Wuf Log - After Cortisol treatment

[Helen]

Maybe the cortisol adjusted receptor sensitivity explaining the effects even after the 9 days ?

of course. but also cortisol downregulates AR.

I talked to wuf all his time on cortisol, I suggested that it can cure his PFS.

he came off, cortisol, felt terrible, and then in a month or 2 , he noticed that his sexual function was better

go on propecia help and read cytochrome recovery.


wuf had low cortisol by the way not high.


also in jinstewart case, he took ru, which upregulated his estrogen and ER receptor, estrogen increases CBG which binds cortisol. thus levels slightly rose after RU.

 

[Walker]

Walker,

You had your bad reaction to methylprednisolone after being completely recovered from PFS correct?

I just read this which puts Methylprednisolone into perspective:

Methylprednisolone is stronger than prednisone:

prednisone is four times as potent as cortisol

methylprednisolone is five times as potent as cortisol.

If I am following correctly Wuf took a cortisol drug to treat ulcerative colitis while already having PFS and felt better to the extent that he recovered PFS sexual sides 100 percent ?

Yes, I had a bad reaction a few months ago. About a year and a half from when I considered myself back to normal from CDs protocol. But keep in mind, I’ve never responded well to prednisone in general. Years before PFS it would really fuck with me too. I’m pretty sure something with PTSD has to do with the cortisol system being F’d up.

 

[5 alpha]

Yes, I had a bad reaction a few months ago. About a year and a half from when I considered myself back to normal from CDs protocol. But keep in mind, I’ve never responded well to prednisone in general. Years before PFS it would really fuck with me too. I’m pretty sure something with PTSD has to do with the cortisol system being F’d up.

Hmmm..

Glucocorticoid Receptor: Genetics and Epigenetics in Veterans With PTSD - ScienceDirect

Posttraumatic stress disorder (PTSD) is conditional on exposure to trauma. Despite this, there is strong evidence from twin studiesand widespread agreement that genetic factorsalso contribute to risk for PTSD. Large-scale genomic studies of PTSD are planned. DNA can be modified by epigeneticprocesses via environmental inputs, thereby influencing how genes are expressed, making this an equally important area of research for PTSD. Results from a succession of studies of PTSD suggested that the negative-feedbacksystem of the HPA axis is overly sensitive, implicating the glucocorticoid receptor(GR) in the pathophysiologyof PTSD

This makes sense. Maybe we are genetically predisposed to having overly sensitive HPA axis involving issue with GR receptor. You had weird reactions to cortisol in the past prior to PFS also experienced severe stress from bing a combat veteran which obviously would not help predisposed issue with GR receptor. Than after you recovered PFS using CD’s protocol again you experienced issues after getting hit with a surge of something 5 times more potent than cortisol. All of these things point towards bad reactions to surges of cortisol

Dam we need a before during and after fin, dut or Saw P experiment. So we can see if the persons cortisol is shooting up while on it

 

[Helen]

@5 alpha RU blocks androgen receptor, which kills further conversions of DHT , kills 3 alpha hsd for a while.

so you basically feel like you are on finasteride again. when you are coming off ru.

this is why jinstewarts progesterone fell. since 5 AR is increased and 3 alpha reduced which slowed gaba activation.

thus estro is higher and cortisol is higher.

 

[Helen]

Hmmm..

Glucocorticoid Receptor: Genetics and Epigenetics in Veterans With PTSD - ScienceDirect

Posttraumatic stress disorder (PTSD) is conditional on exposure to trauma. Despite this, there is strong evidence from twin studiesand widespread agreement that genetic factorsalso contribute to risk for PTSD. Large-scale genomic studies of PTSD are planned. DNA can be modified by epigeneticprocesses via environmental inputs, thereby influencing how genes are expressed, making this an equally important area of research for PTSD. Results from a succession of studies of PTSD suggested that the negative-feedbacksystem of the HPA axis is overly sensitive, implicating the glucocorticoid receptor(GR) in the pathophysiologyof PTSD

This makes sense . Maybe we are genetically predisposed to having overly sensitive HPA axis involving issue with GR receptor. You had weird reactions to cortisol in the past prior to PFS also experienced severe stress from bing a combat veteran which obviously would not help predisposed issue with GR receptor. Than after you recovered PFS using CD’s protocol again you experienced issues after getting hit with a surge of something 5 times more potent than cortisol. All of these things point towards bad reactions to surges of cortisol

Dam we need a before during and after fin, dut or Saw P experiment. So we can see if the persons cortisol is shooting up while on it

I posted this to him many times.

I hope you realize that slow oxidizers feel great on cortisol.

 

[5 alpha]

of course. but also cortisol downregulates AR.

I talked to wuf all his time on cortisol, I suggested that it can cure his PFS.

he came off, cortisol, felt terrible, and then in a month or 2 , he noticed that his sexual function was better

go on propecia help and read cytochrome recovery.


wuf had low cortisol by the way not high.


also in jinstewart case, he took ru, which upregulated his estrogen and ER receptor, estrogen increases CBG which binds cortisol. thus levels slightly rose after RU.

Interesting

Did Wuf take cortisol specifically to treat UC or PFS or both ?

So Wuf had low cortisol and felt better 2 months after coming off of cortisol. Do you know how he felt while on it ?

I’m going to go read about the cytochrome recoveries on PH.

For jinstewart the RU significantly raised his cortisol and after he came off of it his cortisol stayed higher then his pre RU cortisol levels right ?

I wonder if jinstewart’s rise in cortisol prevented his recovery from taking RU and if it would be wise to block cortisol while coming off of RU

 

[Helen]

@5 alpha cortisol is controlled by estrogen, and namely by Cb1 receptor. this is why some people recovered from anandamide reuptake inhibitors.

 

[5 alpha]

I posted this to him many times.

I hope you realize that slow oxidizers feel great on cortisol.

No I did not know that. I need to find out if I am a slow or fast oxidizer

 

[Helen]

Interesting

Did Wuf take cortisol specifically to treat UC or PFS or both ?

So Wuf had low cortisol and felt better 2 months after coming off of cortisol. Do you know how he felt while on it ?

I’m going to go read about the cytochrome recoveries on PH.

For jinstewart the RU significantly raised his cortisol and after he came off of it his cortisol stayed higher then his pre RU cortisol levels right ?

I wonder if jinstewart’s rise in cortisol prevented his recovery from taking RU and if it would be wise to block cortisol while coming off of RU

he did not significantly raised his cortisol. his cortisol barely went up

read the previous post.

Slow oxidzers usually have low cortisol and low acth. since they have slow metabolism, and cortisol is not needed.

estrogen increases CBG , cortisol binding protein, thus if estrogen goes higher. cortisol goes higher. since it is bound.

 

[5 alpha]

@5 alpha RU blocks androgen receptor, which kills further conversions of DHT , kills 3 alpha hsd for a while.

so you basically feel like you are on finasteride again. when you are coming off ru.

this is why jinstewarts progesterone fell. since 5 AR is increased and 3 alpha reduced which slowed gaba activation.

thus estro is higher and cortisol is higher.

Interesting does this suggest that if his cortisol was not higher coming off of the RU it would have helped ?

 

[5 alpha]

@5 alpha cortisol is controlled by estrogen, and namely by Cb1 receptor. this is why some people recovered from anandamide reuptake inhibitors.

Hmm

I kinda figured there is a connection with estrogen and cortisol. I have been trying to figure out why inhibiting estrogen makes me worse while it seems that higher cortisol makes me worse as well

 

[5 alpha]

he did not significantly raised his cortisol. his cortisol barely went up

read the previous post.

Slow oxidzers usually have low cortisol and low acth. since they have slow metabolism, and cortisol is not needed.

estrogen increases CBG , cortisol binding protein, thus if estrogen goes higher. cortisol goes higher. since it is bound.

Wait a sec

Here are Jin’s before and after RU cortisol results:

Pre ru
Cortisol - 411 nmol/L (166-507)

Post ru
Cortisol - 525 nmol/L (166-507) over range, got higher

411 to 525 is not a significant raise? 525 is over the labs range

Either way the connection between estrogen and cortisol is interesting. I know I get worse from inhibiting estrogen so I have been wondering how/if inhibiting estrogen effected cortisol

 

[Helen]

because estrogen increases anandamide. which increases cannabinoids and opiods.

which gives you emotions. and estrogen actually increases cortisol. thru Cb1 receptor .

 

[Helen]

Wait a sec

Here are Jin’s before and after RU cortisol results:

Pre ru
Cortisol - 411 nmol/L (166-507)

Post ru
Cortisol - 525 nmol/L (166-507) over range, got higher

411 to 525 is not a significant raise? 525 is over the labs range

cortisol fluctuates hard while taking blood. it depends on many parameters, 400 and 500 , not a significant difference. but I explained to you why cortisol went up in his case. estrogen increases CBG. which binds cortisol and thus you have higher total cortisol level. plus estrogen increases anandamide which gives you stress response.

 

[Walker]

I posted this to him many times.

I hope you realize that slow oxidizers feel great on cortisol.

Right, I remember you showing me that study before.

If I’m a slow 1, why do I feel like shit on cortisol/methylprednisolone?

 

[5 alpha]

because estrogen increases anandamide. which increases cannabinoids and opiods.

which gives you emotions. and estrogen actually increases cortisol. thru Cb1 receptor .

Hmm maybe my Goal should be higher estrogen and cortisol levels then. I get worse from inhibiting estrogen and don’t really know why I lost my recovery after my first ru cycle. I assumed higher cortisol levels after my cycle made me lose my recovery. Maybe what I needed was more cortisol

 

[Helen]

I explained to you , jinstewart is a slow oxidzier, with very high calcium levels, since his gaba is high.


this calcium inhibits his ESTROGEN

since calcium slows the thyroid, and estrogen slows the thyroid, so when calcium is high estrogen is inhibited.

thus his estrogen level was LOW

why gaba is activated, since DHT converts into its metabolits. 3 adiol

so when you take ru, it blocks AR, which stops convertsion of DHT into 3 adiol and gaba is stopped.

this raises estrogen, since calcium from gaba falls. and estrogen is allowed.

this decreases progesterone, since potassium enters the cell. since calcium is not blocking it.

 

[Helen]

Right, I remember you showing me that study before.

If I’m a slow 1, why do I feel like shit on cortisol/methylprednisolone?

you are 4 highs, with zero potassium

 

[5 alpha]

cortisol fluctuates hard while taking blood. it depends on many parameters, 400 and 500 , not a significant difference. but I explained to you why cortisol went up in his case. estrogen increases CBG. which binds cortisol and thus you have higher total cortisol level. plus estrogen increases anandamide which gives you stress response.

Right you said estrogen increases CBG , cortisol binding protein, thus if estrogen goes higher. cortisol goes higher. since it is bound.

 

[Helen]

@5 alpha

I explained to you , jinstewart is a slow oxidzier, with very high calcium levels, since his gaba is high.


this calcium inhibits his ESTROGEN

since calcium slows the thyroid, and estrogen slows the thyroid, so when calcium is high estrogen is inhibited.

thus his estrogen level was LOW

why gaba is activated, since DHT converts into its metabolits. 3 adiol

so when you take ru, it blocks AR, which stops convertsion of DHT into 3 adiol and gaba is stopped.

this raises estrogen, since calcium from gaba falls. and estrogen is allowed.

this decreases progesterone, since potassium enters the cell. since calcium is not blocking it.


Do you understand now why Jack17 went back on dutasteride and felt totally recovered? he is also a slow oxidizer.

you go on duta , you inhibit 5ar, which stops allo and 3 adiol. less gaba activation, calcium falls, estrogen rises.

as calcium falls, metabolism speeds up and only in higher metabolism both estro and cortisol rise.


this is why Justquitdut , felt recovered on thyroid and test.