Glycine Strongly Upregulates 5-alpha Reductase (5-ar) Activity

TubZy

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Yeah , i read in a pfs forum that a poster cured his pfs by taking low dose prozac.
Now , here is something interesting. I also read there that an MD got pfs like symptoms by taking Accutane and that doc cured it by taking finasteride !! ( since i don't do drugs,alcohol so i am sure i was not high while reading that). How is that even possible ? (I guess there was some study showing that after fin intake , there were strongly upregulated androgen receptors and if you get pfs and survive it, , it's like you will hit a second puberty). Any ideas ?

Regarding fin and liver toxicity, i think they showed that dut was toxic, carcinogenic to the liver by inhibition of all 3 forms of 5-AR enzymes while fin was not. ( i might be wrong here though)

When you say cured by prozac, do you mean he took it for a short period of time and it cured/reversed pfs or as long as he stayed on prozac his PFS symptoms were gone?
 

Dante

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When you say cured by prozac, do you mean he took it for a short period of time and it cured/reversed pfs or as long as he stayed on prozac his PFS symptoms were gone?
That i don't remember much. I think that was the only line written .
 

satsumass

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@haidut re: glycine and its positive effects on steriod pathways. i am curious if in your research you came across any mention of sarcosine having similar effects as glycine on steriod pathways especially the 5-ar upregulation. sarcosine is a GLY-T (glycine transporter) inhibitor which allows for more glycine (at least in the brain) to have its effects, specifically as a coagonist at the NMDA receptor. not sure about elsewhere, but sarcosine is used succesfully in many cases of cognitive dysfunction for schizophrenics.
 
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haidut

haidut

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@haidut re: glycine and its positive effects on steriod pathways. i am curious if in your research you came across any mention of sarcosine having similar effects as glycine on steriod pathways especially the 5-ar upregulation. sarcosine is a GLY-T (glycine transporter) inhibitor which allows for more glycine (at least in the brain) to have its effects, specifically as a coagonist at the NMDA receptor. not sure about elsewhere, but sarcosine is used succesfully in many cases of cognitive dysfunction for schizophrenics.

Sarcosine is simply a precursor to glycine and inhibitor of its degradation, so it raises glycine concentrations in tissues. So, the end goal/target is still glycine. I think the pharma industry simply wanted something more patentable then glycine and went with sarcosine. I don't see what it can offer beyond regular glycine and I am not aware of any direct effects on steroids.
 

bruschi11

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There have been post-mortem studies on people taking Finasteride and committing suicide due to depression. They all had very low ALLO levels. Studies on brains of people not taking Finasteride also showed lower levels but order of magnitude higher than the ones taking Finasteride. Finally, recent study found that one of the SSRI that managed to reverse PFS (in rodents) did this by dramatically increasing ALLO in brain back to control levels. So, I think Finasteride lowering ALLO is pretty widely acknowledged, even in pharma circles. Finasteride has other bad side effects - it is estrogenic and carcinogenic for the liver, so there may very well be other toxic side effects that contribute to development of PFS beyond its effects on ALLO, but getting ALLO back to normal levels definitely won't hurt.

Any link to these studies Haidut?

I totally understand an SSRI is horrible for health. But I'm hearing that researchers are theorizing now that a disregulated GABA-A receptor may possibly be the full reason for PFS. Modulating GABA via allo with an ssri seems scary and risky and just not good for overall health, but if there are studies backing this, not out of the realm to give it a shot if one is in really bad shape.
 
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haidut

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Any link to these studies Haidut?

I totally understand an SSRI is horrible for health. But I'm hearing that researchers are theorizing now that a disregulated GABA-A receptor may possibly be the full reason for PFS. Modulating GABA via allo with an ssri seems scary and risky and just not good for overall health, but if there are studies backing this, not out of the realm to give it a shot if one is in really bad shape.

Where did you see me suggesting modulating GABA via ALLO using SSRI, or saying it is a good idea?
 

Jsaute21

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Anybody have a solid glycine source? I use knox cause it's cheap on Amazon but I noticed @Dan Wich didn't have it on his toxinless page.
 

bruschi11

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Where did you see me suggesting modulating GABA via ALLO using SSRI, or saying it is a good idea?


"Finally, recent study found that one of the SSRI that managed to reverse PFS (in rodents) did this by dramatically increasing ALLO in brain back to control levels."

This was in the quote that I quoted from you.
 
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haidut

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"Finally, recent study found that one of the SSRI that managed to reverse PFS (in rodents) did this by dramatically increasing ALLO in brain back to control levels."

This was in the quote that I quoted from you.

Well, yeah, this was just to elucidate the real mechanism of action of the SSRI drugs in PFS. It is not serotonin, it is the increase in ALLO. But where did you see me suggesting SSRI should be used? If anything, the message that I get from that quote is that we should be increasing ALLO.
 

Kitridge30

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what is the best time to take these aminos? Empty stomach? How much Taurine would be recommended throughout the day along with the glycine and niacinimide?..
 

Kitridge30

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Steroidal inhibitor is usually a chemical with structure similar to a steroid which an enzyme may use as a substrtate. Exemestane is a steroidal aromatase inhibitor and if you look at its structure it is very similar to androstenedione and testosterone, which are two substrates for aromatase. Anyways, glycine, pregnenolone, progesterone, and DHEA should all be able to upregulate 5-AR activity. I don't think finasteride is a suicide inhibitor of 5-AR, but even if it was these substances should be able to help. Saw palmetto is much weaker than finasteride and any effects on lowering libido are probably due to the fact that it contains a natural progesterone-type steroid, not so much due to its inhbition of 5-AR. Either way, again the substances I mentioned should help.
Thank you for getting back to me again Haidut. I believe that the saw palmetto has inhibited my androgen receptors.. My chest and arm hair grows inconsistently now as about half of it does not grow anymore....or if it does it is extremely slow. What substance would you recommend me taking for the specific job of either unbinding or upregulating the androgen receptors? Nicinimide?
 

Lokzo

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Thank you for getting back to me again Haidut. I believe that the saw palmetto has inhibited my androgen receptors.. My chest and arm hair grows inconsistently now as about half of it does not grow anymore....or if it does it is extremely slow. What substance would you recommend me taking for the specific job of either unbinding or upregulating the androgen receptors? Nicinimide?
L-Carnitine L-Tartrate can increase AR density.
 

lvysaur

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This is probably the wrong thread for it, but I've noticed I can become borderline ambidextrous when I drink gelatin regularly.
 

Wagner83

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This is probably the wrong thread for it, but I've noticed I can become borderline ambidextrous when I drink gelatin regularly.
Nice, did you find a brand that you tolerate better than others? How much do you take?
 

sladerunner69

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Someone made the following statement on the PFS board:

"Glycine is an inhibitory neurotransmitter in the central nervous system, especially in the spinal cord, brainstem, and retina. When glycine receptors are activated, chloride enters the neuron via ionotropic receptors, causing an Inhibitory postsynaptic potential (IPSP). Strychnine is a strong antagonist at ionotropic glycine receptors, whereas bicuculline is a weak one. Glycine is a required co-agonist along with glutamate for NMDA receptors. In contrast to the inhibitory role of glycine in the spinal cord, this behaviour is facilitated at the (NMDA) glutamatergic receptors which are excitatory.[20] The LD50 of glycine is 7930 mg/kg in rats (oral),[21]and it usually causes death by hyperexcitability.

This is why chloride is so important. and that is why PFS people @TubZy felt terrible on gelatin . Since without chloride glycine is only excitatoryGlycine is an inhibitory neurotransmitter in the central nervous system, especially in the spinal cord, brainstem, and retina. When glycine receptors are activated, chloride enters the neuron via ionotropic receptors, causing an Inhibitory postsynaptic potential (IPSP). Strychnine is a strong antagonist at ionotropic glycine receptors, whereas bicuculline is a weak one. Glycine is a required co-agonist along with glutamate for NMDA receptors. In contrast to the inhibitory role of glycine in the spinal cord, this behaviour is facilitated at the (NMDA) glutamatergic receptors which are excitatory.[20] The LD50 of glycine is 7930 mg/kg in rats (oral),[21]and it usually causes death by hyperexcitability.

This is why chloride is so important. and that is why PFS people felt terrible on gelatin . Since without chloride glycine is only excitatory."

Any merit to this claim? I have worried about excitotoxicity, as some people claim to get headaches from gelatin. I tend to get wild dreams which bother me at night.
 

Wagner83

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I don't know anything about your specific question but all I can say is I've seen a few people get better with betaine HCL. I'm not sure if they keep the benefits off it.
 

lvysaur

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Nice, did you find a brand that you tolerate better than others? How much do you take?

Oh, I only take it in the form of homemade soup. Chicken/pigs feet, etc.

The amount is important, I used to drink bowlfuls at a time and it would make me almost sedated. I now drink 1 or 2 240mL cups at a time, with rice added. I don't add potatoes because it feels like too much protein.
 

A.R

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I don't know anything about your specific question but all I can say is I've seen a few people get better with betaine HCL. I'm not sure if they keep the benefits off it.
Sorry what benefits did people get from Betaine?
 

Wagner83

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Sorry what benefits did people get from Betaine?
Better digestion mainly (and its consequences), if it improves absorption of nutrients that could be a nice benefit too. Tyw mentioned its use, I don't think he saw it as a digestive aid but rather a way to eliminate pathogens (don't quote me on that). Tarmander uses it, he posted information in his log and on the gbolduev Q and A thread. m_arch had reported good digestion with it.
 

Andman

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Someone made the following statement on the PFS board:

"Glycine is an inhibitory neurotransmitter in the central nervous system, especially in the spinal cord, brainstem, and retina. When glycine receptors are activated, chloride enters the neuron via ionotropic receptors, causing an Inhibitory postsynaptic potential (IPSP). Strychnine is a strong antagonist at ionotropic glycine receptors, whereas bicuculline is a weak one. Glycine is a required co-agonist along with glutamate for NMDA receptors. In contrast to the inhibitory role of glycine in the spinal cord, this behaviour is facilitated at the (NMDA) glutamatergic receptors which are excitatory.[20] The LD50 of glycine is 7930 mg/kg in rats (oral),[21]and it usually causes death by hyperexcitability.

This is why chloride is so important. and that is why PFS people @TubZy felt terrible on gelatin . Since without chloride glycine is only excitatoryGlycine is an inhibitory neurotransmitter in the central nervous system, especially in the spinal cord, brainstem, and retina. When glycine receptors are activated, chloride enters the neuron via ionotropic receptors, causing an Inhibitory postsynaptic potential (IPSP). Strychnine is a strong antagonist at ionotropic glycine receptors, whereas bicuculline is a weak one. Glycine is a required co-agonist along with glutamate for NMDA receptors. In contrast to the inhibitory role of glycine in the spinal cord, this behaviour is facilitated at the (NMDA) glutamatergic receptors which are excitatory.[20] The LD50 of glycine is 7930 mg/kg in rats (oral),[21]and it usually causes death by hyperexcitability.

This is why chloride is so important. and that is why PFS people felt terrible on gelatin . Since without chloride glycine is only excitatory."

Any merit to this claim? I have worried about excitotoxicity, as some people claim to get headaches from gelatin. I tend to get wild dreams which bother me at night.

could explain why i do great on magnesium chloride..calms me down a lot more than even 1g magnesium bicarbonate/day
 
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