cell in exchange for bicarb which is a signalling event for some not-so-good processes like excitatory GABA action.

This is why even in chloride-resistant alkalosis chloride is still part of the treatment in the form of KCl or HCl. Intracellular chloride has been depleted by bicarb, the body is wasting chloride because it's continually being pumped into the extracellular fluid and being filtered out by the kidneys.

 

[Helen]

Cellular transduction requires a lowering in pH from extracellular compartment, to cystosol, and again to the nucleus. So in order for a cell to respond to something like a peptide hormone, by carrying it's signal from the surface to the nucleus, there needs to be a proper pH gradient because this carves out electronegative pathways for the molecules to follow along. Acidity of a molecule is determined by electronegativity and size, so chloride, being a halogen and moderate in size, is quite electronegative. And cells must maintain a certain level of electronegativity (about -60mV to -75mV). This whole pattern is disrupted in alkalosis.

In alkalosis, the negative Cl- ion is displaced by the negative HCO3- ion. In order for the cell to maintain charge, it loses chloride to take in more bicarbonate. The HCO3- creates a condition as if there was excess chloride inside the cell, by increasing the electronegativity of the cell. This causes an upregulation of the Cl- pump, which causes an efflux of chloride out of the intracellular space into the extracellular fluid, upregulating the excitatory nature of the GABA receptor and causing anxiety. This is why most people here with PFS don't report low chloride on their blood tests (and never high chloride).

Chloride is predominantly an extracellular electrolyte, but it is still in high enough concentrations inside of cells to help regulate charge.

Protein is the predominant carrier of negative charge inside the cell. But what is late stage PFS? It's a protein deficiency. So the cells have a hard time maintaining charge, and in alkalosis bicarb will take up the role of providing this charge.

This is why PFS people are responsive to pretty much nothing. Their cells are frozen in bicarb, no minerals are ionized, their signal transduction is disrupted because pH is disrupted and there are no coloumbe pathways carved out to guide signalling molecules, there's a severe lack of amino acids to carry out these functions, and chloride is being dumped out of the cell in exchange for bicarb which is a signalling event for some not-so-good processes like excitatory GABA action.

This is why even in chloride-resistant alkalosis chloride is still part of the treatment in the form of KCl or HCl. Intracellular chloride has been depleted by bicarb, the body is wasting chloride because it's continually being pumped into the extracellular fluid and being filtered out by the kidneys.

In alkalosis yes, I am talking about chloride being stuck in the cell as they write in those articles in epilepsy which POIS PFS people have.. And this will cause high Co2 that we see on tests of people. We need to consider this. No?

Notice you do better on zinc, on active bs. everything that lowers Co2 .

Just playing devils advocate here, trying to look at this from all angles

Сhloride varies Matty. some have it low, some high

 

[mattyb]

In alkalosis yes, I am talking about chloride being stuck in the cell as they write in those articles in epilepsy which POIS PFS people have.. And this will cause high Co2 that we see on tests of people. We need to consider this. No?

Notice you do better on zinc, on active bs. everything that lowers Co2 .

Just playing devils advocate here, trying to look at this from all angles

Chloride doesn't need to be stuck in those cells though. The problem is high anion count and low protein count. The anion could be anything, bicarb or chloride, or whatever.

Most blood tests don't separate CO2 and bicarb from the CO2 reading. So we can't say CO2 alone is high. We can say carbon retention is high, but it could be in the form of CO2 or bicarb.

This is relevant
Bicarbonate Contributes to GABAA Receptor-Mediated Neuronal Excitation in Surgically-Resected Human Hypothalamic Hamartomas

"One alternative factor in the modulation of GABA-mediated excitation is a bicarbonate-driven depolarizing potential. GABAA receptors are known to be permeable to both chloride and HCO3- ions (Bormann et al., 1987), and intracellular accumulation of HCO3- ions from carbonic anhydrase (CA) activity creates an outwardly directed electrochemical gradient for HCO3- (Staley et al., 1995). Moreover, several studies have demonstrated that HCO3--free HEPES buffer is able to suppress GABA-induced membrane depolarization (Staley et al., 1995; Phillips et al., 1998; Dallwig et al., 1999), thus highlighting the relevance of HCO3- to the phenomenon of GABA-mediated neuronal excitation.

It is possible that HCO3- could be affecting neuronal excitability through a mechanism other than L-type calcium channels. A previous study suggested that the intracellular pH (pHi) in excitable cells is higher than that would be expected solely from the normal proton concentration, thus invoking increased intracellular bicarbonate (Thomas et al., 1977). Under such conditions, activation of GABAA receptors would easily lead to bicarbonate efflux through the GABAA receptor ionophore. In support of this, bicarbonate conductance through the GABAA receptor was found to provoke a negative shift of EGABA(Dallwig et al., 1999). Based on these findings, it is reasonable to speculate that changes in pHi under epileptic conditions may in part account for GABA-induced neuronal excitation through bicarbonate efflux. At present, direct evidence for this is lacking."

We also have to keep in mind here that the phenomena you are referring too is isolated to a very specific stage of development, before chloride channels exist in sufficient numbers to allow for efflux of chloride. I'm uncertain if this would happen otherwise, at least in that specific manner.

 

[Helen]

Chloride doesn't need to be stuck in those cells though. The problem is high anion count and low protein count. The anion could be anything, bicarb or chloride, or whatever.

Most blood tests don't separate CO2 and bicarb from the CO2 reading. So we can't say CO2 alone is high. We can say carbon retention is high, but it could be in the form of CO2 or bicarb.

This is relevant
Bicarbonate Contributes to GABAA Receptor-Mediated Neuronal Excitation in Surgically-Resected Human Hypothalamic Hamartomas

"One alternative factor in the modulation of GABA-mediated excitation is a bicarbonate-driven depolarizing potential. GABAA receptors are known to be permeable to both chloride and HCO3- ions (Bormann et al., 1987), and intracellular accumulation of HCO3- ions from carbonic anhydrase (CA) activity creates an outwardly directed electrochemical gradient for HCO3- (Staley et al., 1995). Moreover, several studies have demonstrated that HCO3--free HEPES buffer is able to suppress GABA-induced membrane depolarization (Staley et al., 1995; Phillips et al., 1998; Dallwig et al., 1999), thus highlighting the relevance of HCO3- to the phenomenon of GABA-mediated neuronal excitation.

It is possible that HCO3- could be affecting neuronal excitability through a mechanism other than L-type calcium channels. A previous study suggested that the intracellular pH (pHi) in excitable cells is higher than that would be expected solely from the normal proton concentration, thus invoking increased intracellular bicarbonate (Thomas et al., 1977). Under such conditions, activation of GABAA receptors would easily lead to bicarbonate efflux through the GABAA receptor ionophore. In support of this, bicarbonate conductance through the GABAA receptor was found to provoke a negative shift of EGABA(Dallwig et al., 1999). Based on these findings, it is reasonable to speculate that changes in pHi under epileptic conditions may in part account for GABA-induced neuronal excitation through bicarbonate efflux. At present, direct evidence for this is lacking."

We also have to keep in mind here that the phenomena you are referring too is isolated to a very specific stage of development, before chloride channels exist in sufficient numbers to allow for efflux of chloride. I'm uncertain if this would happen otherwise, at least in that specific manner.

Matty, I agree, we have one case covered , I am just trying to explore another possibility and test it also. Just in case.

I agree that Co2 it can be in form Co2 or bicarb. we dont know. But a lot of those people do better on methylations and adrenaline. So we have to explore both possibilities.

Dont forget that those people were taking drugs constantly activating gaba. like 5 htp, and then went off. So we should not write out the possibility of that phenomena to happen.

IN any case I will try a couple of people on chloride channel blockers. PLus manganese zinc, sulfur.


Have you taken LDN ?

 

[Ghost]

And here we go on Naltrexone

GABA receptor-linked chloride channels and the behavioral effects of naltrexone in rats - ScienceDirect

It seems to effect mainly chloride channels

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[mattyb]

Matty, I agree, we have one case covered , I am just trying to explore another possibility and test it also. Just in case.

I agree that Co2 it can be in form Co2 or bicarb. we dont know. But a lot of those people do better on methylations and adrenaline. So we have to explore both possibilities.

Dont forget that those people were taking drugs constantly activating gaba. like 5 htp, and then went off. So we should not write out the possibility of that phenomena to happen.

IN any case I will try a couple of people on chloride channel blockers. PLus manganese zinc, sulfur.


Have you taken LDN ?

Fair enough. If someone is non-responsive to the electrolyte protocol, they could always try a Cl-CB. It's a bit of a long-shot, but who knows. All of this is experimental.

Wouldn't people high in bicarb do better on methylation/adrenaline too? Increase respiratory drive, increases expulsion of carbon, driving bicarb down. It would temporarily raise pH by lowering CO2, but it would also lower bicarb which is worth the loss of pure CO2. Then the body compensates by retaining hydrogen to raise pH? I don't know, I'm just spitballing here.

I don't really see CO2 and bicarb all that differently, they are both carbon that you want to get out. They transition between each other all the time.