Brainstorming & Ideas (PFS - Gbol)

[mattyb]

Even more important than experimenting is getting some data on yourself first. Find out if you are low prog or high prog (angonized or antagonized receptors) and then choose a protocol that fits that.

 

[TubZy]

I will be starting high dose progesterone with prednisone very soon, I have it ordered just waiting for it to come in.

Planning to do 200mg of prog with 5 mg of prednisone dosed once a day together taken at the same time. Prednisone is stronger than HC so this should work better in theory.

 

[JonnyCraig]

I will be starting high dose progesterone with prednisone very soon, I have it ordered just waiting for it to come in.

Planning to do 200mg of prog with 5 mg of prednisone dosed once a day together taken at the same time. Prednisone is stronger than HC so this should work better in theory.

Finally! TubZy on the Prog train.

I felt FAN-effing-tastic a day ago when I took 100mg of oral prog before bed. Put me in a real nice mood, felt like I really needed that (I have a stressful job/position).

Which progesterone did you buy????

 

[TubZy]

These are the exact cases I outlined. Hypersensitive or the opposite. There are protocols outlined for both. in the beginning of this thread.

Well, I guess people just need to get prog levels tested and then try out a treatment based on that. Sounds pretty straightforward, but I've seen very few people here actually trying out those initial protocols.

I just don't get it. There are hundreds of PFS dudes writing on solvepfs, PropeciaHelp, and on here. I don't see why more haven't given this stuff a shot just yet. It's pretty sad to be honest- we need more people trialing stuff and experimenting.

I was a really bad case with the CFS/mycoplasma/ammonia issues, but I can proudly say I'm all in on this methodology. I am on day 3 of a 3 day RU cycle. I went 75mg, 25mg, 25mg- this morning after a night of RIFING which, normally leaves me waking up feeling quite beat up (herxheimer reaction, body full of toxins due to pathogen die off), I woke up with the stiffest erection I've probably had since I got PFS. Morning erections have been pretty awful since my fast as well (which concluded 16 days ago). This was nice.

The plan from here for me and what many PFS guys should be doing is experimenting. After this cycle I'll know the effect of 75, 25, 25 on my body 2 weeks after an extended fast. Next time in a month or so, I won't fast before other than a intermittent/alternative day here and there, but will likely go low dose with 15-25mg per day for the 3 days. From there, mineral balancing, more experimentation. I'm only 20-30% overall so I'm sure its going to take some time and there may be some frustration at times. This will be a journey.

I know a lot of people are scared to mess with drugs due to their original reaction to fin or trust a dude online ( @gbolduev duev ). But what else are we supposed to do? We lost a part a major part of ourselves with PFS- so much life and happiness we are missing out on. We need to take risks and give this a shot. I don't even see the risk here- honestly is there documentation of any guy ever having a horrible reaction to RU486 or a mineral balancing protocol? Seriously guys.

All I know is that I'm beyond belief thankful we have this site here experimenting while witnessing the significant improvements in several guys here. @5alpha has been in PFS for several years if I recall correctly, same with @@Scenes . Something is happening to us positively for sure employing these practices. Cannot wait to see what the future brings and I really hope more guys jump on and begin experimenting here as well.

X2 RU does work at least in majority of people that used it. Tricky part was getting it to fully stick, if it wasn't so expensive and shipping didn't take forever I would just keep experimenting with it. The only down side is that RU can technically increase cortisol if used for too long so there is a balance. Another good outcome of RU is that we know it lowers progesterone and blocks cortisol and we feel much better on it which just adds some backup info to what really is going on with PFS and gbol actually has a good understanding of PFS which honestly no one has really even came close to explaining at least somewhat of what is going on in the body.

 

[Shadow]

Even more important than experimenting is getting some data on yourself first. Find out if you are low prog or high prog (angonized or antagonized receptors) and then choose a protocol that fits that.

I agree with you, we need data, we need to see what changes, this way we can pinpoint things and develop a better protocol.

 

[bruschi11]

Even more important than experimenting is getting some data on yourself first. Find out if you are low prog or high prog (angonized or antagonized receptors) and then choose a protocol that fits that.

Yes, I plan to order hair test when I get back from my trip next week. Based on everything I've learned, it seems pretty obvious I'm a slow oxidizer, but we need to know more (like prog) and which type.

I'm in a weird spot as the mycoplasma left me depleted of manganese for months if not years on end there, so I found it reasonable to give myself some time to let things balance out before doing the hair test.

I will say that a saliva test showed low end prog early days of PFS 11 months ago or so. I don't know if this has any substance to it though as I was in reallllllly bad shape and it was only a couple weeks after my crash. Also, does saliva prog prove anything worthwhile?

 

[raskolnikov]

Let's be direct here:

1) I have PSSD
2) I want to follow a protocol, but I already don't know which case I am (and to be honest, I'm not a native english speaker, I don't understand biochemistry and there's too much information here, but it looks like I would have to study for months just to start understanding gbolvuev's ideas)
3) I have a health plan that covers almost any blood test and I'm in touch with a doctor who knows nothing about PSSD, but he is open to order any blood test I ask him

So... I already know that I have low testosterone, low LH and low FSH. Prolactin a bit higher than average. These are the parameters I've been monitoring. I want gbolduev or someone who understands gbolduev's ideas to tell me: what should I ask my doctor to see in my next blood test? Progesterone and what else? What about the minerals?

As soon as I get the result, I'll choose a protocol and start. I want to do an organized and clean trial, but I need help to know what to do.

 

[Orion]

So... I already know that I have low testosterone, low LH and low FSH. Prolactin a bit higher than average. These are the parameters I've been monitoring. I want gbolduev or someone who understands gbolduev's ideas to tell me: what should I ask my doctor to see in my next blood test? Progesterone and what else? What about the minerals?

TESTS:

Hair analysis test: sodium, potassium, calcium, magnesium, chloride, phosphorus, zinc, copper, manganese, molybdenum...

Blood test: TSH, free t3, free t4, iron, ferritin, ceruloplasmin, insulin, glucose, progesterone, estrogen, testosterone, cortisol

Blood gases if possible.


this is what is needed to see a good picture.

 

[Jaxx]

Anyone else had difficulty getting prog and estrogen tested as a man? Seems impossible here...at least at the endocriniologist

 

[tanedout]

Anyone else had difficulty getting prog and estrogen tested as a man? Seems impossible here...at least at the endocriniologist

Yep same, I've been unable to get either. You can get some tests done online. I tried to do a prog one where you get the blood from your finger and send it off, but unfortunately when I did it the blood arrived 'haemolysed', but it might be worth a go.

My hair analysis did say I was likely 'progesterone dominant', so I'm assuming it's high, but would be nice to confirm.

 

[BeLikeWater]

Even more important than experimenting is getting some data on yourself first. Find out if you are low prog or high prog (angonized or antagonized receptors) and then choose a protocol that fits that.

I have low progesterone and high potassium. I think I trybto progesterone cycle with 5ar activators fater it finish plus maybe some estrogenic if I feel I need more to DHT become activated.

 

[Ghost]

I’m intrigued by the mineral part of this theory, and I’m excited to talk about it when I learn it more, but let’s start with 5-HT. That’s my comfort zone, as is PSSD.

As mentioned above, PSSD is often caused by Lexapro/Citalopram, which are nearly identical. Lexapro is the more potent enantiomer, and that’s why Lexapro doses are lower and how only 4 doses of 5mg left me fucked up 3.5 years on. Also mentioned above, SSRIs work on hormones at something like 1/50 of the dose that it takes them to work on SERT.

There are two ways to look at a set of non-converging data. First, you may say that there is a “high” and “low” state. From another angle, it looks like a lack of correlation, and that nothing can be taken from these data. I haven’t run the stats on the PFS data, but that is something to keep in mind if people are coming out with both high and low states of Prog. Prog isn’t usually measured in men, and therefore there isn’t a ton of data on reference ranges.

As for PSSD, there really only is a high-prog state. Something like 12/15 tests I’ve seen have high prog. So for PSSD, I see Prog as USUALLY heightened. Again, not always the case, but this is significantly more common than normal or low prog.

Sorry that I’m gonna dive into Serotonin for a bit, but again, it’s my background.

“Progesterone increases MAO< this tanks serotonin.”

I think it’s more complex than this. There is more than MAO activity happening. In the following case, it is hypothesized that Progesterone in pregnancy (it increases a LOT), is actually increasing serotonin activity in the brain, leading to the desensitization of 5-HT1A autoreceptors.


Klink et al., 2002
Gender and gonadal status modulation of dorsal raphe nucleus serotonergic neurons. Part II. Regulatory mechanisms


"During pregnancy, the ED50 for the response to LSD was decreased by about 70%, indicating a partial desensitization of 5-HT1A autoreceptors, which is consistent with the 5-HT neurons higher firing activity. The GABAergic tonic inhibition of 5-HT neurons was assessed using the responses to GABA, bicuculline and isoniazid. Together, they indicate a lower GABAergic tonic inhibition in males and P17 as compared to CF, which is in agreement with their greater 5-HT neurons firing rate. Finally, the efficacy of the long feedback loop, involving postsynaptic 5-HT1A receptors, did not seem affected by gender, ovariectomy or pregnancy since the response to systemic 8-OH-DPAT was similar. These results constitute strong evidence of mechanisms by which gender and hormonal fluctuations can modulate the 5-HT neurons function and influence vulnerability to mood disorders."
"It could, thus, suggest that these modifications of the GABAA receptor function, induced by chronic neurosteroid treatments, are present during pregnancy, when levels of progesterone metabolites are high. This would result in a lesser GABAA receptor responsiveness and would explain the lower GABAergic tonic inhibition of 5-HT neurons observed in the present study."
"Many progesterone metabolites are GABAA receptor modulators. Since we observed a direct correlation between 5-HT neuronal activity and circulating levels of P from P11 to 21, the responsiveness of the DRN 5-HT neurons to GABA, as well as their GABAergic tonic inhibition, had to be explored."
"These results (raising Progesterone) suggest a partial functional desensitization of the 5-HT1A autoreceptor during late
pregnancy."
"During pregnancy, the ED50 for the response to LSD was decreased by about 70%, indicating a partial desensitization of 5-HT1A autoreceptors, which is consistent with the 5-HT neurons higher firing activity."

In addition, Prog blocks the ability of Estrogen and testosterone to protect SERT in the POA. Because of this, SERT levels fall (as they do with SSRIs). This means less 5-HT is cleared, and that 5-HT activity increases.

https://www.ncbi.nlm.nih.gov/pubmed/15225127

“Previous data from our laboratory have shown that during pregnancy, the firing activity of 5-HT neurons increases in parallel with progesterone level”


Something that I’ve noticed for a long time now since PSSD is that I have occasional heart arrhythmias. This isn’t really normal for my age but the cardiologist cleared it and said that it wasn’t dangerous. Regardless, I think now that it may have to do with lowered Potassium levels. It sometimes would happen up to once a day, but after starting potassium supplementation it has gone away completely.
Escitalopram, a selective serotonin reuptake inhibitor, inhibits voltage-dependent K+ channels in coronary arterial smooth muscle cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5507780/


And this happens in the brain too,
The antidepressant citalopram inhibits delayed rectifier outward K+ current in mouse cortical neurons
http://onlinelibrary.wiley.com/doi/10.1002/jnr.22744/full


Other notes:

Has sideroblastic anemia been seen in PFS or PSSD before? I haven’t seen that but I haven’t looked either.


Valid point on Iron. I’ve been eating a lot of spinach recently and I think that helps. It has a lot of Vitamin K, Iron, and Potassium.

Also I agree on Cortisol being high. That’s something we notice in PSSD too. The bad part is that Cortisol can desensitize the 5-HT1A AR, so the cycle can kind of continue for a while.

 

[Aleksandr]

A question that I do have.

Chicken or the egg? High Prog or Low K+?

Which comes first, and I honestly don't know enough of this literature to say yet... Does K+ decrease Prog receptors? I thought I had read that here? The study above seems to paint a different picture: that lowered K+ increases Prog levels. It doesn't seem to me that decreasing Prog would lower receptor levels, but again maybe I'm missing something and I admittedly have only looked at a handful of papers in this field.

By K+ do you mean potassium?

Gbolds theory uses oxidation types. If your talking alopecia pattern hairloss its caused in slow oxidation due to a mineral imbalance. Usually too acidic / too much co2. Can be metabolic or respiratory acidosis. The pattern for this type is (usually) high calcium/magnesium, low sodium/potassium/phosphorus. So the typical mineral balancing is to get ca mg down and na k and p up. To do this various things are recommended: fasting, exercise, chelation, zinc/manganese, reducing carbs.

In this explination i guess you say the potassium comes first, since the minerals usually are intimately tied to enzyme cascades which then influence hormones

 

[Shadow]

By K+ do you mean potassium?

Yes, positively charged(cation) potassium.

 

[Miggie]

I have dexamethasone 4mg per tab. I just wonder do you have to take it in combo with progesterone? and how should this be dosed?

Wont a dose of dexamethasone agonise the receptor and therefor making it even less sensitive to cortisol?

 

[Shadow]

Anyone else had difficulty getting prog and estrogen tested as a man? Seems impossible here...at least at the endocriniologist

Cant you just go to an lab and ask for the test? Here if the doctor dont want to ask some tests I can order ir directly in the lab, problem is that this way my insurance dont pay.

 

[TubZy]

I have dexamethasone 4mg per tab. I just wonder do you have to take it in combo with progesterone? and how should this be dosed?

Wont a dose of dexamethasone agonise the receptor and therefor making it even less sensitive to cortisol?

If you try it make sure you use high dose progesterone with it (100mg or 200mg). You need to both turn off endogenous progesterone and cortisol at the same time otherwise it won't work. Take them together at the same time.

I think the goal is to down regulate both endogenous progesterone and cortisol receptors and snap the body out of the current state it is in. Plus dex, HC or anything that acts as cortisol stimulates 5AR too so I don't technically know how you should feel while on it. This is all in theory as no one has tried it yet, I plan to within the next week just waiting for my stuff to get here except I will try prednisone instead of dex.

You could use the resveratrol example though, it acts as a ER agonist but it can increase estrogen signaling and resensitize it.

 

[Crushed]

I’m intrigued by the mineral part of this theory, and I’m excited to talk about it when I learn it more, but let’s start with 5-HT. That’s my comfort zone, as is PSSD.

As mentioned above, PSSD is often caused by Lexapro/Citalopram, which are nearly identical. Lexapro is the more potent enantiomer, and that’s why Lexapro doses are lower and how only 4 doses of 5mg left me fucked up 3.5 years on. Also mentioned above, SSRIs work on hormones at something like 1/50 of the dose that it takes them to work on SERT.

There are two ways to look at a set of non-converging data. First, you may say that there is a “high” and “low” state. From another angle, it looks like a lack of correlation, and that nothing can be taken from these data. I haven’t run the stats on the PFS data, but that is something to keep in mind if people are coming out with both high and low states of Prog. Prog isn’t usually measured in men, and therefore there isn’t a ton of data on reference ranges.

As for PSSD, there really only is a high-prog state. Something like 12/15 tests I’ve seen have high prog. So for PSSD, I see Prog as USUALLY heightened. Again, not always the case, but this is significantly more common than normal or low prog.

Sorry that I’m gonna dive into Serotonin for a bit, but again, it’s my background.

“Progesterone increases MAO< this tanks serotonin.”

I think it’s more complex than this. There is more than MAO activity happening. In the following case, it is hypothesized that Progesterone in pregnancy (it increases a LOT), is actually increasing serotonin activity in the brain, leading to the desensitization of 5-HT1A autoreceptors.


Klink et al., 2002
Gender and gonadal status modulation of dorsal raphe nucleus serotonergic neurons. Part II. Regulatory mechanisms


"During pregnancy, the ED50 for the response to LSD was decreased by about 70%, indicating a partial desensitization of 5-HT1A autoreceptors, which is consistent with the 5-HT neurons higher firing activity. The GABAergic tonic inhibition of 5-HT neurons was assessed using the responses to GABA, bicuculline and isoniazid. Together, they indicate a lower GABAergic tonic inhibition in males and P17 as compared to CF, which is in agreement with their greater 5-HT neurons firing rate. Finally, the efficacy of the long feedback loop, involving postsynaptic 5-HT1A receptors, did not seem affected by gender, ovariectomy or pregnancy since the response to systemic 8-OH-DPAT was similar. These results constitute strong evidence of mechanisms by which gender and hormonal fluctuations can modulate the 5-HT neurons function and influence vulnerability to mood disorders."
"It could, thus, suggest that these modifications of the GABAA receptor function, induced by chronic neurosteroid treatments, are present during pregnancy, when levels of progesterone metabolites are high. This would result in a lesser GABAA receptor responsiveness and would explain the lower GABAergic tonic inhibition of 5-HT neurons observed in the present study."
"Many progesterone metabolites are GABAA receptor modulators. Since we observed a direct correlation between 5-HT neuronal activity and circulating levels of P from P11 to 21, the responsiveness of the DRN 5-HT neurons to GABA, as well as their GABAergic tonic inhibition, had to be explored."
"These results (raising Progesterone) suggest a partial functional desensitization of the 5-HT1A autoreceptor during late
pregnancy."
"During pregnancy, the ED50 for the response to LSD was decreased by about 70%, indicating a partial desensitization of 5-HT1A autoreceptors, which is consistent with the 5-HT neurons higher firing activity."

In addition, Prog blocks the ability of Estrogen and testosterone to protect SERT in the POA. Because of this, SERT levels fall (as they do with SSRIs). This means less 5-HT is cleared, and that 5-HT activity increases.

https://www.ncbi.nlm.nih.gov/pubmed/15225127

“Previous data from our laboratory have shown that during pregnancy, the firing activity of 5-HT neurons increases in parallel with progesterone level”


Something that I’ve noticed for a long time now since PSSD is that I have occasional heart arrhythmias. This isn’t really normal for my age but the cardiologist cleared it and said that it wasn’t dangerous. Regardless, I think now that it may have to do with lowered Potassium levels. It sometimes would happen up to once a day, but after starting potassium supplementation it has gone away completely.
Escitalopram, a selective serotonin reuptake inhibitor, inhibits voltage-dependent K+ channels in coronary arterial smooth muscle cells
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5507780/


And this happens in the brain too,
The antidepressant citalopram inhibits delayed rectifier outward K+ current in mouse cortical neurons
http://onlinelibrary.wiley.com/doi/10.1002/jnr.22744/full


Other notes:

Has sideroblastic anemia been seen in PFS or PSSD before? I haven’t seen that but I haven’t looked either.


Valid point on Iron. I’ve been eating a lot of spinach recently and I think that helps. It has a lot of Vitamin K, Iron, and Potassium.

Also I agree on Cortisol being high. That’s something we notice in PSSD too. The bad part is that Cortisol can desensitize the 5-HT1A AR, so the cycle can kind of continue for a while.

Ghost, I'm not sure about siderblastic anemia, but I have PSSD from Citalopram, and I have a low platelet count. I noticed another pssd member's set of labs that he also had low platelets.

From a Mayo Clinic lab:

MCV
July 05, 2016
81.0 fL This value is below the normal range. 81.2 - 95.1

Platelet Count
July 05, 2016
148 x10(9)/L This value is below the normal range.150 - 450

 

[Shadow]

Mine are in range:
MCV - 83.52 fL - range (80 - 100)
Platelet Count: 195,000 /mm³ - range 140,000 - 400,000

 

[Area-1255]

Serotonin has a huge role in Platelet function. Mainly causing aggregation and contributing to atherosclerosis.
https://www.ncbi.nlm.nih.gov/pubmed/9491270