ZINC FINGER THEORY DISCUSSION for PFS - 2 cases

Ghost

Well-Known Member
Messages
90
That makes sense, I have high calcium, fibrosis, low copper low K, and my inner bell said no for taking copper as a lonely supp.
Why I got worse only from taking natural progesterone then?

My issues with insuline were there BEFORE, I lack it, as my blood sugar is high.
Can insuline be one pre-requisite for fibrosis problems?


I agree we need to change the theory of molecular biology into practical precision.

One thing interesting for me is that I feel like I can't really gain weight since PSSD. It's like water and food go right through me. I can eat a ton of calories, and it seems to do the same thing to me as eating almost nothing. I've always been fairly lean, but since PSSD I've been more thin. I've gone from size large to medium shirts.
 

Crushed

Member
Messages
29
for me it happened almost overnight, i developed extreme pain in the penis and then all those things happened, i think it took no more than 3 days, i'm very severe in those issues, i think all this traumatized me too

I developed this pain in my glans within a week of stopping citalopram, and the numbness and soft glans continues to this day. The week prior, I felt great and I was completely normal. Stopped Citalopram, and I got extreme headaches, night sweats, hot flashes, then the pain in my genitals and numbness with complete loss of libido etc.
 

Helen

Well-Known Member
Staff member
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5,415
Interesting Theory. Gives a method of ^ Prog, or actually, a method of tanking K+ and Copper, which could be linked to Prog. After we can link this to Prog, we can link it to SERT, and therefore to a mechanism that keeps 5-HT at high levels even after the drug is removed.

The one thing I'm not sure of is the GABA blocking. I've taken various GABA supplements and Ativan while seeing no change in numbness. If you're suggesting that GABA is raised, then wouldn't it also be inhibitory or 5-HT firing?


I am suggesting 2 possibilities with Gaba here. 1) GABA A receptor is upregulated by low or high Allo. And 2) the receptor is missing chloride which deficiency you get along with potassium loss. And GABA A receptor needs Chloride .
 

Steve

Well-Known Member
Messages
69
I am suggesting 2 possibilities with Gaba here. 1) GABA A receptor is upregulated by low or high Allo. And 2) the receptor is missing chloride which you do get in potassium loss. And GABA A receptor needs Chloride .
Will you be coming up with protocols for all these scenarios including pfs?
 

tallglass13

Well-Known Member
Messages
287
the last 5 days, Ive only been taking some glycine and D3. very positive results. My skin around my eyes is looking tighter/younger, and libido is high, and erections are easier. Libido is like really high.
 

Steve

Well-Known Member
Messages
69
So a protocol for pssd is copper, potassium, sodium choloride, potassium chloride, magnesium chloride, plus histidine and cysteine?

When you say potassium, is it any different to the electrolyte potassium chloride?
 

Canari

Member
Messages
1,609
Correct. We need protocols and results with exactly what to take with dosages listed. Hopefully we will get this eventually.
And this is not only for post x syndrom. Biology is for everybody. TEI told me to take Copper because I have the ratio bad with zinc, they did not say more.... Sciences are too seperated one from the other!
I was prescribed GABA from another test...

One thing interesting for me is that I feel like I can't really gain weight
Conservative mode of the body seem to be putting on weight for some, and reverse for others! I am more in the lean category. I think it can come from sympathetic and parasympathetic working at the same time from having stress+numbed stress. It is energy wasting.

and I personally know I'll need years of PTSD therapy after all this.
i think all this traumatized me too
I'm on the same train..this is so depressing..jezz
No need to wait "after" for starting to support the self-regulation of the system. I have just given a tip to shelley that seems nothing but is a start.
We need to emphasize this on the forum.
cdsnuts protocol has stress management, mattyb also published his thoughts about the influence of anger, I have as well and this directly influences the release of hormones. I think some prior sort of shock in life is what made some people more sensitive to the effect of SSRI, as anyway this drug is taken as an intent to regulate the nervous system.

Even people who do not have full ptsd have interest in balancing their nervous system, as this is a prevention in case of accident, and help to bounce back to normal life. There is no shame in this, we were told to be strong and go on, but this is as stupid as telling sb to walk with a broken leg before the known 21 days of healing!!!!!!!!!!!!!!!

I know this because I learned it for my own good! I had poisoning before my birth!

I have worked on many other things, but still have a nervous charge with this, because it involves many aspects. I did work on it 2 days ago, and it was not fun during this moment, as I got stiff as a plank got my throat tightening and choked before it reliesed. Even if the weather is not more dry, my lungs and bronchis do feel different after this. It went away shaking, exactly as animals do and as you can see in videos.... And Ii felt more alive after doing this. And you cannot do it safely if you do not know, though all animals know how to do this, as they do not have the cognitive part.... The cognitive part is not the one that helps most, when you deal with body shocks.
 
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Sam90

Member
Messages
33
I think this is what might be happening in PSSD.

You take SSRI, this increases serotonin, serotonin increases NADPH oxidase. this creates tons of ROS. this is why to increase serotonin you need to increase thyroid and metabolism and not take SSRIs. In slow metabolism there is no ceruloplasmin and low serotonin. Doctors give people SSRIs which is ridiculous forcing serotonin in the wrong body chemistry. Serotonin rises with potassium. and thyroid. And this causes ACTH release. which increases cortisol release in FAST metabolism. People that take SSRI in slow metabolism should never take them they should just increase the metabolism. And if you force serotonin in slow metabolism unfortunately metabolism goes even lower since serotonin will increase ACTH and this will increase cortisol and cortisol willl be getting rid of potassium IN SLOW METABOLISM which should never be the case., NADPH oxidase is activated by cortisol , and this causes ROS, but ceruloplasmin is not there since ceruloplasmin goes up only in fast metabolism and you forced cortisol in the slow oxidation with SSRI. Cortisol should be up only if you have tons of potassium in the cell and fast metabolism. . If you would have lifted metabolism , then this metabolism lift would have increased NADPH oxidase but at the same time would increase ceruloplasmin and the extra ROS would have been blocked by SODS But copper cant rise in the cell with low potassium which you caused with SSRI.

This is why feeding thyroid with copper deficiency is VERY VERY BAD. since ROS will be unopposed. And in copper deficiency you get high RT3.

So end effect of taking SSRI in slow metabolism is copper loss and potassium loss at the same time. Since serotonin activated ACTH which increased cortisol and this cortisol lost all your potassium. Thus you have high progesterone .

This is why it is so tricky, metabolism is already low so when you feed copper you feel bad, and if you feed potassium you get more ROS since raising metabolism creates ROS.

This is why you need to feed copper and potassium in a certain manner, copper always should come with electrolytes and associated aminos.



Fibrosis will be gone on its own. if you lower g6pd and using GHK-CU will totally reverse it.

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Copper is what lowers enzyme G6PD and increases insulin.

Numbness that people are experiencing after SSRI, is from Gaba blocking NDMA signaling, Since from NDMA you get supersensitivity. People even have a disease like that-- tactile supersensitivity .

How do you think we could sort the gaba/nmda signalling issue with regards to numbing?
 

Canari

Member
Messages
1,609
Can you please be more specific?
..like for example if it is enough to take copper gluconate with animal protein meal and HCl and veggies?

About GABA, I was told to take it because of issues with turn over of dopamine and serotonine...
We always come around the same basic elements!
 

Flynn

Well-Known Member
Messages
207
I don't understand how the Zinc Finger works fully but it's a protein substructure that's in loads of transcription factors, so errors could mean over or under transcription. What I do know is that as soon as there's elevated progesterone (from elevated cortisol or whatever) sexual sides can kick in. Androgen/oestrogen signalling imbalance too much either = sexual sides. Too much progesterone = sexual sides. Don't know about too little progesterone but wouldn't be surprised if also = sexual sides.

Right, but does elevated cortisol lead to elevated progesterone? I understand that progesterone can lead to sexual problems. I'm just still struggling to make the link between zinc-finger and progesterone in a significant way. From a quick look online, cortsiol seems to oppose progesterone activity. So if zinc finger problem leads to high cortisol it would reduce progesterone activity. Then there is the flip side, with low cortisol and possibly too much progesterone activity.

As far as I understand zinc-finger, in simple terms, it essentially helps the glucocorticoid receptor function properly (correct me if I'm wrong). So say, FIN or Accutane has damaged zinc finger or damaged glucocorticoid receptor from functioning properly. I'm still struggling to find out how this would affect libido, sexual sides. In one scenario you have excess cortsiol production as its receptor is essential unresponsive or reduced cortisol??? Sorry I'm confusing myself now.
 

Shadow

Moderator
Messages
383
Interesting Theory. Gives a method of ^ Prog, or actually, a method of tanking K+ and Copper, which could be linked to Prog. After we can link this to Prog, we can link it to SERT, and therefore to a mechanism that keeps 5-HT at high levels even after the drug is removed.

We have some problems here, if this was the mechanism all PSSD sufferers would experiment the effects during the drug, and we know that on the majority of cases the problem starts AND worsens after stoping the drug.

Take me as a case:
Lets call SSRI State this: Receptors desensitized, SERT downregulated, a lot of Serotonin.
During the "treatment": SSRI State and extremely minor side effects(mild anorgasmia and ed).
After the drug: Stuck in SSRI State and extreme symptoms in all areas!

Why? If I was already in a SSRI State, why I only had symptoms after stopping IF the problem was that we are still in SSRI State?

@Area-1255 talked about it too, and he is right! We are ignoring the obvious! Btw, @Area-1255 could you tell us more about your Sigma Receptors theory?
 

Ghost

Well-Known Member
Messages
90
Right, but does elevated cortisol lead to elevated progesterone? I understand that progesterone can lead to sexual problems. I'm just still struggling to make the link between zinc-finger and progesterone in a significant way. From a quick look online, cortsiol seems to oppose progesterone activity. So if zinc finger problem leads to high cortisol it would reduce progesterone activity. Then there is the flip side, with low cortisol and possibly too much progesterone activity.

As far as I understand zinc-finger, in simple terms, it essentially helps the glucocorticoid receptor function properly (correct me if I'm wrong). So say, FIN or Accutane has damaged zinc finger or damaged glucocorticoid receptor from functioning properly. I'm still struggling to find out how this would affect libido, sexual sides. In one scenario you have excess cortsiol production as its receptor is essential unresponsive or reduced cortisol??? Sorry I'm confusing myself now.

I think Progesterone is incredibly important, and all roads lead to SERT, and Prog points in that direction.

We have some problems here, if this was the mechanism all PSSD sufferers would experiment the effects during the drug, and we know that on the majority of cases the problem starts AND worsens after stoping the drug.

Take me as a case:
Lets call SSRI State this: Receptors desensitized, SERT downregulated, a lot of Serotonin.
During the "treatment": SSRI State and extremely minor side effects(mild anorgasmia and ed).
After the drug: Stuck in SSRI State and extreme symptoms in all areas!

Why? If I was already in a SSRI State, why I only had symptoms after stopping IF the problem was that we are still in SSRI State?

@Area-1255 talked about it too, and he is right! We are ignoring the obvious! Btw, @Area-1255 could you tell us more about your Sigma Receptors theory?

I can't speak for other people, but this wasn't the case for me. Delayed Ejaculation was the only symptom to resolve after SSRI, and that day that I first noticed that I had it was probably worse function that I have now. I do agree with you though that some people crashed after SSRI, but in my experience, a majority crashed while on the drug.

Cases where it gets worse must be from the body trying to bounce back, but just going further in the wrong direction. I've heard of almost no one say "Oh sex was great on the drug and then fell apart only afterwards". But at the same time, I have heard of people crashing up to 6 months after SSRI. At that point, however, you have to wonder what the odds are that it could be caused by something different entirely. I think we need to get past the idea that it's the drug causing the problem, but rather that it's the persistent state that we are in that is. All I'm saying is that for me these past 3.5 years have jut felt like a big SSRI party. It's like I've been on them for the past 3.5 years. If I had responded well with little sides, I'd probably be off the drugs and anxiety free, because whatever happened on the drugs stuck after I stopped.
 

Helen

Well-Known Member
Staff member
Messages
5,415
We have some problems here, if this was the mechanism all PSSD sufferers would experiment the effects during the drug, and we know that on the majority of cases the problem starts AND worsens after stoping the drug.

Take me as a case:
Lets call SSRI State this: Receptors desensitized, SERT downregulated, a lot of Serotonin.
During the "treatment": SSRI State and extremely minor side effects(mild anorgasmia and ed).
After the drug: Stuck in SSRI State and extreme symptoms in all areas!

Why? If I was already in a SSRI State, why I only had symptoms after stopping IF the problem was that we are still in SSRI State?

@Area-1255 talked about it too, and he is right! We are ignoring the obvious! Btw, @Area-1255 could you tell us more about your Sigma Receptors theory?


I think it all depends on your insulin levels before taking SSRI. Insulin is what controls G6PD and NADPH production .
 
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Shanks

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Messages
165
Do u have first aid ideas what to do when stopping the drug (SSRI)? In my case i am tappering of escitalopram and i get huge side effects like hard brain fog and dizziness. I can t even go running because of this side effects..
 

Shadow

Moderator
Messages
383
I can't speak for other people, but this wasn't the case for me. Delayed Ejaculation was the only symptom to resolve after SSRI, and that day that I first noticed that I had it was probably worse function that I have now. I do agree with you though that some people crashed after SSRI, but in my experience, a majority crashed while on the drug.

Cases where it gets worse must be from the body trying to bounce back, but just going further in the wrong direction. I've heard of almost no one say "Oh sex was great on the drug and then fell apart only afterwards". But at the same time, I have heard of people crashing up to 6 months after SSRI. At that point, however, you have to wonder what the odds are that it could be caused by something different entirely. I think we need to get past the idea that it's the drug causing the problem, but rather that it's the persistent state that we are in that is. All I'm saying is that for me these past 3.5 years have jut felt like a big SSRI party. It's like I've been on them for the past 3.5 years. If I had responded well with little sides, I'd probably be off the drugs and anxiety free, because whatever happened on the drugs stuck after I stopped.

I understand your view and why you have it, and why they clash with mine.

You took SSRI only that time right? When you start taking this shit, its pretty normal to have bad reactions for at least 3 weeks, people call it "adaptation phase". Ive gone through it a couple of times, and 99% of the time, this symptoms subside. I think that you are referring to this state when you say that things stucked to you and you feel like you are on SSRI. If yes, then I agree with you, still, I think that you had an extreme reaction who put you on the "post ssri" crap. I say this because, what you feel while on adaptation can be nasty it doesnt even compare to what happens after stopping, or a crash while on drug(which I think that I had after 12y).

I dont know if you understood what Im trying to say, we should see the big picture.

Do u have first aid ideas what to do when stopping the drug (SSRI)? In my case i am tappering of escitalopram and i get huge side effects like hard brain fog and dizziness. I can t even go running because of this side effects..

By dizziness you mean brain zaps? If yes go even gentle! Dont rush!
 

Helen

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Staff member
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5,415
@Shadow

You are a complicated SSRI case over here, do you want me to try to balance you? I assume POIS PFS PSSD has 2 cases. POIS for sure , people react to the same substance totally differently . I think it all depends on the allo levels, high or low = PFS POIS PSSD. since you will get stuck in parasympathetic state. in both . this is why you see people with really high DHT and people with really low DHT having PFS

Some people were talking about 5AR2 and stuff like that. but it clearly says

Elevated levels of inhibitory neurosteroids, namely allopregnanolone, can produce paradoxical effects, such as negative mood, anxiety, irritability, and aggression.[39][40][41][42] This appears to be because these neurosteroids, like other positive allosteric modulators of the GABAA receptor such as the benzodiazepines, barbiturates, and ethanol,[34][42] possess biphasic, U-shaped actions – moderate levels (in the range of 1.5–2 nM/L total alloprogesterone, which are approximately equivalent to luteal phase levels) inhibit the activity of the GABAA receptor, while lower and higher concentrations facilitate the activity of the receptor.[40][41]


So the same symptoms with high or low ALLO. So you have your 2 cases.

this is why some crash on the drug and some crash when they quit the drug. Same thing with pois people some crash before orgasm and some crash 4 hours after.
 
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